A diabetic male presents with midfoot pain. What’s the Diagnosis?

maryhaasBy Mary Haas, MD, PGY-II

A 60 year old male diabetic with a history of diabetic neuropathy, peripheral vascular disease and left first toe amputation presents to the ED with left foot pain after a recent fall. His pain is worse with weight bearing.

On exam, the patient is noted to have swelling and tenderness to the left midfoot. He has ecchymosis to the plantar surface as well as pain with pronation and supination of the midfoot foot.

You obtain the following X-ray. What is the diagnosis?

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Answer: Lisfranc fracture-dislocation

The Lisfranc injury is a diagnosis that requires a high index of suspicion, as it is easily missed and can lead to significant morbidity including post-traumatic arthritis and midfoot instability.

Lisfranc was the name of a surgeon in Napoleon’s army who described a new method of amputation across the tarsometatarsal joints, which was utilized in situations of wet gangrene from frostbite. The injury itself was later named for horseback riders who got their foot caught in the stirrup upon falling off of the horse.

The lisfranc joint consists of 5 tarsometatarsal joints, with the first through third articulating with the medial, middle and lateral cuneiforms, respectively, while the 4th and 5th articulate with the cuboid bone. The lisfranc ligament originates from the medial cuneiform and extends to the base of the second metatarsal. It is responsible for the stability of the midfoot. A lisfranc injury refers to any fracture or dislocation of a tarsometatarsal joint.

The typical mechanism of injury involves high-energy trauma with plantar flexion and forced pronation or supination. However, up to 1/3 of injuries are from a minor fall. In diabetic patients, especially those with peripheral neuropathy, these injuries can occur from minimal or no trauma.

The clinical presentation includes pain to the midfoot, worse with weight bearing. Physical exam may reveal exaggerated swelling to the midfoot, ecchymosis along the plantar midfoot, pain and tenderness along the tarsal-metatarsal joints, and pain with pronation or supination of the midfoot with the heel fixed in the examiner’s hand. Always look for signs of compartment syndrome as the dorsalis pedis can be injured in severe dislocation.

On radiographs, look for fracture of the base of the second matatarsal. Another hallmark of a lisfranc injury is that the medial margin of the 2nd metatarsal base does not align with the medial margin of the second cuneiform. Dislocations are considered unstable if there is 1 mm or more displacement between the base of the first and second metatarsal. In lateral views, the 2nd metatarsal is higher than the middle cuneiform.

For nondisplaced fractures with < 1 mm between the first and second metatarsal bases, treatment is typically conservative management, with non-weight bearing to the affected foot, splinting and orthopedic follow up. For displaced fractures, emergent ortho consult is required as most of these will require operative management.

References/Further Reading

Trevino, S. Lisfranc Fracture Dislocation. Medscape.

WikEM Lisfranc Injuries

Alrasheedi, A. Foot Injuries in the Emergency Department. 

Yeoh, J et al. Lisfranc fracture-dislocation precipitating acute Charcot arthopathy in a neuropathic diabetic foot: a case report. Cases J. 2008; 1: 290.

Wheeless’ Textbook of Orthopedics

Pope, T and Harris, H. Harris & Harris’ Radiology of Emergency Medicine. Pg 962-965.

Journal Club: Are you hopping on the Ketamine Train?

maryhaasBy Mary Haas, MD PGY-II

Ketamine is undeniably a hot topic right now in the EM world, especially within the community of FOAMed enthusiasts. There are a small but growing number of articles evaluating the safety and efficacy of ketamine in the ED for pain management. We recently had a journal club on the topic, which fueled some excellent discussion among our residents and faculty.

First, let’s go over a little background on ketamine. The May 2015 episode of EM:RAP features a great segment entitled “Doc in the Bay – Ketamine” by Howard Mell, MD. We’ll recap some of the pearls provided in this segment. First, ketamine’s mechanism of action is to antagonize NMDA receptors and thereby serve to limit internal transmission of external stimuli.  Ketamine is dosed on a spectrum, with different effects at different dosing rages, and some overlap in these ranges that can make it difficult to reach your target effect without unintentionally over or undershooting.

0.1 – 0.3 mg/kg IV: Analgesic Dose (Usually 10- 20 mg IV bolus in the average sized person)Journal Club

0.2 – 0.5 mg/kg IV: Recreational dose

0.4-0.8 mg/kg IV: Partially dissociated dose (where emergence reactions tend to occur)

Greater than 0.9 mg/kg IV: Dissociative dose (procedural sedation, RSI, etc.)

Dr. Mell mentions that ketamine actually has a relatively good safety profile, given that increasing the dose serves to bind up more NMDA receptors, and once all of them are saturated, increasing the dose further simply prolongs the duration of the drug.

