Grand Rounds Recap 12.4.19
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Toxicology Pitfalls: Rapid Sequence Execution WITH Dr. Gillian Beauchamp
Salicylate Ingestion
Initially the patient will present comfortably tachypneic with a mixed respiratory alkalosis and metabolic acidosis
If the patient’s HCO3 is low, this is an indication to administer sodium bicarbonate (keep in mind your respiratory rate must be compensatory)
Salicylic acid is a weak acid, and when surrounded by an alkaline environment it dissociates into its anionic form and can no longer cross cell membranes
This traps salicylate in the serum and allows it to be excreted in the urine
Make sure you check and replete the patient’s potassium, because if the patient is hypokalemic they will not be able to excrete salicylic acid - aim for a high normal potassium of 5.0-5.5
A bicarbonate drip can be made with 3 amps of sodium bicarb in 1 L of D5W and 40 mEq of potassium, infused at a rate of 200 mL/hr
A salicylate level over 100 is an indication for hemodialysis
Salicylic acid also disrupts oxidative phosphorylation, which ultimately causes severe neuroglycopenia (serum glucose will be an unreliable marker)
Uncoupled oxidative phosphorylation also depletes ATP, which will quickly result in respiratory fatigue and failure
Intubation and ventilator management
Give D50 prior to intubation to try and prevent intubation all together
Administer additional bicarbonate prior to intubation
Remember that bicarbonate will be converted into CO2, which will cause severe respiratory acidemia especially during the apneic period following paralysis
Aggressively ventilate the patient with a BVM during induction to avoid respiratory acidosis
Also discuss with your respiratory therapist to set the initial respiratory rate much higher than normal - start at the low 30s if possible to match pre-intubation minute ventilation
Succinylcholine is probably a better option for paralysis than rocuronium so that the patient will resume spontaneous respiration
Tricyclic Antidepressant Ingestion
Tricyclics have a myriad of effects on several receptor systems
Antimuscarinic
Antihistaminergic (lethargy)
Na channel blockade
CNS norepinephrine reuptake inhibition (causing seizures)
Alpha adrenergic blockade (causing hypotension)
Potassium rectifier channel blockade (results in a prolonged QT)
GABA antagonism (also causes seizures)
Seizures cause acidemia, which then causes increased free drug and worsening Na channel blockade
If the patient begins to seize, immediately administer a benzodiazepine, as this will worsen acidemia
Give sodium bicarbonate
This will not only decrease the amount of free drug in the serum, but also increases the serum Na which will overcome the Na channel blockade and narrow the QRS
Give BVM ventilation during intubation to decrease acidemia similar to above
Toxicologic Induced Bradycardia Differential
Beta Blockers
Calcium Channel Blockers
Digoxin
Clonidine
Organophosphates
Lithium
Digoxin ingestion
Therapeutic serum levels range from 0.8-1.5
Digoxin increases calcium concentration within cardiac myocytes resulting in increased inotropy as well as increased vascular tone
Digoxin also increases vagal tone to decrease conduction through the SA/AV node
At toxic levels, the myocardium becomes very sensitized and prone to dysrhythmias as well as excessive SA/AV blockade and severe bradycardia
Pathognomonic/Common EKG findings
Biventricular ventricular tachycardia
Slow atrial fibrillation
Digoxin blocks the Na/K ATPase and results in hyperkalemia
A potassium greater than 5.5 is a marker for severe toxicity
Treatment
Atropine, fluids, inotropes/vasopressors
Calcium
Classically has been avoided due to the theoretical stone heart syndrome
In reality, this is almost certainly fine (although ineffective) to give
Pacing often does not work
Digifab
Indications
Hemodynamic instability
Dysrhythmia
Severe bradycardia
Potassium level greater than 5
Digoxin concentration greater than 15 at any time
Digoxin concentration greater than 10 at 6 hours post ingestion
Total digoxin ingestion of 10 mg in an adult or 4 mg in a child
Administered as a slow push over 30 minutes and takes 45 minutes to work
Check a free digoxin concentration before administration
1 vial of digifab binds 0.5 mg of digoxin in acute toxicity
You can also multiply the digoxin concentration by the patient’s weight and divide it by 100 to calculate the amount of digifab to administer
Chronic toxicity - often will occur in older patients who are also on a diuretic - can present with hypokalemia as opposed to hyperkalemia
Give a maximum of 2-3 vials of digifab if the digoxin concentration is less than 8
If the patient is anuric, digifab will not work as a long term solution and other treatments such as plasmapheresis can be performed in the ICU
Beta Blocker Ingestion
Causes decreased inotropy, dromotropy, chronotropy, and vasodilation
Calcium Channel Blocker Ingestion
Causes bradycardia from inhibition of SA and AV nodes
Also causes hypotension from decreased systemic vascular resistance
Patients will often be hyperglycemic from pancreatic B cell calcium channel blockade which inhibits endogenous insulin release
Alpha-2-Agonist Ingestion (Clonidine)
Patients will often present with bradycardia, transient hypertension followed by hypotension, and altered mental status
Treat with IVF, atropine, and vasopressors
Standard approach to the bradycardic overdose patient
1st line: 2 L IVF bolus, calcium (if you suspect this is not a digoxin ingestion), atropine 0.5 mg every 2-3 minutes up to 3 mg total
2nd line: Glucagon 5 mg (this often causes emesis) followed by an infusion if effective, vasopressors, high dose insulin euglycemia therapy (HIET)
HIET causes vasodilation in the microvasulature to allow for perfusion of the gut, heart, and brain and is believed to be pressor-sparing
Start a 1 unit/kg bolus followed by an infusion at 1 unit/kg/hr
Increase the infusion every 15 minutes to a maximum of 10 units/kg/hr
Check a capillary blood glucose every 15 minutes until stable, then every hour
3rd line: Intralipid
Sequesters drug within the serum
Works well for any ingestions that have both cardiovascular and CNS effects
