Grand Rounds Recap 12.15.21
/R1 Clinical Knowledge: Biliary Tract Pathology with Dr. Glenn - R4 Case Follow-up with Dr. Connelly - R3 Taming the SRU with Dr. broadstock - Metrics in our EM Practice with Dr. Pancioli - R4 Simulation and Oral Boards Cases with Drs. Roblee, Gawron, and Berger - Combined Peds EM Lecture with CCHMC Faculty and Fellows: Pediatric Stridor
R1 Clinical Knowledge: Biliary tract pathology WITH Dr. Glenn
Cholelithiasis
80% of patients have asymptomatic cholelithiasis, 20% are symptomatic. About 10% of patients will develop symptoms within 5 years of gallstone formation. This typically presents as biliary colic, or intermittent pain associated with temporary blockage and irritation of the gallbladder by a gallstone.
Diagnosis
Ultrasound is 95% sensitive and 95% specific for the identification of biliary stones.
Management
Asymptomatic patients with gallstones can be managed with watchful waiting, 80% will never have symptoms
Patients with biliary colic can have an elective cholecystectomy. Symptoms can be managed with NSAIDs in the interim.
Patients who elect for non-surgical management who are symptomatic can take ursodeoxycholic acid which alters bile cholesterol homeostasis
Acute cholecystitis
Occurs secondary to gallstones in 90-95% of cases.
Diagnosis
Diagnosed on ultrasound by visualization of a gallbladder wall > 4 mm dilated (sensitivity of 65% and specificity of 91%) , the presence of pericholecystic fluid (sensitivity of 26% and specificity of 94%), and a sonographic murphy sign (sensitivity of 65%, and specificity of 82%)
If clinical suspicion remains high despite a normal RUQ US, you should obtain a HIDA scan which evaluates biliary function. This test is 90-97% and 71-90% specific for diagnosing biliary dysfunction.
Management
Patients with acute cholecystitis are treated with a cholecystectomy or cholecystostomy
Choledocholithiasis
Presents with RUQ pain, +/- Jaundice, nausea and vomiting,+/- fever.
Diagnosis
Typically, the bilirubin and ALP are elevated significantly more than ALT and AST.
RUQ US will have findings similar to that with acute cholecystitis with the addition of common bile duct dilation. Typically, a common bile duct < 5 mm is considered normal, with an additional 1 mm of tolerance for every decade of life after 60yo.
Management
Patients are managed with an elective chole vs MRCP vs ERCP depending on findings of the ultrasound
Ascending Cholangitis
Due to gallstones 65% of the time and malignant stenosis 24% of the time
Characterized by the pentad of fever, jaundice, confusion, shock, and RUQ pain, however 90% of patients will have fever, but only 60% will have jaundice.
R4 Case Follow-up WITH Dr. Connelly
Thrombotic Throbocytopenic Purpura (TTP)
TTP is a consumptive thrombocytopenia that results in hemolytic anemia and end-organ ischemia.
This end-organ ischemia can present as a wide array of findings including myocardial ischemia, cardiogenic shock, cardiac arrest, confusion, headaches, focal neuro deficits, seizure, or coma, AKI, pancreatitis, colitis, and diarrhea.
These symptoms can vary widely and may not all present at once but will present over the course of the disease.
95% of cases of TTP are immune related, 5% are hereditary due to congenital abnormalities in ADAMTS13.
Can also be seen with pregnancy, infection, inflammatory states, or certain medications (clopidogrel, fluoroquinolones)
Notably, 10% of patients with TTP also have SLE.
Has a 90% mortality if untreated, and time is of the essence.
Treatment
Plasma exchange - replaces defective or missing ADAMTS13
Patients can be temporized with FFP transfusion (contains functional ADAMTS13) if plasma exchange is not rapidly available.
Steroids
Monoclonal antibodies
Avoid transfusion of additional platelets as this will further propagate the consumptive thrombocytopenia and anemia. It can also increase renal failure, thrombosis, and risk of death.
R3 Taming the SRU WITH Dr. Broadstock
Complex airway take away points:
Respect the outside hospital report and resources
Patients may look very different when they present to an outside hospital than how they look on arrival to us. Additionally, not every hospital has the resources (in terms of both equipment and manpower) that you have at your facility.
