Grand Rounds Recap 3.16.22
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AIRWAY GRAND ROUNDS WITH DR. CARLETON
Endotracheal Tube Exchange
Some suspected cuff leaks are not cuff leaks, but rather are due to proximal migration of the ETT. Depth at teeth is not a reliable predictor of appropriate ETT position.
Management by ETT removal and attempted DL reintubation had unacceptable failure rate and complications - 46% esophageal intubation, 50% hypoxia, 24% bradycardia, 14% Cardiac arrest (CA).
Management by endoscopy through ETT was more successful but still had significant complications - 1% esophageal intubation, 15% hypoxia, 4% bradycardia, no CA.
There are several options for ETT exchange, all with varying degrees of risk, depending preceding or simultaneous endoscopy or laryngoscopy to confirm extant ETT placement and confirmation of replacement. There is no predictive tool to determine a low v. high risk exchange. Airway exchange catheters (AECs) are important tools in this process to maintain continuous airway access.
Cook Airway Exchange Catheter (CAE) - We have the 14 Fr French CAEs, which will fit inside 5 mm or greater sized ETTs. Complications of using CAEs for exchange include coiling of the CAE with ETT advancement, flopping out of the trachea and passing through the murphy eye with potential for perforation. These are located in EACH SRU against the back wall.
Aintree Exchange Catheter (AIC) - We have 14 Fr and 19 Fr
Stupid airway tricks:
If ETT exchange attempted with an AIC (56 cm long) and insufficient length protrudes to allow the ETT to be exchanged over the AIC, pass a lubricated 14 Fr AEC through the AIC then pass the ETT over the AEC +/- removal of the AIC.
If ETT exchange attempted with an 11 Fr or 14 F AEC and the ETT cannot be passed due to the gap between the AEC and the bevel tip hanging up or the AEC flexing, make the AEC fatter by passing an AIC over it.
If all you have is a bougie for ETT exchange and it is not > 2x the length of the ETT, wedge its butt end into a 4.00 mm-4.5 mm ETT to act as a lengthener and stabilizing rott, ETTs must be > 7.0 mm in this scenario.
Summary Points:
ETT exchange is potentially risky, and difficulty is unpredictable.
Exchange using an AEC is superior to alternative methods.
Pre-exchange airway assessment by laryngoscopy is essential for diagnosing potential exchange difficulties and differentiating cuff rupture from proximal ETT migration.
Laryngoscopy during exchange improves first pass success (FPS) and minimizes complications, compared to exchange with AEC, alone.
VL, not DL, should be used for pre-exchange assessment and during the exchange.
Use the largest AEC that will fit through the ETT to be used. Mind the gap. 19 Fr AEC has higher success rates and lower complication rates than 8F, 11F, or 14 F catheters.
Risk for tracheobronchial injury can be minimized by avoiding passage of AEC beyond ETT tip/carina and by not using jet ventilation.
Rotation of the ETT so the cut of the bevel faces posteriorly minimizes the potential for snagging on glottic structures
Blind passage of an AEC through an LMA is unreliable (30% success rate in one study).
Though shall not:
Pull a malfunctioning ETT without taking a look first.
Use DL for exchange when VL is available
Use an AIC for exchange when an AEC is available.
Ignore the depths of the old ETT, AEC, or new ETT
Lose continuous airway access during exchange.
R4 CAPSTONE: CREATIVE ASSESSMENTS, APPRECIATIVE INQUIRY, AND QUESTIONING BARRIERS WITH DR. LAURENCE
Summary points:
When striving for shared decision making with patients, remember Valerie Billingham’s quote, “Nothing about me, without me.” Patients' views should be considered in and form the basis for any decision that impacts their health. According to one study, more than one reasonable option may be available in more than 50% of ED patient encounters, so it is reasonable in these situations especially to incorporate patient preference with education.
Several ED-based studies have demonstrated room for improvement in our communication with patients. One qualitative study recommended that we strive for transparency when we discuss plans of care and diagnosis; that we aim to be warm and welcoming in our disposition; that we acknowledge anxiety and fear that patients may be experiencing; and that we actively listen and make patients feel heard.
