EM Cases: Decision Making in EM – Cognitive Debiasing, Situational Awareness & Preferred Error
Type 1 & Type 2 Cognitive Decision Making Systems & The Nature of Expertise
“The definition of experience is the capacity to make more and more mistakes with increasing confidence” – Walter Himmel
Type 1: The Intuitive/Reflexive System involves automatic decision making based on pattern recognition. It’s fast and requires little effort.
Type 2: The Analytical/Problem-Solving System is more critical and logical. It involves stepping back and thinking more carefully about the patient’s presentation. It involves estimating pretest probabilities, continuous self-questioning, and considering alternative diagnoses.
The traditional view of this decision making in EM model is that while reasoning will invariably try to default to the Type 1 intuitive/reflexive approach, the most economical and fastest mode, the key to successful decision making is to step back and think analytically when you realize that there are subtle inconsistencies that arise.
The current view of this decision making in EM model is that it’s not a matter of whether Type 2 is better than Type 1 but rather, how expert decision makers blend these two systems. Experts use their experience and past errors/mistakes to reflect on their knowledge and their biases and develop heuristics (cognitive short-cuts) and cognitive forcing strategies that allow them to use their Type 1 system for rapid decision making in EM rather than having to slow down using their Type 2 system.
The Nature of Expertise
“Experts tackle problems that increase their expertise, whereas non-experts tend to tackle problems for which they do not have to extend themselves.” – Carl Bereiter
Decision making in EM expertise comes about, not only through the acquisition of knowledge and gaining experience, but by actively using the knowledge they’ve acquired wisely. How does do we use knowledge wisely?
1. Reflect on your experience – learn from your mistakes by
following up on all but your trivial cases within a few days
developing your own personal heuristics based on on your experience
consider dictating your chart which forces you to reflect on your assessment and plan
before signing off the chart ensure that it has internal congruence – look for disconfirming evidence before you decide on a disposition
2. Understand your personal cognitive biases and your particular system’s biases
3. Employ cognitive debiasing strategies based on 1 and 2
* note that only using your experience without reflection can result in excessive confidence and insecurity which may lead to more errors
“It’s not what you know, it’s what you use– how do you use your knowledge? By developing better heuristics” – Walter Himmel
Cognitive Biases discussed in this Decision Making in EM Episode
Anchoring bias – locking on to a diagnosis early in the assessment and failing to adjust to new information
Diagnosis momentum – accepting a previous diagnosis without considering the differential diagnosis adequately
Confirmation bias – looking for evidence to support a pre-conceived opinion, rather than looking for dis-confirming information
Premature closure– once you have found one diagnosis (eg: a fracture on a set of x-rays) you stop to searching for others (eg: the second fracture on the same set of x-rays)
“Perception is not a passive process. Perception is an active one” – Walter Himmel
In order to identify and help mitigate some of these negative cognitive biases it is not enough to identify them. We must employ cognitive de-biasing strategies for effective decision making in EM.
Cognitive Forcing strategies can be general such as “rule out the most deadly diagnosis” or they can be be related to your own experience based on reflection on previous mistakes.
Examples of Cognitive Forcing Strategies discussed in this Decision Making in EM Episode
Missing trifascicular block on ECG – for any ECG that shows a Right Bundle Branch Block (RBBB), if the axis is pointing left then search for the findings of trifascicular block
Missing a Maisonneuve fracture – For any ankle injury, examine the proximal fibula for tenderness to assess for a Maisonneuve fracture
One important aspect of effective cognitive forcing strategies is to apply them across all clinical encounters of that kind.
Strategies to Mitigate Affective Bias & Decision Fatigue
Overlapping shift start times where the next doc arrives an hour before the first doc finishes
Casino shifts – preserves the anchor period (2am-6am when it is the most important for your circadian rhythm to get some sleep in order to adjust properly) and is associated with more total sleep, reduced sleep debt, shorter recovery time, reduced cognitive impairment, improved work performance and improved career longevity (listen to Episode 11 for details)
Mutual support of colleagues working at the same time, having 2 or more physicians at each resuscitation, and ‘calling a friend’ – asking for an opinion on a case from your colleague, especially when you are at or near the end of your shift and suffering from decision fatigue
Decision Density and Anticipatory Guidance in Resuscitation Management
Human cognition has its limits. There is good evidence to suggest that our brains are not designed to function well during critical events in which multiple points of potentially unrelated information need to processed rapidly.
In critical and stressful situations we tend to ‘tunnel down’ on the task at hand and become less receptive to extraneous information that may be important. Our ability to take in this information is reduced even more when we feel high degrees of stress.
As explained below, a high performance team in which tasks and decision making responsibilities are divided up in ateam huddle, having 2 doctors rather than one at every resuscitation, improving your situational awareness, andstress inoculation training can mitigate the problem of high decision density in stressful situations by cognitive unloading and managing the negative influence of stress effectively.
Mental Rehearsal & Anticipatory Guidance
Practicing or visualizing procedures ‘in your head’ (psychophysical rehearsal) before you do them has been shown to improve performance and success of procedural tasks. There is also some evidence to suggest that it may improve team performance in team-based trauma resuscitation.
The Team Huddle
Take a few minutes when you get the call from EMS about a patient who will soon be arriving in your ED to do a team huddle: predict the potential diagnoses, delegate roles, expectations and responsibilities, think about logistics in your hospital, anticipate which procedures might be necessary and set up the appropriate gear for them.
There is a powerful effect on your team of stating the obvious (e.g. “this patient is in septic shock and they will get worse unless we do x, y and z”).
Anticipatory guidance and team communication is important not only in resuscitation, but in all ED patient encounters. Consider discussing with the nurse and the rest of your team what you think the most likely diagnosis is, what you’re worried about, what your management plan is and what you think the disposition might be, rather than only filling out orders for the nurses. This allows everyone to ‘be on the same page’ and may improve efficiency as well as decrease medical error.
Situational Awareness Checklist
(adapted from ‘Situational Awareness and Patient Safety – A Short Primer’ from The Royal College of Physicians and Surgeons of Canada website)
1. Get Information
Scan and search: be proactive – look for it in your environment or solicit it from your team.
Remain watchful: expect the unexpected
Communicate: openly talk about your thoughts on the situation with your team, the patient and their family
2. Understand the information
Compare: Compare the information to what you know and what you expected
Critique: Think critically about the information – check information integrity (accuracy, completeness, source, and relevance)
3. Think Ahead
Extrapolate and project: beyond the “now”: How will the situation unfold if the current conditions persist? Persist for how long?
Ask “what if?”: Consider various outcomes and contingencies and communicate those possibilities to others
To Act or Not to Act – That is the question: Preferred error & Resilience
From emupdates by Reuben Strayer
Preferred error describes balancing the risks of action vs inaction based on the potential positive vs negative outcome of either. It begs you to consider the consequences of being wrong on both sides of the decision, and determine which course of action fails better. Factoring in how likely you are to be wrong is important in weighing the potential outcomes.
For a detailed explanation of the concept of preferred error visit emupdates
Building Resilience & Stress Inoculation Training
3 steps to building resilience
(adapted from the Harvard Business Review)
Have an accurate understanding of the situation that you’re facing
Give it meaning or purpose
Be prepared to do what ever it takes regardless of the outcome, success or failure
Stress Inoculation Training
The goal of Stress Inoculation Training is to limit the impact of acute stress on performance.
Stress Inoculation Training promotes stress resilience by desensitizing the person to the negative behavioural and physiologic effects of acute stress in a simulated environment. A step-wise process involves increasingly stressful situations in a simulation training environment. During the debriefing period of the simulation the triggers of stress are identified and understood. Then, strategies to minimize the physiologic and behavioural consequences of stress are rehearsed so that the person is better prepared for similarly stressful situations.
Quote of the Month
“The value of experience is not in seeing much, but is in seeing wisely” -William Osler
Key References on Decision Making in EM
Bereiter, C. Scardamalia, M. Surpassing ourselves: An inquiry into the nature and implications of expertise. Open Court Publishing Company. 1993, 77-120.
Chanmugam, A. Avoiding Common Errors in the Emergency Department, Chapter 78: Understand decision-making fatigue and how it influences your clinical judgement, 2010.
Crosskerry, P. The Importance of Cognitive Errors in Diagnosis and Strategies to Minimize Them. Academic Med. August 2003, 1-6.
Crosskerry, P et al. Patient Safety in Emergency Medicine. Lippincott Williams & Wilkins, 2009.
Lorello GR, Hicks CM, Ahmed SA, Unger Z, Chandra D, Hayter MA. Mental practice: a simple tool to enhance team-based trauma resuscitation. CJEM. 2015:1-7.
Petrosoniak A, Hicks CM. Beyond crisis resource management: new frontiers in human factors training for acute care medicine. Curr Opin Anaesthesiol. 2013;26(6):699-706.
Parush A, et al. Situational Awareness and Patient Safety. The Royal College of Physicians and Surgeons of Canada. 2011. Link
Scott Weingart. EMCrit Podcast 49 – The Mind of a Resus Doc: Logistics over Strategy. Link
Reuben Strayer. The Preferred Error. Emergency Medicine Updates. June 11th, 2014. Link
Authors: Drew Long, BS (Vanderbilt University School of Medicine, US Army) and Brit Long, MD (@long_brit) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021)
A 33 y/o man is brought in by EMS after a witnessed tonic-clonic seizure. His vitals are notable for a HR of 124 and BP of 178/86. The patient states he is trying to cut down on his alcohol consumption due to pressure from his wife and hasn’t had a drink in over 24 hours. He is a social drinker and normally consumes “somewhere around 3-4 beers” each day in addition to “a little bit of vodka every now and then.” He appears anxious, has a severe tremor, and is unable to hold a glass of water without spilling its contents. The rest of the physical exam is unremarkable. What is the initial workup and management of this patient? Is he in alcohol withdrawal? What other conditions must be ruled out?
Alcohol use is extremely widespread throughout developed countries. It is estimated that 8 million people in the US are alcohol dependent.1 Approximately 20% of men and 10% of women will at some point in their lives have an alcohol-use disorder.2About half of people with alcohol-use disorders will have symptoms of withdrawal when they cut down or stop their alcohol consumption.3 Extreme complications, including seizures and/or delirium tremens, will occur in 3-5% of these people.3
Alcohol is a CNS depressant: it potentiates GABA receptors to enhance inhibitory tone in the brain and antagonizes the NMDA receptor to inhibit excitatory tone.1,4 Chronic alcohol exposure leads to brain adaptation to the effects of alcohol through changes in receptors. Chronic ethanol use leads to down-regulation and conformational changes of the GABA receptor. Additionally, in chronic alcoholics, NMDA receptors undergo conformational changes and up-regulation. These changes lead to an increased tolerance to ethanol, requiring higher blood alcohol levels to achieve the similar effects of intoxication.1,5-7
The underlying pathophysiology of acute alcohol withdrawal is CNS hyperexcitation.6 After the chronic alcoholic ceases alcohol consumption, they lose the GABA inhibitory effect and have a potentiation of NMDA excitatory effects. These effects lead to CNS hyperstimulation.
