UMEM Educational Pearls - By John Greenwood

Renal Resuscitation using Renal Interlobar Artery Doppler (RIAD)

Shocked patient…. check! Adequate volume resuscitation…. check!  Vasopressors.… check! Mean arterial pressure (MAP) > 65 mmHg….. check!  Adequate urine output…. Wait, why isn’t my patient making urine?

As we begin to understand more about shock, hemodynamics, and the importance of perfusion over the usual macrocirculatory goals (MAP > 65), finding ways to assess regional blood flow is critical.  A recent study examined the effect of fluid administration on renal perfusion using renal interlobar artery Doppler (RIAD) to assess the interlobar resistive index (RI).  See how to perform a RIAD here.

They also recorded the fluid challenge’s effect on the traditional hemodynamic measurements of MAP and pulse pressure (PP) then observed the patient’s urine output (as a clinical marker of perfusion).  The authors reported 3 key findings:
 

1. In the hemodynamically impaired patient, a fluid challenge results in reduced intrarenal vasoconstriction (a reduction in the RI).
2. In the hemodynamically impaired patient, changes in RI are more effective than changes in MAP or PP in predicting an increase in urine output after a fluid challenge.
3. Using RI to guide fluid therapy may be limited by small changes and technical limitations.

Bottom Line: The use of ultrasound to determine intrarenal hemodynamics is an interesting strategy to guide renal resuscitation in the shocked patient.  There is mixed data on the use of RIAD, however this study could explain the findings of SEPSISPAM and also addresses the growing concern that traditional hemodynamic goals may be inadequate resuscitation targets.

References

1. Moussa MD, Scolletta S, Fagnoul D, et al. Effects of fluid administration on renal perfusion in critically ill patients. Crit Care. 2015;19(1):250.
2. Asfar P, Meziani F, Hamel JF, et al. High versus low blood-pressure target in patients with septic shock. N Engl J Med. 2014;370(17):1583-93.

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Advances in Catheter-Directed Therapy for Acute PE - The PERFECT Registry

Earlier this month, initial results from the multicenter PERFECT registry (Pulmonary Embolism Response to Fragmentation, Embolectomy, and Catheter Thrombolysis) were released. In this study, 101 consecutive patients with massive or submassive PE were prospectively enrolled to receive early catheter-directed therapy.

Inclusion criteria:

• Massive or submassive PE
• Presented within 14 days of symptoms
• Had CT evidence of proximal filling defect (main or lobar pulmonary artery)
• Age > 18 years old
• Had no contraindications to therapeutic anticoagulation
• PE not related to tumor thrombus

Therapy provided:

• Submassive PE: Low-dose (0.5 - 1.0 mg/hr of urokinase) infusion directly into clot
• Massive PE: catheter-directed mechanical or pharmacomechanical thrombectomy followed by low-dose thrombolytic therapy used for submassive PE patients.

Outcomes: Clinical success (stabilization of hemodynamics, improvement in pulmonary hypertension and/or right heart strain, and survival to discharge) was achieved in 86% of patients with massive PE and 97% of patients with submassive PE. There were no major procedure-related complications or major bleeding events.

Bottom Line: In patients with massive or submassive pulmonary embolism, there is growing evidence that early catheter-directed therapy may become first-line therapy for selected patients.

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Updates in the Management of Large Hemispheric Infarction

Large hemispheric infarctions (LHI) are estimated to occur in 2-8% of all hospitalized ischemic strokes and 10 15% of all MCA territory infarcts. LHI carry high rates of morbidity and mortality, in fact, if left untreated associated cerebral edema can rapidly progress to transtentorial herniation and death in 40 80% of patients.

Recognized risk factors for progressive cerebral edema include:

• NIH stroke scale > 20 in dominant hemispheric infarct
• NIH stroke scale > 15 in nondominant hemispheric infarct
• Rapid decline in level of consciousness (LOC) indicates effect on contralateral hemisphere (due to ipsilateral swelling)

Evidence based medical strategies for LHI include:

• Positioning: Elevation of the head of the bed (HOB) > 30 degrees
• Glucose control: 140 180 mg/dL (hyperglycemia associated with increased ICP and progression to hemorrhagic conversion)
• Blood pressure control: 15% reduction MAP over 24 hours if BP exceeds 220/120 (likely best accomplished with nicardipine infusion to avoid overcorrection)
• Osmotic therapy: In the deteriorating patient, consider hypertonic saline (23%) with goal Na of 160 mEq/L or mannitol with goal plasma osmolality of 320 mOsm/kg.
• Adjunctive therapies: Prevent fever and hypercapnea

Prophylactic hemicraniectomy

• Consider early neurosurgical consultation for patients with LHI as newer evidence suggests prophylactic hemicraniectomy may improve survival if performed within 24 48 hours.