Trust but verify
Be grateful and utilize the information provided to you from other providers, but always do your own assessment with fresh eyes to prevent bias. Additionally, as above, the patient’s condition may have changed rapidly and you may be dealing with different physiology than the previous provider, even on the same patient.
If you have time, use it. Complex situations require system 2 thinking
If you have a moment to step back and think, take it. Evaluate the problem from multiple views, anticipate the consequences, and develop a plan with a series of back-ups. It’s easy to rush into a situation, but sometimes it is best to take a second and step back.
Start with the least invasive option when possible
Take small steps when you have the time, and make big moves when you have to.
Know your threshold for rescue measures before you enter the room. Aka, choose your number.
We all know the indication for emergent procedures, but when one is anticipated, clarify a firm threshold for the room before you start. Choose your number at which you need to escalate to drastic measures before you enter the room.
Metrics in our EM Practice WITH Dr. Pancioli
Admission is our most ‘expensive’ decision and directly affects boarding
Physicians’ salaries account for about 8% of a hospital’s costs, but the decisions we make as physicians account for about 80% of costs.
As boarding goes up, walkout rates in the ED go up as well. The group with the highest rate of walkout is an ESI 3.
Patients who are admitted but need placement after admission on average stay 2.4 days longer in the hospital than a patient who was admitted for the same illness but can be discharged home.
Social determinants of health
Often admission is a substitute for other things the patient needs such as housing, social support, or connection with resources.
We need to improve outpatient care plug-ins and support with social work for patients to minimize admissions for reasons outside of hospital level medical care.
Improving our care in the ED
Targeting provider variability
Use clinical decision tools to assist with decisions on diagnostic testing, admission, observation utilization, and appropriate imaging.
Work with medicine teams and consultants to arrange short term outpatient follow up
In-person evaluation by a consultant can add several hours to an ED course. Use them when needed, but consider close-term consultant outpatient follow-up instead when appropriate.
R4 Simulation and Oral Boards Cases WITH drs. Berger, Gawron, and Roblee
Toxic Shock Syndrome Simulation
Pathophysiology
Some streptococcus & staphylococcus species secrete superantigens that causes widespread activation of T-lymphocytes and a cascade of inflammatory cytokines leading to multiorgan failure
Presentation
Strep toxic shock is more common
Can affect all ages but trend towards older patients
The source of infection usually fairly evident and is most often a soft tissue infection such as cellulitis or necrotizing fasciitis
Staph toxic shock is less common
Mostly seen in younger patients
Often occurs from colonization w/o invasive infection
Primary focus may be subtle (i.e. small skin abscess, patch of cellulitis)
50% menstrual related to colonization of tampons
50% related to nasal packing, soft tissue infections, or pneumonia
Systemic Features
Both present with a flu-like syndrome including fevers, chills, and myalgias. GI symptoms are common and include nausea, vomiting , and diarrhea.
Skin findings
Patients have a diffuse macular erythematous rash is most common
Erythema of mucous membranes is often present
Skin desquamation is a delayed finding
Lab Workup
Patients will frequently have leukocytosis with a significant leftward shift.
AKI is often the first sign of organ damage.
Some diagnostic criteria include a CK that is at least twice the upper limit of normal.
Elevation of bilirubin, AST, and ALT are common
DIC and thrombocytopenia may be seen late in the disease process.
Treatment
Initial treatment focuses on source control - addressing necrotic tissue with surgery, removing any nidus of infection, and initiating broad spectrum antibiotics (Vancomycin + beta lactam + clindamycin)
Clindamycin is administered because it impairs toxin production
There is some evidence that suggests linezolid may also suppress toxin production and have a synergistic effect with clindamycin.
Patients with hemodynamic compromise should receive fluid resuscitation and early initiation of vasopressors
Boerhaave Syndrome Case
Boerhaave syndrome is a spontaneous rupture of the esophagus which results from a sudden increase in intra-esophageal pressure combined with negative intrathoracic pressure
Frequently seen in the context of vomiting, coughing, straining, or seizures
Exam may show crepitus of the chest wall and Hamman’s crunch
CXR will show mediastinal air or peritoneal air. There may also be a pleural effusion (typically left sided).
Contrast esophagram and/or CT of the neck/chest establishes diagnosis
Initial treatment in the ED includes fluid resuscitation, controlling nausea and vomiting, and initiating broad spectrum antibiotics.
