ACEP Clinical Policy on Acute VTE 2018

The evaluation and management of venous thromboembolism (VTE) in the Emergency Department (ED) is fraught with questions: who should I evaluate, who should get a d-dimer, what should the d-dimer threshold be etc. Answers, unfortunately, are far less common. Due to the enormous volume of literature produced on the topic, it can be difficult for individual clinicians to incorporate all of the information into a comprehensive approach. The ACEP policy subcommittee has taken this job on for the rest of us. This clinical policy addresses five critical questions but does so over 51 pages. We’ve boiled down the major points here.

ACEP Clinical Policies Subcommittee. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department with Suspected Acute Venous Thromboembolic Disease. Ann Emerg Med 2018; 71(5): e59-109. PMID: 29681319

Classes of Evidence

  • Level A Recommendations: Generally accepted principles for patient care that reflect a high degree of clinical certainty (eg, based on evidence from 1 or more Class of Evidence I or multiple Class of Evidence II studies).
  • Level B Recommendations: Recommendations for patient care that may identify a particular strategy or range of strategies that reflect moderate clinical certainty (eg, based on evidence from 1 or more Class of Evidence II studies or strong consensus of Class of Evidence III studies).
  • Level C Recommendations: Recommendations for patient care that are based on evidence from Class of Evidence III studies or, in the absence of any adequate published literature, based on expert consensus. In instances where consensus recommendations are made, “consensus” is placed in parentheses at the end of the recommendation.

Critical Question #1: In adult patients with suspected PE, can a clinical prediction rule be used to identify a group of patients at very low risk for the diagnosis of PE for whom no additional diagnostic workup is required?

Level B Recommendation: For patients who are a low risk for acute PE, use the PERC to exclude the diagnosis without further diagnostic testing.

Comment: A number of blog posts have looked at the PERC score developed by Jeff Kline in 2004. Prior to using this tool, the clinician must first establish that the patient is low risk for the diagnosis of PE. The initial pretest probability is often stated at 15% though many of the studies have a much lower incidence of PE (around 5-6%). Overall if the risk of PE is ~ 10% for your patient, a negative PERC brings the patient down to a 1.9% risk. This risk is below the testing threshold meaning that further evaluation is more likely to harm the patient that provide benefit.

The PROPER trial (RCT of PERC vs. standard assessment) was not included in this clinical policy (Freund 2018). This RCT demonstrated a very low risk of PE occurrence in low-risk patients who were negative by PERC (0.1% vs 0%). Additionally, imaging was reduced by 10% with application of the PERC criteria.

Some keys to applying the PERC:

  1. Do not apply to patients with no risk or high risk of PE based on your clinical assessment
  2. Be sure that you are using the rule in its entirety. It is most likely better to use a decision support program like MDCalc as opposed to relying on your memory

PERC Decision Tool (MDCalc.com)

Critical Question #2: In adult patients with low to intermediate pretest probability for acute PE, does a negative age-adjusted D-dimer result identify a group of patients at very low risk for the diagnosis of PE for whom no additional diagnostic workup is required?

Level B Recommendation: In patients older than 50 years deemed to be low or intermediate risk for acute PE, clinicians may use a negative age-adjusted D-dimer result to exclude the diagnosis of PE.

Comment: When used correctly, the D-dimer assay can be a valuable tool in risk stratifying patients in whom PE is a possibility. Though specificity of the test is poor, a normal D-dimer level virtually rules the diagnosis out. However, as patients age, higher baseline circulating levels of D-dimer are the norm. Therefore, the static cutoff of 500 FEU (or 250 DDU) may be inappropriate. Raising the D-dimer threshold with age, thus, can help to increase specificity of the test and reduce unnecessary advanced imaging (i.e. CTPA). Numerous studies (cited in these guidelines) demonstrate the safety of the age-adjusted D-dimer and this approach has been endorsed by the American College of Physicians and the European Society of Cardiology. For assays using FEUs with a cutoff of 500, age-adjustment is performed by multiplying the patients age X 10 and using this number as the upper limit of normal (i.e. a 85 year-old patients would have an age-adjusted cutoff of 850 FEU).

These guidelines additionally endorse using an age-adjustment of age X 5 for the DDU assay (standard cutoff 250 DDU). This recommendation is based off of a single study (Jaconeli 2017) which we have reviewed previously. Though a number of clinicians we have spoken with have already embraced age adjustment with the DDU assay, the presence of this in the ACEP guidelines provides important support for this approach.