The anesthesia and surgery literature has shown ketamine to mitigate pain and reduce opioid consumption in patients with chronic pain, cancer pain and acute post-operative pain. Although a paucity of literature exists for evaluating the use of ketamine for analgesia in the ED specifically, the number of studies looking into this is expanding, especially as both poorly controlled pain and opioid overuse and addiction are both understood to be major public health issues.

In journal club this week, we reviewed a recent article entitled “Intravenous Subdissociative-Dose Ketamine Versus Morphine for Analgesia in the Emergency Department: A Randomized Controlled Trial.” The primary author of this study is Dr. Sergey Motov, an emergency physician out of Maimonides Medical Center who has a particular interest in pain management in the ED. See his awesome website “The Pain-Free ED” here, and a shout out he received on the EMCrit blog here.

This study was performed at a single center site as a prospective, randomized, double-blind trial evaluating ED patients between the ages of 18-55 who presented with acute pain (< 7 days duration) that was moderate to severe (defined as at least a 5 on the 0-10 point traditional pain scale). Eligible patients were randomized to either receive 0.1 mg/kg morphine by IV push versus ketamine 0.3 mg/kg IV. The study was powered to detect  a difference of at least 1.3 at 30 minutes by enrolling 90 total patients (45 in each treatment arm). The study found no statistically significant difference in its primary outcome, which was defined as reduction in pain at 30 minutes. No difference in the secondary outcome, which was defined as incidence of rescue analgesia with fentanyl at 30 or 60 minutes, was observed. There was an increase in minor adverse effects in the ketamine group relative to morphine 15 minutes post drug injection, including dizziness, disorientation, mood changes and nausea. However, there was no serious adverse effects in either group. The study concluded that subdissociative IV ketamine at 0.3 mg/kg  provides analgesic effectiveness and apparent safety comparable to that of IV morphine for short-term treatment of acute pain in the ED.


Overall, the conclusion was that this was a fairly well-designed study. The outcome measures were clearly defined. The study’s randomized design allowed it to directly compare IV morphine to IV ketamine individually. However, several limitations must be acknowledged – this was a relatively small study, with the sample size near minimum for adequate power. It was a single-center study, with potential for unblinding given some ketamine-specific effects (i.e. nystagmus). Using pain scales as a metric for pain improvement is also fraught with potential issues, although some would argue it’s the best metric we’ve got (see here for interesting commentary on the difficulty interpreting studies evaluating effects on pain such as this study and the Beaudoin study that also looked at ketamine use in the ED).

The main issues the majority of us had with this article came down to the data’s generalizability to our every day practice, and whether or not this study (or the other studies currently out there on the topic) is enough to be practice changing given the barrier’s that currently exist for the routine use of ketamine for acute pain.

The study exclusion criteria was quite extensive (pregnancy, breast-feeding, altered mental status, allergy to morphine or ketamine, weight less than 46 kg or greater than 115 kg, unstable vital signs, medical history of acute head or eye injury, seizure, intracranial hypertension, chronic pain, renal or hepatic insufficiency, alcohol or drug abuse, psychiatric illness, or recent opioid use – 4 hours before). Given the extensive exclusion criteria, some would argue that the study can’t be effectively applied to many of the particular patients in which ketamine may actually be uniquely useful over opioids: for instance, those patients who have been given initial doses of opioids but continue to have poor controlled pain, patients with chronic pain, and patients who are relatively hypotensive/unstable in which you may be concerned to use opioids due to the side effects of respiratory depression and hypotension, but still wish to administer something for acute pain management.

Several of our faculty also made the point that this study is most applicable to patients with an acute cause of their pain, such as a femur fracture, for whom most faculty already feel comfortable simply using IV opioids and questioned the need for an alternative method such as ketamine. In counterpoint, others expressed concern that introducing opioid-naive patients to opioids, even in the acute setting, could potentially increase that person’s future risk of addiction, and thus there is a real need to have a non-opioid alternative up front. Some cited the recent study by Hoppe et al, which suggested that opioid-naive patients prescribed oral opioids for acute pain are at increased risk for additional opioid use at 1 year (although note that this study did not evaluate the effect of giving IV opioids acutely in the ED on subsequent narcotic use).

Additionally, this study compares one time dosages of morphine and ketamine, when in reality the more appropriate way to manage pain is often to titrate repeating dosing of a given agent to the goal effect.

Another practical issue that arose in the discussion was nursing discomfort with ketamine use for acute pain given that it is relatively less established than IV opioid use and is traditionally understood by nursing staff as a medication used for procedural sedation. Defining protocols for dosage and clarifying the type and extent of monitoring necessary to ensure patient safety when IV ketamine is used for acute pain is a potential solution.

