Grand Rounds Recap 8/31

Inhalation Injury and Hyperbaric Oxygen: Dr. Dale

Burn degree evaluation on physical exam:

  • 1st degree: pink base, sunburn in quality
  • Superficial 2nd degree: when blisters are unroofed underlying tissue is red in coloration and will blanch
  • Deep 2nd degree: when blisters are unroofed underlying tissue doesn’t blanch due to thrombosis in blood vessels
    • Important regarding healing prognosis as thrombosis in vasculature impedes healing
  • 3rd degree: full thickness burns

Keep in mind that grease transfers heat more readily than water (cooks things, including us, faster)

Burn extent (% TBSA)

  • >20% sends patient into distributive shock
  • Burning eliminates selective filtration properties of blood vessels, becoming so porous that plasma and proteins freely leak

Parkland formula: For administration of LR 4 ml/kg/%burn in 24 hours

  • 50% in first 8 hours
  • 25% in 2nd 8 hours
  • 25% in 3rd 8 hours
  • Consider placement of foley catheter as administration is later titrated hourly by urine output goal
  • This formula does not account for inhalation injury, concomitant trauma, comorbidities including age, heart failure, renal failure, etc.      

Inhalation injury: 

  • Responsible for 50% of all burn deaths
  • Doubles burn mortality
  • Present in 5-30% of all burn admissions
  • Separated into 3 categories:
    • 1. Airway injury
      • Rapid flash burns to face usually has almost negligible injury to airway due to high convective capacity of oropharynx.
        • Classic example of smoking while on nasal cannula.  Dr. Dale recommends evaluating these patients for COPD exacerbation of CHF exacerbation if history and exam suggest it and may need further monitoring if these comorbidities are present.  However, often these patients may need 2-3 hours of monitoring in ED and likely able to be discharged home.
      • True airway risk lies in edema secondary to burn injuries to face and neck or for extended exposure in closed space fires
        • Keep in mind the sheer volume of fluid resuscitation these patients may often receive, they can develop an impressive amount of airway edema
    • 2. Lung injury
      • Pulmonary parenchymal injury leads to shedding of bronchial epithelium and transudate progressing to ARDS
    • 3. Systemic Toxicity
      • Carbon Monoxide (CO) poisoning
        • Half life of 320 minutes, reduced to 71 minutes on NRB O2 and 21 minutes with hyperbaric oxygen at 1.5 atm
        • Can present with non-specific symptoms of headache, confusion, fatigue, nausea, visual changes, or severe presentations with coma, shock, and cardiac arrest
        • Important to consider delayed neurologic sequelae (DNS)
          • Neurologic symptoms including parkinsonian symptoms, akinetic mutism, persistent deficits in executive function presenting 3-8 weeks after exposure
          • Dr. Dale suggests insufficient evidence to support hyperbaric oxygen therapy for treatment and prevention of same, citing out of 6 randomized controlled trials performed in study of same, only one showed improvement (Weaver et. al NEJM, 2002).   
            • Follow up replication study found no difference between room air and HBO therapy in regards to outcomes of DNS
            • Cochrane database stating HBO lacks sufficient evidence to support its efficacy, ACEP and American Burn Association reportedly in agreement with this statement
          • Theories include not only impaired O2 delivery is responsible for DNS, also consider free radical generation causing degradation of myelin sheaths and cellular membranes
            • Future therapies being studied include inhaled H2 and ion channel specific therapies
      • Cyanide poisoning
        • May present with many similar symptoms to that of severe CO poisoning
        • Treat with cyanokit (hydroxycobalamin) empirically if suspicious for this toxicity of patient with severe bradycardia, hypotension, or arrest after closed space fire

Dr. Dale suggest consideration for intubation of inhalation injury patient before transport if patient has been involved in closed space fire or significant smoke exposure, if prolonged transport of patients involving face or neck, and also if patient has significant fluid resuscitation requirements based on amount of surface area burned (remember delayed airway edema).

In Dr. Dale’s opinion, blisters from burns should be unroofed.      

Dr. Kircher’s Clinical Soapbox: Pneumonia

Pneumonia defined as a new infiltrate on imaging plus clinical evidence that the infiltrate is of infectious origin.

ED clinical exam sensitivity for detecting pneumonia alone is only about 60%

  • CXR boasts only sensitivity (44-79%) and specificity (67-93%)
  • CT scan of chest reaches near 100% sensitivity and specificity
  • But do all patients need a CT of their chest then?
    • Experienced providers in lung ultrasound (>100 credentialed and reviewed studies performed) found to have 94% sensitivity and 96% specificity
      • Not ready for prime time within our organization, but consider for training in your career as useful diagnostic adjunct

Keep in mind that blood cultures are no longer recommended in evaluation of community acquired pneumonia (CAP).