Differential Diagnosis and Evaluation
First and foremost, alcohol withdrawal syndrome (AWS) is a clinical diagnosis (cannot be confirmed by any laboratory tests) and a diagnosis of exclusion. Even in the withdrawing chronic alcoholic, the Emergency Physician must evaluate for an underlying process resulting in the patient’s presentation. It is vital to consider and rule out other pathologies that can mimic alcohol withdrawal syndrome (Table 1), while keeping in mind that chronic alcoholics are prone to malnutrition, trauma, and electrolyte abnormalities. At the same time, the Emergency Physician must strive to recognize AWS early to prevent progression of minor symptoms to life-threatening complications.
Table 1. Differential Diagnosis of Alcohol Withdrawal Syndrome6
Neuroleptic malignant syndrome
Sepsis and septic shock
The diagnosis of AWS is driven by the history and physical. The patient’s history of alcohol abuse, including amount of alcohol consumed per day in addition to number of years of alcohol use, must be quantified. The Emergency Physician should keep in mind that patients with alcohol use disorder commonly minimize their alcohol consumption. Furthermore, it is very important to recognize that a patient can have alcohol in their system and still be withdrawing. For example, if a patient typically has a basal alcohol level of 0.30 g/dL, then a serum level of 0.15 g/dL would be a significant reduction for this patient. The patient should also be asked why they decided to cease consumption of alcohol. A quick and easy method of screening a patient with a positive history of alcohol use is the CAGE questionnaire (http://www.mdcalc.com/cage-questions-for-alcohol-use/). The Emergency Physician should also inquire about illicit drug use.
In approaching the patient with alcohol withdrawal, the Emergency Physician should additionally consider underlying pathologies, such as pancreatitis or severe gastritis. In tachycardic patients, further evaluation for PE, MI, sepsis, or dehydration may be warranted.6
Testing in patients with suspected alcohol withdrawal syndrome should be driven by the differential diagnosis, in which the Emergency Physician should rule out mimicking or potential coexisting conditions. Helpful laboratory and imaging evaluations are shown in Table 2.
Table 2. Tests in AWS6
Serum pH and osmolality
CMP (evaluate for alcoholic hepatitis)
Serum salicylate and APAP levels
Ethanol level (controversial)
Coagulation panel (PT/INR, PTT)
A CBC may show pernicious anemia from vitamin B12 deficiency. The CMP may show hypokalemia, hypomagnesemia, hyponatremia, and/or elevated liver enzymes. Chronic alcoholics are prone to electrolyte abnormalities due to malnutrition and dehydration. In regards to LFTs, remember that in alcoholic hepatitis, AST is elevated to a greater degree than ALT. Especially if the patient is altered, a rapid glucose is necessary to evaluate for and if necessary correct hypoglycemia. If concerned with another ingestion, it is helpful to order serum salicylate and APAP levels. An ECG can assist in evaluating for ischemia or other toxic ingestions. If fever or hypoxia is present, a CXR is useful in ruling out pulmonary pathologies (most likely pneumonia). A head CT is warranted if there is a concern for any type of trauma or the patient is altered. Coagulation studies may reveal elevated INR.5,6
Stages of Withdrawal
Reductions in the concentration of alcohol in the blood lead to symptoms that are generally the opposite of the acute effects of alcohol intoxication. Symptoms from alcohol withdrawal usually start within 6-8 hours (after the blood alcohol level decreases), peak at 72 hours, and diminish by days 5 to 7 of abstinence.1,7 Broad withdrawal symptoms from alcohol include insomnia, anxiety, GI upset (nausea/vomiting), tremulousness, headache, diaphoresis, palpitations, increased body temperature, heart rate, and blood pressure.1,3 Of note, patients taking beta blockers or alpha-2 agonists may have blunted autonomic hyperactivity.5 If the patient’s withdrawal does not progress, these withdrawal symptoms will often resolve within 24 to 48 hours.8
Alcohol hallucinations generally occur 12-24 hours after the patient’s last drink.9 Alcoholic hallucinations occur in 7-8% of patients with AWS.10 These hallucinations are most commonly tactile but may also be visual. Importantly, alcoholic hallucinations can be differentiated from delirium tremens in that patients with alcoholic hallucinations will have an otherwise normal sensorium.
Withdrawal seizures generally occur 12-48 hours after the patient’s last drink.11 These seizures, while generalized tonic-clonic, are typically minor (isolated, short in duration, little post-ictal period). In the seizing alcoholic patient, alternative causes of seizures must be considered (i.e. infection, subdural hematoma, or metabolic abnormalities).6 Of note, AWS patients who have withdrawal seizures have a higher likelihood of progressing to delirium tremens, as 1/3 of patients with withdrawal seizures progress to DT.11
Delirium tremens (DT) is a rapid-onset, fluctuating disturbance of attention and cognition (sometimes with hallucinations) plus alcohol withdrawal symptoms and autonomic instability.5 DT occur in 3-5% of patients who are hospitalized for alcohol withdrawal.7,12,13 DT usually begins 3 days after the appearance of withdrawal symptoms and lasts for 1 to 8 days.7,14,15 The mortality of hospitalized patients with DT is currently estimated to be 1-4%.7,13-15 DT can be predicted by the following factors:16-18
History of previous DT
History of sustained drinking
CIWA scores > 15
Patients with SBP > 150, or patients with HR greater than 100
Recent withdrawal seizures
Prior withdrawal delirium or seizures
Recent misuse of other depressants
Concomitant medical problems
Like every patient presenting to the ED, the initial management for any patient with suspected alcohol withdrawal is the ABCs (airway, breathing, circulation). The mainstay of treatment of mild, moderate, and severe alcohol withdrawal is benzodiazepines.7,14,19 Benzodiazepines act as central GABAA agonists, addressing the underlying problem being alcohol withdrawal (CNS hyperexcitation). Benzodiazepines treat the psychomotor agitation experienced by withdrawing alcoholics in addition to preventing progression to more serious withdrawal symptoms. While benzodiazepines are the optimal treatment for AWS, there is debate regarding which benzodiazepine is best. No single benzodiazepine has been shown to be superior.
Four benzodiazepines to be aware of in the management of AWS are Valium (diazepam), Ativan (lorazepam), Versed (midazolam), and Librium (chlordiazepoxide). For acute symptom control, most clinicians prefer diazepam or lorazepam. Diazepam has a faster onset of action (1-5 minutes) compared to lorazepam (5-20 minutes), which may allow for easier titration and avoidance of dose stacking.20Diazepam also has active metabolites, nordazepam and oxazepam, which extend the duration of sedating effects. On the other hand, lorazepam has a short half-life and no active metabolites, which may help prevent prolonged effects of oversedation. Another benzodiazepine to consider is chlordiazepoxide, which is available in only oral format. Chlordiazepoxide has a slow onset of action and relatively long half-life, making it ideal for an outpatient setting. These properties also provide chlordiazepoxide with a lower potential for abuse. Table 3 compares various benzodiazepines in the treatment of AWS.
Table 3. Benzodiazepines for AWS6
Time to onset
1-5 min IV
10-20 mg IV
10-20 mg PO
5-20 min IV
2-4 mg IV
2-4 mg PO
2-5 min IM/IV
2-4 mg IM/IV
2-3 hrs PO
50-100 mg PO
The decision to give benzodiazepines is often based on symptom-triggered therapy, as evaluated by the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) scale. Symptom-triggered therapy was validated by Saitz et al in 1994. This study was a randomized double-blind controlled trial comparing patients receiving chlordiazepoxide for AWS with either a fixed schedule or symptom-triggered therapy. This study found patients in the symptom-triggered therapy group required less medication (median 100 vs. 425 mg) and a shorter treatment period (median 9 vs. 68 hours).21 The maximum score of the CIWA scale is 67. A mild score is 15 or less, moderate is 16-20, and severe withdrawal is a score greater than 20. For CIWA monitoring, evaluations as frequent as every 10-15 minutes may be appropriate for patients with severe AWS receiving treatment with benzodiazepines. Once symptoms are under control, hourly reassessment with CIWA is effective.22
For patients with severe AWS, repeating escalating doses of IV diazepam (20, 40, 80 mg) or lorazepam (2, 4, 8, 16 mg) are recommended. An escalating dose of diazepam can be given every 10-15 minutes as required, while an escalating dose of lorazepam can be given every 15-20 minutes as required. The clinician should utilize this regimen of escalating doses based on the patient’s vital signs and clinical appearance. For severe withdrawal, titrating benzodiazepines to achieve a state of somnolence with arousal to minimal stimulation is a reasonable goal. This method of escalating benzodiazepines dosing and front-loading has been shown to reduce seizures, DT, and the need for mechanical ventilation in patients with severe AWS.6,23,24
A pitfall to avoid in the management of AWS is attributing complications from AWS to another condition and administering the incorrect treatment. For example, in alcoholic hallucinosis, the management is benzodiazepines, with limited data showing that antipsychotics are actually detrimental in acute AWS.25For withdrawal seizures, there is no role for antiepileptic medications, and benzodiazepines are again the treatment of choice.26
A small subgroup of patients may have benzodiazepine-resistant alcohol withdrawal and DT. Early aggressive treatment of these patients is warranted, including fast escalation of doses of benzodiazepines.24A reasonable choice in these patients not responding to benzodiazepines is a barbiturate such as phenobarbital, which has been associated with a decrease in ICU admissions when utilized early in the course of management of AWS.27Additionally, intubation should be at the forefront of patients with severe AWS not responding to benzodiazepines, with propofol being ideal as an induction agent due to its GABA agonist and NMDA antagonist effects.28,29 Some preliminary evidence also supports the use of dexmedetomidine in these patients
Other therapies to consider in patients with AWS include re-orienting the patient to time, place, and date. The patient should be placed in a well-lit room, provided reassurance, receive frequent monitoring of vitals, and receive adequate volume resuscitation. Severe alcohol withdrawal has an important impact on a patient’s fluid and electrolyte status, and almost all patients with AWS are hypovolemic. In addition, thiamine and multivitamins should be given to the chronic alcoholic. Any electrolyte abnormalities should be corrected.
Disposition of the AWS patient depends on accurate identification of the patient’s degree of withdrawal. Patients who have a very mild CIWA score and are not currently intoxicated may be considered for discharge. On the other end of the spectrum, patients with severe AWS and/or medical comorbidities will need ICU admission. Table 4 outlines aspects to consider in the disposition of patients with AWS.
Table 4. Disposition for AWS6
Discharge with detoxification referral31
-CIWA Score <8
-Patient not currently intoxicated (alcohol or other drugs)
-No history of complicated AWS (seizures, hallucinosis, DT)
-No significant medical or psychiatric comorbidities
Inpatient detoxification or medical unit
-No underlying medical or surgical condition requiring ICU-level care
–Normalization or near-normalization of vitals in ED
-Responsive to 10-20 mg diazepam
–Tolerates 2-4 hours between benzodiazepine doses
-Presence of medical or psychiatric condition requiring inpatient admission
Intensive Care Unit
-Underlying medical or surgical condition requiring ICU-level care
-Patient requires >100-200 mg of diazepam to control symptoms in ED
-Requires benzodiazepines more frequently than every 2 hours
-Requires phenobarbital or other adjunctive therapy to control AWS
-Altered sensorium or recurrent seizures present
After your encounter with this patient, you remember that while he is likely going through alcohol withdrawal, this is a diagnosis of exclusion. You evaluate the patient for other etiologies of his seizure (including infection, subdural hemorrhage, and metabolic abnormalities). While considering other conditions, you place this patient on the CIWA scale, for which he scores 23. A head CT is negative for any abnormalities, and his laboratory analysis is remarkable for an AST of 92, ALT of 41, and Tbili of 5. His UDS comes back positive for cocaine and methamphetamine.
