Grand Rounds Recap 05.06.20
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Airway Grand Rounds WITH Dr. Carleton
Airway QI: Critical documentation pearls
If EGD is in place on arrival, type
Indication for intubation
Difficulty indicators - anatomic and physiologic
Route
Pharmacology
Device choice
Number of courses and attempts (courses are based on device/meds and correlate with cognitive approach to airway; attempts reflect the technical skill of the operator)
Glottic view
Intubation complications
Need for rescue
Who tried, who succeeded
Lessons learned
Glycopyrrolate takes 10-15 minutes to work
Anticipate need for suction and set it up early - know how to attach the suction tubing to the endoscope
Jaw thrust during endoscopy will improve your view even during endoscopy - opens up and can clear secretions
Have a syringe with 4% lidocaine set up and ready to augment your topical anesthesia, especially of the cords
COVID intubation practices
Deviation from standard procedures increases potential for error - have a plan for your PPE, airway equipment, preoxygenation, primary/secondary/tertiary approaches
Mac 4 VL with bougie is the recommended primary approach in most cases, with the caveat that a D blade may be better when the anatomy will not allow a Macintosh blade
Plan if you can maintain oxygenation
Plan if you can’t maintain oxygenation
Principles
Minimize aerosolization
Intubate in negative airflow room
Intubate early if getting to the point of needing positive pressure devices
Caveat - some are advocating for the use of HFNC with caution in selected patients as a way to avoid need for intubation (patients who are still <88% on 15lpm on reservoir mask)
HEPA filters for PPV if needed
RSI for apnea and cough prevention with supranormal doses of RSI meds (we frequently underestimate patient’s weight and there is little downside to more paralytic)
Sucinylcholine 2mg/kg
Rocuronium 1.5mg/kg
Clamp ETT until bag/circuit attached
Inflate ETT cuff before first breath, and consider connecting patient to ventilator for the first breath rather than the bag if you can for one less disconnect
Pre-oxygenation critical because patients drop fast
Keep upright/reverse trendellenberg15L reservoir mask if not critically hypoxic
If critically hypoxic consider HFNC at 30-60 lpm vs NIPPV using vent circuit
HEPA filters need to be placed between patient and circuit/bag and exhaust port of bag
If using facemask BMV use an OPA, lowest effective volume
Consider iGel as opposed to facemask for BMV if paralyzed - this effectively creates a closed circuit because the iGel allows negligible airflow around their margins
Apneic oxygenation probably doesn’t work in this population
Intubate to the upper end of depth by gender to reduce need for repositioning/disconnection
Minimize vent/bag disconnects
Deliver first breath with vent if able
Do not use colorimetric capnography if you have waveform
Stop CPR during airway attempts
Risk for aerosolization greatly increases
Patients in arrest from critical hypoxia in COVID have poor survival rates
Maximize first pass success - (minimizes aerosols, overcomes physiologic fragility)
Preplanning - room and equipment set up, personnel placement and assignment of roles
Closed-loop communication
Checklists
Equipment/meds/personnel roles
Plan A/B/C/… (A and B should be in the room always; C and onwards should be outside and acquired by a “runner” to avoid contamination)
Optimize safe preoxygenation
Positioning
Plane of earhole to plane of sternal notch
Consider intubating with HOB up to 25-30
RSI with supranormal paralytic dosages
Best device? King vision - we have these available to practice with, and so familiarize yourself
C-mac blades are approaching critical shortage
Best operator should intubate
Failed first-pass?
Continue intubation attempts vs rescue
If you have to bag use filters/thenar grip/lowest effective volume/OPA/under drape
Strongly consider iGel - allows closed-circuit ventilation and a conduit for intubation
Intubating through iGel
Blind success rate 67-74%Endoscopic success rate very high but unqualified
Initiate attempt at the end of a breath
Consider performing endoscopy through a bronch adaptor with side-port blocked
Have suction prepared
Cric if you have to
Limit contamination
Enhanced PPE/double-gloving
Checklist for donning/doffing vs coached donning/doffing
Minimize in-room personnel and assign roles
Attending
Resident
Nurse
RT
Runner at the door
Communicating outside the room? Baby monitor vs radio vs yelling through the door to the runner
Equipment for plans A and B inside the room
Cric tray, direct laryngoscope, code cart, etc outside the room
Aerosol mitigation - NatMat, tent, box
Intubation pods are arriving soon for use in both the SRU and the respiratory pod
Summary
Stay safe
Pre-plan and communicate
Do what’s best for the patient - use HFNC or BiPAP appropriately when needed
Develop systems and plans to
Minimize aerosolization
Maximize first pass success
Limit contamination
Consider early use of EGD for rescue
R1 Diagnostics - Urine Drug Screen WITH Dr. Mullen
Check out Dr. Mullen’s post on Taming the SRU for some background and additional information.