The take home point that can be drawn from this particular study is that ketamine is a relatively safe and similarly effective alternative to morphine for patients with acute pain in the ED, with a potential for increase in minor adverse effects with ketamine. This study does not prove whether ketamine is a better alternative to opioids in the ED for acute pain, either in general or for certain patient populations who remain to be fully defined. The more relevant question may be whether ketamine is safe and efficacious as an adjunct to opioids compared to opioids alone, which multiple other studies have explored, and may be the more relevant question (see the further reading section below, including the study by Beaudoin et al).

References and Further Reading

Journal Jam 4 – Low Dose Ketamine Analgesia 

 Mell, H. Doc in the Bay – Ketamine. EM:Rap May 2015

Beaudoin FL, Lin C, Guan W, Merchant RC. Low-dose ketamine improves pain relief in patients receiving intravenous opioids for acute pain in the emergency department: results of a randomized, double-blind, clinical trial. Acad Emerg Med. 2014;21(11):1193-202.

Lester LM, Braude DM, Niles CM, et al. Low-dose ketamine for analgesia in the ED: a retrospective case series. Am J Emerg Med. 2010;28:820-827.

Richards JM, Rockford RM. Low-dose ketamine analgesia: patient and physician experience in the ED. Am J Emerg Med. 2013;31:390-394.

Miller J, Schauer S, Ganem V, et al. Low-dose ketamine vs morphine for acute pain in the ED: a randomized controlled trial. Am J Emerg Med. 2015; http://dx.doi.org/10.1016/j.ajem.2014.12.058.

Ahern T, Herring A, Stone M, et al. Effective analgesia with low-dose ketamine and reduced dose hydromorphone in ED patients with severe pain. Am J Emerg Med. 2013;31:847-851.

What’s the deal with Bicarb?

By Beau Stokes, MD, PGY-2, with commentary by Dr. Sage Whitmore, MD

beaustokesThe topic of acid base physiology came up in a recent M&M. I know that one of my biggest weaknesses was acid/base physiology until I sunk a bunch of time into reading about it. It was just conceptually hard for me to wrap my mind around it for a while. I’m hoping that this post can help save other people the amount of time it took me to sort through all of this complicated physiology.

For the longest time, I couldn’t understand why giving bicarb wasn’t the treatment for acidosis. There have been multiple studies that have shown in various situations where giving bicarb in acidosis not only does not improve mortality, but can even increase mortality. It seemed backwards that giving a base to someone with acidosis could actually increase mortality.

What's the deal with bicarb (2)It turns out that it all comes down to physiology. When you give someone bicarb, it buffers pH through the equation we all learned back in med school: HCO2 + H < > H3CO2 < > H2O + CO2.  When you give someone bicarb, the only way it can make the pH more “basic” is by turning the H+ ions into water and generating carbon dioxide. However, if that patient can’t breathe out the carbon dioxide, they will just become hypercapnic, and the excess CO2 will diffuse intracellularly which traps acid inside body compartments, like the CSF and myocardium. Most acidemic patients already have increased respiratory rate and are already maximally compensated from a respiratory standpoint. If you give them bicarb, all you are doing is causing increased CO2 that they can’t ventilate out. This will then cause worsening hypercapnia and potentially worsened acidosis (which is a possible explanation for the paradoxical increased mortality in some patients given bicarb).

This also applies to the fluids we give. There has been a movement towards LR as a more “balanced” fluid with less potential to cause acidosis. This is not because of the lactate conversion to bicarb in the liver, but rather because of the composition of LR. We’ve all heard by now that normal saline has the propensity to cause a hyperchloremic metabolic acidosis, which you don’t get with LR. If you also look at the pH of LR versus normal saline, the pH of normal saline is around 5.5, and the pH of LR is around 6.5. The strong ion difference of LR is also closer to physiologic range compared to normal saline. There’s just less acidosis caused with LR and it is indeed a more balanced fluid, although as we can imagine, there would be certain clinicaly situations depending on the physiology of the patient where NS would be preferred. Although there is not much data about improved mortality in these acidotic patients with LR vs. NS (that I could dig out, seems limited), physiologically it just makes sense to use LR more that we probably do.

This is a great podcast for acid/base of fluids and how they effect physiology: http://emcrit.org/podcasts/acid-base-4-use-of-fluids/

This is a great podcast for why giving bicarb physiologically doesn’t help in these patients: http://emcrit.org/podcasts/enough-with-the-bicarb-already/

I’d also recommend listening to Jan. 2015 EMRAP they had a nice segment about giving bicarb to these patients and why it doesn’t work. https://www.emrap.org/episode/2015/january/criticalcare (starts at 19 minutes in for DKA management, 24:30 for why not to use bicarb).