Bottom Line: Early recognition of large hemispheric stroke is critical as it is associated with a high rate of morbidity and mortality. Aggressive medical management and early neurosurgical involvement may improve outcomes.

References

1. Zha AM, Sari M, Torbey MT. Recommendations for management of large hemispheric infarction. Curr Opin Crit Care. 2015;21(2):91-8.

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Stop looking for the “Best PEEP”, aim for a “Better PEEP”

Mechanical ventilation settings in the patient with acute respiratory distress syndrome (ARDS) need to provide adequate gas exchange and prevent ventilator induced lung injury (VILI). Positive end-expiratory pressure (PEEP) is often prescribed with consideration of the patient’s FiO₂ requirement, estimated chest wall compliance, and hemodynamic tolerance. 

So what is the best strategy for PEEP prescription?

In a recent review, Gattinoni & colleagues analyzed a number of the recent studies examining PEEP optimization.  In this paper, the authors conclude that there is no “Best PEEP,” and regardless of the level chosen there will be some degree of intratidal recruitment-derecruitment and VILI.  They go on to recommend a PEEP prescription strategy that reflects the severity of ARDS using the patient’s PaO₂/FiO₂ or P/F ratio.  

• Mild ARDS (P/F 200 – 300): 5-10 cm H₂O
• Moderate ARDS (P/F 100 – 200): 10-15 cm H₂O
• Severe ARDS (P/F < 100): 15-20 cm H₂O
   

Bottom line: There is no “Best PEEP” however, a “Better PEEP” is one that is primarily tailored to the severity of the patient’s ARDS, but also compensates for chest wall resistance and minimizes hemodynamic compromise.    

References

1. Gattinoni L, Carlesso E, Cressoni M. Selecting the 'right' positive end-expiratory pressure level. Curr Opin Crit Care. 2015;21(1):50-7.
2. ARDSnet PEEP table: http://www.ardsnet.org/system/files/Ventilator%20Protocol%20Card.pdf

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The Role of the CVP in a Post- “7 Mares” Era
 

The role for using central venous pressure (CVP) as a measure of volume responsiveness has largely fallen out of favor over the years.¹ There are certainly better indices for fluid responsiveness, but don’t be fooled – the CVP isn’t a one trick pony.  In fact, a high or rapidly rising CVP should raise a significant concern for impending cardiovascular collapse.

Consider the following differential diagnosis in the patient with an abnormally high or rising CVP ( >10 cm H₂O).

• Excessive pressures outside of the heart or impediments to venous return (juxta-cardiac pressures)
  • Cardiac tamponade
  • Auto PEEP or breath stacking during mechanical ventilation
  • Tension pneumothorax
• Venous return that’s more than the right ventricle can handle
  • RV failure
  • Severe tricuspid valve disease
  • Massive increase in pulmonary vascular resistance (massive PE, pulmonary hypertension, ARDS, LV failure)

Bottom Line: In a time where the utility of the CVP has been largely dismissed, remember that an abnormal CVP offers great deal of information beyond a simple measure of volume status.

References

1. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134(1):172-8.
2. Berlin DA, Bakker J. Starling curves and central venous pressure. Critical Care. 2015;19(1):55.

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Extracorporeal Treatment Strategies for Acute Methanol Poisoning (When to Dialyze)

Methanol toxicity is classically included in the differential for the intoxicated patient presenting to the ED. Add a negative EtOH level, anion/osmolar gap, blindness and you have yourself a slam dunk diagnosis. The goal is to stop the liver from metabolizing methanol to formic acid. Outside of fomepizole (or old school ethanol therapy), dialysis is often discussed, but when should you actually get the nephrologist on the phone?