How does the urine drug screen work?
Samples can come from urine, hair, saliva, or blood. Urine is the most common sample obtained in the ED.
The type of assay that we use in the ED is an immunoassay, although mass-spectrometry is another option for confirmatory testing.
Immunoassays are fast and cheap, but positive results are always “presumptive” positive and require confirmation with mass-spec.
There are five main drugs that can be detected:
Amphetamines, cocaine, marijuana, opiates, PCP.
Other drugs such as TCAs and barbiturates may also be included on specific assays.
Drug Detection Times
Urine detection times can be affected by a variety of factors including patient body habitus, urine pH or concentration, drug half life, last use, etc.
See the post above for specific detection times of common drugs.
Cases and Learning Points
General Pearls
Results are qualitative, not quantitative.
Urine drug screens rarely change our ED management.
Only drug classes are tested for, not specific drugs (e.g. benzodiazepines but not diazepam or alprazolam specifically).
Thresholds and numeric cutoffs are affected by drug concentration, so there is possibility for false negative results.
Most importantly, there is a large amount of cross-reactivity with common over-the-counter drugs, which lead to false positive results.
Cocaine
Overall the UDS is a good test for cocaine with high specificity.
Stays positive for 2-4 days after use.
Cocaine can induce an MI through sympathomimetic surge, vasoconstriction, and promotion of thrombus formation.
Benzodiazepines
Many benzodiazepines are not detected by the UDS. It only tests for metabolites of chlordiazepoxide (Librium) and diazepam (Valium). Alprazolam, lorazepam, and clonazepam won’t be detected.
Sertraline and oxaprozin (an NSAID) are important cross-reactants.
Tricyclic antidepressants
There are many cross-reactants for TCAs: carbamazepine, cyclobenzaprine, diphenhydramine, hydroxyzine, and quetiapine to name only a few.
Opioids
These also have an extensive list of cross-reactants including dextromethorphan, diphenhydramine, doxylamine, verapamil.
You need additional testing for many of the synthetic opioids including oxycodone and methadone.
CPC thyrotoxicosis secondary to molar pregnancyWITH Drs. Wolochatiuk and Paulsen
Hyperthyroidism in normal pregnancy and molar pregnancy can be missed due to assuming that symptoms are from normal pregnancy (nausea, mild abdominal cramping, tachycardia/palpitations).
Normal pregnancy is a mildly hyperthyroid state, so have a low threshold to check a TSH in your pregnant patients with tachycardia.
Hyperthyroidism in a normal pregnancy can cause low birth weight, premature labor, spontaneous abortion, and preeclampsia.
Most of the complications of molar pregnancy (hyperemesis, hyperthyroidism, early preeclampsia) are due to high circulating levels of beta-hCG.
Beta-hCG has homology with the TSH hormone, thus can stimulate the downstream effects of increased TSH.
Molar pregnancies will presents with higher than normal levels of beta-hCG, likely will not manifest signs and symptoms of hyperthyroidism until levels are >100,000.
The symptoms of thyrotoxicosis in molar pregnancy differ slightly from that of a typical hyperthyroid state. Notably, no exophthalmos, pretibial edema, or enlarged thyroid.
Molar pregnancies often first present with vaginal bleeding, so don’t assume that your patient's tachycardia is simply due to bleeding. Go looking for concomitant thyrotoxicosis.
Symptoms of thyrotoxicosis will resolve with decreasing beta-hCG levels.
Complete molar pregnancies require D&C - check a TSH pre-operatively due to the risk of inducing thyroid storm with anesthesia induction.
R1 Clinical Knowledge - Ear Pathology WITH Dr. Ijaz
General approach to ear pain
Through varying etiologies such as infectious, neoplastic, etc
Anatomic approach, e.g. from outside to inside
Or some of each
Auricular hematoma
Due to shearing of blood vessels from underlying cartilage.
Hematomas larger than 2cm need to be incised and drained. Be sure to place a bolster dressing to prevent reaccumulation.
Some smaller studies suggest that needle aspiration may be effective, but standard of care remains I&D with bolster.
