Right Ventricular Strain on Bedside Echocardiography

As we know, point-of-care ultrasound has become an extremely useful tool in the ED, allowing providers to glean disposition-altering information from a quick and non-invasive bedside study.  On my ultrasound month, I helped out with a patient who presented with shortness of air for 2-3 days.  The patient was a fairly poor historian, but she reported progressive dyspnea on exertion for several weeks along with cough and orthopnea.  She had no formal diagnosis of COPD or CHF, but she had an extensive smoking history.  I was asked to perform a bedside echo to help narrow down the differentials. The images I obtained demonstrated some classic findings of right heart strain, and I felt like this would be a good opportunity to review some of them.

  1. RV dilatation
Screen-Recording-2021-12-30-at-10.39.53-PM

As you can see in this parasternal long axis view from our patient, the RV is massively dilated in comparison to the LV. A normal RV : LV ratio is approximately 0.6:1. Anything larger than this is considered abnormal, with 0.6-0.9:1 representing mild enlargement, 1:1 moderate enlargement, and > 1:1 severe enlargement. When looking at the parasternal long axis view, you can use the “rule of thirds”. According to this, the left atrium, LV outflow tract, and RV outflow tract should be roughly the same size. In this video, the RVOT is clearly much larger than it should be. You can also get a sense of the relative sizes of the ventricles in the other three windows on transthoracic echo.

  1. RV systolic dysfunction

In our patient’s apical four chamber view, you can again appreciate the size of the RV compared to the LV. In addition, there appears to be relative hypokinesis of the free wall of the RV, suggesting there is systolic dysfunction. The right atrium enlargement seen in this video also suggests that this patient’s RV strain was more of a chronic process.

  1. Paradoxical septal wall motion

In a normal heart, the LV should be fairly circular in the parasternal short axis view, and the RV will appear more crescent-shaped. Additionally, the walls surrounding the LV should move inward equally during systole. In the setting of elevated RV pressures, you can often see the interventricular septum bowing in towards the LV, creating a “D” shaped left ventricle, as seen in the clip above. Interestingly, there are different variants of the so-called “D sign”, helping to distinguish between right ventricular pressure vs. volume overload. In pressure overload, the RV presses on the septum during systole AND diastole. Conversely, in volume overload, the septal bowing is much more pronounced in diastole compared to systole. Our patient has a D-shaped LV throughout the cardiac cycle, suggesting RV pressure overload.

  1. McConnell’s Sign

This finding refers to RV wall hypokinesis with apical sparing. As you can see in the video above, the apex of the RV appears to bounce up and down while the rest of the RV remains stationary. In the right clinical setting, McConnell’s sign is considered highly specific for acute pulmonary embolism. Disclaimer: this clip came from one of Dr. Nichols’s patients who was later found to have an extensive saddle embolus.

  1. Lack of respiratory variation in the inferior vena cava

The normal IVC diameter is less than 1.7 cm and there is a 50% decrease in the diameter during inspiration when the RA pressure is normal (0-5 mmHg). When the inspiratory collapse is less than 50%, the RA pressure is usually between 10-15 mmHg. If there is no collapse with respirations in a spontaneously breathing patient, this suggests markedly increased RA pressure > 15 mmHg. This is usually best evaluated using M mode, measuring the diameter of the IVC during inspiration and comparing to its diameter during expiration. Our patient has an enlarged IVC with almost no collapsibility throughout the respiratory cycle.

Conclusion

If you identify any of these findings on a patient in the emergency department, you should consider common causes of RV failure and strain, such as PE, pulmonary hypertension, left heart failure, ARDS, severe tricuspid regurgitation, volume overload, etc. Our patient received a CT PE in the ED, which was negative. She was subsequently admitted to the cardiology service, where right heart catheterization found evidence of severe pre-capillary pulmonary hypertension. After a few days of monitoring, she was subsequently discharged back into the world with a prescription for diuretics and follow up in the pulmonary clinic.