Due to his severe withdrawal as graded by the CIWA score, requirement for frequent monitoring and administration of benzodiazepines, he is admitted to the ICU for further management of his alcohol withdrawal.
The underlying pathophysiology of AWS is CNS hyperexcitation.
AWS is a diagnosis of exclusion; it is vital to rule out other mimicking conditions (including other toxins, head trauma, and sepsis).
AWS must be recognized early based on the presentation and history of alcohol use and cessation of alcohol consumption.
Patients can withdraw from alcohol even if they still have alcohol in their system
Stages of withdrawal include withdrawal symptoms, hallucinations, seizures, and delirium tremens.
Delirium tremens is a rapid-onset fluctuating disturbance of attention and cognition (sometimes with hallucinations) plus alcohol withdrawal symptoms and often autonomic instability. It usually begins about 3 days after the appearance of symptoms and can last anywhere from 1-8 days.
The mainstay of treatment for all stages of AWS is benzodiazepines.
Symptom-triggered therapy is recommended for dosing and administration of benzodiazepines.
Even in AWS patients who develop DT, early symptoms may be mild.
In the tachycardic alcoholic patient, be sure to consider PE, myocardial infarction, sepsis, dehydration, and other potential diagnoses other than AWS.
Alcoholics commonly present with a range of metabolic abnormalities, some of which can be life-threatening. Be sure to check for these abnormalities and correct as appropriate.
The presence of confusion or altered mentation in a patient with AWS may be due to DT and warrants admission to a higher level of care such as an ICU.
AWS is a diagnosis of exclusion: consider structural CNS pathology, metabolic abnormalities, infection, other toxicologic causes, and other conditions before diagnosing AWS.
A seizure in a patient with AWS who has never had a previous seizure warrants a complete neurological work-up and cranial imaging.
Patients with alcohol use disorder commonly minimize their alcohol consumption, often understating the true degree of how much alcohol they consume on a daily basis.
Benzodiazepines are always your first line treatment for alcohol withdrawal syndromes.
Kosten TR, O’Connor PG. Management of drug and alcohol withdrawal. N Engl J Med. 2003 May 1;348(18):1786-95.
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Schuckit MA. Recognition and management of withdrawal delirium (delirium tremens). N Engl J Med. 2014 November 371;22:2109-2113.
Yanta JH, Swartzentruber GS, Pizon AF. Alcohol withdrawal syndrome: Improving outcomes through early identification and aggressive treatment strategies. EB Medicine. 2015 June 17;6:1-20.
Mainerova B, Prasko J, Latalova K, et al. Alcohol withdrawal delirium—diagnosis, course and treatment. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2013;157:1-9.
Etherington JM. Emergency management of acute alcohol problems. Part 1: Uncomplicated withdrawal. Can Fam Physician. 1996;42:2186.
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Tsuang JW, Irwin MR, Smith TL, et al. Characteristics of men with alcoholic hallucinosis. 1994;89(1):73-78.
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Eyer F, Schuster T, Felgenhauer N, et al. Risk assessment of moderate to severe alcohol withdrawal—predictors for seizures and delirium tremens in the course of withdrawal. Alcohol Alcohol. 201146:427-33.
Berggren U, Fahlke C, Berglund KJ, Blennow K, Zetterberg H, Balldin J. Thrombocytopenia in early alcohol withdrawal is associated with development of delirium tremens or seizures. Alcohol Alcohol. 2009;44:382-6.
Mayo-Smith MF, Beecher LH, Fischer TL, et al. Management of alcohol withdrawal delirium: an evidence-based practice guideline. Arch Intern Med. 2004;164:1405-12.
Hjermo I, Anderson JE, Fink-Jensen A, Allerup P, Ulrichsen J. Phenobarbital versus diazepam for delirium tremens—a retrospective study. Dan Med Bull. 2010;57:A4169.
Cushman P Jr. Delirium tremens. Update on an old disorder. Postgrad Med. 1987;82(5):117.
Schuckit MA, Tipp JE, Reich T, Hesselbrock VM, Bucholz KK. The histories of withdrawal convulsions and delirium tremens in 1648 alcohol dependent subjects. 1995;90(10):1335.
Amato L, Minozzi S, Vecchi S, Davoli M. Benzodiazepines for alcohol withdrawal. Cochrane Database Syst Rev. 2010;3:CD005063.
Stehman CR, Mycyk MB. A rational approach to the treatment of alcohol withdrawal in the ED. Am J Emerg Med. 2013;31(4):734-742.
Saitz R, Mayo-Smith MF, Roberts MS, Redmond HA, Bernard DR, Calkins DR. Individualized treatment for alcohol withdrawal. A randomized double-blind controlled trial. JAMA. 1994;272(7):519.
Hoffman RS, Weinhouse GL. Management of moderate and severe alcohol withdrawal syndromes. UpToDate. 12 November 2015.
Muzyk AJ, Leung JG, Nelson S, et al. The role of diazepam loading for the treatment of alcohol withdrawal syndrome in hospitalized patients. Am J Addict. 2013 Mar-Apr;22(2):113-8.
Gold JA, Rimal B, Nolan A, et al. A strategy of escalating doses of benzodiazepines and phenobarbital administration reduces the need for mechanical ventilation in delirium tremens. Crit Care Med. 2007;35(3):724-730.
Kaim SC, Klett CJ, Rothfeld B. Treatment of the acute alcohol withdrawal state: a comparison of four drugs. Am J Psychiatry. 1969;125(12):1640-1646.
D’Onofrio G, Rathlev NK, Ulrich AS, et al. Lorazepam for the prevention of recurrent seizures related to alcohol. N Engl J Med. 1999;340(12):915-919.
Rosenson J, Clements C, Simon B, et al. Phenobarbital for acute alcohol withdrawal: a prospective randomized double-blind placebo-controlled study. J Emerg Med. 2013;44(3):592-598.
Hans P, Bonhomme V, Collette J, et al. Propofol protects cultured rat hippocampal neurons against N-methyl-D-aspartate receptor-mediated glutamate toxicity. J Neurosurg Anesthesiol. 1994;6(4):249-253.
Irifune M, Takarada T, Shumizu Y, et al. Propofol-induced anesthesia in mice is mediated by gamma-aminobutyric acid-A and excitatory amino acid receptors. Anesth Analg. 2003;97(2):424-429.
Tolonen J, Rossinen J, Alho H, Harjola VP. Dexmedetomidine in addition to benzodiazepine-based sedation in patients with alcohol withdrawal delirium. Eur J Emerg Med. 2013 Dec;20(6):425-7.
Asplund CA, Aaronson JW, Aaronson HE. 3 regimens for alcohol withdrawal and detoxification. J Fam Pract. 2004;53(7):545-554.
Arendt RM, Greenblatt DJ, deJong RH, et al. In vitro correlates of benzodiazepine cerebrospinal fluid uptake, pharmacodynamics action and peripheral distribution. J Pharmacol Exp Ther. 1983;227(1):98-106.
Authors: Captain William Dirkes (EM Resident Physician, Madigan Army Medical Center), Captain Joshua Kessler (EM Resident Physician, Madigan Army Medical Center), Lieutenant Colonel Jay Baker (EM Attending Physician, Madigan Army Medical Center), and Colonel Ian Wedmore (EM Attending Physician, Madigan Army Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021)
A 59 year-old male presented to the emergency department with a chief complaint of difficulty concentrating and loss of vision. He had presented to the same facility the day prior for chest pain, chills, and a cough. During his prior visit, the patient underwent a chest x-ray which demonstrated a consolidation suggestive of a lobar pneumonia and was subsequently discharged home with a prescription for Azithromycin as well as instructions to follow-up with his primary care doctor. However, he was unable to fill his prescription. Upon attempting to drive home, the patient was pulled over by law enforcement because he was acting “delirious.” Despite the traffic incident, he was allowed to return home. The patient reported that once he arrived at home he began bumping into furniture, experiencing difficulty with concentration, and suffered vision loss. In addition, he continued to experience chills, chest pain, and shortness of breath. He denied experiencing any abdominal pain, dysuria, focal numbness or weakness, headache, hematuria, hematochezia or melena, speech disturbances, or a rash. His medical history included diabetes, hypertension, hyperlipidemia, and an unprovoked DVT (deep venous thrombosis) approximately 5 months prior. He denied any surgical history. His medications included Atorvastatin, Lantus, Metformin, Rivaroxaban, Sitagliptin, and Telmisartan. He reported smoking a ½ pack of cigarettes per day for the last 15 years, consuming alcohol occasionally, and denied any current or prior illicit drug use.
His initial vital signs in the emergency department were a blood pressure of 150/95, a heart rate of 106, a respiratory rate of 24, an oxygen saturation of 95% on room air, and a temperature of 97.8F, taken temporally. His physical exam demonstrated a male appearing his stated age, in no apparent distress but with mild tachypnea, diminished breaths sounds in the left posterior lung fields, and no cardiac murmurs on auscultation. His neurologic examination demonstrated that he was alert and oriented, but had intermittent periods of confusion and difficulty with recall during the interview. His speech was normal and his cranial nerves were grossly intact. He had a right hemianopsia on visual confrontation. He had full strength in all of his extremities and normal sensation to light touch. No dysmetria on finger-nose testing and heel-shin was normal.
He underwent a non-contrasted computed tomography (CT) scan of his head which demonstrated multifocal cortical abnormalities concerning for embolic infarcts with a dense left middle cerebral artery sign indicative of an evolving territorial infarct. A portable chest x-ray demonstrated a moderate left lung pleural effusion and prompted further imaging to characterize the lesion. A CT pulmonary arteriogram demonstrated a segmental pulmonary embolism of the right lower lung lobe with an enhancing mediastinal mass concerning for malignancy in addition to the already visualized left-sided pleural effusion. Abnormal laboratory findings included a white blood cell count of 10.4 and a platelet count of 58. The remainder of the CBC was unremarkable and his lactate, liver function tests, coagulation panel, troponin, and urinalysis were within normal limits. His electrocardiogram demonstrated a normal sinus rhythm with a rate of 85 beats/minute.
He was admitted to the inpatient medicine service which included a neurology consultation. An inpatient MRI of his brain was obtained which demonstrated an acute ischemic infarct in the left parieto-occipital lobes. These findings were consistent with multiple chronic infarcts versus vasogenic edema possibly representing metastatic disease. A trans-esophageal echocardiogram demonstrated tricuspid vegetations. He was subsequently diagnosed with Non-Bacterial Thromboembolic Endocarditis (NBTE) and discharged home on the following day.
