Grand Rounds Recap 1.5.22
/MORBIDITY AND MORTALITY WITH DR. WALSH - R4 CASE FOLLOW-UP: COMPLICATED GAS WITH DR. THODE - R1 CLINICAL KNOWLEDGE: SUBMERSION INJURIES WITH DR. HARWARD - COLLABORATION WITH MEDICAL DEVICE INNOVATION AND ENGINEERING WITH DRS. PANCIOLI AND BROWN - R1 CLINICAL DIAGNOSTICS & TREATMENT: FACIAL FRACTURES WITH DR. BROWER - CPC: HYPERTHYROIDISM WITH DRS. FABIANO AND THOMPSON
MORBIDITY AND MORTALITY WITH DR. WALSH
Hypokalemia
In general, a potassium ≥ 3.0 is well tolerated, and oral replacement is appropriate. IV potassium should be used for patients with DKA requiring insulin, patients with GI losses who likely cannot tolerate or would have inadequate PO absorption, severely low levels and patients with GI anatomic changes or issues with motility. As a reminder, a serum change of 0.3 mEq/dL is roughly equivalent to a total deficit of 100 mEq.
IV potassium replacement has several known complications, including extravasation, phlebitis, and risk of asystole. The designated rates for repleting potassium IV are:
Peripheral Line 10 mEq/hr
Central Catheter 20 mEq/hr
Consider: 20 mEq can be achieved with 2 IVs
Potassium repletion in ESRD/AKI requires some additional consideration. While the rate of repletion acceptable is unchanged, there is concern for rapid accumulation. In light of these, providers should decrease the total body potassium deficit by half and either check a repeat potassium after 50% of the dose has been administered or at 4 hours.
Similarly, providers should be mindful of the risks of hypokalemia in patients with a history of heart failure. Hypokalemia leads to prolonged repolarization and can subsequently contribute to long QT intervals, increased risk of ventricular arrhythmias (which account for 50% of CHF related deaths), increased risk of sudden cardiac death, and worsened diastolic dysfunction. In light of this, the goal is for potassium homeostasis in patients with heart failure with an ideal K > 4.0 mEq/dL.
Hypokalemia is associated with increased mortality in both the ED and ICU settings. Across several studies, a U-shaped curve is observed for patients with either hyperkalemia or hypokalemia, though admittedly, untreated hyperkalemia has a larger mortality increase. In one study, there was increased mortality if the potassium remained unbalanced by day 2 of hospital stay, and, interestingly, no change in mortality was noted if the initial K was less than 2.5 compared to more mild hypokalemia.
With respect to hypokalemia in cardiac arrest, the AHA Guidelines state that providers can replete potassium at 2 mEq/min via any route in cardiac arrest or in the presence of a malignant arrhythmia. The rate of repletion should be decreased once ROSC or NSR is achieved. However, there is minimal evidence to support this save case reports. At UC, our pharmacists stipulate that the max dose is 40 mEq during either of these scenarios. Furthermore, it is compatible with Mg sulfate, CaCl, Epinephrine, Amiodarone, Lidocaine, and Vasopressin.
Summary:
Hypokalemia can be replaced at the usual rate in ESRD patients.
CHF patients have an increased risk of arrhythmia and sudden cardiac activity with hypokalemia.
Overall mortality is increased in ICU patients with dyskalemia.
Delays in potassium repletion increase mortality in critically ill patients.
Potassium can be replaced at 2 mEq/min in cardiac arrest and malignant arrhythmias
Safe disposition for opioid overdoses
Opioid overdose data is somewhat limited by body of research performed during the “Heroin era,” which may not reflect increase in fentanyl analogue and prescription drug abuse seen clinically. Opioid overdose duration of action is affected by route of administration (IM v. IN v. IN), opioid used, CYPD6 enzymes, and renal function.
Naloxone remains our go-to competitive antagonist with onset in 1-2 minutes, peak effect in 15 minutes, and a duration of action of 30-90 minutes. Of note, Naloxone’s duration of action intranasally may be longer since the dose is higher.