There is no conclusive evidence as to benefit of prophylactic antibiotics.
Perichondritis is a known complication. Usually due to Pseudomonas aeruginosa, often spares the lobule, and is treated with PO ciprofloxacin 500-750mg BID x one week outpatient.
Otitis externa
Breakdown of skin-cerumen barrier allows P. aeruginosa and S. aureus to cause infection.
Commonly presents with otalgia, otorrhea, pruritis, and hearing loss.
Be sure to visualize the tympanic membrane and verify that it is intact.
If the TM is ruptured then avoid ototoxic medications. Go with either ofloxacin or ciprofloxacin + dexamethasone.
Place an ear wick if the TM is not visible due to swelling.
Important for patients to follow up in 48-72 hours and know that it can take up to 2 weeks for resolution.
Malignant otitis externa
Complication of otitis externa, usually in a patient with poorly-controlled diabetes.
IV antibiotics and ENT consultation are a must.
CT head or other imaging may be indicated if you suspect a brain abscess or DVST, which may further complicate malignant OE.
Acute otitis media
Common causes include S. pneumoniae, H. flu, M. catarrhalis.
General approach is “wait and see" instead of immediate abx, unless there are red flags:
< 6 months old
6-23 months with bilateral AOM
> 6 months with severe pain, fever > 102.2, or symptoms > 48 hours
First line abx amoxicillin, second line amox + clavulanate
R4 Sim - Crush Injuries and Hyperkalemic Arrest WITH Drs. Golden, Ham, and Spigner
Crush Syndrome
In general, there is no good evidence for any of the management strategies for crush syndrome. Management is largely based on animal studies, expert opinion, and anecdotes.
Crush syndrome is cause by compression of muscle that leads to release of myoglobin, electrolyte derangements, edema, and volume loss.
With release from the compressive force there is reperfusion.
This all causes renal failure, acidosis, dysrhythmia, and shock.
Decline can be precipitous.
Prior to 1940 crush syndrome was virtually universally fatal.
Early studies included
Rabbit models of alkaline rehydration to prevent renal failure in induced acidosis.
Urine alkalinization following the bombing of London in WW II.
Mannitol or mannitol/bicarbonate “cocktail” to protect against myoglobinuric renal failure.
Bicarbonate and mannitol have been studied in retrospect, but no clear benefit was detected. This contradicted prior animal studies and lower quality evidence.
Scene safety is paramount.
There is a large body of knowledge surrounding structural collapse incidents.
Consider airborne contamination (dust, asbestos, etc.).
Liquid and biohazard contaminants
Sharps/cut, electrical, fire hazards
Temperature and lighting
Despite lack of high-quality evidence, a reasonable approach to such incidents includes:
Scene safety, PPE, environmental optimization
Primary survey to assess life threats
Consider indications for amputation if necessary for extrication, or placement of tourniquets to crush limbs prior to extrication.
Dr. Otten recommends adding a tourniquet if the patient has been entrapped longer than one hour.
Resuscitate before release with volume +/- bicarbonate.
“Crush injury cocktail” recommended by Dr. Gonzalez with FDNY: 1.5L 0.9% NS +/- 1 amp bicarb and 10mg mannitol in each liter
Ongoing volume post-extrication, urine pH > 6.5, mannitol if urine < 200-300 ml/hr, consider early dialysis for oliguria
Dr, Otten recommends volume resus before release and add bicarb.
Hemodynamic monitoring for cardiac dysrhythmias or shock
Hyperkalemic arrest
This is a possible complication of crush syndrome and as such should be anticipated.
Hyperkalemia falls into broad categories of mild, moderate, and severe from 5.5-6, 6.1-6.9, and >7, respectively.
There are characteristic EKG changes that correlate well with adverse outcomes including PR prolongation, QRS widening, 2nd degree heart blocks, and junctional rhythms.
Treatment principles include
Membrane stabilization
Calcium gluconate or chloride; only chloride is carried on Air Care currently. Take great care to avoid extravasation if you administer it through a peripheral IV.
Transcellular shift
Insulin/glucose
Albuterol
Epinephrine - works through a similar beta-agonistic mechanism and is also useful as a pressor.
Sodium bicarbonate - only useful if the patient is also academic, but in reference to crush syndrome this may also be helpful even outside of hyperkalemic arrest.
Removal
In the case of crush syndrome with rhabdomyolysis and acute renal failure, dialysis is the go-to for removal.