Conference 12/8

Neck Trauma
Dr. McMurray

Zone 1: Clavicles to cricoid

  • Highest mortality rate due to proximity to mediastinal structures

Zone 2: Cricoid cartilage to angle of mandible

  • Most commonly injured
  • Classically, zone II injuries undergo surgical exploration, zone I and III undergo further evaluation

Zone 3: angle of mandible to base of skull

Penetrating trauma:

  • Has to penetrate the platysma which demarcates superficial from deep wounds
  • Most common cause of immediate death is involvement of carotid artery

Hard signs of vascular injury:

  • Hypotension
  • Arterial bleeding
  • Rapidly expanding hematoma
  • Deficits (pulse/neuro)
  • (bruit/thrill)

Hard signs of aerodigestive trauma:

Air bubbling, massive hemoptysis, respiratory distress

Soft signs

subQ air

dysphonia

dysphagia

Blunt Trauma

  • Blunt vascular injury have up to 60% risk of stroke; if no operative intervention, consider ASA/Plavix/heparin etc

Denver Screening Criteria

  • Used to screen for vertebral and carotid artery dissection and/or injury after blunt head/neck trauma
  • CTA if 1 or more criteria present
  • Reduces number of missed injuries to <5%

Strangulation

  • Most common cause of death is neck vessel occlusion rather than airway obstruction
  • Also can have laryngotracheal fx, C-spine injury
  • If dyspnea, dysphonia, odynophagia, etc need laryngobronchoscopy

Ophthalmic Trauma
Dr. Nelson

Corneal abrasions:

  • Richly innervated = very painful
  • Short healing time 24-48 hours
  • Common causes: mechanical trauma, foreign body, contact lenses, flash burns
  • Clinical features: foreign body/gritty sensation, injection, tearing, relief with topical anesthetic, can also have photophobia and vision change
  • Workup and diagnosis: eyelid exam with eversion, fluorescein exam looking for uptake
  • Consider corneal ulceration in contact lens wearers
  • Treatment: Removal of foreign body, PO/topical NSAIDs, abx (erythromycin in general population, fluoroquinolone drops in contact wearers for pseudomonal coverage)
  • Ophtho follow up

Open globe:

  • Full thickness disruption of sclera or cornea
  • Clinical pictures: pain, decreased visual acuity, teardrop shaped pupil
  • AVOID pressure on the eye = do NOT perform tonometry
  • May have positive Seidel’s test on fluorescein exam
  • CT orbit if concern for foreign body
  • Management: urgent ophtho consult for repair, cover eye, elevate HOB, bed rest, tdap, abx
    • If no foreign body, IV fluoroquinolone
    • If foreign body, IV vanc+ceftaz

Eyelid Lacerations:

  • Ophtho consult for repair:
    • Lid margin
    • Within 6-8mm of medial canthus
    • Lacrimal duct/sac
    • Inner surface of lid
    • If ptosis is present
    • Tarsal plate or levator palpebrae involvement
  • Full thickness (through and through): high risk for ocular injury, eval for corneal lacs and globe rupture
  • Partial thickness: most simple horizontal lacs can be repaired by ED physician, ends of sutures should be kept away from cornea to prevent further abrasion
  • Lid margin lacerations: very small <1mm do not need repair and will heal spontaneously, if larger consult ophtho for repair