Safe Discharge for opioid overdoses per the 2018 HOUR Study by Clemency et al
This was a prospective observational study that evaluated 358 patients who received Naloxone pre-hospital and compared outcomes, including adverse events within 24 hours, between patients discharged according to clinician gestalt v. modified St. Paul Early Discharge Protocol
The modified protocol includes the following criteria for discharge:
1 hour of observation since administration of Naloxone
Mobilize, as usual
O2 saturation > 95% (*increased from 90% in original study)
RR 10-20 bpm
HR 60-100 bpm
Normothermic between 35-37.5 degrees Fahrenheit
GCS 15
Results: Sensitivity of gestalt and protocol were roughly equivalent with respect to AE. Gestalt alone was 85.4% sensitive which increased slightly to 87.8% when combined with the protocol.
Predictors of longer observation included: oral ingestion, body-packing, long-acting formulation (ie, Methadone), need for additional doses of Naloxone and/or a drip
There are no studies that suggest when you should start a Narcan drip, but a rule of thumb is to do so if a second or third dose is required or if there is another predictor of a longer duration such as known Methadone use.
Narcan IV/IM intermittent dosing: 0.4 mg-2mg IV/IM with repeat dosing at 1-3 minutes
Narcan gtt:
Initiate at ⅔ bolus dose/hr
Titrate 0.1-0.2 mg/hr increments
Wean 0.1-0.2 mg/hr every 2 hours
Summary:
Duration of opioid effect in overdose is hard to predict.
Narcan has a known duration of action around 60 to 90 minutes.
Normalization of vital signs, mobilization, and normal mental status at 1 hour suggest safe discharge.
If known, the route or type of opioid can be useful in predicting prolonged intoxication.
Antibiotics to treat pyelonephritis
IDSA Guidelines (2011) for treatment of pyelonephritis in women:
Urine culture should be sent for all patients with suspected pyelonephritis. (A-III)
Oral ciprofloxacin BID is appropriate when resistance is < 10%. (A-I)
If resistance is > 10%, a one time dose of Ceftriaxone should be used. (B-III)
Once daily Ciprofloxacin ER or Levofloxacin can be used in lieu of BID dosing. (B-II)
TMP-SMX can be used if a pathogen is susceptible. (A-I)
If pathogen is unknown, a one time dose of Ceftriaxone should be used (B-II)
Oral 𝛃-lactams are less effective than other agents. (B-III)
Common pyelonephritis pathogens include the following: E. coli 70-90% >> K pneumoniae, P. mirabilis > Enterococcus, Pseudomonas, S. Aureus, S. Saprophyticus
According to our antibiogram, we should use Ceftriaxone regardless of outpatient or inpatient disposition given generally favorable sensitivities. Our additional treatment options include the following:
Fluoroquinolone + 1 dose of Ceftriaxone
Consider risk/benefits discussion of fluoroquinolone AEs, including tendinopathies, AMS, seizures, and dissection
TMP-SMX + 1 dose of Ceftriaxone
Call back to previous M&M to beware of risk of worsening renal function with TMP-SMX
In one prospective randomized, open label study, treatment with Ceftriaxone 1 g daily x 10 days was compared with Ceftriaxone 1x followed by Cefixime daily and outcomes assessed at three days with 100% bacterial eradication in both groups and equivalent clinical care. Another study evaluated performance of TMP-SMX or a fluoroquinolone v. Cefixime for outpatient treatment of pyelonephritis and found that TMP-SMX and fluoroquinolones had a 23% failure rate v. 0% failure rate for Cefixime.
Based on one retrospective study that assessed the predictive utility of prior urine cultures for a new infection, they found that isolated organisms corresponded about 57% of the time at 4-8 weeks and 49% at greater than 32 weeks. The susceptibility profile was the same or better with 83% at 4-8 weeks and 75% at greater than 32 weeks. E Coli isolate predicted correspondence with an OR of 1.39. However, it is important to note that sensitivities really only predict local resistance.
Summary:
Pyelonephritis is largely a clinical diagnosis.
A one time dose of Ceftriaxone should be used with fluoroquinolones or TMP-SMX.
Oral 3rd generation cephalosporins have excellent cure rates.
Culture data predicts organism and resistance.
Antibiograms are local.
Ultrasound in cardiac arrest
Ultrasound can be used to identify 5/10 H’s and T’s: hypovolemia (flat IVC, poor LV filling), cardiac tamponade (free wall rupture, dissection), tension pneumothorax (difficult to assess lung sliding, but B lines may be present), thrombosis (RWMA for AMI, RHS pre-arrest or DVT findings for PE), trauma (FAST exam could also signal ruptured AAA or ectopic in the right patients).