Critical Question #3: In adult patients with sub-segmental PE, is it safe to withhold anticoagulation?

Level C Recommendation: Given the lack of evidence, anticoagulation treatment decisions for patients with sub segmental PE without associated DVT should be guided by individual patient risk provides and preferences [Consensus recommendation].

Comment: Multiple studies in recent years show that while more patients are being diagnosed with PE, those diagnoses and subsequent treatments have not changed overall patient outcomes. Advances in imaging technology may be to blame in part as smaller and smaller clots are able to be seen but increased workups are at least equally if not more responsible for this trend. Some small studies have shown an absence of bad outcomes in patients with isolated subsegmental PE without DVT but these studies are inadequate to base a broad recommendation on.

Critical Question #4: In adult patients diagnosed with acute PE, is initiation of anticoagulation and discharge from the ED safe?

Level C Recommendation: Selected patients with acute PE who are at low risk for adverse outcomes as determined by PESI, simplified PESI (sPESI), or the Hestia criteria may be safely discharged from the ED on anticoagulation with close outpatient follow up.

sPESI Tool (MDCalc.com)

Hestia Criteria

Comment: A number of countries outside the US routinely discharge hemodynamically stable patients from the ED on anticoagulation. In the past, the reliance on low-molecular weight heparin (LMWH) with transition to a vitamin K antagonist (VKA), often necessitated admission. However, the advent of novel oral anticoagulants (NOACs – rivaroxaban, apixaban, dabigatran, edoxaban) has changed this paradigm. Patients can now be started on a NOAC and rapidly achieve appropriate anticoagulation. The key is to identify patients who are at low risk for decompensation. Clinicians typically use the sPESI and Hestia scores in order to aid in these decisions.

The safety outcomes of interest (recurrent VTE, major hemorrhage, death) were comparable between those treated as inpatients and those treated as outpatients across the included studies.

Unfortunately, the Level C Recommendation in this clinical policy is unlikely to be strong enough to lead to a marked shift from admission to discharge home. Further research is necessary but, for now, careful selection of patients for outpatient management along with close follow up can be considered. Shared decision making with the patient may be helpful as well.

Critical Question #5: In adult patients diagnosed with acute lower extremity DVT who are discharged from the ED, is treatment with a NOAC safe and effective compared with treatment with LMWH and VKA?

Level B Recommendation: In selected patients diagnosed with acute DVT, a NOAC may be used as a safe and effective treatment alternative to LMWH/VKA.

Level C Recommendation: Selected patients with acute DVT may be safely treated with a NOAC and directly discharged from the ED.

Comment: While the LMWH/VKA approach to DVT treatment is tried and true, it is complicated by requiring frequent INR testing and dietary restrictions. Many patients spend significant periods of time outside of the therapeutic window (both over and under-anticoagulated). The NOACs appear to have solved this problem. The studies we have on the drugs show non-inferiority to LMWH/VKA with reduced major bleeding and nonmajor bleeding.   Most patients can be started on this drug although the “-xabans” are contraindicated at differing renal function levels. Though only a level C recommendation is given for discharge from the ED, this is routine care for most patients (i.e. most DVTs aren’t being admitted for anticoagulation monitoring).

Take Home Points

  1. The PERC risk stratifies low risk PE patients (~10%) to a level low enough (1.9%) as to obviate the need for additional testing.
  2. Age-adjusted D-dimers are ready for use and it doesn’t matter if your assay uses FEU (cutoff 500) or DDU (cutoff 250). For FEU use an upper limit of 10 X age and for DDU use an upper limit of 5 X age.
  3. For now, subsegmental PEs should continue to routinely be anticoagulated even in the absence of a DVT. Keep an eye out for more research on this area.
  4. Although outpatient management of select PE patients (using sPESI or Hestia criteria) may be standard practice, the evidence wasn’t strong enough for ACEP to give it’s support
  5. Patients with DVT can be started on a NOAC and discharged from the ED

Read More:

References:

  1. Jaconelli T, Eragat M, Crane S. Can an age-adjusted D-dimer level be adopted in managing venous thromboembolism in the emergency department? A retrospective cohort study. European journal of emergency medicine : official journal of the Eur Soc Emerg Med. 2017. PMID: 28079562
  2. Freund Y et al. Effect of the Pulmonary Embolism Rule-Out Criteria on Subsequent Thromboembolic Events Among Low-Risk Emergency Department Patients: The PROPER Randomized Clinical Trial. JAMA 2018; 319(6): 559-66. PMID: 29450523

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

The post ACEP Clinical Policy on Acute VTE 2018 appeared first on R.E.B.E.L. EM - Emergency Medicine Blog.