This month the Extracorporeal Treatments in Poisoning Workgroup released a systematic review and consensus statement to help clinicians decide when to pull the HD trigger. Their suggestions are below.

When to start HD:

1. Neurologic dysfunction: Coma, seizures, new vision deficits
2. Metabolic acidosis: blood pH ≤7.15 or persistent metabolic acidosis despite adequate supportive measures & antidotes
3. Serum anion gap higher than 24 mmol/L
4. Serum methanol concentration:
   • > 700 mg/L (21.8 mmol/L) if fomepizole therapy is given
   • > 600 mg/L or 18.7 mmol/L if ethanol treatment is given
   • > 500 mg/L or 15.6 mmol/L in the absence of an alcohol dehydrogenase blocker

Which Modality: Intermittent HD (IHD) should be used over continuous renal replacement therapies (CRRT), as you can clear the toxin faster with higher HD flows.

When to stop HD: Extracorporeal treatment can be terminated when the methanol concentration is less than 200 mg/L or 6.2 mmol/L and a clinical improvement is observed.

Bottom Line:  Consider early hemodialysis in most patients presenting with methanol toxicity.  Clinical exam and routine lab testing will likely provide enough information to determine the need for IHD, but specific methanol levels can be helpful to guide adjunctive treatment options.

Reference

Roberts DM, Yates C, Megarbane B, et al. Recommendations for the Role of Extracorporeal Treatments in the Management of Acute Methanol Poisoning: A Systematic Review and Consensus Statement. Crit Care Med. 2015;43(2):461-472.

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Cartoons Kill: A new high-risk patient for critical illness & death

This past month, the BMJ published an impressive retrospective review that analyzed nearly 80 years of data to find that animated characters in children’s films are in fact at a very high-risk for death when compared to characters in adult dramas.

Films ranged from 1937 (Snow White) to 2013 (Frozen) and were compared against the two highest gossing dramatic films in that same year.  The authors found that nearly two thirds of the children’s animated films contained an on-screen death of an important character compared to only half in adult dramas. 

Fatalities were most commonly the result of:

• Defenestration/falls (11%)
• Animal attacks (11%)
• Drowning (6.7%)
• Gunshot wounds (6.7%)
• Other mystical causes (6.7%)

Other high-risk animated characters include the parents of the protagonist (17.8% mortality) and nemeses (28.9% mortality).  Median survival time was approximately 90 minutes (much less than the usual ED LOS!)

Notable early on-screen deaths included Nemo’s mother being eaten by a barracuda 4 minutes into Finding Nemo, Tarzan’s parents being killed by a leopard 4 minutes into Tarzan, and Cecil Gaines’ father being shot in front of him 6 minutes into The Butler.

The author’s intention  was to point out the psychological impact of death on young children, but I think the authors also highlight an important, high-risk patient population that could present to your ED.

Bottom Line: Animated characters should be aggressively resuscitated and strongly considered for admission to a higher level of care should they present to your ED, as they appear to be at high-risk for death and rapid decompensation.

May all of you have a happy and safe 2015!

Reference

1. Colman I, Kingsbury M, Weeks M, et al. CARTOONS KILL: casualties in animated recreational theater in an objective observational new study of kids' introduction to loss of life. BMJ. 2014;349:g7184.

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Dynamic Measures of Intravascular Volume Assessment

The resuscitation of a patient in shock often requires the administration of intravenous fluid.  Excessive fluid resuscitation can lead to worsening pulmonary edema, systemic edema, acid-base disturbances, as well as many other complications. There are a myriad of techniques to try and figure out if the patient needs more intravascular volume, but each has it’s pitfalls.

Recently, experts have recommend that we move away from using static measures of preload assessment such as central venous pressure (CVP) and instead focus on using dynamic measures for volume responsiveness.

Volume Responsiveness Defined: An increase of stroke volume of 10-15% after a 500 mL IV crystalloid bolus over 10-15 minutes.

Below is a chart describing key values, requirements, and contraindications for each of these dynamic measures of non-invasive intravascular volume assessment. 

Important notes:  PPV and SVV require the patient to be intubated with controlled tidal volumes.  Arrhythmias and right heart failure make many of these measures invalid (except for PLR).  Other methods of assessment not discussed include systolic pressure variation, left ventricular outflow track velocity time integral (LVOT VTI), and end-expiratory occlusion pressure (EEO).

