Grand Rounds Recap 4.1.20
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Hypoxemia in the Ed WITH Dr. Shaw
Initial Approach
Consider any patient who remains hypoxemic (SpO2 < 90%) on greater than 50% FiO2 to be refractory hypoxemia
Classification of the severity of hypoxemia using P/F ratios informs decision-making regarding escalating therapy, but does not necessarily require an arterial blood gas immediately as initially SpO2 can approximate PaO2 (rough memory tool seen on the right)
Evidence-based management of ARDS requires lung protective ventilation (LPV), consisting of appropriate weight-based tidal volumes, minimizing plateau pressure, minimizing oxygen toxicity, and titration of PEEP based on FiO2 needs
The ARMA trial (2000) – established a mortality benefit for low tidal volume ventilation (4-8mL/kg predicted body weight based on measured height) in ARDS patients assuming no significant underlying acidosis or other indications for high minute ventilation.
However relatively few patients in the ED receive low tidal volume ventilation and many ARDS cases go unrecognized. Hypoxemia was managed by increasing FiO2, but infrequent PEEP titration. Ventilator settings started in the ED often continued in the ICU from therapeutic momentum
In a follow up before-and-after study, Fuller (2017) showed that implementation of a ventilator protocol consisting of low-tidal volume ventilation, lower FiO2, amongst other interventions improved adherence to LPV principles and mortality in the ED setting.
The provider should assess the ventilator at the bedside and ensure that the targeted volumes are actually being delivered. If tidal volumes are not being delivered appropriately, consider augmenting analgesia/sedation, working with RT to change flow parameters or inspiratory time (to maximize patient comfort), or paralysis
FiO2 should be minimized, and if patients require increasing amounts of supplemental oxygen, PEEP should be titrated in accordance with the ARDSnet table
Elevate the head of the bed to optimize V/Q matching and place a gastric drainage tube to minimize aspiration risk
Obtain a blood gas (venous or arterial) 30 minutes after initiation of mechanical ventilation to ensure appropriate minute ventilation. These patients usually deserve an arterial line for frequent hemodynamic instability and trending of ABG’s
Adjunct medications & modes
Sedation promotes patient-ventilator synchrony, decreasing discomfort and allowing for total control of ventilation and oxygenation.
Paralysis can be considered if dysynchrony is persistent despite deep sedation, and has been shown in at least one large RCT to improve mortality in severe ARDS patients (ACURASYS, 2010).
A recently published large scale RCT (ROSE, 2019) showed no difference between paralysis and placebo, however still remains common practice pattern
Rescue Therapies
Proning has been shown to significantly improve mortality in the PROSEVA trial (2013), and can be considered if maximal therapy has had no effect in the ED, but requires experience to be done well. Can be more technically challenging in the ED setting.
Consider contacting critical care specialists (intensive care nurses, RT’s, or critical care physicians) to help with logistics and ensure patient safety if attempting in the ED (or anywhere it is not typically performed).
Inhaled pulmonary vasodilators (nitric oxide, epoprostenol) have been shown to improve oxygenation but not affect patient centered outcomes, including mortality – consider as a bridge to ICU admission, transfer, or salvage therapy (i.e. VV ECMO). Given that V/Q mismatch seems to be among the primary etiologies of hypoxemic failure in COVID patients, has potential, although will all COVID patients, data in lacking.
US Grand Rounds mimics WITH Dr. Minges
Case #1: Where is the common bile duct?
First identify the portal triad (cystic duct, hepatic artery, hepatic portal vein). Vein is larger and deep to the artery and duct which is the classic “mickey mouse” view. The left “ear” of the mickey mouse is often the common bile duct.
The main lobar fissure is a bright hyperechoic line that connects the portal vein to the to the gallbladder fossa.
Tips for identifying the CBD:
1. Inspiratory Pause
2. Use color or power doppler to distinguish between vessels
3. Left lateral decubitus positioning
Case #2: False positive hydronephrosis
Mimic #1: Prominent renal vasculature can be confused for mild to moderate hydronephrosis. Putting color or power doppler on these areas can help distinguish vessels from the collecting system.
Mimic #2: Perinephric cysts can be confused for hydronephrosis, however often have a rounded appearance and doesn’t connect to the rest of the collecting system.
Mimic #3: Extrarenal pelvis notably located outside the renal hilum. Appears as a hypoechoic mass. However it is not associated with dilated calyces, parenchymal thinning or enlarged kidney.
Case #3: Right heart strain that isn’t really there
Left ventricle can appear to have a false D sign in parasternal short axis view if cut at an angle / foreshortened.
PSSA view can be obtained at several different levels (basal, apical, mid), however we most often use the mid-papillary view to asses RV pressure increase
Apical 4 view is the most difficult to obtain but very useful in assessing chamber size. Should see LV apex and atria should be rounded (not appearing to be cut in half).