Be creative when asking questions of patients as clinicians and the communities we serve as a leader. While not necessarily applicable to patient care, Photovoice is one means of creatively asking questions of communities and engaging them in the process of developing an action plan from the results.
Appreciative inquiry offers a unique way of acknowledging strengths and values of individuals to achieve change.
While it is important to incorporate strengths based assessments into our conversations, it is equally important to ask about and question barriers that exist for our patients.
R1 CLINICAL DIAGNOSTICS: ATYPICAL HEADACHES WITH DR. GLENN
Factors that make headaches atypical - SNOOP2:
Systematic symptoms - fever, chills, weight loss, immunocompromised status
Neurologic symptoms - confusion, AMS, vision changes, seizures, abnormal neurologic exam
Onset - acute, sudden, or “thunderclap” headaches
Old - patient age < 50 with no onset or progressive headache
Previous HA history - changes in headache character, severity, or frequency
Pregnant or Postpartum
Idiopathic Intracranial Hypertension (IIH) is caused by an imbalance of CSF secretion versus reabsorption.
The frequency of IIH is thought to be approximately 1 case per 100,000 per year, though frequency is increasing with the obesity epidemic.
Clinical presentation typically involves headache worse on waking (84%), vision changes (70%), and tinnitus (60%).
On exam, you may find evidence of bilateral, symmetric papilledema, but important to also assess visual acuity, visual fields, blood pressures, fundoscopy.
To diagnose of IIH, MRI is preferred, but CT is reasonable if MRI is unavailable. CT or MRI Venogram is an essential part of the work up to exclude CVST as a cause of papilledema. Providers also need to perform a lumbar puncture with opening pressure > 250 (measured in lateral decubitus position) diagnostic with normal CSF studies.
Management of IIH
Precipitous vision loss warrants neurosurgical consultation for potential VPS.
In the short term, IV steroids and serial LPs are recommended.
For long term management, weight loss, salt and H2O restriction, acetazolamide (+/- Topiramate and Furosemide) are recommended.
Giant Cell Arteritis is a large and medium vessel vasculitis that can present with headache with the potential complication of vision loss.
It is more common in females than males (2-3:1), in a Northern European population, and in patients older than 50.
30-50% of patients with GCA also have polymyalgia rheumatic
Clinical presentation of GCA often includes headache (30-80%), fever (20-50%), scalp tenderness (40-70%), and vision loss (12-40%).
To work up GCA, secure elevated ESR and CRP, which are admittedly imperfect markers for GCA, though highly sensitive.
To diagnose GCA, perform a temporal artery biopsy.
1990 Criteria for the Classification of GCA by American College of Rheumatology. Can make diagnosis when ⅗ below criteria are met with 93.5% sensitivity and 91.2% specificity.
Age > 50 at disease onset
New headache
Temporal artery abnormality (tenderness)
ESR > 50
Abnormal temporal artery biopsy
Management of GCA
Prednisone - 1000 mg/day x 3 days if vision loss; 40-60 mg/day x 2-4 weeks if no vision loss
ASA 81 mg qD
Ophthalmology consult
Rheumatology follow-up
Treatment of GCA should never be deferred until biopsy given risk of permanent vision loss
Acute angle closure glaucoma (AACG) is an eye and vision threatening disease characterized by narrowing or closure of the anterior chamber angle, and is often associated with a headache.
It is the second leading cause of blindness in the world.
Clinical presentation often involves headache, blurred vision, eye pain, and “halos” around lights. Patients may also report nausea and vomiting. It can be precipitated by walking into dim rooms, anticholinergics, sulfa drugs, serotonergic drugs.
To diagnose AACG, physical exam is your best tool and may demonstrate a monocular red, painful eye, pupil asymmetry with a sluggish or non-reactive pupil to light, elevated IOP > 30-40, optic nerve cupping
Management of AACG - Beta-blocker (Timolol) > Alpha-2 agonist (Brimonidine) > Carbonic anhydrase inhibitor (Dorzolamide) + Acetazolamide
Trigeminal neuralgia (TN) typically arises as a result of compression of the trigeminal nerve by an aberrant loop of artery or vein, though some cases may come from multiple sclerosis and brainstem lesions.