Simplifying Mechanical Ventilation – Part 2: Goals of Mechanical Ventilation & Factors Controlling Oxygenation and Ventilation

In part 1, we discussed that the ventilator can deliver 3 types of breaths: controlled, assisted or spontaneous breaths. These breaths can be delivered either by a set pressure or a set tidal volume. Then we closed with a discussion of the common ventilator modes, which is simply just combining all these types of breaths together.

There are many aspects to consider in post-intubation management such as hemodynamic variations, analgesia & sedation, confirmation of the correct position of your endotracheal tube, and setting up the ventilator based on your patients physiology. Too often physicians pay little or no attention to how our amazing respiratory therapists set up the ventilator. Respiratory therapists have expertise in setting up, weaning and trouble-shooting the ventilator, but clinicians need to communicate important clinical physiologic information and their goals for their patient on mechanical ventilation. If you don’t feel comfortable setting up the ventilator at this point you at the very least need to communicate with your respiratory therapist when the ventilator is being set up.

Before we can start spinning dials on the ventilator, I think it’s important to discuss the goals of mechanical ventilation, the factors that control oxygenation and ventilation (removal of carbon dioxide), and in the next few parts we will discuss the 3 main physiologies we need to consider before we can set up the ventilator.

As both a pediatric and adult critical care physician, I will discuss some of the pediatric considerations for mechanical ventilation, but the concepts I will discuss throughout will apply to both pediatric and adult patients.

Goal of Mechanical Ventilation:

The ventilator is not a magical therapy that makes patients better, but simply a supportive therapy used until more definitive therapies have time to work. Lets consider the practical indications for intubation and mechanical ventilation: (1) refractory hypoxemia, (2) increased work of breathing (3) apnea/hypopnea leading to inadequate ventilation (4) inability to protect their airway.

So the goals of mechanical ventilation are simply to provide adequate (not perfect) oxygenation and ventilation, reduce our patient’s work of breathing, and to minimize the damage to the lung caused by the ventilator known as ventilator induced lung injury (VILI).

 Oxygenation & Ventilation:

It has been classically taught that oxygenation is controlled by 2 main factors, PEEP or positive end expiratory pressure, and the fraction of inspired oxygen (fi02). Ventilation (removal of carbon dioxide) is also controlled by 2 main factors, tidal volume (Vt) and respiratory rate (RR). You can more simply say that ventilation is controlled by 1 factor, minute ventilation, which is simply the RR multiplied by Vt.

These facts are taught to help simplify the understanding of mechanical ventilation, but unfortunately can limit your understanding especially in grasping advanced modes or techniques specifically targeted to improve oxygenation in patients with Acute Respiratory Distress Syndrome (ARDS).

The truth is that the main determinants of oxygenation are your mean airway pressure (MAP) and fi02. Your mean airway pressure is the average pressure your lung is exposed to during mechanical ventilation both during inspiration and expiration. Mean airway pressure improves oxygenation by allowing the re-distribution of oxygen from highly compliant alveoli (more stretchy) too less compliant alveoli (stiffer).

When the ventilator delivers a breath, regardless of whether it’s a volume or pressure delivered breath, the mean airway pressure is increased and therefore improves oxygenation. Since oxygenation occurs by simple diffusion, it actually occurs throughout the respiratory cycle both during inspiration and expiration. It’s classically taught that the main factor besides fi02, controlling oxygenation is PEEP because our inspiratory to expiratory ratio (I:E) is typically 1:2 or 1:3 and therefore we spend more time in exhalation and at PEEP. Since more time is spent in exhalation, the expiratory pressure in the airways (PEEP) is more heavily weighted when calculating the mean airway pressure.

If this doesn’t make sense, think about another MAP that you are more familiar with, mean arterial pressure. Your ventricle spends more time in diastole than it does in systole, so your diastolic blood pressure is more heavily weighted when calculating the mean arterial blood pressure.   The systolic blood pressure is higher than the diastolic blood pressure, but your higher systolic blood pressure is maintained for much less time than your lower diastolic blood pressure. As a result, your mean arterial blood pressure is closer to your diastolic blood pressure.