Commentary by Dr. Sage Whitmore, MD (critical care trained EM faculty):

whitemore blog picI completely agree. Pushing bicarb is indicated for NO OTHER condition than for frank hemodynamic collapse. A sudden jump in HCO3 and pH can cause decreased oxygen delivery to tissues (leftward shift of oxy-hgb curve and tissue arteriolar constriction), increased lactate production, decreased ketone clearance, hypocalcemia, and hypokalemia. “Slow push” might be needed for QRS widening with hyperkalemia or sodium channel blocking agents, or as a poor-(wo)man’s hypertonic fluid for impending brain herniation. In NON-anion gap metabolic acidoses, as well as renal failure (bicarbonate wasting processes), you can give bicarb but in the form of a drip: 150mEq (3 amps) in a liter of D5W. If your patient is on a ventilator, ALWAYS be thinking about how you’re going to ventilate the iatrogenic CO2 load off. Otherwise, just say no; never for a lactic acidosis or respiratory acidosis, unless there is cardiovascular collapse. Not to mention, most patients can tolerate a much worse pH than you as their physician can tolerate to look at on your blood gas

Regarding NS versus LR, there was just a recent meta-analysis associating mortality from severe sepsis/septic shock with normal saline use, and plenty of other literature on worse systemic inflammation, worse bleeding, worse acid base status, worse renal function, increased need for dialysis, etc. all associated with normal saline.

NOW, for the exceptions: there are FIVE groups of patients who cannot tolerate acidemia or permissive hypercapnia, and we must correct their pH whether by improving their minute ventilation or by giving bicarb: Cardiogenic shock, pulmonary hypertension, elevated ICP, certain overdoses—specifically salicylate and sodium channel poisons, and pregnancy. Furthermore, there are groups of patients for whom LR is NOT appropriate (due to its lower sodium concentration): intracranial pathology at risk for cerebral edema, chloride losses such as severe vomiting, hypovolemia accompanied by alkalemia, adrenal failure (hyponatremia/hyperkalemia), hypercalcemia, and in small children/infants. Furthermore, for logistics, know that LR cannot be run in with blood products (but plasmalyte can), and additives such as KCl are not easily added (which is why I begrudgingly still use half-normal saline for DKA).

Yo! know your IO!

Image obtained from Wikimedia commons Vidacare Corporations: EZ-IO ® Intraosseous Infusion System

By Mary Haas, MD, PGY-II


Few things instill fear in the emergency physician more than caring for a crashing patient without a line. If you’ve got a patient with impending cardiorespiratory collapse and a lack of good IV access, know your IO!

Why do IOs work well in patients with shock/cardiac arrest?

  • Can be performed quickly,  often faster than peripheral lines in settings where there is peripheral vasoconstriction (bone marrow is a noncollapsible venous access route).
  • Requires less skill and practice than central and umbilical line placement
  • Fewer serious complications than central lines

Which medications can be given through an IO?

  • Any medication that can be safely given through a peripheral vein can be given safely through an IO
  • IO and IV doses are the same, however each medication administration via IO should be followed by 3-5 mL fluid flush

In which sites can you place IOs?

  • Proximal tibia:
    • Palpable landmarks (2 cm below patella, 2 cm medial to tibial tuberosity)
    • Away from airway/chest during simultaneous resuscitative efforts
  • Proximal humerus:
    • Palpable landmarks (rest patient’s hand on their abdomen with elbow adducted, palpate directly up the humerus to the most prominent aspect of the greater tubercle, and use the yellow need if the pt is  40 kg)
    • Better flow rates
    • Less painful (preferred in awake patients)
    • Less risk of compartment syndrome
  • Distal tibia
  • Sternum
  • Distal femur (last resort)

How do you place an IO?

Proximal humerus:

Proximal tibia:  

What sizes exist for IOs?

  • For patients 3-39 kg: Pink (15 mm)
  • For patients 40 kg and above: Blue (25 mm)
  • For patients with excessive tissue/obesity: Yellow (45 mm)

What are the potential complications of IOs?

  • Extravasation of fluid (most common): can lead to compartment syndrome or muscle necrosis
  • Infection: osteomyelitis, cellulitis
  • Local hematoma
  • Pain
  • Fracture
  • Growth plate injuries with incorrect placement
  • Fat microemboli

How long can you keep an IO in?

  • Ideally, remove within 3-4 hours, but IOs can remain in 72-96 hours (risk of infection increases with time that it remains in place)
  • Remove once more definitive venous access is achieved

How do you know you’re in the right place?