Overturning all we know about pneumonia treatment: is hospital acquired pneumonia (HCAP) really a thing anymore?

  • Dr. Kircher suggests importance of evaluating for PES (pseudomonas, ESBL, MRSA) organisms instead of archaic rules regarding hospitalizations
    • Meta-analysis found poor sensitivity of HCAP diagnostic criteria in predicting multi-drug resistant organism pneumonias
    • Blanket administration of broad spectrum antibiotics when patient is technically HCAP criteria but without high risk for MDR organisms may be contributing to growing antibiotic resistance
    • Consider the following MDR organism risk factors:
      • Age (risk increasing for ages 40-65 and again for those >65)
      • Male gender
      • Antibiotic use in last 30 days
      • Chronic respiratory disorder
      • Chronic renal disease
      • Altered mental status in ED

Consider the patient as an individual in presentation, evaluate, assess and treat each encounter utilizing these suggestions as a playbook rather than strict marching orders, allowing you to make real time decisions.  

Dr. Kircher’s proposed management and disposition triple option

  • Going home: CAP coverage for + infiltrate, supportive care, return precautions
  • Admitted: cover all for CAP, risk stratify of PES or influenza, consider steroids, consider broad spectrum
  • ICU: guns blazing, low threshold for broad coverage, source confirmation, low threshold for steroids, cx mandatory

Dr. Polsinelli Taming the SRU: Cardiogenic Shock

71 yo M with severe SOB, hx of CABG, CHF with BiVICD, COPD, L MCA stroke.  Tachypneic, hypotensive, 87% on non-rebreather.  Clear lungs, clear heart, no JVD, narrow pulse pressure, cold extremities without edema.  Cardiology US with diffuse hypokinesis.

Cariogenic shock: decreased CO and evidence of tissue hypo perfusion with adequate IV volume.  

  • Systolic BP less than 90 for greater than 30 minutes or requiring vasopressors
  • Pulmonary congestion or increased LVEDP
  • Signs of decreased organ perfusion

80% of patients in cardiogenic shock are due to acute MI, but only minority with acute MI have cariogenic shock.  

  • If signs of ischemia on EKG, go straight to cath lab

So, how do you intubate somebody who is hypoxic and hypotensive?

  • NIPPV for oxygenation, but keep in mind possible hypotension due to decreased preload
  • Arterial line for BP monitoring during intubation
  • Vasopressor support on hand (push dose epinephrine, etc)
  • Try IV fluid administration if hypotensive, even if in cardiogenic shock

RSI Induction agent choices

  • Etomidate with clear safety profile advantage over propofol
  • Can consider ketamine, however, sympathomimetic properties can be risky, in vitro studies in some species also show calcium channel blockade properties in ketamine

Inotrope Choices

  • Dobutamine is favored by our cardiology colleagues.  No loading dose required, easily accessible in ED, fast onset
  • May consider milrinone as well

Vasopressor Selection

  • Levophed is clearly superior to dobutamine in cardiogenic shock
    • Dopamine has been shown to be hazardous in this patient population
  • Epinephrine with potential for more tachydysrhythmias as well as some decreased splanchnic perfusion
  • Vasopressin and epinephrine both showed trend towards mortality (not statistically significant, in a non-randomized prospective trial)
  • Consider use of IV calcium for inotropic support with vasopressors

Special considerations: try inotropic support with dobutamine before vasopressors for aortic stenosis or acute mitral regurgitation patients in cardiogenic shock

Dr. Carleton: Airway Grand Rounds

Case 1:

Middle aged man at scene with self inflicted deep neck laceration.  Hypertensive, tachycardia, tachypnea, 97% on room air

Large laceration above hyoid from ear to ear, no active bleeding, no bubbling. Supraglottic airway laceration.

Apply the universal airway algorithm. Crash airway? No.  Routine RSI? No.  Difficult airway algorithm.  Consider awake technique in this patient.  

In general: NEVER pass a blind device when there ia a possibility of a supraglottic airway injury

    ⁃    may include site of bleeding in the trapped gas space

    ⁃    may disrupt a stable clot

    ⁃    may enlarge existing wound

An anticipated bloody airway may be the only situation where DL is the best first choice

Prepare for failure and have plans to address it.

You can’t bag a supraglottic airway perforation!

Case 2:

Young male patient riding go-cart with a scarf, gets caught in clutch and hyperextends his neck.  Vital signs good, can’t talk.  Inspiratiory stridor.  No vocalization.  Neck balloons on expiration.  On CT, 6 cm discontinuity between cricoid cartilage and proximal trachea.  Still stable after CT .  Send to OR, underwent awake tracheotomy.  

Bottom line: sometimes the best action is NO action.  He’s stable.  Don’t mess with it.  Send to the OR.

