Airway Subtleties in Critically Ill Patients

Airway Subtleties in Critically Ill Patients: Salicylate Poisoning, Hypotensive/Septic, and Obtunded DKA

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‘Fish in the oropharynx.’ Sim training on Kangaroo Island, rural Australia via KIDocs.org. Reposted with permission (thanks!).

Salicylate-Poisoned Patients

When salicylate-poisoned patients are ventilated using standard settings you may harm your patients by diminishing the respiratory alkalosis, which facilitates the passage of salicylate into the CNS. Also the use of sedatives and paralytics can result in CO2 retention and respiratory acidosis, which can further facilitate the shift of salicylate into the CNS.

Because of this many toxicologists believe that intubation should be avoided if possible and performed only if the patient has true respiratory failure (worsening acidosis, hypoxemia). Endotracheal intubation and mechanical ventilation can be associated with rapid worsening of clinical salicylate toxicity and increased mortality unless a normal or slightly alkalemic blood pH is maintained via hyperventilation and achievement of a low PCO2 and/or intravenous sodium bicarbonate.

The following are recommendations for salicylate-poisoned patients based on a retrospective case series using the New York City Poison Control Center (NYCPCC) database for cases of salicylate poisoning, defined as a peak serum concentration >50 mg/dL, who had mechanical ventilation:

  • Avoid intubation if possible. Intubation should only be performed if patient truly has respiratory failure (worsening acidosis, hypoxemia).
  • Ensure that alkalinization of plasma and urine are initiated early and prior to intubation if possible.
  • Avoid paralytics and high doses of sedatives during rapid sequence intubation. Try to minimize the time that patient’s ventilatory drive is compromised.
  • Place an arterial line for frequent blood gas monitoring.
  • Frequent blood gas monitoring to ensure that an appropriately high minute ventilation is achieved. The goal is to maintain an arterial pH of 7.5–7.6.
  • Consider pressure-controlled ventilation. Adjust the rate to obtain the desired minute ventilation. This will allow delivery of maximal tidal volumes while controlling peak airway pressures. Any mode can be used as long as physiologic goals are being met. Adjust the settings based on the arterial blood gas to achieve goal pH.
  • Monitor closely for ‘‘breath-stacking’’ and ventilator asynchrony due to tachypnea.
  • Collaboration with intensivist recommended.

Further Reading

  1. American College of Medical Toxicology, Guidance Document: Management Priorities in Salicylate Toxicity, Available at: http://www.acmt.net/cgi/page.cgi/zine_service.html?aid=4210&zine=show
  2. Stolbach AI, Hoffman RS, Nelson LS. Mechanical ventilation was associated with acidemia in a case series of salicylate-poisoned patients. Acad Emerg Med 2008;15(9):866-9.
  3. http://www.ncbi.nlm.nih.gov/pubmed/12705252

Sepsis-Induced ARDS

Sepsis is the leading cause of death in U.S. hospitals, affecting 750,000 Americans and killing between 28 and 50 percent of those people each year. Managing the airway and ventilation settings in a patient with sepsis-induced ARDS can be challenging. The following are guidelines from the Surviving Sepsis Campaign, a joint collaboration of the Society of Critical Care Medicine and the European Society of Intensive Care Medicine committed to reducing mortality from severe sepsis and septic shock worldwide.

Mechanical Ventilation

  • Target a tidal volume of 6 mL/kg predicted body weight in patients with sepsis-induced ARDS (grade 1A vs. 12 mL/kg).
  • Plateau pressures should be measured in patients with ARDS and initial upper limit goal in a passively inflated lung be ≤ 30 cm H2O (grade 1B).
  • Positive end-expiratory pressure (PEEP) should be applied to avoid alveolar collapse at end expiration (atelectotrauma) (grade 1B).
  • Strategies based on higher rather than lower levels of PEEP should be used for patients with sepsis-induced moderate or severe ARDS (grade 2C).
  • Recruitment maneuvers should be used in sepsis patients with severe refractory hypoxemia (grade 2C).
  • Prone positioning should be used in sepsis-induced ARDS patients with a PaO2/FiO2 ratio ≤100 mm Hg in facilities that have experience with such practices (grade 2B).
  • Mechanically ventilated sepsis patients should be maintained with the head of the bed elevated to 30-45 degrees to limit aspiration risk and to prevent the development of ventilator-associated pneumonia (grade 1B).
  • Noninvasive mask ventilation (NIV) should be used in that minority of sepsis-induced ARDS patients in whom the benefits of NIV have been carefully considered and are thought to outweigh the risks (grade 2B).
  • A weaning protocol should be in place and that mechanically ventilated patients with severe sepsis undergo spontaneous breathing trials regularly to evaluate the ability to discontinue mechanical ventilation when they satisfy the following criteria: a) arousable; b) hemodynamically stable (without vasopressor agents); c) no new potentially serious conditions; d) low ventilator and end-expiratory pressure requirements; and e) low FiO2 requirements which can be met safely delivered with a face mask or nasal cannula. If the spontaneous breathing trial is successful, consideration should be given for extubation (grade 1A).
  • Against the routine use of the pulmonary artery catheter for patients with sepsis-induced ARDS (grade 1A).
  • A conservative rather than liberal fluid strategy for patients with established sepsis-induced ARDS who do not have evidence of tissue hypoperfusion (grade 1C).