Non-Bacterial Thromboembolic Endocarditis (NBTE)
NBTE is also known as Libman-Sacks Endocarditis or formerly, as Marantic Endocarditis. It is a rare condition, often diagnosed on autopsy, most often found between the fourth and eighth decades of life. [1, 2, 4] NBTE is the result of platelet and/or fibrin aggregation on a heart valve secondary to an underlying hypercoagulable state. Usually, the hypercoagulable state is induced by a metastatic process or rheumatologic condition such as Systemic Lupus Erythematosus (SLE), Anti-Phospholipid Syndrome, or Rheumatoid Arthritis. [1-3] These disorders are known to have a higher prevalence in female patient populations (approximately 5-9 times their male counterparts), more specifically in African American and Hispanic ethnicities. As such, the clinician should maintain a higher degree of suspicion when treating these patient populations. Unlike bacterial vegetations, the vegetations of NBTE are symmetric with a smooth or verrucoid texture and contain little evidence of polymorphonuclear leukocytes, microorganisms, or inflammation. The disease affects the heart valves with the following predilection: aortic valve > mitral valve > tricuspid valve > pulmonary valve. Clinically, the disease presents with embolic events including stroke, delirium, pulmonary embolism, renal/splenic infarction, acute myocardial infarction, digital ischemia, and/or rash. Because of the non-invasive nature of NBTE, clinical examination may or may not reveal a new cardiac murmur. An embolic stroke may be the initial presentation to suggest a diagnosis of NBTE and if the clinician is suspicious, an Echocardiogram should be obtained to assess for valvular lesions. Emergency Department management should include evaluation for Disseminated Intravascular Coagulation (obtaining coagulation panel, d-dimer, fibrinogen), as this complication has been found in 18% of cases of NBTE.
Treatment of NBTE consists of anti-coagulation and therapy directed at the underlying metastatic process or rhematoogical condition. Unfractionated heparin should be the anti-coagulant employed as warfarin is less effective and has been associated with increased rates of thromboembolic events. Novel anticoagulants, such as Dabigatran, Apixaban and Rivaroxaban, should also be avoided as they have not been evaluated for use in this disease process. Surgical intervention may be considered in select cases where the risk-benefit ratio is favorable. Anticoagulation should be continued indefinitely, since recurrent thromboembolism has occurred in patients following its discontinuation.  The indications for surgical intervention in NBTE are similar to those in infective endocarditis, namely heart failure, valve rupture, and most commonly recurrent embolization despite anticoagulation. Follow-up should be considered on an individual basis. However, patients should be monitored for known complications of NBTE, specifically infective endocarditis and emobilzation despite anticoagulation. Additionally, Echocardiogram 6 weeks to 3 months after initiation should be considered to follow the progression or resolution of valvular vegetations. Prognosis is generally grim despite anticoagulation due to the underlying predisposing medical condition rather than NBTE itself; a strong association between advanced malignancy and NBTE has been demonstrated in retrospective studies. Similarly, in patients with SLE, a longitudinal, cross-sectional study reports poor outcomes due to recurrent embolic events (25%), cognitive disability (24%) and death (9%). 
el-Shami, K, Griffiths, E, and Streiff, M. Nonbacterial Thrombotic Endocarditis in Cancer Patients: Pathogenesis, Diagnosis, and Treatment. The Oncologist. 2007;12:518-23.
Evan Miller, DO (EM Resident Physician, Allegheny General Hospital) and Maxim Dzeba, MD (EM Attending Physician, Allegheny General Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021)
You are the overnight senior resident in the ED managing a 27 year-old asthmatic male who has been in respiratory distress for the past few hours. You make the decision to intubate given the patient’s declining mental status and increasing fatigue. The respiratory therapist asks if you want to set the patient’s respiratory rate at his current 24 breaths per minute.
You received sign-out from the day resident about an intubated patient in room 5. The patient is an 81 year-old female who presented seven hours prior and was intubated after being diagnosed with severe sepsis due to pneumonia. The patient’s blood pressure has been steadily decreasing and repeat chest xray showed diffuse bilateral opacities which was worse than prior imaging. The patient is 80 kg and 5’3” tall. She was started on VCV rate 14, tidal volume 600, PEEP 10, FiO2 80%. Are these the correct settings?
Your overnight junior calls for your help with his decompensating intubated patient. The patient is a 54 year-old male with a history of COPD who was intubated ten minutes ago. The ventilator is alarming due to high pressures. The patient’s current vitals are HR 140, BP 80/50, SpO2 82%. The ventilator settings are VCV rate 12, tidal volume 450, PEEP 15, FiO2 100%. You quickly disconnect the circuit but the patient is not improving. What do you do next?
As you are managing these critical patients, a nurse tells you that the 16 year-old female in room 1 who was intubated for airway protection for a suspected drug-induced encephalopathy has a low pressure alarm. You enter the room and see an obese young female who is bucking the vent and thrashing around. You perform an inspiratory pause and find the plateau pressure to be low with a continuously low peak pressure.
The care of critically ill, mechanically ventilated (MV) patients is essential to the practice of emergency medicine. While emergency physicians are experts at securing even the most difficult airways, much less time is spent on learning the intricacies of mechanical ventilation. Increasing emergency department (ED) boarding time has been associated with negative outcomes.1Fuller et al (2015) found emergency physicians had suboptimal adherence to best practice guidelines for mechanically ventilated patients in the ED. This was correlated with increased intensive care unit (ICU) length of stay (LOS) and higher rates of morbidity and mortality. In that study the median ED LOS was 3.4 hours with a range of 1.1 to 18.3 hours. Due to this increased ED LOS, it is imperative ED physicians are comfortable with initial ventilator settings, best practices, and perhaps the most difficult yet most important task of ventilator troubleshooting.2
Basics of Mechanical Ventilation
Indications and Pathophysiology
The emergency physician will intubate for one of four main reasons: a) inability to ventilate; b) inability to oxygenate; c) anticipated clinical course; and d) airway protection.3
There are two main goals of respiration: supplying oxygen demand and eliminating carbon dioxide (CO2). Ventilation is defined as the elimination of CO2 from the body. Adequate ventilation is matching minute ventilation with metabolic demand, while hypoventilation is the inability to keep up with metabolic demand resulting in hypercapnia and eventually acidosis.
Minute ventilation (VE) is the measurement of air inhaled or exhaled per minute and is found by multiplying the respiratory rate (RR) by the tidal volume (VT) [VE = RR x VT]. When dealing with a patient who was intubated for inability to ventilate, these two parameters (RR, VT) can be modified to correct the hypoventilation. Common causes of low RR include any CNS depressant/injury, while causes of low VT include poor respiratory muscle contraction due to neuromuscular disorders or poor chest wall mechanics.4
Oxygenation is any process that leads to the delivery of O2 to the tissues. There are many causes of hypoxemia including low inspired FiO2 (altitude, medical error), V/Q mismatch, hypoventilation, diffusion defect, and low mixed venous oxygen.5 Shunt and dead space ventilation are the two major mechanisms that cause significant abnormalities in gas exchange.
Shunt is perfusion without ventilation. This occurs when the blood passes from the right heart to the left heart without passing any areas of ventilation. An intra-cardiac right to left shunt is an easy representation of this. Intrapulmonary causes include consolidation, pulmonary edema, and atelectasis. In these situations, increasing the FiO2 to 100% will not improve the oxygenation as the blood is not being exposed to areas of ventilation. The treatment for shunt induced hypoxemic respiratory failure is positive end expiratory pressure (PEEP).6,7 PEEP recruits collapsed alveoli and works to decrease the shunted areas. One method to determine the proper amount of PEEP is to use the Acute Respiratory Distress Syndrome Network (ARDSNet) PEEP/FiO2 table (http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf). Ideally, the goal is to use the lowest amount of PEEP to maintain an oxygen saturation of 88 – 95%.8
Dead space is any area of ventilation without perfusion. The traditional example of dead space is seen with a massive pulmonary embolism, but this can also be seen in cases of low cardiac output. Iatrogenic causes of dead space include alveoli over distension secondary to breath-stacking in an intubated COPD patient. Increased dead space can lead to both hypoxemia and hypercapnia.4
Modes and variables
There are several different modes and variables to understand when setting up MV.
Breath types: There are three main types of breaths that a ventilator can supply. The most basic is a mandatory breath which is initiated, controlled, and ended by the machine itself. The second type is an assisted breath which is initiated by the patient but controlled and ended by the machine (based on variables set by the provider). The third type is a spontaneous breath which is initiated, controlled, and ended by the patient.
Trigger: An assisted breath is triggered by a set negative airway pressure or flow. When an intubated patient attempts to take a breath, the negative pressure or change in flow is sensed by the vent and a breath is delivered. This setting is generally standard and not often manipulated by ED physicians.
Cycle: The cycle is the main distinction between ventilator modes. The “cycling” is when the ventilator switches from inspiration to expiration. Volume-cycled: the machine delivers a set volume at which point it stops the flow and allows for expiration. Pressure-cycled: the machine delivers a breath until it reaches a set pressure at which point it stops the flow and allows for expiration. The volume will vary with each breath depending on lung compliance.
Respiratory rate: This variable sets a minimum number of breaths that must be given per minute. For example, in an assist mode, if you set the rate at 12 the ventilator will break the minute up into 12 five second blocks. If the patient initiates a breath during these five seconds, the ventilator will count that breath. If the patient does not initiate a breath by that time, the ventilator will deliver a mandatory breath ensuring a minimum number of breaths per minute.9
Inspiratory to expiratory (I:E) ratio: This variable is a factor of the inspiratory time which is the VT divided by the flow rate (VT / FR). The standard flow rate is 60 L/min. The I:E can be increased by: 1) decreasing the tidal volume; 2) increasing the inspiratory flow; or 3) decreasing the respiratory rate. A normal I:E would be 1:2 or 1:3 vs. a patient with COPD where an appropriate I:E would be 1:4 or above.
Positive end-expiratory pressure: PEEP is used to increase functional residual capacity (FRC) by preventing alveolar collapse at the end of expiration and recruiting fluid filled or atelectatic alveoli. The starting PEEP is usually set at 5 cm H2O as this is believed to be equivalent to physiologic levels. In patients with ARDS, the PEEP is adjusted based on the PEEP / FiO2 tables.8
Fraction of inspired oxygen: FiO2 is usually started at 100% and is titrated down to a SpO2 of > 88% (or PaO2 > 55 mm Hg) with a goal FiO2 of < 60% as soon as possible.10 In patients who are intubated for airway protection and have no issues with ventilation or oxygenation, it is reasonable to start the FiO2 at lower levels. Increased FiO2 allows for a higher PAO2 at a low alveolar ventilation L/min.
Tidal Volume: VT is set in volume-cycled modes and is the minimum volume delivered per breath. It is important to note that the tidal volume should be calculate using the ideal body weight (aka predicted body weight) rather than the actual weight.
Predicted body weight (in kg) Males: 50 + 2.3 (height [inches] – 60) Females: 45.5 + 2.3 (height [inches] – 60)
Assist-control ventilation (ACV) provides the highest level of ventilatory support3. In this mode, every breath is supported by the ventilator, including any breaths above the set rate. ACV can be either volume-cycled (volume-targeted) or pressure-cycled (pressure-targeted).
In volume-cycled ACV the physician will establish a set VT to be delivered with each breath ensuring a minimum volume per breath. The trigger can either be an elapsed time (minimum set rate) or a spontaneous breath. Major disadvantages of this include auto-PEEP with associated lung injury (discussed later) and decreased cardiac output.