The REASON Trial by Gaspari et al published in 2016 was a multicenter, non-randomized protocol observation study that evaluated the outcomes (survival to admission, survival to discharge, ROSC) associated with POCUS performance at the beginning and end of ACLS. They found that:
Of the 33% of patients with a PEA cardiac arrest, 3.8% of those with cardiac activity on US survived to discharge v. 0.6% of those without cardiac activity
Of the 5% of patients with a pericardial effusion, 15.4% had discharge survival after pericardiocentesis vs. 1.3% that had discharge survival without pericardiocentesis.
There is a valid concern that the use of ultrasound prolongs pulse checks during cardiac arrests (17-21s for US v. 11-13 by palp in one study). Importantly, shorter POCUS delays are associated with increased ROSC and survival to discharge. Factors that may prolong pulse checks include provider inexperience (US faculty 4.1s faster) and single provider resuscitations (6.1s slower).
However, the CASA (Cardiac Arrest Sonographic Assessment) Protocol proposed that specific studies be performed during each pulse to reduce duration of pulse checks:
Evaluate for cardiac tamponade
Evaluate for right heart strain
Evaluate for cardiac activity
Consider eFAST for AAA, PTX, or ectopic
There should be a 10 second pause during pulse check for US, which should be performed by a second provider.
When the CASA Protocol was evaluated, they found that the duration of pulse checks decreased by 4s (though still about 15 s), that having the probe in position decreased pulse checks by 3.1s, and that US faculty were 3.1s faster.
Other tips and tricks for use of POCUS in cardiac arrest:
Find your window 15s before the pulse check
Subxiphoid and apical 4 chamber views are ideal during an arrest
Have someone count the time and stop at 8 seconds
No window should equal no cardiac activity and resumption of compressions
Review the image after CPR is restarted
Lung sliding will be absent, look for B-lines
Consider evaluating the carotid or femoral artery during pulse checks
Summary:
Ultrasound can determine the cause of cardiac arrest.
Ultrasound improves survival in treatable conditions.
The CASA protocol decreases cognitive load and time to obtain images.
Put the probe on the chest before pausing compressions
Have a second provider perform the ultrasound
Limit your pause to 10s, even if you don’t get a window
Tracheal stenosis
Tracheal stenosis is defined as infraglottic stenosis extending as far as mainstem bronchi. Patient presentation with tracheal stenosis is non-specific, but may include dyspnea, cough, and wheezing. It often will take patients a few ED presentations to be diagnosed because, interestingly, they may experience transient improvement with beta-2 agonist therapy.
Tracheal stenosis most often occurs as a result of iatrogenic intervention, specifically intubation, (54.7% of patients with stenosis), followed by idiopathic etiology (18.5%), autoimmune (18.5%), and traumatic (8%). Stenosis typically develops greater than 7 days after extubation and occurs in 1-21% of intubated patients and 16% of tracheostomy patients.
The gold standard for diagnosis is bronchoscopy; however, CT scan is 100% sensitive for obstruction, so it’s really quite good.
Why is this important? We are likely to see an increase in patients who experience this complication given increased number of tracheostomies in COVID patients.
The Empey Index (FEV1:PEFR) is a way of predicting an upper airway obstruction that can be performed at the bedside. At high lung volumes, flow is dependent on effort and the pressure within the alveoli. Upper airway obstruction increases the resistance and reduced flow at high volumes. At low lung volumes, the collapse of the bronchioles plays a greater role in flow. FEV measured over 1s compiles these two factors and is less affected by airway obstruction whereas PEFR is measured at initial 2ms of maximal expiration so more affected. A normal ratio is < 10. Greater than 10 suggest subglottic stenosis. The Empey Index has high sensitivity (96%) and high specificity (94%) for subglottic stenosis.
Summary:
Tracheal stenosis is largely iatrogenic after intubation or tracheostomy.
Prolonged intubations from COVID will likely increase the number of cases.
CT scan of the neck is diagnostic.
The Empey Index is a bedside test with great sensitivity and specificity.
CVC Line Placement and Confirmation
The risk of central line associated bloodstream infections (CLABSIs) with site selection has been frequently studied. One meta-analysis by Marik et al published in 2012 included 2 RCTs and 8 cohort studies and found no difference in infection risk between catheter site location, though removed two studies that were reportedly outliers and which found an increased risk of infection in femoral lines compared to IJs with a RR 1.90.