Sedation, Analgesia, and Neuromuscular Blockade in Sepsis

  • Continuous or intermittent sedation should be minimized in mechanically ventilated sepsis patients, targeting specific titration endpoints (grade 1B).
  • Neuromuscular blocking agents (NMBAs) should be avoided if possible in the septic patient without ARDS due to the risk of prolonged neuromuscular blockade following discontinuation. If NMBAs must be maintained, either intermittent bolus as required or continuous infusion with train-of-four monitoring of the depth of blockade should be used (grade 1C).
  • A short course of NMBA of not greater than 48 hours for patients with early sepsis-induced ARDS and a PaO2/FiO2 < 150 mm Hg (grade 2C).

Use of Etomidate

The Surviving Sepsis Campaign Guidelines also discourage the use of etomidate if adrenal suppression is suspected. “Although the clinical significance is not clear, it is now recognized that etomidate, when used for induction for intubation, will suppress the hypothalamic-pituitary-adrenal axis. Moreover, a subanalysis of the CORTICUS trial revealed that the use of etomidate before application of low-dose steroids was associated with an increased 28-day mortality rate. An inappropriately low random cortisol level (< 18μg/dL) in a patient with shock would be considered an indication for steroid therapy along traditional adrenal insufficiency guidelines.”

Further Reading

  1. Surviving Sepsis Campaign, International Guidelines for Management of Severe Sepsis and Septic Shock. Crit Care Med. 2013 Feb;41(2):580-637. Available at http://www.sccm.org/Documents/SSC-Guidelines.pdf
  2. http://www.ncbi.nlm.nih.gov/pubmed/23903852
  3. http://www.ncbi.nlm.nih.gov/pubmed/23859579
  4. http://www.ncbi.nlm.nih.gov/pubmed/21394520

Diabetic Ketoacidosis with Severe Metabolic Acidosis

Diabetic Ketoacidosis is very common and is responsible for more than 500,000 hospital days per year at an estimated cost of 2.4 billion USD. Patients in DKA can look terrible. They may be obtunded, hypotensive, have respiratory fatigue after compensating for a while with Kussmaul breaths, and may have underlying sepsis. Their electrolytes are usually off and they can have severe metabolic acidosis. Patients are usually breathing at a maximum for respiratory compensation and trying to intubate them using standard approaches can cause a period of apnea which can kill your patient who is dependent on that respiratory compensation.

Fluid Therapy

The ADA recommends a gradual correction of glucose and osmolality as well as the judicious use of isotonic or hypotonic saline, depending on serum sodium and the hemodynamic status of the patient. In the absence of cardiac compromise, isotonic saline (0.9% NaCl) is infused at a rate of 15–20 ml/kg during the first hour. Subsequent choice for fluid replacement depends on hemodynamics, the state of hydration, serum electrolyte levels, and urine output. In general, 0.45% NaCl infused at 250–500 ml/h is appropriate if the corrected serum sodium is normal or elevated; 0.9% NaCl at a similar rate is appropriate if corrected serum sodium is low.  Once the plasma glucose is 200 mg/dl, 5% dextrose should be added to replacement fluids to allow continued insulin administration until ketonemia is controlled while at the same time avoiding hypoglycemia.

VBG vs ABG

You can feel confident sending off a VBG instead of an ABG. A VBG gives you the same information as an ABG except for the PO2 and O2 sat, but we have our monitors that we can use instead to give us this information (EMRAP May 2013).