To understand this analogy, you must think of ventricular systole, where the ventricle achieves a higher pressure (compared to diastolic pressure) for a shorter time (compared to diastolic time) similar to inspiration where your airway pressure is high (compared to your expiratory pressure/PEEP) but again, only stays high for a short period of time (compared to your time to expire). So our higher inspiratory pressure is maintained for a shorter period time compared to our lower expiratory pressure (PEEP), then our mean airway pressure is closer to the PEEP.

So why take the time to explain this? There are some ventilator maneuvers you can perform to increase oxygenation other than simply increase the fi02 and the PEEP. You can increase the inspiratory pressure and therefore increase the MAP, but that may cause barotrauma (high pressures that cause VILI) in the lungs and not the best idea. The other maneuver is to increase the inspiratory time, increasing the time at this higher inspiratory pressure (increased MAP) and helping to redistribute gas flow throughout the lungs and therefore improve oxygenation.

Figure 1: Mean Airway Pressure

You can actually lengthen the inspiratory time and maintain this higher inspiratory Pressure for longer periods of time to improve oxygenation. In fact, you can lengthen the inspiratory time to be equal to the expiratory time, which is called inverse ratio ventilation (IRV) a maneuver used in ARDS to improve oxygenation. Another advanced mode, which we haven’t discussed yet, is airway pressure release ventilation (APRV), which delivers higher pressures (P-High) for a longer time (T-High) with very short pauses (T-Low) at low pressure (P-Low) to help exhale carbon dioxide. These are more advanced techniques and modes to improve oxygenation.

PEEP, or optimal PEEP, is highly important for many reasons other than just increasing mean airway pressure. Setting PEEP optimally is important so that during expiration your alveoli do not collapse (atelectasis) which will help maintain adequate alveolar surface area for oxygen diffusion to continue. Also, optimal PEEP will prevent higher pressures from being delivered from the ventilator to have to re-open closed alveoli.

Recall, during part 1, we compared our lungs to a balloon and described how hard it is to initially start blowing up a balloon, but once you expand that balloon it take a lot less pressure to inflate that balloon after this initial phase. We used this to discuss the concept of airway resistance and PIP, but here I want you to think about it in the context of inadequate PEEP and atelectasis. If you are going to breath air in and out of a balloon over and over, it will make your life easier if you do not let the balloon completely deflate. If the balloon completes deflates in between breaths, then you will have to blow harder each time you attempt to re-inflate the balloon. The key is to keep some air in the balloon, keeping the balloon partial inflated, and then you will save energy, as you don’t have to overcome that initial resistance each time.

Now imagine you let your alveoli completely collapse between breaths (inadequate PEEP), this will not allow for adequate oxygenation during expiration and you have give more pressure just to open the alveoli let alone then expand the lung. This repetitive opening and closing of the alveoli will lead to shear stress or atelectotrauma (another form of VILI) and can worsen the patient’s lung injury.

Figure 2: Optimal PEEP

For More on this Topic Checkout:

Frank Lodeserto at REBEL EM: Simplifying Mechanical Ventilation – Part I

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

The post Simplifying Mechanical Ventilation – Part 2: Goals of Mechanical Ventilation & Factors Controlling Oxygenation and Ventilation appeared first on R.E.B.E.L. EM - Emergency Medicine Blog.

Salicylate Toxicity

Definition: Salicylate toxicity is characterized by a constellation of symptoms caused by acute or chronic overdose of salicylate containing compounds. The most common salicylate is aspirin, but the group also includes topical forms of salicylates, methyl salicylate (Oil of Wintergreen), and bismuth subsalicylate (such as in Pepto-Bismol).