Considerations in site selection:
Subclavian:
Non-compressible site in hemorrhage
Increased risk of subclavian stenosis/clot
Acute angle of brachiocephalic to SVC can cause lower flows
Internal jugular:
Right side preferred due to less acute angle of the vessel
Femoral:
Possible increased infection risk
Recirculation rates: 8% with 24 cm catheter v. 30% catheter with 15 cm catheter
Increased life of CRRT circuit when compared to SCV and IJ.
Ultrasound guidance tips and tricks:
Puncture 2-3 cm proximal from the clavicle for IJs to decrease risk of puncturing lung.
Gradually track needle tip in small increments until in the vessel
Evaluate wire in long axis view to assess position in vessel
Means for using ultrasound to confirm CVC position/malposition include dynamic US guidance during procedure, evaluation for lung slide after placement, and confirmation by evaluating the vessel or with an agitated saline study. Several studies, including two metaanalysis, have evaluated these approaches found 100% sensitivity for pneumothoracies and more efficient evaluation than CXR.
Summary:
Femoral access infection risk may be lower than previously thought.
Subclavian vein should be avoided for dialysis access.
Femoral dialysis access should use the longest available catheter.
Ultrasound can be used to rapidly determine catheter misplacement.
R4 CASE FOLLOW-UP: COMPLICATED GROUP A STREP WITH DR. THODE
Group A Streptococcus (GAS) infection is caused by S. pyogenes and is the most common cause of bacterial pharyngitis and can also manifest as cellulitis. Complications are categorized as suppurative and nonsuppurative. Suppurative complications include necrotizing fasciitis, bacteremia, peritonsillar abscess/cellulitis, otitis media, and sinusitis. Nonsuppurative complications include scarlet fever, acute rheumatic fever, poststreptococcal glomerulonephritis, PANDAS, and strep toxic shock syndrome.
The primary reasons we treat GAS is to prevent suppurative complications and acute rheumatic fever, to prevent transmission, and to reduce duration and severity of symptoms.
Scarlet fever is caused by the GAS exotoxin and classically manifests as a sandpaper rash (diffuse erythema that blanches with pressure and numerous small “papular” elevations giving it a sandpaper quality), circumoral pallor, and a red strawberry tongue. Treat with Penicillin or Amoxicillin.
Acute rheumatic fever (ARF) typically occurs 2-4 weeks after GAS pharyngitis infection. To diagnose ARF, patients must have evidence of either 2 major manifestations or 1 major and 2 minor manifestations, which also vary depending on whether the patient falls into a low-risk or moderate/high-risk population.
Major criteria: clinical/subclinical carditis, arthritis, chorea, erythema marginatum, subcutaneous nodules
Minor criteria: arthralgias, fever, ESR ≥ 30 and/or CRP ≥ 3.0, prolonged PR interval
ARF Treatment: Patients with acute rheumatic fever should start on therapy for the symptomatic management of acute rheumatic fever, including salicylates and anti-inflammatory medicines to relieve inflammation and decrease fever, as well as management of cardiac failure. These patients should also be started on antibiotics for treatment of group A strep pharyngitis, regardless of the presence or absence of pharyngitis at the time of diagnosis, in order to eradicate any residual group A strep carriage
Poststreptococcal glomerulonephritis is the most common cause of acute nephritis in children and can range from asymptomatic to the edema, hematuria, and hypertension classic for nephritic syndrome. Treatment is supportive care.
Explosive pleuritis was first characterized in 1986 as the rapid development over 24 hours of a pleural effusion involving more than 90% of the hemithorax, which is often, but not always associated with GAS. The pathogenesis is from streptococcal debris that blocks peribronchial and subpleural lymphatics. Most data we have at this point are case reports. Based on these, the pleural effusion is often loculated and patients fare better with antibiotics and prompt surgical drainage, often requiring a VATS procedure.
Reminder for various tube sizing in children:
1 x ETT = (age/4) + 4 (formula for uncuffed ETT)
2 x ETT = NG/OG/foley size
3 x ETT = depth of ETT insertion
4 x ETT = chest tube size (max for hemothorax)
R1 CLINICAL KNOWLEDGE: SUBMERSION INJURIES WITH DR. HARWARD
A submersion injury is essentially drowning. Drowning is a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium.