Cardiothoracic surgery should be consulted early. Severity of illness dictates conservative vs operative management
Congenital Long QT Syndrome Case
Occurs in ~1 in 2,000 patients
Primary symptoms including syncope, syncope followed by generalized seizure, or sudden cardiac arrest
Any child with unexplained syncope should have an EKG
Prolonged QT syndrome has the potential to decompensate into fatal ventricular arrhythmias, including torsades de pointes
Treatment for torsades includes IV magnesium, defibrillation, and overdrive pacing (At about 100 bpm) for refractory cases
Isoproterenol can be utilized in patients who have torsades secondary to bradycardia prior to initiating overdrive pacing.
Long Treatment
Avoid QT prolonging medications
Replace potassium and magnesium aggressively during any illnesses
Beta blocker - reduces the incidence of syncope and sudden cardiac death.
ICD - placement of an ICD is not necessary in all patients with congenital prolonged QT syndrome but should be considered in patients whose initial presentation was sudden cardiac arrest or in patients who have significant recurrent events (such as recurrent syncope)
Combined Pediatrics Emergency MEdicine LEcture - Pediatric Stridor
Stridor is a high-pitched sound resulting from air flowing through a narrowed airway.
Inspiratory stridor typically indicates an extra-thoracic obstruction, as the upper airways narrow with inspiration
Expiratory stridor typically indicates intrathoracic obstruction, as the increased intrathoracic pressure in expiration causes intrathoracic airways to collapse.
Biphasic stridor typically suggests a fixed central airway obstruction
Pediatric differential for stridor
Croup - accounts for 90% of pediatric stridor. Most common in children 6 months to 3 years old. Stridor is typically gradual and preceded by viral URI symptoms.
Bacterial Tracheitis - Most common in school aged children. Typically preceded by viral URI type symptoms, however on presentation patients are more toxic appearing.
Epiglottitis - less common with widespread vaccination. Most common in patients over the age of 7 but can occur at any age. Untreated it can rapidly progress to a life-threatening airway obstruction.
Retropharyngeal or peritonsillar abscess. - Retropharyngeal abscesses are more common in younger patients because they have a larger mass of lymph tissue in that area.
Foreign body aspiration
Caustic ingestion
Anaphylaxis
Congenital/Anatomic causes include tracheomalacia, laryngomalacia, vascular rings, bronchogenic cysts, and infantile hemangiomas (look for facial hemangiomas as a clue).
Initial management and evaluation
Minimize further agitation of the child
Gather information and try to figure out what is causing the stridor based on history and physical exam (allergies, aspiration, infection, injury)
Assessment
Mild obstruction - hoarse cry, good air entry, stridor with agitation or exertion, absent or minimal retractions/nasal flaring/grunting/or head bobbing
Moderate to severe obstruction - tachypnea, stridor at rest, airway posturing (tripoding or sniffing position), prolonged inspiratory time with increased work of breathing, decreased air entry, hypoxia.
Management
Severe or complete obstruction
Suspected foreign body - attempt to dislodge the foreign body with basic BLS maneuvers (back blows in infants, abdominal thrusts in children). If the patient becomes unresponsive initiate CPR which may also dislodge the foreign body. If the foreign body is not successfully dislodged and removed within 1 minutes, the patient should be intubated. If possible, visualize and remove the foreign body with laryngoscopy. If you are unable to visualize the obstruction, you should intentionally mainstem the intubation on initial ETT passage and then retract to the correct depth - this maneuver is performed in an attempt to force the obstruction distal enough that adequate oxygenation and ventilation can be emergently achieved.
No suspected foreign body - attempt to optimize the patient with BVM. IF adequate oxygenation can temporarily be achieved the patient should be maintained with BVM and then undergo emergent but controlled intubation in the OR. If the patient cannot be temporized effectively then an attempt to intubate the patient should be completed and if unsuccessful followed by management via the failed airway algorithm.
Imaging (largely airway films) can give you clues to the etiology and location of the obstruction but may be non-diagnostic and should not interfere with acute stabilization of an ill patient
Croup may have a steeple sign on lateral neck x-ray
Epiglottis may have a thumbprint sign indicating an enlarged epiglottis
Bacterial tracheitis may show a shaggy appearance of the trachea
Retropharyngeal abscesses present as distention of the retropharyngeal tissue (should be smaller than width of the adjacent vertebrae)