Case #4: Do B lines always equal pulmonary edema?
B lines can be seen in multiple disease processes, however the pattern of B lines can be more helpful to distinguish:
Diffuse - cardiogenic pulmonary edema, pulmonary fibrosis
Focal/scattered: ARDS, pneumonia, pulmonary contusion/hemorrhage
CPC WITH Dr. Pulvino vs Dr. Goel
Case: Elderly male with a history of L MCA stroke, HTN, DM, remote cranial tumor resection presenting with ataxia. Also reports increased thirst and urination and has been out of his insulin. Physical exam notable for ataxia with leaning to the left with ambulation. Diagnosis: Dorsal medullary stroke found on MRI
Ataxia: “the loss of control of one’s body movements” or “impaired coordination”
Causes of Ataxia:
Sensory: often a proprioception problem; can co-exist with a cerebellar problem, but need to ask “what is the dominant feature”
nystagmus often absent, romberg’s often positive
Cerebellar: long differential including stroke, acute disseminated encephalomyelitis, basilar migraine, MS, wernicke encephalopathy, paraneoplastic syndrome, abscess/tumor, vasculitis, alcohol related cerebellar degeneration
nystagmus often present, romberg’s classically negative
Vestibular: inner ear problem contributing to gait changes
Diabetes Insipidus: a condition characterized by “large amounts of dilute urine and increased thirst”
Central DI: No ADH
Nephrogenic DI: can’t “see” ADH (can be seen in lithium toxicity)
Psychogenic DI: just can’t stop drinking water
Dorsal Medullary Stroke:
Presents with acute isolated vestibular syndrome
Medullary infarcts constitute 7% of ischemic strokes
Isolated dorsal medullary stroke is rare
Most common risk factors are age and diabetes
Over half of patients studied show signs of both peripheral and central vestibulopathies
MRIs often initially negative
Long term prognosis is excellent
CPC Dr. Irankunda vs Dr. Continenza
Digoxin Toxicity
Reversibly inhibits Na/K pump causing an increase intracellular sodium and decrease in intracellular potassium which can cause myocardial irritability
Digoxin has very good oral absorption. With an acute ingestion, levels peak at 6 hours after ingestion vs 4-6 days with those patients with renal dysfunction
3rd most common adverse drug event resulting in hospitalizations
Digoxin is inactivated in the GI tract and many antibiotics cause inhibition of inactivation (especially macrolides) which can lead to increased levels of toxicity, along with many other drug interactions
Narrow therapeutic window: 0.5-1.0 ng/ml is normal, with >2.0 ng/ml toxic
Presentation
Headache, confusion, delirium, visual disturbance (yellow ring distortion classic, although blurred vision is more common), GI symptoms (nausea, vomiting, anorexia), cardiac symptoms (palpitations, dyspnea, bradycardia)
EKG findings that are common include PR prolongation with scooping of ST segment. These findings do not necessarily mean toxicity, but can be seen at therapeutic levels.
Treatment
Based on K and digoxin levels; also need to know if acute or chronic
Acute: Treat if K>5, digoxin level >15 or digoxin level >10 six hours post ingestion or arrhythmia
Treatment for acute poisoning is often 10-20 vials of DigiFab
Chronic: patients usually have underlying renal dysfunction and hypokalemia can actually worsen toxicity. Will treat if arrhythmia, hemodynamic instability, but if normal vital signs and no ectopy will not treat.
Treatment for chronic poisoning is often 3-6 vials of DigiFab
Of note, DigiFab is very expensive.
Can treat other symptoms as well:
Tachydysrhythmias with lidocaine and magnesium, but no cardioversion as this can lead to VT or VF
For high block AV block, can do atropine and transvenous pacing
r4 capstone WITH Dr. jarrell
“The recipe calls for a tablespoon of sprinkles, but I don’t think anyone should limit their sprinkle intake.”
- the great Dr. Jarrell
Vanilla Mug Cake
Ingredients:
2 tablespoons unsalted butter
1 tablespoon milk
1/2 teaspoon vanilla extract
1 large egg yolk (*do not add in the egg white)
2 tablespoons white sugar
4 tablespoons all-purpose flour
1/2 teaspoon baking powder
1 tablespoon sprinkles (optional - but highly encouraged by Dr. Jarrell)
Recipe:
Add the butter to your mug and microwave until melted (about 30 seconds).
Whisk in the milk, vanilla extract, egg yolk & sugar with a fork.
Then whisk in the flour and baking powder. Stir in the sprinkles.
Microwave for 60-90 seconds on medium power. The top should look set when it's done.
Cool for at least 1 minute before enjoying.