Epidemiology of drowning:
Who: 25-30% of drownings occur in those ages 0-3 years old, 25% in those 4-18 years old, and 65-70% occur in males.
Why: 40-60% of drownings involve EtOH, 25% other substances, 1-2% arise secondary to cardiac issues (esp long QT syndrome)
When: 60% of drownings occur during the summer
Where: Older individuals tend to drown in natural water whereas younger patients tend to drown in bathtubs, private or public pools
Pathophysiology:
When someone drowns, they experience a reflex inspiration with subsequent surfactant washout and dysfunction and possible pulmonary edema, hypoxia, cardiac arrhythmia, and hypoxic ischemic brain injury as sequelae.
Pulmonary edema occurs due to disruption of the alveolar/capillary membrane and may occur irrespective of liquid type (chlorinated or non chlorinated, isotonic or hypertonic).
Is “dry drowning” real?
Previously, drowning was categorized into “dry drowning” and “wet drowning;” however, “dry drowning” as a concept, though sometimes discussed in the media, has been further investigated and is not likely a real clinical entity based on several studies, including one by Lunetta et al.
This was a retrospective study of drowning victims, which found that there was a very low incidence of “death of persons found in water who have normal lungs and do not have penetration of liquid in the airway.”
In sum, “all drownings occur in liquid, and therefore, all drownings are wet.”
Drowning Management: This depends on the grade of injury.
Grade 1 drowning are defined by if the patient is awake with normal lung auscultation and a cough.
Grade 1 drownings typically do not require further care and have 100% survival; however, you can consider transport for further evaluation if concerning events preceding the drowning or significant injuries unrelated to the drowning.
Grade 2 drownings are defined as abnormal lung auscultation with rales in some lung fields in awake patients.
Appropriate to supply some low flow O2 by NC with 6-8 hour period of observation and to discharge if adequate arterial O2. Estimated 99% survival.
Grade 3 drownings are defined as abnormal lung auscultation with rales in all fields and a normotensive blood pressure.
Appropriate to supply high flow supplemental O2 and consider ICU admission for respiratory monitoring. Estimated 95-96% survival.
Grade 4 drownings are defined as abnormal lung auscultation with rales in all fields and hypotensive blood pressure.
Appropriate to supply high flow supplemental O2 or consider intubation as well as crystalloid resuscitation +/- pressor support. Estimated 78-82% survival.
Grade 5 drownings are defined by patients who are not awake or breathing spontaneously, but do have a pulse.
Plan to intubate, provide crystalloid resuscitation +/- pressor support. Respiratory arrest may reverse quickly in these cases. Estimated 56-69% survival.
Grade 6 drownings are defined by patients who are not awake or breathing spontaneously and do NOT have a pulse.
Management: Only initiate resuscitation if submerged for < 1 hour
Resuscitate according to ACLS protocols with rewarming
Estimated 7-12% survival
Resuscitation futile if submerged for > 1 hr
Drowning can be a fatal insult due to ARDS, pneumonia, atypical infections, bronchospasm, hypoxic pulmonary vasoconstriction, and myocardial ischemia that can occur as a result.
With respect to hypothermia in hypoxic drowning victims, hypothermia preceding hypoxia is a poor prognostic factor in part because it suggest a possible cause for the drowning and prolonged exposure time whereas hypothermia following hypoxia suggests possible neuroprotective effect and improved prognosis.
Focus on special population - scuba and CCRB divers:
Remember: Gas dissolves in solution under high pressure. When pressure relieved, the gas is released. Some gases have narcotic effects at high pressures, and others become toxic.
To mitigate these effects, some divers blend different gases together.
An unresponsive diver may be hypoxic or hyperoxic and may be breathing Helium or H2.
Summary points:
Drowning is defined by primary respiratory impairment.
Surfactant washout and pulmonary edema lead to shunt physiology.
Hypoxia leads to bradyarrhythmias and cardiovascular collapse.
Hypothermia may help or hurt, depending on when, how cold, and how long it lasts.
Pediatric drowning should prompt further medical and social investigation.
Not all divers breathe air, and physiology changes with depth.