  • Needle will stand firmly upright when released
  • Aspirate marrow upon entry
  • Bolus 5-10 ccs of isotonic sodium chloride: High resistance to flow or visible extravasation means it’s likely in the wrong place. Can also use ultrasound in addition to physical exam to evaluate for extravasated fluid.

Which laboratory values from IOs correlate with peripheral venous levels?

  • Some data on this comes from this small study.
  • Good correlation: Hemoglobin/hematocrit, chloride, glucose, BUN/Cr, albumin, total protein

  • Not as good of a correlation: CO2 (lower), platelet (lower), WBC (higher), Potassium (often hemolyzed), CO2, calcium

  • Before obtaining/sending IO sample for labs, aspirate and discard the first 2 mL.

Sources & Additional Reading: 

Miller, LJ. A new study of intraosseous blood for laboratory analysis. Arch Path Lab Med 134(9):1253-1260, 2010. 

Dolister M et al. Intraosseous vascular access is safe, effective and costs less than central venous catheters for patients in the hospital setting. J sac Access. 2013 Jul-Sep; 14(3):216-24

Lee et al. Intraosseous versus central venous catheter utilization and performance during inpatient medical emergencies. Crit Care Med. 2015 Jun;43(6):1233-8

Paxton et al. Proximal humerus intraosseous infusion: a preferred emergency venous access. J Trauma. 2009 Sep;67(3):606-11

Van Hoff et al. Does intraosseous equal intravenous? A pharmacokinetic study. Am J Emerg Med. 2008 Jan;26(1):31-8

Gluckman, W. Intraosseous Cannulation. Medscape

Rogers et al. Intraosseous (IO) Access. WikEM

Guthrie, K. Seizing and No Access!! Life in the Fast Lane

EZ-IO by Vidacare: The 5 Rights of Intraosseous Vascular Access

Sage Advice: ED Management of the LVAD patient

Written by Sage Whitmore, MD

whitemore blog pic

Here are some key points and pearls to take away with regard to management of the critical Left Ventricular Assist Device (LVAD) patient after a recent related simulation case.

Ventricular Fibrillation Defibrillate Early, even with LVAD. The LVAD is helping the LV but not the RV, so shock can occur.

Other arrhythmias, like VT, A-fib, flutter, etc. Can usually be treated with antiarrhythmics and watchful waiting

Chest compressions are NOT indicated unless there is a lack of pulses AND no measurable BP with Doppler AND a lack of LVAD function (out of battery, not whirring on auscultation, no flow). If there is any flow from the LVAD or measurable BP, conduct a “chemical code” without compressions. Compressions may dislodge the device and lead to rapid exsanguination (debatable). Alternative to chest compressions are LUQ abdominal compressions (debatable)

Hypotension BP should be obtained by manual cuff and Doppler of the brachial pulse. The first whooshing sound you hear is the MAP. Normal MAP is 70-90.

The differential for shock in the LVAD patient is the same for anyone. More details below

HYPOVOLEMIC—bleeding, overdiuresis, GI losses

DISTRIBUTIVE—septic, anaphylactic

CARDIOGENIC—RV overload, tamponade, arrhythmia, pump thrombosis, hypertensive crisis. (PE is relatively uncommon)

Bedside echo and then formal echo are absolutely essential to differentiating shock type and figuring out whether to give volume vs. pressors vs. inotropes

Pump thrombosis In our recent LVAD simulation case, our patient had cardiogenic shock with LV > RV overload on bedside echo, meaning his LV was not being drained or assisted by the LVAD. In the context of a warm battery pack, high power, and high flow, this points to pump thrombosis. If the LVAD was working properly, we might have seen the RV > LV with septum bowed from Right to Left, indicative of RV overload (which is how most of these guys walk around).

The treatment is immediate heparinization and discussion with CT surgery. At our institution, they tend to emergently replace the VAD rather than use tPA to open the thrombus.

Hemolysis Hemolysis is a common problem leading to anemia and poor O2 delivery, and is common with pump thrombosis. Every VAD patient needs the following labs added on to the usual labs/coags:

–          LDH

–          Haptoglobin

–          Plasma (free) hemoglobin

–          Fibrinogen

–          Urine Hgb/Mgb

Mesenteric Ischemia In our simulation case, our patient was is in cardiogenic shock from LVAD failure and had an elevated lactate and vague abdominal pain, suggestive of Mesenteric Ischemia. His CTAP would show thickened bowel walls.

One must ALWAYS think about gut ischemia in the LVAD patient. This may be due to shock/hypoperfusion in general, venous outflow diminished from RV failure, or from pump thrombosis flicking clots out into the mesenteric circulation.