PEM Lecture-Abdominal Trauma:
Dr. Elmore

  • Trauma is the most common cause of death in children from 1-18 years old in the US
  • Blunt abd trauma accounts for more than 90% of childhood injuries
  • It is the most unrecognized cause of fatal injuries
  • Children are at greater risk due to immature skeleton and they have higher abd organ to body mass ratio
  • Children are able to compensate in the face of significant blood loss
  • Clinical prediction rule may rule out intraabdominal injury in blunt trauma
    • No sign of abd wall injury
    • No TTP
    • No evidence thoracic wall trauma
    • No abdominal pain
    • No decrased bowel sounds
    • No vomiting
  • HDS but concern for intraabdominal injury if:
    • Hct<30
    • UA>5 RBCs
    • AST>200,ALT>125
    • Elevated lipase
    • Low systolic BP
    • Femur fx
  • Spleen most commonly injured intraabdominal organ, liver second
  • Pancreatic injury = classic “handlebar” injury from bike accident (also consider duodenal injury/hematoma with this mechanism)
  • Hollow viscera injuries are rare, but most common causes are lap belt injuries, peds vs. auto, NAT (rapid acceleration/deceleration)
  • As many as 50% of children with Chance fx have intra-abdominal injury such as duo perf, mesenteric disruption, transection of small bowel, panc injury, bladder rupture
  • TEN-4 rule for NAT
    • Bruising on torso, ears, or neck of child >4 years old
    • Any bruising in an infant 4 months old or less

Small Group: Abdominal Trauma
Dr. Harmon

  •   Indications for immediate lap in penetrating abdominal trauma:
    • Peritonitis (rigid abdominal wall, rebound tenderness)
    • Hemodynamic instability
    • Evisceration of abdominal contents
    • Hematemesis or gross blood per rectum
  • Literature varies widely on sensitivity of CT for bowel/mesenteric injuries
  • CT findings that may indicate bowel injury:
    • Stranding, bowel wall thickening, pneumoperitoneum
  • Findings concerning for diaphragm injury:
    • Elevated/blurred L hemidiaphragm, bowel sounds in chest, gastric bubble/air fluid level in chest, mediastinal shift away from affected side
    • Gold standard for diagnosis of diaphragm injury is exploration in OR; cannot be ruled out by CT or CXR

 Traumacology
Dr. Senn, PharmD

  • Triad of trauma: hypothermia, coagulopathy, acidosis

  • TXA for trauma patients:
    • CRASH-2 trial compared TXA vs. placebo
      • In hospital mortality within 4 weeks of injury
      • Reduction in all cause mortality, greatest benefit SBP<75 and if given within 3 hours of initial injury
    • MATTERS trial 1g TXA given, greater impact on those requiring MTP
  • Take-home points for TXA: consider using in adult trauma patients with severe hemorrhagic shock (SBP<90), ideally <3h from injury
    • Dosing: 1g over 10 min followed by 1g over 8h
  • Trauma patients, hypocalcemia, and blood transfusion
    • Twice mortality for those with iCal <0.9
    • Calcium plays vital role in coagulopathy
    • Consider administration 1g CaCl or 3g Ca gluconate when giving 3-4 PRBCs/FFP

Not All “Knee Dislocations” Are Created Equally

“Can you come see this patient in triage? Their knee is definitely dislocated.”
“Hey, doc, we’re bringing in this guy involved in an MVC, his knee was dislocated but it reduced on its own.”

It is important to be able to tell the difference between a true knee dislocation and a patellar dislocation.

Patellar Dislocation
A normally functioning patella is nestled within the trochlear groove of the distal femur. Patellar dislocations can occur either from a direct blow to the knee or from planting the ipsilateral foot and rapid change of direction/twisting, either of which can cause the patella to become displaced from the trochlear groove. Usually the patella becomes displaced laterally.

Reduction of the patellar dislocation involves extending the leg at the knee. Gentle pressure can be applied from the lateral aspect, directed medially, while extending. Post-reduction plainfilms should be obtained to evaluate for any associated fractures. If no fracture, the patient can be placed in a knee immobilizer for 7-10 days and follow up with orthopedics. Patellar dislocations are recurrent around 40% of the time.

Knee Dislocation
Knee dislocations are most commonly high mechanism injuries and have a high rate of neurovascular injury. They are rare, but it is difficult to know how many there truly are as up to 50% of them reduce spontaneously. The most common nerve injury is to the common peroneal nerve, with the popliteal artery being the most commonly affected artery. 60% of knee dislocations have associated fractures.