COLLABORATION WITH MEDICAL DEVICE INNOVATION AND ENGINNEERING WITH DRS. PANCIOLI AND GORDON
The MDIEP Program supports 60-70 biomedical engineering (BME) students annually and collaborates with 35-40 clinical partners, including faculty in Medicine, EAS, DAAP, and Business Schools and at CCHMC, UCMC, and area industries.
These collaborations are intended to tackle real problems and yield the complete creation of 15-20 design programs that progress from concept to feasibility.
These collaborations benefit from lab space that includes 3D printing, electronics prototyping, VR/AR simulation suites, and verification and validation labs.
Collaborative Overview:
Opportunity to work with top student teams
Needs assessment and assessment of competitive landscape
Proof-of-concept prototyping (2D/3D design)
Exploration of alternative designs
What they need from us if interested:
Identify unmet clinical needs
Guide a student design team
Provide clinical insight, exposure through observation, interviews, active participation.
Sample projects: Maxillofacial stapler collaboration with Dr. Krishnan of Oral Maxillofacial Surgery
MDIEP Capstone Project Timeline:
June/July: project identification, student team applications
Aug-Dec: team assignment, clinical on-ramp, initial designs delivered
Jan-March: device testing and design iteration, clinical immersion
April/May: DHF delivery, end-of-year showcase, project lifecycle evaluation
R1 CLINICAL DIAGNOSTICS AND TREATMENT: FACIAL FRACTURES WITH DR. BROWER
Emergency evaluation of maxillofacial trauma begins with the primary survey.
Airway management:
Ensuring airway patency is of the utmost importance as up to 42% of patients with severe maxillofacial trauma require intubation.
Airway management in maxillofacial trauma is complicated by three primary factors:
Midface/mandibular instability, especially Le Fort 2/3 fractures, which impeded adequate mask-seal and BMV.
Soft tissue edema, posteriorly displaced tongues, and foreign bodies (such as dislodged teeth) impede placement of extraglottic devices
Soiled airways due to hemorrhage or emesis complicate laryngoscopy and limit video laryngoscopy and awake looks with endoscopy.
Airway management pearls:
Don’t let the patient drown. Clear their C-spine and sit them up if you are able to or use manual in-line cervical immobilization.
Suction, suction, suction. Get the DuCanto, have pediatric bougie ready to thread through suction if need be.
If you can’t BVM, consider placing an EGD (especially, an i-Gel given ability to intubate through it); however, you must make sure the airway is not obstructed before placing.
When life gives you a bloody facial trauma, make SALAD (Suction Assisted Laryngoscopy for Airway Decontamination)
Control hemorrhage aggressively
Given increased vascularity of facial structures, the incidence of severe and life-threatening hemorrhage in maxillofacial trauma ranges from 1-11%.
Control hemorrhage early with direct pressure - press on it or pack it.Consider that midface fractures can lead to significant epistaxis, so providers should quickly proceed to more aggressive control measures like posterior nasal packing with tampons, Foley catheters, double lumen balloon catheters, or other materials early.
Patients may require surgical arterial ligation or IR for embolization if unsuccessful.
Next, we proceed to the secondary survey. If patients can talk, talk to them. Use these questions to guide your exam:
Focused history: How is your vision? Any facial numbness? Do your teeth fit together normally? Any anticoagulation or antiplatelet medications?
Inspection and motor function:
Look for certain telltale signs (ie, Racoon eyes, Battle’s sign)
Assess motor function - close your eyes, raise your eyebrows, purse your lips, smile, frown
Sensation, Palpation, and Stability
Test sensation from top to bottom (forehead to lips and chin)
Palpate for tenderness, step-off’s, including the zygoma intraorally, and for crepitus.
Assess stability (for possible Le Fort fractures) by gently rocking the patient’s hard palate back and forth while the other hand palpates the central face.
Eyes - assess visual acuity, for abnormalities such as pupillary asymmetry in shape or response, diplopia; measure intraocular pressure assuming appropriate; check extraocular eye movements for pain or limitation
Ears, Nose, and Oropharynx:
Ears: Look for auricular hematoma, hemotympanum, CSF leaks
Nose: Look for epistaxis, CSF leak, nasal lacerations, septal hematoma or deviation
Oropharynx: Evaluate for malocclusion, jaw deviation, missing or injured teeth, lacerations, sublingual hematomas, alveolar ridge fractures
The tongue blade test can be performed as a screening tool to identify mandibular fractures with sensitivity ranging from 85-95%.