In pressure-cycled ACV the physician will establish a set rate, flow, and pressure. Each breath will cycle after the set pressure is reached thereby decreasing peak inspiratory pressure (discussed later). However the tidal volume is variable which each breath and is dependent upon the lung compliance.
Pressure-support ventilation (PSV) is used primary for weaning purposes or during stable ventilatory support periods. Each breath is patient-triggered and pressure-cycled. This mode provides extra pressure support to help the patient overcome the inherent resistance of the ventilator circuit.
Other available modes include synchronized intermittent mandatory ventilation, bilevel, and control mode ventilation.
General settings for initiation of MV using the “lung-protective” strategy are as follows:8,10
Assist control mode – volume-cycled
Tidal volume 6 mL/kg IBW
Alternatively starting at 8 mL/kg IBW and reducing by 1 mL/kg every 2 hours until tidal volume is 6 mL/kg4
RR 14-16 breaths/min (can titrate to a max of 35 to keep pH above 7.15)
FiO2 100% with rapid titration based on SpO2
PEEP 5 to 7 cm H2O
Keep plateau pressures below 30 cm H2O
For patients with contraindications for permissive hypercapnia (discussed below):
Tidal volume 8 mL/kg IBW
RR 12-20 breaths per minute
Acute Respiratory Distress Syndrome (ARDS)
Acute respiratory distress syndrome is a severe cause of hypoxemic respiratory failure. ARDS is caused by both direct and indirect lung injury which causes an exudative alveolar filling. This leads to a severe VQ mismatch. While ARDS is not commonly encountered in the ED due to its delayed time of onset, most patients that are intubated in the ED have significant risk factors for its development. These risk factors include severe sepsis, chest trauma, and pneumonia.
Historically, tidal volumes were set as 10-12 mL/kg even though the normal tidal volumes of spontaneous breathing is 5-7 mL/kg IBW. It was later discovered that these elevated volumes lead to alveolar over distension causing alveolar rupture and release of inflammatory cytokines. These effects in turn can lead to: 1) Barotrauma, which includes pneumothorax, pneumomediastinum, and pneumopericardium, occurs when the structural integrity of the alveolus is disrupted due to elevated transalveolar pressures; 2) Volutrauma is due to the overdistention of the alveolus resulting in lung parenchyma damage; and 3) Biotrauma which is a multi-organ injury due to the inflammatory cytokines.11
The high mortality of ARDS led to a randomized control trial performed by ARDSNet in 2000 which found a significant reduction in morbidity and mortality when volumes were set at 6 mL/kg IBW and plateau pressures were kept below 30 cm H2O.8 The low tidal volume strategy is designed to prevent worsening lung injury that could be caused by alveolar over-distension. These lower tidal volume are combined with higher respiratory rates to provide adequate minute ventilation.8
The lung-protective settings usually result in a retention of CO2 and therefore a degree of acidosis, this is referred to as permissive hypercapnia. Previously, MV was used to normalize arterial blood gas numbers, specifically the pH and arterial carbon dioxide tension (PaCO2). The current thought process is to minimize the risks of MV while still maintaining an adequate gas exchange. Permissive hypercapnia is acceptable as long as the pH remains above 7.15-7.20. If the pH falls below 7.15, you can increased the RR to a maximum of 30-35 breaths/min.10 Due to this acidosis, permissive hypercapnia is contraindicated in patients with acute brain injury, fulminant hepatic failure, severe pulmonary hypertension, or severe metabolic acidosis.9,13
Asthma and COPD
The major concern for mechanically ventilated patients with obstructive airway disease is dynamic hyperinflation (also known as auto-PEEP, intrinsic PEEP, breath stacking, or air trapping). This condition occurs when gas becomes trapped in the lungs during mechanical ventilation. The air trapping is caused by inadequate time for exhalation allowing for delivery of the next breath before the patient has time to completely exhale. This leads to increased alveolar pressures, decreased venous return, and decreased cardiac output ultimately leading to hemodynamic instability. Auto-PEEP can be detected on the ventilator waveform because the flow will not return to zero before the next breath (figure 1).
Strategies to avoid auto-PEEP would be any factor that increases the I:E ratio which include decreasing the respiratory rate and/or tidal volume, or increasing the inspiratory flow rate (the standard flow rate is 60 L/min, this can be increased up to 80-100 L/min).6 These factors allow more time for the patient to complete exhalation minimizing the risk of hyperinflation. In severe cases, deep sedation and paralysis may be necessary to improve ventilator synchrony and avoid auto-PEEP.11
Other special topics
Elevated intracranial pressure: Ii any case of elevated ICP, hypoxia and hypercapnia need to be avoided. Permissive hypercapnia is contraindicated due to association with cerebral vasodilatation which could lead to increased cerebral blood flow and therefore increased intracranial pressure.11
Severe metabolic acidosis: Patients with severe metabolic acidosis (e.g. diabetic ketoacidosis or salicylate toxicity) usually increase their minute ventilation to help compensate for the acidosis. This is usually accomplished by increasing their respiratory rate. When these patients are placed on MV, it is important to consider setting the RR close to the pre-intubation rate as well as closely monitoring the pH.6
Shock: High amounts of PEEP can result in increased intrathoracic pressures which decrease cardiac preload and exacerbate hypotension. Addressing volume status, preferably prior to intubation, and keeping PEEP at 5 cm H2O is advised.7
Troubleshooting the ventilator
General effects of intubation include:
Decreased venous return due to increased intrathoracic pressure
Maintaining endotracheal tube cuff pressure at 20 cm H2O
Placing a naso- or oro-gastric tube to avoid overdistention
Oxygen toxicity – the exact cause and mechanism is still controversial however supraphysiologic levels of oxygen has been associated with increased mortality and worse neurologic outcomes in post arrest patients
There is a broad differential in any mechanically ventilated distressed patient including anxiety and pain as well as tension pneumothorax and auto-PEEP. The first step is identifying the level of distress as well as the overall hemodynamic stability.
In a hemodynamically stable patient, a focused systematic approach can be safely utilized.7,15
1) Obtaining a history from the bedside staff – this includes reason for and difficulty of intubation, ETT depth, current ventilator settings, and any recent changes including ventilator settings, new medications, or invasive procedure attempts (e.g. chest tube, central line).
2) Performing a physical exam – this includes examining the ETT for migration, air leak, or kinking. This also includes assessing need for continued intubation. For example, if a previously healthy patient was intubated for airway protection for a suspected drug overdose and is now awake and following commands, weaning to extubate could be an option. Evaluation for equal breath sounds and chest rise should be performed as well. Assess for hypoxia via pulse oximetry and/or arterial blood gas.
3) Checking the ventilator – evaluate the patient’s synchrony with the machine as well as the waveform searching of possible auto-PEEP.
5) Examining a chest x-ray or bedside ultrasound – examine the chest x-ray for worsening clinical condition, pneumothorax, and ETT tube position. Bedside ultrasound can be utilized for evaluation of pneumothorax.
6) Evaluating adequacy of analgosedation – after all other causes have been evaluated, the patient’s need for analgesia, sedation, and possibly paralysis should be assessed (e). The modified Society for Critical Care Medicine’s algorithm for sedation and analgesia on UpToDate can be utilized.
Measuring pressures – monitoring lung mechanics
Peak airway pressure (PAP): The peak pressure (Ppeak) is the amount of pressure that is required to deliver the set tidal volume from the ventilator circuit to the alveoli. The PAP is measured at the end of inspiration and is a function of both the airway resistance and the compliance of the lung. Therefore, if the tidal volume remains constant, a change in the PAP would be due to either a change in the airway resistance or in the compliance. In VCV, the increase in PAP would not affect the delivery of the set volume. However, in PCV, the increase in the peak pressure would result in less volume be delivered (since the set pressure is constant).
Ppeak ≈ (Resistance + Compliance)
Plateau pressure (Pplat): The plateau pressure is measured by using the “inspiratory hold” technique. After the ventilator completes delivery of the breath, the machine will pause resulting in no airflow between the ventilator and patient; this allows for the equalization of pressures. Since the plateau pressure is measure when there is no airflow, it is therefore only a measurement of compliance.
Pplateau ≈ Compliance
Based on the above information, the difference between the Ppeak and Pplat would be proportional to the airway resistance.
Ppeak — PPlateau≈ Airway resistance
The normal measured airway resistance should be less than 10 cm H2O (with an adequate sized ETT).11
Using Pressures to troubleshoot
We can now apply the above information in a case of a crashing ventilator-dependent patient.
If the peak pressure is elevated while the plateau pressure remains unchanged, that means there is an issue with the airway resistance. [ΔPPeak – PPlat would be increased]
If both pressures are increased, then this would mean there is an issue with the compliance of the lungs and chest wall. [ΔPPeak – PPlat would be unchanged or decreased]
If the peak pressure would be decreased, then there is either an air leak or the patient is hyperventilating enough to pull the air instead of having it pushed under pressure.
No change in peak or plateau and patient still having respiratory distress, pulmonary embolism should be considered.11
Using pressures to troubleshoot
High peak pressure
High peak and plateau
· ETT obstruction by kinking or patient biting tube
· Airway obstruction (secretions, mucus, blood)
· Abdominal compartment syndrome
· Large body habitus
· Pulmonary edema
· R mainstem intubation
· Cuff Leak
· ETT dislodgement
· Ventilator malfunction
· Vent circuit is disconnected
Abdominal compartment syndrome is due to elevated abdominal compartment pressures. These elevated pressure result in compression of the diaphragm and lead to elevated peak and plateau pressures. Symptoms include hypotension, difficulty ventilating, decreased urine output, and cardiac arrest. Treatment includes decompression, sedation and/or paralysis, and urgent surgical consultation.6
In a hemodynamically unstable patient, the EM physician must know how to quickly react in order to prevent worsening patient condition and death. A common mnemonic used to respond to a deteriorating patient is DOPE. This stands 1) Dislodgement, 2) Obstruction, 3) Pneumothorax, and 4) Equipment failure.7,11
The first step should be disconnecting the patient from the ventilator and proceeding to manually bag with a bag valve mask and 100% FiO2. This step alone will help identify if the distress is due to the equipment failure or auto-PEEP. If there was a large exhalation immediately after disconnecting the circuit with immediate improvement in stability, auto-PEEP was likely to be the cause. If the patient improves with BVM then the ventilator needs to be investigated for equipment failure or patient-ventilator asynchrony due to inadequate sedation. Asynchrony can be improved by addressing adequacy of sedation as well as tailoring vent settings to match the patient’s efforts with required support.11 Double-cycling is an example of asynchrony in which there are back to back ventilator delivered breaths. This occurs when the patient wants a higher flow rate than what is set. This can be alleviated by increasing the flow rate.13
If the patient does not improve, next assess the difficulty of ventilation. If it is “too easy” to ventilate, a dislodgement or air leak could have occurred. If it is “too difficult” to ventilate, a suction catheter should be passed through the tube to asses for ETT obstruction or kinking.
If the above measures fail and the patient continues to decline, pneumothorax must be considered. This can be evaluated with auscultation, chest x-ray, or bedside ultrasound. If necessary, a needle chest decompression followed by a decompressive chest tube should be performed.
Case #1: No. This patient is at risk for auto-PEEP. If this patient’s vent was set for a rate of 24 this would allow for 2.5 seconds per breath. Even if the inspiratory flow would be increased to 100 L/min, that would only allow for a maximum of 2.4 seconds for exhalation. This would result in an I:E of 1:2.4 which is significantly less than the recommended 1:4 to 1:5.