Bottom Line: None of these measures are perfect and shouldn't be used in isolation to determine if the patient’s “tank is full”.  Combine clinical judgment with these measures to get a best estimate of whether or not to give that next fluid bolus.  

Reference

1. Enomoto TM, Harder L. Dynamic indices of preload. Crit Care Clin. 2010;26(2):307-21, 

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Back 2 Basics Series: Your Simple RSI Checklist - SOAP ME

The use of a checklist during high stress medical procedures is often recommended.  Rapid sequence intubation (RSI) is a classic situation where having a checklist can ensure adequate preparation however, if you don’t have a checklist – this simple mnemonic will make sure you are well prepared for a successful intubation.

The SOAP ME mnemonic is a quick and useful technique to remember only the basics of airway management and preparation.  Always remember to also assign roles to team members and communicate clearly to maximize your chances of success.  

The ARISE Trial

Early, aggressive resuscitation and attention to detail are essential element of managing critically ill patients.  This past week the ARISE trial was published - a 2nd large, randomized control study to examine the benefit of protocolized vs. usual care in patients with severe sepsis and septic shock. 

What were the main findings?  After enrolling 1,600 patients who presented to the ED in severe sepsis or septic shock:

• They found no difference in mortality between the control (usual care) and treatment arm (early goal-directed therapy)
• Mortality was 18.6% vs. 18.8% at 90 days
• No evidence that continuous ScVO2, Hgb target > 10 mg/dL (check out the TRISS trial), or use of inotropes with a normal cardiac index improved mortality

Bottom Line:  Resuscitation goals for the patient with septic shock should include:

• Early antibiotics (source control)
• Adequate volume resuscitation (preferably balanced, crystalloid solution)
• End-organ perfusion (lactate normalization)

Additional therapeutic goals should be made on a patient by patient basis.  Reassess your patient frequently, pay attention to the details, and you will improve your patient’s mortality.

Suggested Reading

1. The ARISE Investigators and the ANZICS Clinical Trials Group.  Goal-Directed Resuscitation for Patients with Early Septic Shock. N Engl J Med. 2014. [PubMed Link]
2. Wessex ICS: The Bottom Line Review

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Goal-Directed Resuscitation During Cardiac Arrest

Focusing on high-quality CPR is by far one of the most effective methods to ensure your arrested patient has the best chance to survive.  However, emerging evidence suggests that there are additional goals that we should try and accomplish during our resuscitation.

 As we continue to move toward goal-directed resuscitation strategies, optimizing coronary perfusion pressure (CPP) may be our next target in “personalizing” the care we provide to those in cardiac arrest.

A recent AHA consensus statement recommended the following physiologic goals during cardiac arrest care:

• CPP > 20 mmHg: Estimated by diastolic BP [DBP] – [CVP] using an arterial line & central line.
• DBP > 25 mmHg: When an a-line is present without an appropriate CVC.
• EtCO₂ > 20 mmHg: When an a-line & CVC are not present.

Each of these variables can give the provider valuable feedback about how their patient is responding to their resuscitation.  Some argue that the DBP target should be much higher (>35 mmHg), with the caveat that pharmacologic optimization can only occur once high quality CPR is confirmed.  The goal should always be to minimize the use of epinephrine whenever possible!

Bottom Line:  During your next cardiac arrest resus, consider using a goal-directed strategy by monitoring the patient’s CPP, DBP, & EtCO₂ to determine the effectiveness of your resuscitation.

Suggested Reading

1. Meaney PA, Bobrow BJ, Mancini ME, et al. Cardiopulmonary resuscitation quality: [corrected] improving cardiac resuscitation outcomes both inside and outside the hospital: a consensus statement from the American Heart Association. Circulation. 2013;128(4):417-35.
2. Sutton RM, Friess SH, Maltese MR, et al. Hemodynamic-directed cardiopulmonary resuscitation during in-hospital cardiac arrest. Resuscitation. 2014;85(8):983-6.

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Should I Give My Patient with Septic Cardiomyopathy Fluids? 

The incidence of acute LV dysfunction in septic shock is estimated to occur in 18 - 46% of patients within the first 24 hours of shock.  Unlike the "classic" pattern of cardiogenic shock where LV filling pressure is high, in septic shock there are normal or low LV filling pressures.