Diagnostic imaging: CT face without contrast is the test of choice, though CT head can capture some facial fractures and may be warranted in addition to CT cervical spine to evaluate for concomitant injuries. Consider CTA if you have penetrating to the lateral face given branching arteries from external carotid artery. Ultimately, to facilitate definitive diagnosis and operative planning, most specialists request CT face.
Fracture patterns and anatomy
Orbital, zygoma, and nasal fractures often occur together given their close proximity.
Ethmoid bone fractures require different management. Specifically, nasoorbitoethmoid fractures occur when significant force is applied to the nasal bridge and often are accompanied by lacrimal duct injuries, disruption of the cribriform plate, dural tears, and TBI necessitating neurosurgical intervention.
Also, be mindful of oculo-cardiac reflex, which can occur when stretch receptors in the ophthalmic nerve are activated in response to pressure in the ocular and periorbital soft tissue leading to stimulation of vagal response and bradycardia.
All Le Fort fractures involve the pterygoid plate.
Le Fort I fractures are transverse fractures that separate the maxilla from the pterygoid plate and nasal septum. This leads to a “floating palate” wherein only the hard palate and teeth move, similar to a loose a denture.
Le Fort II fractures are pyramidal fractures that extend into the orbital floor and inferior orbital rim separating the central maxilla and hard palate from the rest of the face. Le Fort II fractures result in movement of the hard palate and nose, but not the eyes.
Le Fort III fractures, also known as craniofacial disjunction, cause mobility of the entire face with the globes only held in place by the optic nerve and occur due to fractures of the frontozygomatic suture line, orbit, nose, and ethmoids.
Le Fort IV fractures are Le Fort III fractures with frontal bone involvement.
Mandibular fractures most commonly occur at the mandibular condyle, body, and the angle. Due its ring shape, the mandible is often broken in more than one location. These fractures require careful intraoral examination for breaks in the oral mucosa that indicate an open fracture.
For additional information on specific management and considerations for different facial fractures, please see THIS fantastic post on Taming the SRU by Dr. Brower
R2 CPC: THYROTOXICOSIS WITH DRS. FABIANO AND THOMPSON
The Case: middle aged female who presents with tachycardia to 140s-150s for the past few months. On arrival, patient normotensive, but tachycardic to 138. PMH of anxiety and on the following medications: Acetyl-L-carnitine, Chromium picolinate, hawthorn berry, Kava Kava, melatonin, selenium, and Valerian root. ROS notable for significant weight loss of 60 lbs in past year with severe calorie restriction. Exam generally unremarkable save tachycardia, anxious mood, rapid speech. Work up notable for unremarkable VBG, BMP, Hs troponin, CBC and a negative pregnancy test. CXR with irregular multifocal airspace disease. EKG with sinus tachycardia. After 1 L of LR, she remained mildly tachycardic to 115. And then a test was ordered…
An approach to persistent tachycardia by David Thomspon (on ALiEM): https://www.aliem.com/paucis-verbis-an-approach-to-persistent-tachycardia/
Differential for tachycardia includes:
EtOH withdrawal, anemia, anxiety, cardiac arrhythmia, dehydration, electrolyte imbalances, fever, hypoglycemia, ingestion, occult shock, pian, pulmonary embolism, respiratory distress, thyroid disease, trauma
Consider what’s possible and what’s dangerous
Differential for this patient:
Anxiety
Sedative withdrawal syndrome
Stimulant toxidrome - amphetamine, cocaine, caffeine
Drug toxicity - to include serotonin syndrome and arcane stimulants such as kava kava toxicity, which is associated with hepatotoxicity
Dehydration
Hyperthyroidism
Test of choice: Tsh/T4 to diagnose thyrotoxicosis
Hyperthyroid Emergencies
Epidemiology:
US incidence ~ 0.5%
5:1 female predominance
Often affects those aged 20-50
80% occur due to Grave’s Disease
Potential etiologies and manifestations of hyperthyroidism include thyrotoxicosis, thyroid storm, drug-induced thyroiditis, toxic multinodular goiter, toxic adenoma, Grave’s disease, postpartum thyroiditis, subacute thyroiditis.
Thyrotoxicosis is defined as excess thyroid hormone resulting in clinical symptoms that warrant evaluation and treatment.