Case #2: The tidal volume in the scenario was set to 600 mL. Given this patient’s current condition she would be at risk for ARDS and the lung protective strategy should be utilized. The patient’s height is 5’3” and an appropriate tidal volume would be 400 mL (http://www.mdcalc.com/ideal-body-weight/).
Case #3: This is an example of a hemodynamically unstable patient. In the case, the patient was removed from the ventilator and BVM was utilized. In going through the stepwise approach you find that the ETT is in good place and is not obstructed. You place the ultrasound on the left chest and quickly identify an acute tension pneumothorax. You perform a needle decompression with immediate patient improvement. Afterwards you place a tube thoracostomy and decrease the PEEP to 5.
Case #4: On your physical exam you notice the patient has “tongued” the tube out of place and therefore has self-extubated. You reassess the patient’s mental status and confirm that the patient is currently alert and oriented, following commands, and is able to protect her airway. The patient is eventually discharged from the department in the custody of her concerned parents.
Must Know Information
Understand the importance of the initial ventilator settings
Utilize the lung protective settings when applicable
Use 6-8 mL/kg using predicted/ideal body weight
Understand how permissive hypercapnia can be utilized to prevent ARDS
Have a standardized approach to a crashing patient
Understand how peak and plateau pressures can be utilized to help diagnose an acutely crashing patient
References / Further Reading
Chalfin DB, et al. Impact of delayed transfer of critically ill patients from the emergency department to the intensive care unit. Crit Care Med 2007;35:1477-1483
Fuller BM, Mohr NM, Miller CN. et al. Mechanical ventilation and acute respiratory distress syndrome in the emergency department: a multi-center observational, prospective, cross-sectional study. Chest. 2015;148:365-374
Adams J. Emergency Medicine: Clinical Essentials. Philadelphia, PA: Elsevier/Saunders; 2013.
Marino, P. L., & Sutin, K. M. (2007). The ICU book. Philadelphia: Lippincott Williams & Wilkins.
Mosier JM, Hypes C, Joshi R, Whitmore S, Parthasarathy S, Cairns CB. Ventilator Strategies and Rescue Therapies for Management of Acute Respiratory Failure in the Emergency Department. Annals of Emergency Medicine2015;66(5):529–541.
Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. New England Journal of Medicine N Engl J Med2000;342(18):1301–1308.
Rosen, P., Marx, J. A., Hockberger, R. S., Walls, R. M., & Adams, J. (2006). Rosen’s emergency medicine: Concepts and clinical practice. Philadelphia, PA: Mosby Elsevier.
Wood S, Winters ME. Care of the Intubated Emergency Department Patient. The Journal of Emergency Medicine2011;40(4):419–427.
Archambault PM, St-Onge M. Invasive and Noninvasive Ventilation in the Emergency Department. Emergency Medicine Clinics of North America30:421–449.
Written Summary and blog post by Clarie Heslop, edited by Anton Helman January, 2013
Fight Bites & Boxer Fracture
Suspect a “fight bite” when there is a laceration over an MCP joint. 10% of “fight bites” develop septic arthritis;these injuries need prophylactic antibiotics. For metacarpal fractures, assess for rotation & compare to contralateral hand:
Phalanxes should point to the scaphoid in a closed fist (image below, left), or
Look head on at the fingertips for rotation of fingernails, or
Looking for scissoring with MCP in flexion (image below, right).
Reduce if rotation is present!
Rotational deformity of the 5th digit: note that the 5th digit does NOT point towards the scaphoid
Metacarpal Fracture Acceptable angulation
40° for 5th MC, 30° for 4th MC, 20° for 3rd MCP, and 10° for 2nd. Reduce if greater angulation is present.
Pearls for Boxer Fracture Reduction
Provide good anesthesia (i.e. ulnar nerve block).
Consider using finger-traps for traction. Reduce by pushing dorsally on the distal bone fragment while providing counter pressure on proximal fragment, and immobilize in position of safety (MCP 90′ flexion, IP extension).
Early follow-up (<7 days) in clinic to confirm stability is necessary.
Have a high index of suspicion.
Inspect & test function of tendon against minimal or no resistance.
For <50% extensor tendon injury, a splint may be sufficient.
Our experts suggest ED physicians may repair extensor tendons cut >50% if ends are easily visible and easily opposed.
Use a single horizontal mattress suture and splint the hand.
All flexor tendon and all complex extensor tendon injuries should be splinted and seen by plastics in <7 days.
Is suturing indicated? Simple hand lacerations <2 cm in healthy individuals have the same outcome without sutures. Digital nerve block: Single palmar injection of 2-3mL of 1% xylocaine at the base of the digit just distal to the proximal skin crease. Irrigation: Use 19g needle with 35cc syringe to irrigate copiously with saline or even tap water, under pressure.
Gamekeeper’s Thumb or Skier’s Thumb
Mechanism: Valgus force to abducted thumb. Exam: point of maximal tenderness is usually over the volar/ ulnar aspect of 1st MCP. Pincer grasp often painful with partial tears.
Assess stability by applying radial stress to the distal thumb while immobilizing the proximal thumb and compare to contralateral thumb.
If >30′ deviation, assume instability. Get an X-ray to rule out avulsion # of proximal phalanx. For a partial injury, a 6-week splint may heal the tendon, but a complete tear requires surgery, so surgical exploration is often necessary for cases where a partial tear cannot be confirmed. All patients should be placed in a thumb spica splint and seen early for follow up (7 days) as nonunion of a complete tear requires extensive reconstruction.
Gamekeeper’s thumb with fracture
High Pressure Injection Injury
Injury Liquid under high pressure causes severe injury when injected into the hand by: 1) Direct dissection of tissue planes and tissue ischemia, 2) Cytotoxicity of materials, and 3) Possible secondary infections. These injuries can result in extensive damage and lead to amputation. Don’t be fooled: these can appear benign but pain, pallor, and edema progress like a hand “compartment syndrome”. If history suggests a high pressure injection, contact plastics urgently for definitive exploration and debridement. X-ray can help determine the extent of injury.
High pressure injection injury
4 cardinal signs (Kanavel signs):
Finger held in slight flexion,
Fusiform swelling of the digit,
Tender along tendon sheath, &
Pain with passive extension.
Time is key because adhesions can form and permanently disable the digit. These must be urgently evaluated by plastic surgery, treated with IV antibiotics, and often admitted for either close monitoring, or urgent surgical irrigation and drainage. Start antibiotics, splint and elevate the hand, and refer to plastics.
Hook of the Hamate Fracture
Mechanism – either FOOSH, or an impact of a club or racket forced into the palm. Hook of the hamate fractures may not be seen on usual Xray views of the hand. The “carpal view” (supinated lateral view) should be ordered if suspicious about this fracture, and/or if pain is felt over the hypothenar eminence.
Carpal View for hook of the hamate
Not all hamate fractures appear on Xray. Some need further imaging (CT), and nonunion is very common. Excision of the fracture fragment is often necessary if there is nonunion. If a fracture is seen, immobilize the hand (in a volar slab, with MCP joints in flexion) and refer for follow-up within 4 weeks.
Paronychia (nail edge infections, image at right) should be managed depending on the extent of the infection. A small infection without an abscess may improve with soaking the finger, and oral antibiotics.
However, if an abscess has formed, it needs blunt dissection with a surgical blade, elevation of the lateral nail fold (image at right) and drainage of the sulcus between the lateral nail plate and the lateral epithelium.
Irrigate copiously, and instruct the patient to soak the finger to keep the abscess open, or place a wick.
If the abscess tracks under the nail, consider wedge resection of the nail plate, or nail plate removal if the entire nail plate is involved.
Compartments of the volar skin may form abscesses which need careful and thorough surgical decompression. See image (right). If urgent referral to a hand surgeon is not available, these must be managed in the ED. Cut and detach septae along whole length of distal phalanx nearest to the abscess site, releasing and irrigating very thoroughly. Avoid making incisions across the lateral aspect, to avoid injuring the digital nerve. After releasing all septae, swab, pack and treat with IV antibiotics, splinting, and elevation. Ensure urgent follow-up.
Tips for Hand Injuries
When considering when to remove sutures in the hand, leave sutures that are over areas of tension (i.e. over a joint) for longer (at least 12 days) so they heal completely.
If controlling bleeding is an issue, do NOT clamp any digital arteries, as the digital nerve is very nearby and hard to visualize. Use pressure, limited tourniquet and elevation to control bleeding safely.
Prophylactic antibiotics are indicated for for all animal bites to the hand, and for certain complex injuries (crush wounds, wounds over a joint, or for immune compromised patients).
If referring a hand abscess to a clinic, consider swabbing the drained fluid so MRSA status can be determined.
Immobilizing the PIP joint in extension can stiffen the collateral ligaments causing permanent disability, so don’t splint PIP joint for greater than 1–2 weeks unless necessary, and if splinting, ensure an early referral time. (within 1–2 weeks).
Dr. Helman, Dr. Tate and Dr. Arcand have no conflicts of interest to declare.
infection such as osteomyelitis, or spinal epidural abscess,
fracture (trauma or pathologic),
disk herniation & cord compression,
cancer in spine causing cord compression,
vascular – leaking/ruptured AAA, retroperitoneal bleed, and spinal epidural hematoma.
Red flags for Low Back Pain Emergencies
Age <18 or >60,
Symptoms or history of cancer,
Immunodeficiency (including diabetes, IVDU), previous spinal interventions, or recent infections,
Pain not resolved by analgesia,
History of trauma or coagulopathy,
Cauda equina/cord compression symptoms (bowel, bladder or erectile dysfunction, saddle paresthesia, progressive bilateral leg weakness)
Pearls: *Constant, unrelenting, severe pain, especially if it is worse lying down is a red flag for infection or cancer.* Discogenic pain is worse with flexion, and spain from spondylolysis is worse with extension
A challenge in the ED?
Upwards of 90% of low back pain presentations in the ED are due to benign causes. However there are several important life/limb- threatening diagnoses we must consider in the low back pain patient, and most of these diagnoses are easy to miss. Furthermore, lumbosacral sprain is often associated with significant morbidity, and ED docs should provide specific education and evidence based treatments (see page 3).
Physical exam for Low Back Pain Emergencies
Physical Exam Maneuvers:
Percuss the spinous processes for tenderness, a red flag for infection and fracture,
Test for saddle anesthesia (sensation changes may be subtle and subjective),
DRE looking for tone/sensation
Look for fever, or signs of infection,
Check carefully for bilateral, or multi-level neurologic findings in lower extremities, and assess for gait disturbances.
Straight leg raise (SLR):
Non-specific test, only positive pain is produced distal to the knee between 30–70°.
Pain with contralateral SLR is more specific for siatica.
Slump test: Helps discriminate radicular pain from hamstring pain. With thoracic and cervical flexion, and knee in extension, dorsiflex the foot and flex the neck to determine if pain is produced, with release of cervical flexion to see if symptoms improve (image below).
Abdomen exam and ED ultrasound: look for AAA and bladder distention post-void.
Cognitive Forcing Strategy to Remember Serious Pathologies:
Considering renal colic?
think about AAA!
think about spinal infection!