Pathophysiology of Salicylate Toxicity

  • Basics
    • Aspirin is rapidly converted to salicylic acid.
    • The therapeutic range of salicylate concentration for anti-inflammatory effects is between 15 and 30 mg/dL.
    • Concentrations higher than 30mg/dL can be associated with signs and symptoms of toxicity
  • Salicylate Metabolism (Goldfrank’s Toxicology)

    Salicylic acid acts to uncouple oxidative phosphorylation, leading to accumulation of lactic acid and pyruvic acid, causing a primary elevated anion gap metabolic acidosis. (Figure 3 Oxidative Phosphorylation)

  • Salicylic acid also directly stimulates the respiratory drive in the medulla, leading to a primary respiratory alkalosis.
  • Salicylic acid is a weak acid: exists mostly in charged/ionized state at physiologic pH. As pH decreases, shifts more towards uncharged/ non-ionzed state and can cross blood-brain barrier to worsen neurotoxicity.
  • Neuroglycopenia (Thurston 1970)
    • Even at normal plasma glucose levels, salicylate toxicity causes decreased brain glucose due to uncoupling of oxidative phosphorylation and compensatory stimulation of brain glycolysis.
    • This can cause CNS effects of hypoglycemia at normal plasma glucose levels

Salicylate Effect on Oxidative Phosphorylation (http://www.derangedphysiology.com)

Signs and Symptoms/Presentation:

  • Tachypnea and hyperpnea: due to central stimulation of respiratory drive
  • Tinnitus: not completely understood mechanism, inhibition of COX and Na/K ATPase in ear. In the elderly, may see decreased hearing instead of tinnitus
  • Nausea/vomiting: disruption of mucosal barrier, local gastric irritation
  • CNS: uncoupling of neuronal oxidative phosphorylation and neuroglycopenia lead to confusion, altered mental status, seizures, coma
  • Hyperthermia, due to uncoupling of oxidative phosphorylation (this may represent a peri-mortem presentation)

Acute

  • Often present with known / intentional ingestion
  • Often younger patients without medical problems
  • Co-ingestants are common

Chronic

  • Often unintentional and not initially obvious overdose, older patients, salicylate usually used for chronic medical problem
  • Increased mortality, likely due to delay in diagnosis and underlying medical comorbidities

Differential Diagnosis: 

  • Anion gap metabolic acidosis
  • KULTS
    • Ketoacidosis (DKA, alcoholic ketoacidosis)
    • Uremia
    • Lactic acidosis
    • Toxins (ethylene glycol, methanol, metformin)
    • Salicylates
  • Consider the diagnosis in any elderly patient with altered mental status that is taking aspirin. Chronic salicylate toxicity is often confused with a simple UTI leading to delayed diagnosis

Diagnostics

  • Blood Gas (VBG or ABG)
    • Classical finding: primary metabolic acidosis with primary respiratory alkalosis
    • Winter’s Formula: In patient with primary metabolic acidosis, you must determine if decrease in CO2 is a compensation, or if there is another primary acid/base disturbance
    • Patients will often present with normal pH to slightly alkalemic.
    • Patients who are acidemic on presentation are more likely to be critically ill
  • BMP
    • Look for elevated anion gap metabolic acidosis
    • However, salicylate can interfere with lab assay for chloride, causing falsely elevated chloride and making it appear as though anion gap is normal
    • Acute kidney injury
    • Hypokalemia secondary to acidemia
  • Salicylate concentration: can give you an indication of how severe toxicity is and influence management considerations
  • Acetaminophen level (concomitant acetaminophen ingestion common in all overdoses)

Management

  • Alkalinization (Goldfrank’s Toxicology)