Electrolyte Repletion

After IVF the next step in management is electrolyte repletion, especially potassium. Repleting electrolytes should be done prior to starting a patient on an insulin drip.  The ADA recommends that potassium replacement should begin with fluid therapy, and insulin treatment should be delayed until potassium concentration is restored to >3.3 mEq/l to avoid life-threatening arrhythmias and respiratory muscle weakness. The ADA also recommends repleting phosphate to avoid cardiac and skeletal muscle weakness and respiratory depression due to hypophosphatemia.

Sodium Bicarbonate

The use of sodium bicarbonate is controversial. Studies have shown that it may have little effect on patient outcome and can actually cause harm by causing increased risk of hypokalemia, decreased tissue oxygen uptake, cerebral edema, and development of paradoxical central nervous system acidosis. The ADA recommends that adult patients with a pH <6.9 should receive 100 mmol sodium bicarbonate (two ampules) in 400 ml sterile water (an isotonic solution) with 20 mEq KCI administered at a rate of 200 ml/h for 2 h until the venous pH is >7.0. If the pH is still <7.0 after this is infused, they recommend repeating infusion every 2 h until pH reaches >7.0. Some believe that giving sodium bicarbonate won’t work as patients are already breathing at their maximum. Unless they blow off the bicarb-generated CO2, they won’t increase their pH significantly (EMCrit Episode 3; EMRAP May 2013).

Insulin Bolus vs Insulin Drip

The ADA recommends an insulin bolus for adults, but no bolus in pediatrics when you start an insulin infusion. Some recommend not giving the bolus since studies have shown that patients are more likely to have hypoglycemic episodes when started with a bolus and have no difference in the change of anion gap (EMRAP May 2013).

RSI Medications

In cases requiring intubation, the ADA recommends that the paralytic succinylcholine should not be used if hyperkalemia is suspected; it may acutely further elevate potassium.

Airway Pearls

In Scott Weingart’s EMCrit Episode 3 he describes his method for intubating a DKA patient with severe metabolic acidosis. For preoxygenation he recommends using the “pseudo-NIV technique,” which is placing a NIV mask on the patient and connecting it to a ventilator on SIMV mode to allow the patient to take spontaneous breaths. Below are notes from his podcast.

Vent Settings during Preoxygenation

  • Mode Volume SIMV
  • Vt 550 ml
  • FiO2 100%
  • Flow Rate 30 lpm “aim nice, slow breaths, over 1 second (on normal ventilator setting usually less <1sec)”
  • PSV 5-10
  • PEEP 5
  • RR 0 (most important part, pt breaths on their own)

Getting ready to intubate

  • Attach ETCO2 and observe value (try and keep this value at all times)
  • Push the RSI Meds
  • Turn the Resp Rate to 12 (note we are giving breaths at all times so there is no apneic period)
  • Perform jaw thrust (while the pt is still wearing the BiPAP mask)
  • Wait 45 seconds. This violates the tenets of RSI, but keeping the pt alive is probably more crucial right now.
  • Most experienced operator should intubate the patient (first pass success most important).
  • Attach the ventilator
  • Confirm tube placement by observing ETCO2
  • Immediately increase Respiratory Rate to 30
  • Change Vt to 8 cc/kg predicted IBW
  • Change Flow Rate to 60 lpm, this is the normal setting for intubated patients

Why 30 BPM? To maintain eucapnea (normal capnea) you need 60 cc/kg/min. After intubation you need 120 cc/kg/min (because of additional dead space) to stay at a PCO2 of 40. But we want a PCO2 of at least 20 so we need to double it so 240 cc/kg/min, which when divided by 8 cc/kg comes out to 30 BPM to get the tidal volume we need.

  • Make sure ETCO2 is at least as low as it was when you started
  • Check blood gas (check pH and pCO2)
  • Pat yourself on the back

Further Reading

  1. www.EMCrit.org, Episode 3, Intubating the Patient With Severe Metabolic Acidosis. Available at http://emcrit.org/podcasts/tube-severe-acidosis/
  2. www.EMRAP.org, May 2013 Episode, DKA Myths
  3. American Diabetic Association Consensus Statement, Kitabchi A, et al. Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care. 2009 July; 32(7): 1335–1343. Available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699725/
  4. Viallon A et al. Does bicarbonate therapy improve the management of severe diabetic ketoacidosis? Crit Care Med. 1999 Dec;27(12):2690-3.
  5. http://www.ncbi.nlm.nih.gov/pubmed/?term=%22DKA%22+%22intubation%22+%22emergency+medicine%22
  6. http://www.ncbi.nlm.nih.gov/pubmed/16911005
Edited by Alex Koyfman, MD

16 thoughts on “Airway Subtleties in Critically Ill Patients”