Clinical presentation of TN involves paroxysmal electric/sharp pain in one or more of the nerves in the V1-V3 distribution, occurring for 1-5 seconds.
The diagnosis of TN is clinical, though often patients will get head imaging with MRI or CT/CTA at some point to rule out other causes.
Management of TN:
First line - Carbamazepine, Oxycarbazepine
Second line - Gabapentin, Lamotrignine, Baclofen, Botulin injection
Rescue agents - IV lidocaine, IV phenytoin, SQ sumatriptan
Beware adverse agents with Carbamazepine, Oxcarbazepine
R2 CPC: DIGOXIN TOXICITY WITH DRS. KEIN AND ADAN
Digoxin reversibly inhibits Na+-K+ ATPase pump in the myocardium, increased intracellular Na+, decreased intracellular K+ inhibiting Na+-Ca2+ exchange and increasing intracellular calcium concentration. Increased intracellular Ca2+ concentration increases cardiac contractility.
In toxic doses, intracellular calcium elevates further and triggers afterdepolarizations. This increases the risk of arrhythmias while shortening the refractory period and increasing automaticity
Acute toxicity:
GI: nausea, vomiting, abdominal discomfort
CV/pulm: palpitations, dyspnea, syncope, dysrhythmias
CNS: lethargy, confusion, delirium, weakness
Hyperkalemia
Chronic toxicity:
Similar to acute presentation, though with fewer GI symptoms and more CNS symptoms; may have green-yellow visual disturbances and blurred vision; hypokalemia secondary to concomitant diuretic use
EKG findings of scooped ST segments or T wave flattening do not necessarily indicate toxicity and can also be present with therapeutic dosing. Arrhythmias are more common secondary to increased automaticity and decreased AV conduction.
Evaluation and Management:
Dig level
Initial and 6 hours for acute, single level for chronic if >6 hours from ingestion
>4 in chronic, >10 in acute
Poor correlation with toxicity overall, especially in chronic
Electrolytes, renal function
Correct hypomag, hypoK
Tx for hyperK: digifab, can temporize in interim
EKG
Best tx for bradycardia/tachycardia: digifab
Can use atropine to temporize
Avoid pacing, cardioversion --> can precipitate Vtach
?Lidocaine for Vtach
When to bind
Controversial
Acute: K>5, level 15+ ng/mL (any time) or 10+ (>6 hrs post ingestion), life threatening dysrhythmia
Chronic: life-threatening dysrhythmia, supratherapeutic concentration with AMS/HD instability/dysrhythmia
How much to use
Ask MDCalc, pharmacy, poison control
If unknown: peds= 5 vials, acute= 5 (stable)/10 (unstable)/20 (arrest), chronic= 3-6
PEDIATRIC SIMULATION WITH PEM COLLEAGUES
Types of ductal dependent lesion: truncal atresia, transposition of the great vessels, truncus arteriosus, pulmonary atresia or critical pulmonary stenosis, tetralogy of fallot, hypoplastic left heart syndrome, critical aortic stenosis, coarctation of or interrupted aortic arch
Key elements of history and clinical presentation: poor feeding secondary to work of breathing or fatigue, potential inconsistent prenatal care
Management:
Ensure you are getting a pre- and post-ductal dependent lesion saturation - should aim for right upper extremity (to ensure you are not picking up on a lesion before the left subclavian) and one of the lower extremities
You can access an umbilical vein up to 7-14 days after birth.
Do not administer significant supplemental oxygen because it can worsen shunt. Try not to intubate. Nasal cannula at 2 LPM should not do too much damage.
Cautious fluid administration (small aliquots) to avoid volume overload - aim for 5 cc/kg bolus and reassess
Prostaglandin E1 (Alprostadil) is administered to maintain the patency of the ductus arteriosus when a cyanotic lesion or interrupted aortic arch presents in a newborn.
Dosing: 0.05-0.1 mg/kg IV bolus
Risk of prostaglandin administration includes apnea.