CCB, BB, bupropion, TCA, diphenhydramine, cocaine, lamotrigine
Administer 100 mL over 5 minutes, then 400 mL over 20 minutes with a maximum dose of 1 L
4th line: Methylene blue
Inhibits nitric oxide production and vasoplegia
5th line: ECMO
Consider this in young patients who have a quickly reversible disease process such as a CCB or BB overdose
For additional FOAMed toxicology learning, check out Tox Shorts and Tox in Ten
Deep Thoughts
Finding your niche in EM
Start with wellness - exercise, eat healthy, find time to rest and recover, and remember your emotional well being
Start with small steps during residency - micro wellness
Try to make one mindful choice per day - find out what is important to you and make time for this, even if it is only brief
Think about the aspects of your life as layers as opposed to pieces of a pie, with there always being a full supportive layer underneath what you’re choosing to bring to the forefront of the moment
This will allow you to be mindful amidst the chaos and truly find your calling
Air Care Grand Rounds
Pneumothorax
Needle thoracostomy
Place 10 gauge angiocath in the 4th or 5th intercostal space along the anterior axillary line - this has a lower failure rate and is safer than placing the catheter in the 2nd intercostal space of the anterior chest
Finger thoracostomy
Incision is made in the anterior axillary line at the 4th or 5th intercostal space, insert kelly clamp into the pleural space followed by your finger to confirm the track actually communicates with the pleural space
Indications: traumatic cardiac arrest or refractory tension physiology after attempted needle thoracostomy
Ultrasound
Check out Dr. Harty’s instructional video on use of the new V-scan machines on Air Care
Emergency Procedures
In flight emergencies
3 different procedures
Land as soon as practical - extended flight not recommended, landing site and duration determined by the pilot
Land as soon as possible - landing site determined by pilot
Land immediately - engine fire that will not extinguish or if both transmission oil pressure gauges are low
The blue checklist booklet is in the cockpit and provides a step by step approach to any emergencies
Medical Crew Emergency Responsibilities
Responsible for the patient and making sure everything is secure in the cabin
Know how to exit the aircraft if the doors are not operational for both aircraft types
Know where the survival kit is located - either behind or below the doc seat
Fire extinguishers are located on the clamshell doors and between the pilot/co-pilot seat
During emergency landings, extinguish any fires in the cabin and turn off any medical equipment that may be causing smoke while also opening the windows
Types of emergencies: Loss of tail rotor, both engine failure, one engine failure, engine fire, airframe fire, smoke in cockpit, inadvertent instrumental meteorologic conditions
Emergency Landing Procedures
Transit a may day call, exit the aircraft after the rotors stop turning (unless there is a fire) and meet at the nose of the aircraft, stay close to the aircraft to help search and rescue teams
Airway grand rounds WITH Dr. Carleton
Angioedema
Caused by either histamine or bradykinin release (ACE-I, tPA, hereditary angioedema)
Histamine mediated
Associated with urticaria
Treat with steroids and antihistamines
Airway involvement is often early in the patient’s course
Bradykinin mediated
Steroids and antihistamines are ineffective
FFP, ecallantide, icatibant, and C1-esterase inhibitor concentrate may be helpful
The time course is both more insidious (up to 72 hours) and migratory - progressing from the tongue to the pharynx and finally the supraglottic space
Airway involvement is often later in the patient’s course
Who should we intubate?
Retrospective chart review in 1999 showed that no patients with lip or soft palate involvement were intubated, 7% with tongue edema were intubated, and 24% with laryngeal edema were intubated
No patients were intubated prophylactically and were only intubated for respiratory distress
Patients who had voice change or hoarseness were more likely to be intubated
Anterior edema appears to be less dangerous than diffuse lingual edema
Retrospective review of 66 cases of angioedema in 2000
Cause of angioedema (histamine or bradykinin) was not predictive of need for intubation
Involvement of the oral cavity but not the face or lips was associated with airway intervention
Retrospective review of 311 ACE-I angioedema cases in the ED in 2015
Only 17% had an airway intervention with 1 surgical airway
Patients who needed to be intubated had a more prolonged hospital course compared to those who were not intubated
Patients were more likely to be intubated if they had dysphagia, dysphonia, or drooling
When endoscopy was performed, aryepiglottic fold edema was the highest predictor for intubation
Retrospective chart review 108 ACE-I angioedema cases in 2010
No cases of isolated supraglottic edema were seen
No patient needed airway intervention if they presented more than 12 hours after symptom onset
Patients with oropharyngeal floor/base of tongue edema were most likely to be intubated
In summary, there is no definitive evidence or answer to this question based on the current body of literature
How should we intubate?
This should almost always be done using the awake technique
Administer glycopyrrolate, 4% lidocaine, and sedation to effect
Driver & McGill, Annals of Emergency Medicine 2017 - first method success rates
Fiberoptic nasal - 57%
Blind nasal - 40%
Fiberoptic oral - 67%
VL - 86%
If you can see the patient’s soft palate, you will likely be able to use a standard or video blade and successfully intubate the patient
If performing an endoscopic intubation, sub-totally intubate the patient and pass the scope through the ETT for better first-pass success rates
Be aware that there is an increased bleeding risk, patient’s do not tolerate this as well, and there is therapeutic momentum to complete the intubation when it is not really necessary
Consider splitting a nasopharyngeal airway to allow for diagnostic nasopharyngoscopy without having to sub-totally intubate with an endotracheal tube