Treatment is emergent reduction and neurovascular examination. Presence of pulses does not exclude vascular injury. ABIs can be performed if pulses are normal. If ABI normal, may elect to observe the patient. If ABI abnormal, CTA indicated. If pulses are unequal, decreased or absent, you must ensure that the joint was reduced appropriately, and if still unable to locate pulses, immediate surgical intervention may be required.

Especially since both patellar dislocations and knee dislocations may spontaneously reduce, it is helpful to ask the patient and/or EMS about the initial appearance of the knee. A self-reduced patellar dislocation likely only requires plainfilms, while a self-reduced knee dislocation merits further evaluation for neurovascular injury.

Conference 12/1/21

Pelvic Trauma
Dr. Ferko

  • Signs of pelvic trauma: hematuria, inability to void, abnormally positioned prostate
  • Diagnosis:
  • Hematuria, but severity of hematuria on UA does not equal severity of injury
    • Plainfilms to evaluate for fx near kidney/bladder/urethra
    • Retrograde urethrogram
    • Retrograde cystogram
  • Retrograde urethrogram-when?
    • Male with external signs of trauma
    • Perform ideally before foley placement
    • Females-urology consult needed
    • Defer if CTA pelvis needed as it will interfere with contrast
  • Retrograde urethrogram-how?
    • Patient supine
    • Obtain baseline KUB
    • 60cc syringe with 10% contrast, in last 10cc repeat KUB
    • For stretch injury/partial disruption, usually conservative management with catheter
  • Retrograde cystogram
    • Fully fill bladder; inject until full and then 50cc further (usually around 400cc)

(from Journal of Urology)

Le Fort Fractures
Dr. Lehnig

  • Complete or partial separation of mid face from skull
  • Pterygoid involved in all
  • Usually caused by blunt trauma
  • LeFort I most common
  • Higher velocity more likely to cause II/III
  • LeFort I: palate-facial separation (think dentures)-mobility of the maxilla
  • LeFort II: (nose and mouth) Nasal bridge, maxilla, lacrimal bones, orbital floor, and rim
  • LeFort III: across nasal bridge, orbital walls, zygomatic arch (“floating face”)
  • Endotracheal intubation preferred over nasal, prep for difficult airway
  • LeFort II/III: CTA indicated
  • Complications: Vascular injury (internal carotid as high as 7%), nerve injury, eye injury
  • Treatment: definitive tx is surgical, ophtho consult, NES if CSF leak
  • No specific guidelines on abx, many get augmentin

(From Journal of Oral and Maxillofacial Surgery)

Prehospital Airway Management
Dr. Price

  • Methods available? ET tube (oral or nasal), BVM (with OPA/NPA), supraglottic, needle cric (methods vary by state per state regulations)
  • Variables to consider: patient (age, condition), provider (level, experience, training), setting (environment, distance)
  • Study with 4 Key questions addressed
    • BVM vs SGA
    • BVM vs ETI
    • SGA vs ETI
    • Benefits and harms comparison based on pt type, technique, and devices
    • Methods: 1990-2020, >9000 abstracts, 99 studies
    • Results…inconclusive benefits, but harms: no difference in reported aspiration, airway trauma, regurgitation with any devices; BUT number of attempts less with SGA than ETI
    • Conclusion: current evidence does not favor more invasive airway approaches based on survival, neurologic function, ROSC, or successful airway insertion
  • More research needed, may be more useful to study ventilation management as it may reveal clinically relevant differences

Oral Boards Prep
Dr. Shaw

Learning Points:

  • In every patient, unless something requires emergent intervention, perform physical exam head to toe
  • Remember to request repeat vitals
  • Use a systematic approach
  • Primary survey in trauma:
    • MARCH
      • Massive hemorrhage
      • Airway
      • Respiration
      • Circulation
      • Hypothermia/Head injury
    • Massive hemorrhage:
      • Tourniquet: place proximal to bleed, write time of placement
      • Twist tourniquet until you lose pulses in the extremity
      • 2 inches, 2 hours
      • 2 inches proximal to wound
      • On for up to 2 hours (can be left up to 6 hours, but can have neurovascular damage)
    • Airway:
      • Oxygenate
      • Ventilate (apnea)
      • Protect airway (secretions, mental status)
      • Clinical course (too agitated for CT)
    • Respiratory:
      • Rate, breath sounds, stridor, tracheal deviation, JVD
      • Needle decompression can be done either anteriorly at mid-clavicular line or laterally at anterior axillary
      • If needle decompression or chest tube for penetrating trauma, remember to place occlusive dressing over the initial injuries/wounds
    • Circulation:
      • BP, HR
      • 14G (250ml/min) and 16G (150ml/min) peripheral IVs have higher flow rate than Cordis (130ml/min)
    • Head Injury/Hypothermia:
      • GCS, pupillary exam, neuro exam
  • Primary survey for every trauma patient, every time

Conference 11/10/2021

Tumor Lysis Syndrome – Dr. Aher

typically occurs within days after chemotherapy.

Findings of: Hyperkalemia, Hyperuricemia, Hyperphosphatemia, HYPOcalcemia (2/2 phosphate binding Calcium

Dialysis indications: Potassium >6, Cr. >10, Uric Acid >10, symptomatic hypocalcemia, Phos >10, Volume overload

Methemoglobinemia – Dr. Norby-Hill

Can happen with dapsone overdose

Dissociation between SPaO2 and PaO2

Acquired cases from medications and environment, commonly dapsone, local anesthetics, nitrites, h202

50% is fatal

Features: refractory to supplemental o2, color of blood, cyanosis, respiratory depression

Tx: methylene blue (Not in G6PD or those on SSRIs as MB is MAOI), ASCORBIC ACID, EXCHANGE TRANSFUSION

Pediatric Surgical Emergencies – Dr. Robin Lund

Early blood tinged emesis – cracked nipples

Pyloric stenosis: M>F 4:1, 3 to 5 weeks, veracious eaters, NBNB projectile every feed, dehydration, malnutrition

Appy’s usually missed the younger they are

Intuss – 6 mo to 3 yo; ddx Meckels and hsp. 

Features: colicky severe, 20 min, emesis, sausage mass

NEC: sudden feeding intolerance, distention, tenderness, bilious vomiting, diarrhea, rectal bleeding

Malrotation: <1* vomiting, sick, abd distension, peritonitis.

Heme emergencies – Dr. McGee

1 single unit of donor platelets raises plts by 30k

Transfusion indications: <10k (20k if febrile or septic), <50k active bleeding, <100k CNS bleeding or neuraxial surgery

-vwb dz tx for minor bleeding is ddavp

Post transfusion purpura: alloantigen on transfused plts: t penia, purport, clinically significant bleeding. Tx IVIG

Don’t forget about HIIT if recent inpatient stint

MAHAs – non immune HA.

TMAs: microvascular hemolysis; tap, has, drug, complement, pregnancy, htn emergency

High Sensitivity Troponin – Dr. Adam Ross

6 or above reported. Anything less than 20 nl in males; <15 normal in females

>88 MI

15 or greater (change in either direction) increase is clinically significant (2 hours)

TBD if there will be poc trop in R9

Single trop undetectable with >3 hours of symptoms

Hemophilia Lecture

A is Factor VIII deficiency

B is Factor IX

Both are 

VWD: VWf “chaperones” Factor VIII and facilitates its efficacy

Emicizumab: bispecific mab. Helps factor 9 and 10 work. Subcutaneous injection prophylactically.

Meds ending in -ate are for VIII deficiency.