Common LVAD settings and problems

Speed (RPM) This is the only setting that is actually “set” by the LVAD team. They set the RPM in the OR under TEE guidance, looking for the magic RPM that drains the LV adequately without allowing the RV to bulge too much. The best RPM is where the septum sits nicely between the RV and LV. Normal RPM is 6000-15000 for Heartmate II This value does not change
Power The POWER is the wattage needed by the LVAD to maintain its set RPM. This is a variable. Normal Power is <10 watts. The patient/family and LVAD team are told to watch this number over time for rising/falling Increasing power (14 watts in our case) tells you that the LVAD is trying to overcome resistance to maintain the set RPM; think of pump thrombosis or hypertensive crisis (too much afterload in the aorta).

Decreasing power tells you the afterload is reduced, as in distributive shock (sepsis) or aortic insufficiency

Pulsatility Index (PI) The PI tells you in general about the equilibrium between the native cardiac function and the device (how much the heart squeezes compared to how much blood the LVAD is moving).

If the LVAD had a low speed, not much flow, but the heart was squeezing well, there would be a HIGH PI.

If the LVAD has a high speed, high power, cranking away and moving a lot of blood, and the heart is sick and not contracting, there is a LOW PI

Normal PI is 3.5-5.5. A low PI (1.5 in our case) tells you the heart is either not contracting at all, is underfilled, or the pump is thrombosed. Need an echo to figure it out.
Flow In liters/min, the FLOW is a CALCULATED product of RPM and POWER. This is not the actual output of the device or the patient’s cardiac output Normal Flow can be 4, 6, 8 LPM, anywhere in there. In pump thrombosis, the flow is FALSELY elevated (power is high)

In bleeding, hypovolemia, or cardiogenic shock, the flows can be low.

Useful Head-to-Toe DDX for the sick LVAD Patient

Intracranial Hemorrhage High MAP, High INR
Embolic Stroke Pump Thrombosis
Pump Thrombosis High Power, High Flow, Big LV with shock, Hemolysis

INR might be subtherapeutic

Start heparin and inotropes (Dopamine, Epi, or Levophed+Milrinone)

RV overload Progressive RV failure, fluid overload, RV infarct

Edema, JVD, Liver tenderness, ascites

Huge RV with R > L septal bowing and obliterated LV cavity

Start Norepinephrine, Milrinone, 100% O2, INO, do not intubate

Arrhythmia Shock VF

Otherwise, Amio is the usual go-to

Suction Event Bleeding or Hypovolemic patient has underfilled LV cavity, –OR–

Huge RV overload has obliterated LV cavity

Sudden drop in all parameters: RPM, PI, Flow, Power

Give fluids or treat RV failure, depends on echo

Team may adjust the speed

Suction events often present with sudden/recurrent syncopal episodes, usually associated with tachydysrhythmias

Tamponade Recent placement or instrumentation
Aortic Insufficiency New appearance of big LV, pulmonary edema, low afterload state, hypotension and shock. The LVAD is essentially recirculating blood without moving it forward. Start inotropes (dopamine, epi) to increase heart rate and contractility and limit time spent regurgitating during diastole
Hypertensive crisis Patient’s MAP is much higher than usual

Risk for head bleeds

Increased afterload will limit the LVAD flow

Afterload reduction (Nicardipine, Nitroprusside)

Hemorrhage GI bleed, retroperitoneal bleed, hypovolemic shock

Look for IVC variability on inspiration to know you can give fluids/blood

CAREFUL with transfusion—if patient is a potential heart transplant recipient, run the Hgb low and use Irradiated or Leuko-Reduced blood to reduce the chances of antibody formation

Sepsis Drive Line infection, Pocket infection, other typical sources
Mesenteric Ischemia Maintain low index of suspicion. Fix hypotension. Think about scanning the belly
Limb Ischemia Flickin’ clot
Hemolysis Add those special labs


Pratt et al. LVAD management in the ICU. Critical Care Medicine 2014

Higgins et al. LVAD Guidelines. Main Medical Center 2010.

MyLVAD.com, EMS Field Guide, 2012

Sage Advice: Using NIV for Pre-oxygenation prior to Intubation

Written by Sage Whitmore, MD

whitemore blog picReferenced below are three of the better articles on this subject, which provide fairly convincing evidence that in hypoxic patients (PNA, ARDS, etc.), a few minutes on NIV prior to intubation will get you a higher starting saturation, safer apnea time, and much less of a drastic desaturation during the attempt. I invite our providers and RTs to be familiar with this concept so that we have it as an option in the right patients if the airway doc is inclined to use it.