SPINAL EPIDURAL ABSCESS
Suspect epidural abscess in a patient with:
back pain or neurologic deficits andfever,or
back pain in an immune- compromised patient, or
patient with a recent spinal procedure and either of the above.
CRP and ESR may help, depending on the clinical suspicion for epidural abscess. If suspicion is low after the history and physical, low ESR and CRP levels support not doing an MRI, and discharging the patient home with close follow up. If there is a high index of suspicion, an MRI is indicated *regardless of CRP and ESR*.
Remember the normal ESR cutoff is: (age+10)/2.
In one study of epidural abscesses, 98% had ESR >20, and most were much higher (>60).
Is there any role for CT scan? CT cannot rule out epidural abscess because it does not show the epidural space, spinal cord, or spinal nerves. CT can lead to the pitfall diagnosis of osteomyelitis, missing coexistent abscess (and the urgent indication for surgery).
Remember if the suspicion is epidural abscess, the entire spine must be imaged by MRI. Spinal cord obstruction and paralysis can happen very quickly from epidural abscess, so there needs to be definitive imaging and surgical decompression as quickly as possible.
Start antibiotics while awaiting definitive diagnosis: include appropriate coverage for MSSA and MRSA, and cover gram negatives.
Spinal Epidural Abscess Pearls and Pitfalls
Spinal epidural abscess is rare (1–2/10,000 of hospitalized patients).
The classic triad of fever, back pain, and neurologic deficit is present in only 15% of patients, depending on stage of disease. Spinal epidural abscess is often missed on first ED visit. Fever is present in only 50% of patients, and neuro deficits start very subtly.
Risk Factors: Diabetes, IVDU, indwelling catheters, spinal interventions, infections elsewhere (especially skin), immune suppression (i.e. HIV), and “repeat ED visits.”
CAUDA EQUINA SYNDROME
Definition of Cauda Equina Syndrome:
urinary retention or rectal dysfunction or sexual dysfunction (or all of the above)
saddle or anal anesthesia and/or hypoesthesia (1).
Urinary retention is non-specific for spinal cord compression, but sensitive. Post void residual <100cc has a very high NPV to rule out cauda equina syndrome.
When are steroids indicated:
Evidence supports dexamethasone for metastasis to spine causing cauda equina.
There is no indication for IV steroids for patients with cord compression by other causes
SPINAL METASTASIS – A LOW BACK PAIN EMERGENCY
Known cancer + new back pain = spinal metastases until proven otherwise!
Time is Limbs: Spinal metastases are one of the most common causes of cord compression. Pre-treatment neuro status predicts outcome for this emergency.
X-ray to look for compression #, soft tissue changes, blastic/lytic lesions, pedicle erosion (see image below)
Consider testing ESR and CRP, and calcium profile if signs are consistent with hypercalcemia (e.g. polyurea)
Give dexamethasone as soon as mets are suspected (at least 10mg IV) if the patient has neurologic symptoms. Consider bisphosphonate* and calcitonin if patient is hypercalcemic, or if you suspect compression # or bony metastasis.
Get an urgent MRI if there are symptoms of cord compression. If there are hard neurologic findings, MRI is needed within 24 hours. If the x-ray findings are consistent with mets, but there are no neuro findings, an MRI should be done within 7 days.
*Bisphosphonates may decrease bone resorption in patients with metastatic disease to the bone, and relieve pain better than placebo.
Authors: Joe Walter, MD (@joewalter9999, EM/Hyperbaric Attending Physician, Hennepin County Medical Center/ Healthpartners), R. Eric Minnihan, MD (EM Attending Physician, Hyperbaric Medicine fellow, Mayo Clinic Health System, Hennepin County Medical Center), Tom Masters, MD (EM/Hyperbaric Attending Physician, Hennepin County Medical Center), Chris Logue, MD (EM/Hyperbaric Attending Physician, Hennepin County Medical Center), Bjorn Westgard, MD (EM/Hyperbaric Attending Physician, Hennepin County Medical Center/ Healthpartners), Stephen Hendriksen, MD (EM/Hyperbaric Attending Physician, Hennepin County Medical Center) // Edited by: Alex Koyfman, MD (EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital, @EMHighAK) & Justin Bright, MD (EM Attending, Henry Ford Hospital, @JBright2021)
An 82 year-old man with a history of dyslipidemia, hypertension, and CAD s/p stenting was driving home from the grocery store when he experienced sudden vision loss in his right eye around 2:30 pm. He has no previous history of vision problems and is puzzled but eventually concerned. By the time he presents to the ED he has light perception only in his right eye. He cannot not recognize motion. Central retinal artery occlusion (CRAO) is first in the differential.
Central Retinal Artery Occlusion is characterized by a sudden painless loss of vision in one eye. It occurs when there is a blockage of the central retinal artery causing ischemia and infarction to the retina. Incidence is 1-10/100,0001 with a mean age of 60-65 and over 90% of cases occurring in those over 40.2,3,4Providers are increasingly recognizing this as a cerebral vascular accident that shares the same risk factors commonly associated with stroke: hypertension, hyperlipidemia, diabetes, and tobacco use1. Recent studies have shown that acute cerebral infarcts often accompany CRAO and a marked incidence in stroke and acute myocardial infarction occur in the month following a CRAO.5,6
The first branch off of the internal carotid artery is the ophthalmic artery which splits into the posterior ciliary and central retinal arteries which supply the eye. In CRAO there is an occlusion of the central retinal artery causing a profound vision loss. In some cases the ciliary arteries are able to perfuse the periphery of the retina and maintain perfusion to the central portion of the retina. Research has shown that the retina can only survive 90-100 minutes of ischemia prior to permanent damage.7,8 However, cases with visual recovery beyond this timeframe have been reported, potentially due to incomplete occlusion, an intact cilioretinal artery, or collateral flow.
Although there are many etiologies for CRAO, carotid artery stenosis is thought to be the most common cause and is present in up to 70% of cases.2Cardioembolic disease is another prevalent etiology and is more likely in those under 40 and in those with a history of atrial fibrillation or valvular disease. Giant cell arteritis, vasculitis, Sickle cell, carotid artery dissection, Moyamoya, hypercoagulable states (SLE, antiphospholipid, hematologic cancers), and iatrogenic causes (injections, cerebral angiogram, carotid endarterectomy) are less common causes of CRAO.
A patient typically presents with acute, profound, painless, monocular vision loss with potentially a small amount of temporal sparing. Approximately 20% of the population has a cilio-retinal artery which can lead to some central sparing in case of a CRAO.7 On exam, patients will demonstrate a complete or relative afferent pupillary defect, though this need not be present. Funduscopic exam will show retinal whitening (a “cherry red spot,” described in 90% of patients with acute CRAO) or “box-carring” (vascular attenuation with stacking of red cells within the vasculature, only seen in 15% of patients with acute CRAO).9
The particular history of past and present illness is important in each patient, as additional symptoms may lead to a specific etiology. Headache and/or temporal tenderness may suggest Giant Cell Arteritis while neck pain or recent cervical trauma may suggest dissection. It is also important to remember the differential diagnosis, which includes occipital stroke, retinal detachment, complex or atypical migraine, and other ischemic optic neuropathies.
Recent painless vision loss is an ocular emergency that should prompt immediate ophthalmology consultation. Concerns about vasculitis or Giant Cell Arteritis deserve the addition of an ESR/CRP to the workup. A complete stroke and cardiovascular work up is needed either in the ED or during inpatient admission, as there is a high correlation with additional stroke or myocardial infarction in the period immediately following onset of a CRAO (Incident Rate Ratio of 14.0 (95% confidence interval, 8.90-22.00)).5,6 Despite this only one-third of ophthalmologists transfer patients with incident CRAO to an emergency department for immediate evaluation.5
As this in an ophthalmologic emergency, management is usually in coordination with ophthalmology and early consultation is recommended. No clinical trials have demonstrated improvement with any treatment compared with observation10 and historically CRAO has an abysmal prognosis.10,11 Despite the unlikely chance of improvement, maneuvers are usually attempted if a patient presents within 24 hours including:10,12
Ocular pressure lowering agents / maneuvers
Topical agents such as timolol
IV agents such as acetazolamide or mannitol
Anterior chamber paracentesis
Breathing into a bag (to increase CO2 which causes vasodilatation)
Again, there is little data to show that any of these methods improve outcomes over control and there is some evidence to suggest that that these interventions may actually be associated with worsened visual outcomes and recovery rates.13
As CRAO is a vaso-occlusive phenomenon, there is a great deal of interest in the use of tPA in its treatment. While there are published reports of vision improvement after the administration of tPA,13 there is debate about whether or not this improvement is greater than the natural history of CRAO.11 Additionally, there is concern regarding hemorrhage associated with the administration of tPA and as such, the use of tPA in patients with CRAO is not currently considered standard of care. As a result of this, the traditional “treatment” of CRAO has been observation alone.11
Hyperbaric Oxygen Experience/Data:
Recently, the undersea and hyperbaric medicine society made a recommendation for the consideration of hyperbaric oxygen therapy (HBOT) in patients with a CRAO.14 While experiencing a CRAO, the inner retinal layers become ischemic due to poor perfusion / oxygenation. Animal models have shown that under hyperbaric conditions, the collateral circulation from the choroid is capable of supplying 100% of the retina’s oxygen needs.15,16 Additionally, as mentioned before, approximately 20% of the population has cilioretinal artery, which supplies blood to the area around the macula. This ability to hyperoxygenate and meet the retina’s oxygen demands while the central retinal artery re-cannulates is part of the rationale behind the use of hyperbaric oxygen. Additional proposed mechanisms are related to hyperbaric oxygen’s effect on edema reduction and its ability to blunt ischemia-reperfusion injury after re-canalization occurs.17
There are a number of clinical trials looking at the effect of hyperbaric oxygen on patients affected by a CRAO. In a literature summary of 476 patients treated with hyperbaric oxygen, 306 (65%) experienced vision improvement after their treatment.18 Overall, the American Heart Association classification of evidence was considered IIB with fair to good evidence with retrospective control case series, but no prospective randomized controlled trials.18 Additionally noteworthy is that therapy with hyperbaric oxygen is generally considered to be benign and safe with proper patient selection and medical control.
To add to the existing evidence, Hennepin County Medical Center has one of the largest single cohorts of CRAO patients treated with hyperbaric oxygen therapy. Patients found to have a CRAO are being treated with hyperbaric oxygen and seeing significant results. In patients who are treated in <6 hours from time of onset, 83% are seeing improvement in their vision, averaging 6 lines of improvement on a Snellen eye chart. Overall, patients had 4.6 lines of improvement when treated with HBOT.19 Though this is a small and promising study, further investigation is needed. As with all strokes, it appears that time is crucial.
Our patient is transferred to a hospital that has emergent hyperbaric capabilities and is evaluated by the Emergency Staff, Neurology and Ophthalmology. CRAO is confirmed and he is taken for hyperbaric oxygen therapy at 9:30 that evening (7 hours after onset of vision loss). During treatment, his vision improves to 20/200 (he can read the big E), and after treatment examination shows that he has improved to 20/100. On examination the following day, he is able to count fingers but is no longer able to read the eye chart. Immediately after his second treatment, he is again 20/100. Ophthalmology evaluation later that day shows a corrected vision of 20/20 -1. The patient reports some small gray spots, but otherwise marked improvement. He is then treated BID for a total of 10 treatments. During his hospitalization he had a stroke work up including an MRI, CTA of the neck and an echo. On reevaluation 6 weeks later, he continues to see 20/20 with correction.