Three therapeutic options should be strongly considered in the patient with a septic cardiomyopathy [CM]:

• FLUIDS:  Most patients with septic CM need fluids to restore adequate preload/afterload.  Severe vasoplegia requires volume resuscitation - even if the bedside ECHO suggests reduced contractility. Give fluids generously.
• Vasopressors: Catecholamine supplementation (norepi) improves patient's preload & afterload, but can often unmask septic CM. Consider epinephrine as a second line agent (over vasopressin) for inotropic support.
• Inotropes: Consider adding epinephrine (1 to 5 mcg/min) or dobutamine (start at 1-5 mcg/kg/min) to target an improved cardiac index (>2.5 L/min/m2) or ScVO2 > 70%.

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Patient Positioning During Mechanical Ventilation

In any patient with acute respiratory failure, it is extremely important to consider patient positioning after initiating mechanical ventilation.  Both ventilation (V) and perfusion (Q) of the lungs can be significantly altered by manipulating the way you position your patient.  

• Routine Care: A good rule of thumb is to alays keep the patient's head of bed > 30 degrees whenever possible to maximize diaphragmatic excursion, increase lung expansion, and prevent downstream incidence of ventilator associated pneumonias.
   
• Lateral Decubitus Positioning: Severe unilateral lung disease may warrant alternative patient positiong.
  • Good lung DOWN: In general, the good lung should be placed in the dependent position to improve V/Q matching.
  • Good lung UP: Exceptions where the patient should be placed so the bad lung is in the dependent position include massive hemoptysis (prevent blood from filling the good lung), large pulmonary abscesses (prevent pus from filling the good lung), & unilateral emphysema (prevent hyperinflation)
     
• Reverse Trendelenburg:  In the morbidly obese patient, or those who must remain flat in bed, a trick of the trade to achieve a pseudo-semirecumbent position is to utilize reverse trendelenburg to > 30 degrees.

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Thrombelastography for Management of Non-Traumatic Hemorrhagic Shock

The use of thrombelastography (TEG, ROTEM) has traditionally been utilized and studied in the management of acute coagulopathy of trauma (ACoT) developed by patients in hemorrhagic shock secondary to trauma.

Functional coagulation tests such as the TEG may provide valuable information when resuscitating the hemorrhaging patient, especially if there is any concern for an underlying coagulopathy.  

The following is a TEG recently returned during the resuscitation of a 60 y/o male with a history of HCV cirrhosis presenting with hemorrhagic shock secondary to a massive upper GIB.  The University's Massive Transfusion Protocol was promptly activated and at this point, the patient had received approximately 4 units of PRBCs & FFP along with 1 liter of crystalloid.  His Hgb was 5, PT/PTT/INR were undetectable, and his fibrinogen was 80.

Below is a table that simplifies the treatment, based on the test's abnormalities:

• Prolonged R:  Fresh frozen plasma
• Prolonged K or reduced α angle: Cryoprecipitate
• Low MA: Platelets, desmopressin (DDAVP)
• Elevated LY 30%: Consider antifibrinolytics (aminocaproic acid, TXA)

After reviewing the initial TEG, all perameters were abnormal in addition to the presence of significant fibrinolysis.  The patient was given an additional 4 units of FFP, DDAVP, cryoprecipitate, a unit of platelets, and aminocaproic acid.  The patient still required significant resuscitation, however bleeding had significantly decreased as well has his pressor requirement.  Below is the patient's follow-up TEG 2 hours later.

There is growing enthusiasm for the use of functional coagulopathy testing in the patient with hemorrhagic shock.  Early resuscitation with blood products as your fluid of choice with limited fluid administration while arranging for definitive source control are critical, but also consider early thrombelastography to detect additional causes for uncontrolled hemorrhage.

References

1. Walsh M, Thomas SG, Howard JC, et al. Blood component therapy in trauma guided with the utilization of the perfusionist and thromboelastography. Journal of Extra-Corporeal Technology. 2011 Sep; 43(3):162-7.
2. The Use of TEG & Goal Directed Blood Component Therapy.  MarylandCCProject.org

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email: johncgreenwood@gmail.com

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Carbapenem Resistant Organisms are HERE

We've all heard Dr. Bryan Hayes warn us that, "Vanc & Zosyn is NOT the Answer for Everything" but things just got a little more serious, on a whole 'nother level...