Clinical features include anxiety, restlessness, myalgias, weakness, dyspnea, fatigue, tremor, flushing, oligomenorrhea, infertility, tachycardia, and palpitations
Diagnostic testing: Tsh/T4 as well as additional basic labs (CBC, BMP, liver function tests, glucose, and pregnancy test); ESR if concern for thyrotoxicosis, Thyrotropin receptor Ab, and Tsh IG for Graves disease; EKG, CXR; TTE, and extended cardiac window
Management of thyrotoxicosis:
Assess disease severity through good H&P and cardiac testing
Laboratory testing as noted above
Symptomatic treatment with 𝛃-blockers, fluids, and BZDs
Endocrinology consult for hospital admission v. outpatient referral, discussion of PTU or Methimazole
Admit if symptoms poorly controlled, comorbidities, age, urgent work up needed, other active problems requiring management
Discharge if symptoms reasonably controlled, few comorbidities, and are able to arrange for rapid follow up.
Treatment of concomitant disease process (ie, DKA, atrial fibrillation, infection)
𝛃-blocker dosing in thyrotoxicosis
Propranolol 10-40 mg 2-4 PO daily, can use XR formulation (helps with sxs, inhibits peripheral conversion of T4 to T3, preferred in pregnancy, lactation)
Atenolol 25-100 mg 1-2 x PO daily (safer for asthmatics, increased pt adherence, avoid in pregnancy)
Metoprolol 25-50 mg 2-3x PO daily (useful for patients w/ other indications to take cardiac BB)
Thyroid storm is defined as a life-threatening response to excess thyroid hormone leading to shock, multi-organ failure, and possible death. It is often caused by a reaction to a physiological stressor such as DKA, MI, PE, trauma, surgery, infection or drugs, in the setting of preexisting hyperthyroidism resulting in adrenergic hyperactivity. Mortality ranges between 10-30% even with treatment and is 100% if untreated.
Clinical manifestations: Pyrexia, AMS, seizure, tachycardia, arrhythmias including atrial fibrillation, heart failure, pulmonary edema, possible liver dysfunction
Burch & Wartofsky Score is a clinical scoring system that grades thyroid storm severity.
Management of thyroid storm:
Rapid diagnosis and supportive care (typically IV fluids, antibiotics, monitoring, possible cooling, glucose monitoring)
Inhibit peripheral adrenergic effects with 𝛃-blockers (Propranolol or Esmolol)
Propranolol - 0.5-1 mg IV over 10 minutes with repeat 1-2 mg dosing every 15 minutes until HR controlled. This is preferred if no concern for heart failure, and it has the added benefit of decreased peripheral conversion of T4 to T3.
Esmolol - 250-500 µg/kg loading dose followed by an infusion of 50-100 µg/kg/min. This is preferred if concern for heart failure or with asthma and need for quick titration.
Inhibit new thyroid hormone synthesis with PTU or Methimazole
PTU - 500-1000 mg PO or NG load > 250 q4h
Methimazole - 60-80 mg/day q8h PO or NG (teratogenic in 1st trimester)
Inhibit thyroid hormone release with either potassium iodide or Lugol’s solution, which must be given at least 1h after antithyroid drugs.
Prevent peripheral conversion of T4 to T3 with Hydrocortisone 300 mg load > 100 mg q8h
Identify and treat precipitating factors
Disposition: ICU
Special considerations:
For patients with Afib - rate control and avoid Amiodarone given concomitant thyroid toxicosis. Digoxin contraindicated if 𝛃-blockers administered.
For patients with heart failure, consider treatment with 𝛃-blockers for high output heart failure and cautious treatment with Esmolol, ACE-i, furosemide in those with low output heart failure.
For patients who are pregnant, give PTU in the first trimester, and Methimazole for 2nd/3rd trimester. Labor can precipitate thyroid storm.
For patients undergoing emergency surgery, use Esmolol infusions.
Case follow-up: She underwent additional evaluation with CTPA and CTH to rule out PE and pituitary mass, which were unremarkable. Endocrinology was consulted, and she underwent additional diagnostics, including Thyrotropin receptor Ab and Thyroid-stimulating Ig, which were elevated suggesting Grave’s Disease. She was initiated on Propranolol 80 mg XR q24h and Methimazole 10 mg BID, admitted, and later transitioned to Atenolol.