Presentation: Painless vision loss
Early ophthalmology consultation (true eye emergency)
Should be treated as a stroke
Traditionally poor prognosis overall
Promising HBO experience thus far. Consider early consultation with an emergent hyperbaric treatment center if available
Hayreh SS. Ocular vascular occlusive disorders: Natural history of visual outcomes. Progress in Retinal and Eye Research. 2014;41:1-25.
Tintinalli, Judith, Gabor Kelen, and J. Stephan Stapczynski. Emergency Medicine: A Comprehensive Study Guide -6th Edition. New York: The McGraw-Hill Companies, Inc., 2004. Print.
Schrag M, Youn T, Schindler J, Kirshner H, Greer D. Intravenous fibrinolytic therapy in central retinal artery occlusion. A patient-level meta-analysis. JAMA Neurology. 2015;72(10):1148-1154.
Murphy-Lavoie H, Butler F, Hagan C. Arterial Insufficiencies: Central Retinal Artery Occlusion. In: Weaver LK, ed. Hyperbaric Oxygen Therapy Indications. 13th ed. North Palm Beach: Best Publishing Company; 2014.
Patz A. Oxygen inhalation in retinal artery occlusion. American Journal of Ophthalmology. 1955;40:789-795.
Li HK, Dejean BJ, Tang RA. Reversal of visual loss with hyperbaric oxygen treatment in a patient with Susac Syndrome. Ophthalmology. 1996;103(12):2091-2098.
Buras JA, Garcia-Covarrubias L. Ischemia-reperfusion injury and hyperbaric oxygen therapy. Basic mechanisms and clinical studies. In: Neuman TS, Thom SR, eds. Physiology and Medicine of Hyperbaric Oxygen Therapy. 1st ed. Philadelphia, PA: Saunders Elsevier; 2008.
Murphy-Lavoie H, Butler F, Hagan C. Central retinal artery occlusion treated with oxygen: a literature review and treatment algorithm. Undersea and Hyperbaric Medicine. September-October 2012;39(5):943-953.
Masters T, Westgard B, Hendriksen S, Walter J, Logue C. Central retinal artery occlusion treated with hyperbaric oxygen. A retrospective review. Paper presented at: UHMS Annual Scientific Meeting, 2015; Montreal.
Dr. Arun Sayal and Dr. Natalie Mamen discuss the key diagnostic considerations in commonly missed occult fractures and dislocations. They review the indications and controversies for the use of Bone Scan, CT and MRI in occult fractures and dislocations and give you some great clinical pearls to use on your next shift.
Missed occult fractures and dislocations, in general, may result in significant morbidity for the patient and law suites for you. Six cases are presented in this episode, ranging from common scaphoid fractures to rarer dislocations. Dr. Sayal & Dr. Mamen answer questions such as: Which fractures can mimic ankle sprains and how do you avoid missing them? What are the most reliable signs of scaphoid fracture? In which occult orthopaedic injuries should we anticipate limb threatening ischemia? Which is better to diagnose occult fractures – MRI or CT? Which calcaneus fractures require surgery and which ones can be managed conservatively? and many more……
Case 1 – Occult Hip Fracture
67 y.o. woman with severe COPD on long-term steroids who fell from standing height
Ambulating well at current time, but with groin pain
Findings suspicious for hip fracture:
New inability to weight bear
Hip pain on axial loading of leg
Inability to straight leg raise are highly specific for hip fracture
Percuss patella bilaterally while listening with stethoscope on symphysis pubis. Unilateral diminished sound (due to effusion) should increase suspicion.
Don’t forget hip injury can present as knee pain, especially in children and elderly
Pelvic ring and femoral neck fractures are mutually exclusive: In a study with >100 elderly patients unable to weight bear after a fall, no patient with a fracture of the femoral neck had an associated fracture of the pelvic ring or vice versa found on MRI.
Imaging choices in occult hip fracture:
CT scan: in general, very good at identifying fractures involving bone cortex. Most studies compare 4-slice CT vs MRI and show that MRI is far superior for identifying occult hip fractures. However, newer-generation CT scans (64-slice) may be as sensitive and specific for hip fractures compared to MRI, especially when 3D reconstructions are available (no studies to confirm this yet).
MRI: The gold standard. Allows better look at bone marrow (trabecular bone), but might overcall certain injuries that are not clinically relevant.
Bone scan: Very sensitive at 48-72hrs (24hrs for newer 3-phase array scans) but not specific and poor localization, and potential for complications while patient is bedridden waiting for scan (VTE, pneumonia, pressure ulcers, delays to surgery).
Ultrasound: May demonstrate effusion in occult hip fracture
A study from Israel had 100% sensitivity for identifying post-traumatic hip fracture, but not ready for ‘prime time’
Safran et al. J Ultrasound Med 2009; 28:1447–1452
A proposed algorithm for suspected occult hip fracture:
In young patients with high-energy trauma, a fracture in the cortex will likely be seen
If x-rays are negative but clinical suspicion is high, move on to CT scan
In elderly with low-energy trauma, occult fractures are less likely to involve cortex
If x-rays are negative but clinical suspicion is high, move on to MRI (preferred) or 64-slice CT if MRI not available
18 y.o. woman landed “funny” while snowboarding and had immediate left ankle pain
Very swollen inferior and anterior to the tip of fibula, with tenderness over the anterior talofibular ligament (ATFL)
Ankle sprain mimics:
Snowboarder’s fracture (lateral process of talus)
Posterior talus process fracture
Achilles tendon rupture
Anterior process calcaneus fracture
Talar dome fracture
In snowboarder’s fracture (see image below) the feet are fixed in dorsiflexion, and the anterior foot usually everts as the snowboarder lands (very different mechanism than classic inversion ankle sprain). The fibula impacts the lateral process of the talus causing a fracture.
Broden’s view (Mortise view) x-ray:
Foot in plantar flexion; lateral aspect of the talus better visualized The plantar talus should show a “symmetric V” in normal x-ray
An asymmetric “V sign” indicates a displaced fracture requiring surgery
When in doubt, place a posterior slab and make the patient non weight-bearing until follow-up
Case 3 – Occult Knee Dislocation
40 y.o. male in belted MVC (frontal collision at 80km/h)
Severe knee pain and tenderness and limited ROM, but no deformity
Pearls of occult knee dislocation:
50% self-reduce before presenting to the ED, and with distracting injuries can be easily overlooked
Common mechanisms: pedestrian-vs-car, contact sports injuries and knee-to- dashboard mechanism
1/3rd will have neurovascular injuries, with significant morbidity
if decreased sensation in peroneal nerve distribution, assume concomitant popliteal artery injury
Findings suspicious for occult knee dislocation:
3 out of 4 knee ligament laxity (ACL, PCL, MCL, LCL)
Ankle-Brachial Index (ABI): >90% is reassuring, and can be monitored serially
CT-angiogram if suspicious of vascular damage, and consult vascular
In patients with knee dislocation associated with vascular injury, 15% will develop ischemia when repair is delayed by > 8hrs
Case 4 – Occult Scaphoid Fracture
10 y.o. boy with FOOSH and lone snuff box tenderness
Pearls of occult scaphoid fracture:
Epidemiology: Less likely in children < 15y.o., adults > 50 y.o., 15% of fractures will be occult on initial x-rays
Physical exam – 3 key maneuvers for scaphoid fracture:
Palpation of snuff box with wrist ulnarly deviated
axial loading of thumb with pain in the anatomical snuffbox
palpation of volar aspect of scaphoid with wrist radially deviated
3 of 3 gives 90% risk of scaphoid fracture (70% with 2 of 3)
X-ray imaging for suspected scaphoid fracture:
Order specific scaphoid views
Consider clenched fist view to splay carpals, especially if tenderness is more at the lunate bone
Might reveal a dynamic “Terry Thomas sign” (or “David Letterman” sign) (as the gap in their teeth similar to the gap between scaphoid and lunate) if >3mm between scaphoid and lunate consistent with a scapho-lunate ligament tear
In negative x-ray with high clinical suspicion:
Immobilization with thumb spica splint is most commonly used
precise position of immobilization does not effect outcome
Other options: CT in ED, Bone Scan at 72hrs, MRI
must weigh time off work/sport if immobilize vs expense and radiation exposure of early advanced imaging
Longer follow-up (10-14d) necessitates longer immobilization period, but allows for more time for the fracture to reveal itself compared to shorter period (7d)
many scaphoid fractures take up to 16 weeks to heal
Case 5 – Posterior Shoulder Dislocation
56 y.o. male found down by wife, found to have glucose of 1 by EMS
Holding bilateral shoulders in internal rotation, and there is resistance to external rotation attempts
2-3% of shoulder dislocations, 15% bilateral and often missed on first visit (50-80%!)
Associated with 3 Es: epilepsy, ethanol and electricity
Mechanism: axial force with shoulder internally rotated and abducted
Prominent coracoid, and humeral head posteriorly displaced (vs. squared shoulder of anterior dislocation)
Patients hold arm internally rotated, and reversed Hill-Sachs lesion (engagement of humeral head on posterior glenoid rim) often prevents external rotation
Axillary view on x-ray very useful, as well as the subtle “light bulb” sign on AP (loss of asymmetry of the humeral head created by greater tuberosity due to the internal rotation of the humerus – see image below)
Reduction of Posterior Shoulder Dislocation:
Physician’s contralateral hand puts anterior pressure on the patient’s posterior humeral head (eg, left hand on right shoulder)
Physician applies gentle longitudinal downward traction of patient’s arm
Assistant externally rotates patient’s arm
Immobilization of Posterior Shoulder Dislocation:
Arm hanging in neutral position, with internal or external rotation (recent studies show external rotation may be better, but impractical)
Length in weeks: “8 minus decade of life, to max of 3”, maybe even shorter
For an excellent evidence-based review of posterior shoulder dislocations visit Brent Thoma’s Boring EM blog
Case 6 – Occult Calcaneus Fracture
29y.o. male jumped from height while under the influence of crack cocaine
Tender to palpation L-spine and entire bilateral extremities, ankles and feet swollen, positive pulses
X-rays all normal lower extremities, but multiple L-spine compression fractures
Fall from height onto feet:
Look for associated injuries: spinal injuries (esp. L-spine), contralateral calcaneal fracture, and ankle fractures
Calcaneal injuries have high morbidity with 20% of patients debilitated at 3yrs
Calcaneal fracture imaging:
Bohler’s angle on lateral view x-ray of foot measured between the line formed by posterior tuberosity of calcaneus apex to anterior process, and line formed by apex to anterior process (see image)
Normal is 20-40°, <20° suggestive of compression fracture of calcaneus
Harris view (axial view of calcaneus)
Usually needs CT scan to determine whether fracture is extra-articular (conservative management) or intra-articular (operative management)
Any displacement typically requires operative repair
ED management centres around minimizing soft tissue swellling and preventing fracture blisters and skin sloughing, with application of a bulky compressive dressing with a posterior splint, combined with elevation and icing