Within the past few months, 2 cases of NDM-producing carbapenem-resistant pseudomonas have been reported in the area - one in Delaware and one in Pennsylvania.  Previously, the only reported cases were found in Europe.  

It's important for EM physicians to be aware of carbapenem resistant organisms and infections because:

• They have been independently associated with an increase in mortality
•  Are increasing in frequency around the world
• Are a major threat to our antimicrobial armamentarium

Risk factors for carbapenem resistance 

• Stem cell transplant patients
• History of mechanical ventilation
• Recent ICU stay
• Previous exposure to antibiotics

Antimicrobial options

Few treatment options are currently available for carbapenem resistant organisms.  

• Polymixins (colistimethate & polymyxin B)
• Tigecycline
• Fosfomycin
• Some aminoglycosides (amikacin, gentamicin, & tobramycin)

Appear to have retained some in vitro activity against these organisms, but are generally used as, "drugs of last resort". 

What should you do about it?

Know it exists, take a good history, & know your local antibiogram.  Prior to selecting a broad spectrum antimicrobial regimen, try to obtain previous antimicrobial culture data for patients with resistant organism infectious risk factors.

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Direct vs. video laryngoscopy in the patient with an acute TBI

Hypoxia and hypotension are considered the "lethal duo" in patients with traumatic brain injury.  In a recent randomized control trial (by our own Dr. Dale Yeatts at the Shock Trauma Center) mortality outcomes were compared between 623 consecutive patients who were intubated with either direct laryngoscopy (DL) or video laryngoscopy (VL).  Here is what they found:

1. No significant difference in mortality for all comers (Primary Outcome)
2. In the subset of patients with severe head injuries, there was:

• A significantly higher mortality in patients with TBI if VL was used
• A significantly longer intubation duration for VL (74 sec) than DL (65 sec)
• A greater incidence of low oxygen saturations of 80% or less in the VL group (27 patients) than DL (15 patients) - objectively recorded data, not self reported.

There is a reasonable amount of literature that shows hypoxia and hypotension significantly contribute to morbidity & mortality in the TBI patient, and a growing body of literature that suggests intubation with VL takes longer than DL.

Bottom Line: When choosing a method of intubation for the TBI patient, remember the "Lethal Duo" and consider direct laryngoscopy with manual inline stabilization first.

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Nitric Oxide appears to have NO role in ARDS

Background: The use of inhaled nitric oxide (iNO) in acute respiratory distress syndrome (ARDS) & severe hypoxemic respiratory failure has been thought to potentially improve oxygenation and clinical outcomes.  It is estimated that iNO is used in up to 14% of patients, despite a lack of evidence to show improved outcomes. 

Mechanism: Inhaled NO works as a selective pulmonary vasodilator which has been found to improve P_aO₂/F_iO₂ by 5-13%, but is costly ($1,500 - $3,000 per day) and increases risk of renal failure in the critically ill.

Study: A recent systematic review analyzed 9 different RCTs (N=1142) and compared mortality between those with severe (P_aO₂/F_iO₂ < 100) and less severe (P_aO₂/F_iO₂ > 100) ARDS and found that iNO does not reduce mortality in patients with ARDS, regardless of the severity of hypoxemia.

Bottom Line: Inhaled NO is an intriguing option for the treatment of refractory hypoxemic respiratory failure, however there does not appear to be a mortality benefit to justify it's high cost and potentially negative side effects.  In the ED, it is important to focus on appropriate lung protective ventilation strategies (TV: 6-8 cc/kg IBW) and maintaining plateau pressures < 30 cm H₂O in the initial stages of ARDS to prevent ventilator induced lung injury while awaiting ICU admission.

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Intensive BP Control in Spontaneous Intracranial Hemorrhage

Managing the patient with hypertensive emergency in the setting of spontaneous intracerebral hemorrhage (ICH) is often a challenge.  Current guidelines from the American Stroke Association are to target an SBP of between 160 - 180 mm Hg with continuous or intermittent IV antihypertensives.  Continuous infusions are recommended for patients with an initial SBP > 200 mm Hg.
 

