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

Conference Highlight from July 7th, 2015: Clinical Analgesia Pearls

Clinical Analgesia Pearls: Recap of Lecture given by Dr. Michael Cole


  • Defining procedural sedation: giving an IV anxiolytic and an IV analgesic together does not necessarily always count as procedural sedation. Key point: It’s not the combination of medications you use, but rather the intent behind using them. A procedure is a painful event (cardioversion, shoulder reduction, etc.) followed by relief. Post-procedurally, there is diminished adrenergic drive once relief has been achieved, which can lead to a potential cardiovascular and respiratory collapse if drugs remain on board. Thus, following administration of medications for the purpose of performing the procedure, patients require continued monitoring for this. In contrast, giving an anxious patient with abdominal pain both ativan and dilaudid would not count as procedural sedation, as once these medications wear off, the patient is likely to continue to have pain.
  • Hypoxia during procedural sedation is always an emergency that should be promptly addressed. A normal, healthy adult can maintain apneic oxygenation for ~7 minutes until desaturating to 90%. However, once desaturated to 90%, it takes only 2 minutes to get down to an oxygen saturation of 0%. Interventions include maneuvers to open the airway such as jaw thrust, BVM, and use of reversal agents such as narcan.Exert caution with using the benzodiazepine antagonist flumazenil in ALL patients. Although it is typically safe in pediatrics (used ONLY as rescue med for procedural sedation), we recommend that it NEVER be used in Adults in light of the constant uncertainty related to the practice of emergency medicine and the fact that the risk of inducing intractable seizures is too great. The answer for the patient with benzodiazepine related adverse event is typically supportive care with the potential need for intubation (and possibly vasopressors, in severe overdose).
  • There are many options when it comes to analgesics. Tylenol is generally considered the safest first line pain relief medication and is good for most mild types of pain. Exert caution when using in patients with liver disease, renal disease, or on coumadin (tylenol dose > 2 g/day has been demonstrated to increase INR while on coumadin). NSAIDs work by inhibiting prostaglandins which leads to anti-inflammatory effects. Contraindications include PUD/gastritis, renal disease, Coumadin use (can exacerbate bleeding), allergy. Please click here for the latest FDA Warning on the cardiovascular risk related to NSAID use. There is no great evidence that NSAIDs inhibit bone healing, and use of NSAIDs in pediatric fractures is generally accepted at our institution by our orthopedic colleagues. A good practical rule of thumb (until we get better evidence on this topic) is the older and sicker the patient is (i.e. the more difficult it is for them to heal) the less likely it is that you should be plowing them with NSAIDs. Toradol is another option, but should only be used in the short term due to its increased side effect profile. Morphine, dilaudid and fentanyl are commonly used opiates in the ED. Use caution with morphine in ESRD patients as its metabolites are renally excreted, leading to an increased risk of side effects such as respiratory depression. Ketamine has gained increasing popularity as an analgesic when used at the appropriate dose, as it provides both analgesia and amnesia. It can be associated with an emergence reaction. Dr. Cole emphasized that it is better used in combination with other medications as it has an opiate sparing effect, rather than as a monotherapy, and suggested the dosage of 0.1-0.5 mg/kg bolus followed by a drip 0.05-0.4 mg/kg/hr.


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