  1. Oi! Thats a pic from my resus room – the infamous ‘fish in the oropharynx’ sim (based on a real case, Weinberg et al if you google it)

    Not sure what has to do with salicyclate poisoning! You are of course welcome to use the photo, but pls acknowledge as from ‘sim training on Kangaroo Island, rural Australia via KIDocs.org’

    Many thanks

    1. It’s very cool to hear where the picture came from, and looks like a great sim case! I just put the acknowledgment in the caption. Sincere thanks for the permission, and we hope you liked the article. 🙂

  2. The case report on which this sim is based is fascinating , more details at

    http://kidocs.org/2013/08/warming-up-for-rural-masterclass/

    It’s referenced as Tam T et al BMJ Case Reports 2013 doi 10.1136/bcr-2013-010486 and tells the story of ‘accidental fish ingestion’ – until then universally fatal!

    “The bizarre mishap occurred when the 22-year-old, on a fishing trip to the Murray River, decided to pucker up and kiss his first catch of the day. Unimpressed by his romantic advances, the fish wriggled free and slid headfirst down the man’s throat, complete with fishing line and hook attached. Its fins and spines swiftly became hooked in his oesophageal and hypopharyngeal mucosa — defying multiple attempts to pull it out. What followed was a life-saving medical marathon, involving three hospitals, over 150km of driving and an array of quick-thinking doctors.

    “In severe respiratory distress, the man was first driven to the hospital in Barham, a country town of 1200 people on the NSW-Victorian border, where an emergency cricothyrotomy was performed.

    “With some oxygen getting in, but deteriorating fast, he was transferred to a larger regional hospital at Kerang, Victoria, where the only local GP with advanced airway training was called in to perform an orotracheal intubation. The procedure proved extremely tricky – the now-dead fish was completely obscuring the oropharynx — but a size 4 microlaryngoscopy tube was eventually squeezed past, allowing the patient to be properly ventilated at last.

    “But this was not the end of his woes: now surgeons at a third hospital, Bendigo, were left with the challenge of getting the dead critter out. In what is thought to be a unique procedure, they opted to cut off the fish’s tail and core out its upper body with a bone rongeur. This “collapsed” the remaining part of the fish, so scissors could be passed down its side to snip the scales and spines that were holding it in place. The leftover carcass was eventually pulled out with forceps.

    “Dr Laurence Weinberg, who reported the case this week, said to his knowledge it was the only Australian case of airway obstruction caused by a whole live fish. Similar cases from overseas had all proven fatal. The man developed aspiration pneumonia and sepsis, and spent eight days in hospital, but has since made a complete recovery.”

  3. Nice post on tough topic. My concern with intubating patients with ASA overdose is a bit different. They have metabolic acidosis with concomitant respiratory alkalosis from hyperventilation. Paralysis leads to apnea and CO2 retention. Even a brief period of apnea can lead to rising PaCO2 and lethal acidosis. These patients will often have a peri-intubation arrest from this critical acidemia. Additionally, even after a successful intubation, ventilatory strategy must mimic preintubation conditions. High respiratory rates are necessary to keep the PaCO2 low to counterbalance that metabolic acidosis.

    1. ‘Paralysis leads to apnea and CO2 retention. Even a brief period of apnea can lead to rising PaCO2 and lethal acidosis.’

      Is there real evidence that the PaCO2 in any type of severe acidosis significantly rises during a period of apnea? I tried searching for this but I can’t find any data. What I’m specifically asking is if during the 1-2 minutes of apnea — how much will the PaCO2 increase? If it’s 20, that’s a drop of pH of 0.16 (0.08 decrease ~ 10 mmHg CO2 increase), does this make a clinically significant difference? Most of the studies and papers on this mention ‘post-intubation ventilatory rates’ as the may factor leading to arrest. I can’t find any data to support the above statement and my ICU attendings have never thought it to be as big of a deal as it is made out in EM.

      1. ‘breathing at a maximum for respiratory compensation and trying to intubate them using standard approaches can cause a period of apnea which can kill your patient who is dependent on that respiratory compensation.’

        This is the same concept — wondering if there’s evidence to make this universal statement. Is it 1-2 minutes of apnea or 5 minutes, etc.

        I don’t want people to read this and take away from it ‘never intubate a severely acidotic patient because I might kill them’ because not intubating that same patient can cause harm and possibly kill them as well.

        1. Matt, a reasonable point. I’ve never seen any lit on it either. I agree that people should not take away the idea that they shouldn’t intubate these patients but rather that caution, preparation and expectation are vital.

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