An emerging concept is that rapid and aggressive BP control (target SBP of 140) may reduce hematoma formation, secondary edema, & improve outcomes.
 

Recently published, the INTERACT 2 trial (n=2,829) compared intensive BP control (target SBP < 140 within 1 hour) to standard therapy (target SBP < 180) found:

• No difference in mortality (11.9% vs 12%, respectively)
• Improved functional status (secondary outcome) with intensive BP control
• Intensive lowering of BP in patients with acute ICH appears safe 

Study flaws: Patients treated with multiple drugs - combinations of urapadil, labetalol, nicardipine, nitrates, hydralazine, and diuretics.  Management variability away from protocol seemed high. (Interesting editorial)
 

A Post-hoc analysis of the INTERACT 2 published just this month suggests that large fluctuations in SBP (>14 mmHg) during the first 24 hours may increase risk of death & major disability at 90 days.

Bottom Line:  INTERACT 2 was a large RCT but not a great study (keep on the look out for ATACH II).  However, in patients with spontaneous ICH, consider early initiation of an antihypertensive drip (preferably nicardipine) in the ED to reduce blood pressure fluctuations early with a target SBP of 140 mmHg.

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Arterial Catheter-Related Blood Stream Infections

Whether arterial lines are a potential source of catheter-related blood stream infections (CRBSIs) is highly-debated; however, based on a recent systematic review they are an under recognized and significant source of CRBSIs.

• Incidence: In systematically cultured arterial catheters, the infection rate was 1.6 infections/1,000 catheter days which is similar to what has been reported for infections associated with short-term CVC's.
   
• Location: Femoral a-lines are more likely than radial a-lines to be a source of a CRBSI. Femoral a-line CRBSIs occurred in 1.5% of all catheters (95% CI, 0.8–2.2%), which is higher than radial CRBSI, with a relative risk of infection 1.94 times greater than those placed at the radial site.
   
• Technique: Only one study specifically evaluated the impact of full barrier precautions versus using sterile gloves only for peripheral a-lines, and it did not find any significant difference in BSI. No study has evaluated the impact of maximal barrier precautions for femoral, axillary, and brachial arterial catheters.
   
• Dressing: The risk of infection was significantly decreased with the use of chlorhexidine-impregnated dressings (ex: BioPatch).

Bottom Line(s) 

1. Arterial lines appear to be a significantly under recognized source of CRBSI's in critically-ill patients.  If you are deciding to place an a-line for invasive blood pressure monitoring, strongly consider the radial site and use a chlorhexidine sponge or dressing to try and minimize the risk of future BSI.
    
2. There is a paucity of data regarding the utility of maximal barrier techniques when inserting peripheral arterial lines.  With arterial catheter infection rates approaching that of central venous catheters, we should probably be inserting a-lines with the same sterile technique.

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VAD thrombosis: A Must Know VAD Complication

The HeartMate left ventricular assist device (LVAD) is one of the most frequently placed LVADs today. Originally, it was thought to have a lower incidence of thrombosis due to its mechanical design. However, a recent multi-center study published in the NEJM reported a dramatic increase in the rate of thrombosis since 2011 in the HeartMate II device.  The report found:

• An increase in pump thrombosis at 3 months after implantation from 2.2% to 8.4%

• The median time from implantation to thrombosis was 18.6 months prior to March 2011, to 2.7 months after.

Pump thrombosis is a major cause of morbidity and mortality (up to almost 50%!!) and is a can't miss diagnosis.  It's important to keep thrombosis on the differential for any VAD patient presenting with:

• Power spikes or low pump flow alarms on the patient's control box

• Pump (VAD) failure

• Recurrent/new heart failure

• Altered mental status

• Hypotension (MAP < 65)

• Signs of peripheral emboli (including acute CVA)

Useful lab findings suggestive of thrombosis include:

• Evidence of hemolysis

• LDH > 1,500 mg/dL or 2.5-3 times the upper limit of normal

• Hemoglobinuria

• Elevated plasma free hemoglobin

Bottom Line: In the patient with suspected VAD thrombosis, it is important to contact the patient's VAD team immediately (CT surgeon, VAD coordinator/nurse, VAD engineer).  Treatment should begin with a continuous infusion of unfractionated heparin, while other treatment options can be discussed with the VAD team.

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