My practice is to wheel the vent to the bedside, set it to Spontaneous/Pressure Support 5 over 5, FiO2 of 100%, back-up rate of nothing (4 or 6, something very low so there is no asynchrony), hook the hose up to a NIV mask and place on the patient for a few minutes while I set up for the airway. Then after drugs are pushed, I hold the NIV mask over the mouth with a jaw thrust, let the patient take their last few breaths, and then hold the mask there for 45-60 seconds while the drugs kick in (NOT giving any breaths—still technically an RSI). This keeps the patient PEEPed open and maintains an O2 gradient flowing from circuit to alveoli. Then I pop the mask off, intubate, and hook the circuit up to the tube with an ETCO2 detector, and start them on lung-protective settings right away.

Delayed Sequence Intubation: A Prospective Observational Study. Weingart, Scott D. et al. Annals of Emergency Medicine , Volume 65 , Issue 4 , 349 – 355.

An intervention to decrease complications related to endotracheal intubation in the intensive care unit: a prospective, multiple-center study. Jaber et al. Intensive Care Med. 2010 Feb;36(2):248-55.

Noninvasive ventilation improves preoxygenation before intubation of hypoxic patients. Baillard et al. Am J Respir Crit Care Med. 2006 Jul 15;174(2):171-7. Epub 2006 Apr 20.

Sage Advice: Indications for Non-invasive Ventilation

Written by Sage Whitmore, MD

whitemore blog picMy favorite thing to do on Thursday nights at 2:30am is pontificate on non-invasive ventilation, so…whatever that says about me…

It came up on a shift the other day that there are some patients with respiratory failure who are best served by a trial of BiPAP, and some patients who are best served by an early intubation. I wanted to review some of the literature and make some (generally agreed-upon in the ICU community at large) recommendations on this controversial topic. The major issue at play here is whether the patient in front of you is likely to be helped by BiPAP (avoid intubation, decrease LOS, decrease nosocomial infection, get better quicker, die less), or ultimately harmed (delayed intubation, more complications, worsened condition, die more).

There are generally 5 categories of patients for whom BiPAP is preferred over intubation:

COPD STRONG evidence.

–       Reduced need for intubation

–       Reduced mortality

–       Reduced nosocomial infections

–       Decreased LOS

CHF STRONG evidence.

–       Reduced need for intubation

–       Decreased LOS

Severely Immunocompromised MEDIUM evidence in patient with Neutropenic Fever, recent Solid Organ Transplant, Active Chemotherapy

–       Reduced intubation rate

–       Reduced mortality (if they avoid intubation)

–       Reduced nosocomial infections

Cystic Fibrosis/Advanced Interstitial Lung Disease (who are NOT transplant candidates) MEDIUM evidence

–       Less nosocomial infections

(ALSO, these are terminal condition at the time that the patient would need intubation, and they are VERY unlikely to come off the vent without a trach. Would rather have a palliative conversation than intubate these guys)

Asthma WEAK evidence

(But we know it works, and asthma is very difficult to manage with a high mortality on a ventilator )

Obesity-Hypoventilation Syndrome (often misdiagnosed as OSA +/- COPD) responds nicely to BiPAP as well, IF they are awake enough to participate and can be positioned sitting straight up to take the weight off their diaphragm.

There are generally 5 categories of CONTRAINDICATIONS to non-invasive ventilation

Decreased LOC Your patient should be a GCS of 14 or better, should be able to participate. Should be able to take a deep breath when you instruct them, should be able to give you a thumbs up, should be able to press their call light if they feel worse
Airway Issues Facial trauma, upper airway mass, obstruction, stridor, vomiting, hematemesis, poor swallow, poor cough, any recent Thoracic, Esophageal/Upper GI, ENT, or craniofacial surgery, or spine precautions = don’t do it!
Respiratory Conditions Respiratory arrest (duh), hypoventilation, initial presentation of myasthenia gravis, guillan barre, cervical cord injury, de novo pneumonia/ARDS in the absence of COPD/CHF*
Circulatory Issues Hemodynamic instability (diaphragm steals up to 50% of cardiac output during septic shock), active ischemia (new ECG changes, trop rising), malignant arrhythmias
Prognosis Cause of respiratory failure unlikely to resolve within 24-36 hours

*On the issue of BiPAP for Pneumonia/ARDS: There is no randomized trial comparing NIV to invasive mechanical ventilation in PNA/ARDS that I know of. There are old trials showing that compared to plain supplemental oxygen, NIV reduces the need for intubation (duh). The most important is the data is looking at how often patients with PNA/ARDS fail a trial of NIV, and what happens to them after they fail. Here is what I look at, based on studies that are referenced at the bottom:

  1. Predictors of NIV failure include: presence of pneumonia, hemodynamic instability
  2. NIV failure rates are >50% in presence of severe pneumonia and/or ARDS
  3. Overall mortality rates for patients who fail NIV are anywhere from 50-92% (highest being in neutropenic patients with HCAP/ARDS)
  4. Mortality rates for patients who fail NIV are 2x higher than otherwise predicted by severity of illness scores
  5. Patients with de novo hypoxic respiratory failure (i.e. PNA/ARDS) are >3x more likely to die if they fail NIV
  6. in a review from our QI database at U of A over the last two years, patients who were intubated after failing NIV are >2x more likely to significantly desaturate, become hypotensive, or aspirate during intubation, also associated with increased odds of death

The take home point is: patients with PNA/ARDS are more likely than not to fail NIV, and when they do, their intubation is more complicated and they are more likely to die. So, prevent an ugly crash intubation in the middle of the night; intubate your septic pneumonia patient early.


  1.       Kramer et al AJRCC 1995 – reduced intubation in COPD group
  2.       Keenan et al. Crit Care Med 1997 – reduced mortality and intubation in COPD
  3.       Antonelli et al. NEJM 1998 – non-COPD patients
  4.       Pan et al. Chest 1998 – metaanalysis, reduced intubation
  5.       Wood et al. Chest 1998 – small ED trial, included PNA patient
  6.       Confalonieiri et al. AJRCCM 1999 – benefits for severe pneumonia
  7.       Antonelli et al. J Crit Care 2000 – Review article, helps in CHF, COPD
  8.       Wysocki et al. Chest 1995 – non-COPD pts, no benefits of NIV
  9.       Antonelli et al. JAMA 2000 – NIV in fresh transplant is good
  10.    Cheung et al. Hong-Kong Medical Journal 2000 – failed NIV worsened mortality, esp PNA
  11.    Girou et al. JAMA 2000 – NIV decreased nosocomial infections in COPD and CHF
  12.    Martin et al. AJRCCM 2000 – need for intubation decreased in all comers
  13.    Moretti et al. Thorax 2000 – prediciting NIV failure in COPD
  14.    Sinuff et al. CMAJ 2000 – no clear predictors of NIV failure in mixed population
  15.    Ambrosino et al. Thorax 1995 – precense of PNA and low pH predict NIV failure
  16.    Azoulay, Alberti et al. Crit Care Med 2001 – NIV decreased mortality in Cancer Pts
  17.    Gilles, Didier et al. NEJM 2001 – NIV in immunosuppressed
  18.    Hilbert, Gruson, et al. Crit Care Med 2000 – NIV in neutropenic, all responders lived
  19.    Madden, Kariyawasam, et al. Europ Resp J 2002 – NIV in cystic fibrosis improves PaO2
  20.    Carrillo, Gonzales-Diaz. Inten Care Med 2012 – NIV for CAP, delayed ETI = mortality
  21.    Ferrer, Esquinas. AMJRCC 2003 – RCT of NIV v O2 for hypoxic resp failure
  22.    Gristina et al. Crit Care Med 2011 – NIV for heme malignancy, 5yr experience.
  23.    Jolliet, Abajo, et al. Intens Care Med 2001 – cohort of NIV for ARDS, 66% failed
  24.    Rana, Jenad, et al. Crit Care 2006 – risk factor for NIV failure in ALI
  25.    Carron, Freo, et al. J Crit Care 2010 – severe CAP on NIV, 56% failed
  26.    Demoule, Girou, et al. Intens Care Med 2006 – NIV for de novo vs chronic resp failure
  27.    Ferrer, Cosentini, et al. Europ J Intern Med 2012 – Review of NIV for PNA
  28.    Sorksky et al. Europ Resp Review 2010 – NIV for asthma, review
  29.    Zhan, Sun et al. J Crit Care Med 2012 – RCT of NIV vs simple O2 for Acute Lung Injury
  30.    Antonelli, Conti, Moro et al. Intens Care Med 2001 – predictors of NIV failure
  31.    Keenan et al. Crit Care Med 2004 – systematic review of NIV for hypoxic resp failure
  32.    Delclaux et al. JAMA 2000 – RCT of NIV vs simple O2 for Acute Lung Injury +/- CHF
  33.    Carron, Freo et al. British J Anaesth 2013 – Review of NIV complications
  34.    Emeriaud G, Crulli B, Ducharme-Crevier L, Nishisaki A. 429: Safety of pediatric tracheal intubation after non-invasive ventilation failure (POSTER). Critical Care Medicine 2012;40(12) Supplement 1