    Initial Management

    • Basics: ABC’s, IV, O2 (if hypoxic), cardiac monitor
    • GI decontamination: activated charcoal if patient awake and alert to tolerate
    • Alkalinization with Sodium Bicarbonate
      • Goal in treatment is to increase pH of both serum and urine to shift towards charged state to prevent neurotoxicity and enhance elimination through the urine. (Goldfrank 2015)
      • (Figure 2 Alkalinization)
      • Start with 1-2 mEq/kg bolus followed by a drip
      • Bicarb drip can be made with 3 ampules of NaHCO3(150 mEq) in one liter of D5W
      • Do not make bicarb drip with normal saline because this will be hypertonic solution due to sodium in sodium bicarbonate
      • Run bicarb drip at 1.5-2X maintenance fluid rate. These patients are fluid down and need to replace losses
      • Goal serum pH around 7.55, urine pH 8.0
      • No benefit of forced diuresis
    • Treat hypo or normoglycemia to prevent neuroglycopenia (Thurston 1970, Kuzak 2007)
      • No human studies showing a “goal” serum glucose concentration
      • If patient is altered, consider glucose supplementation regardless of serum glucose concentration
    • Treat hypokalemia to goal K of 5.5 mEq
            • If hypokalemia, renal tubules will reabsorb potassium ions in exchange for hydrogen ions
            • This prevents alkalinization of the urine
  • Airway and Respiratory Management (Mosier 2015)
    • Tachypnea alone is not an indication for intubation
      • Tachypnea and hyperpernea leads to respiratory alkalosis
      • This is necessary compensation for the metabolic acidosis
    • Avoid intubation if possible
      • Hypoventilation during the apneic period causes respiratory acidosis
      • Associated with peri-intubation period morbidity and possible cardiac arrest (Stolbach 2008)
    • Indications for airway management include hypoxia, pulmonary edema, hypoventilation/tiring out, worsening acidosis despite appropriate therapy
    • Give bicarb 1-2 mEq/kg bolus peri-intubation
    • Consider awake intubation or ketamine facilitated intubation to minimize or eliminate apneic time
    • Ventilator settings very important post-intubation
      • Need to match minute ventilation of patient pre-intubation to prevent respiratory acidosis
      • High tidal volumes and high rate needed
    • Frequent blood gas monitoring post-intubation, as well as need for frequent BMP, salicylate concentrations. Consider A-line placement
  • Hemodialysis (HD) (McCabe 2017)
    • If unable to appropriately alkalinize and eliminate salicylate with bicarbonate, HD may be indicated
    • Consult nephrology early to be able to ensure prompt HD
    • Indications include: persistent altered mental status, renal/hepatic/cardiac failure, persistent acidemia, and requiring intubation
    • No definite cutoff for salicylate concentration requiring HD, however acute toxicity patients with concentrations greater than 80 or 100 mg/dL will likely require HD
    • In chronic salicylate toxicity, may require HD at much lower levels

Take Home Points:

  • Always consider salicylate toxicity
    • In patients with tachypnea, hyperpnea, AMS and clear lungs
    • In the presence of an anion gap metabolic acidosis with a respiratory alkalosis
  • Treat salicylate toxicity by alkalinizing the blood and urine to increase excretion
  • Avoid intubation until absolutely necessary. If you do have to intubate, minimize apneic time and consider awake intubation and nake sure your ventilator settings match the patient’s necessary high minute ventilation
  • Think about chronic salicylate toxicity in unexplained altered mental status, tachypnea or metabolic acidosis in elderly
  • Know indications for hemodialysis in salicylate toxic patients

Guest Post By

Max Berger
PGY2 Resident
Bellevue/NYU Emergency Medicine Department

Guest Peer Reviewed By

Rana Biary MD
Assistant Professor of EM
Board Certified Toxicologist and the director of the NYU School of Medicine Toxicology Fellowship

Read More:

References:

  1. Anderson, RJ et al. Unrecognized adult salicylate intoxication. Ann Intern Med 1976; 85: 745-748. PMID 999110
  2. Goldberg, MA. Barlow, CF. Roth, LJ. The Effects of Carbon Dioxide on the Entry and Accumulation of Drugs in the Central Nervous System. J Pharmacol Exp Ther. (1961) 131: 308-318. PMID 13706469
  3. Hoffman, RS. Howland, MA.  Lewin, NA.. Nelson, LS. Goldfrank LR. Goldfranks’s Toxicologic Emergencies (10th ed.) New York: McGraw-Hill Education. 516-527.
  4. Kuzak N. Brubacher JR. Kennedy JR. Reversal of saliycate –induced euglycemic delirium with dextrose. Clinical Toxicology. 45:5; 526-529. PMID 17503260
  5. McCabe, D et al. The association of hemodialysis and survival in intubated salicylate-poisoned patients. Am J Emerg Med 2017; 35: 899-903. PMID 28438446
  6. Temple AR. Acute and Chronic Effects of Aspirin Toxicity and Their Treatment. Arch Intern Med 1981; 141: 364-369. PMID 7469627
  7. Thurston JH et al. Reduced brain glucose with normal plasma glucose in salicylate poisoning. J Clin Invest. 1970: 49 (11); 2139-45. PMID 4319971
  8. Stolbach, AI. Hoffman, RS. Nelson, LS. Mechanical Ventilation Was Associated with Acidemia in a Case Series of Salicylate-poisoned Patients. Soc Acad Emerg Med 2008; 866-869. PMID 18821862
  9. Mosier JM et al. The physiologically difficult airway. West J Emerg Med 2015; 16(7): 1109-17. PMID: 26759664

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie) and Anand Swaminathan, MD (Twitter: @EMSwami)

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