  • However, manage airway early if you anticipate decline
  • Be cautious in administering positive pressure in airway injury
  • Never place a blind device down an injured airway
  • Never paralyze a patient you are not confident that you can intubate or rescue
  • Be highly suspicious of airway injury if mechanism is supportive of same.  Do not delay diagnostics or consultation.  
  • Tracheal separation may be perilous for RSI, could potentially push distal stump further into chest if it is truly in discontinuity

But what if he crashes?

- Desperate times call for desperate measures, consider bedside surgical airway and attempt to locate distal retracted trachea for direct intubation

Case 3

Young female patient found down at home, in asystole, intubated in field, got ROSC.  Contusions everywhere of various ages.  ETT 28 cm at lip, decreased breath sounds on left, retracted to 24 cm with bilateral breath sounds noted.  CXR shows ETT still at right mainstream opening.  ETT pulled back to 21 cm.  Brief PEA arrest, responds to epi.  PH 6.7, subdural, uncal herniation, lots of rib fractures, large right posterolateral distal tracheal tear with pneumomediastinum with RA/RV flattening suggesting tamponade from pneumomediastinum. Selectively intubate below tear via fiberoptic into right mainstem bronchus.

Blunt airway trauma 25% of time is located at right mainstem/tracheal junction

Keep in mind the RUL bronchus comes off so high, consider preferential selective intubation of left mainstem to preserve an entire lung function as opposed to 2/3 of one.

Bottom line:

  • Be aware that airway disruption in blunt trauma is possible in thorax
  • Be aware of typical location (have to get balloon past the hole, consider anatomy for best lung preservation) 
  • Recognize the consequences of one lung ventilation (keep in mind tidal volume, compensate with rate etc accordingly)
  • ALWAYS re-assess an outside airway

Case 4

Female patient in her 60s with history of a-fib, comes in with dyspnea and palpitations.  Concern for PE.  Shortly thereafter develops severe respiratory distress.  HR 136, RR 36 and labored, O2 saturation 87% on NRB.  Becomes unresponsive, atonal respirations, brady down. Crash intubation successful, however:

    ⁃    no color change

    ⁃    breath sounds distant

    ⁃    no gurgling in epigastrium

Tube visualized again, switched out.  Each bag afterwards results in further subcutaneous emphysema.  

ET tube on autopsy protruding through posterior membranous portion of trachea

Iatrogenic tracheal injury:

  • 86% female
  • 66% older than 50
  • 77% proximal to carina
  • 92% in posterior membranous wall
  • 28x more common without paralytics
  • High correlation with chronic steroid use
  • Associated with stylet use.  Be very cautious with infraglottic portion of airway   

Bottom line:

  • These things must be done delicately
  • Be aware of high risk populations
  • If tear is suspected, re-intubate past area of tear

Case 5

Mid-40s female patient after MVC, combative and flailing.  tachicardic, 95% on NRB, chubby with short neck.  Obvious flail mandible fracture.  Intubated for projected clinical course.  RSI with DL/VL, video obscured by blood.  Best DL view is CL-III, bougie passed with no clicks, “held up” at 36 cm, intubated over bougie to 23 cm at teeth, taken to CT scan, comes back with significant subcutaneous emphezyma.  Right mainstem on CT

Bougie trauma:

  • Trachea is generally only 10-15 cm long 
  • In the US, holdup tends to be mostly at 28 cm.  If resistance is not felt by         that depth you must be concerned about either esophageal passage or             mainstem passage
  • Introducer trauma estimated in 5% of bougie intubations
  • If you don’t firmly hold onto bougie while passing ETT, it will migrate distally
  • The more you “choke up” on the bougie the higher force you can generate and higher potential for injury

Bottom line:

  • NEVER pass the bougie to 45 cm to see if it “holds up”
  • Once the bougie has passed the cords, be gentle
  • Pay close attention to bougie depth
  • Feel for tracheal click after 22 cm
  • If no feedback after 30 cm, be concerned
  • Consider retracting 3 cm once “hold up” is felt
  • Anchor butt of bougie while passing ETT

Small Group Sessions with Drs. Goel, Miller, Renne, and Titone

Transvenous Pacemaker Primer

Why not Transcutaneously Pace?

People are sweaty

People have a pacer

10x the mA needed (uncomfortable)

Don’t want to give sedatives to patients in cardiogenic shock

Can’t palpate carotid well for mechanical capture

Sometimes you’ll miss V-fib/V-tach because of all the artifact

When to do to it:

  1. Unstable bradycardia: easy
  2. Stable third degree: more complicated
  3. MI
    1. Up to 43% of patient’s with third degree, new LBBB or RBBB with LAD due to MI can develop a high degree AV block
  4. Patient with second degree?

Consider placing a Cordis just in case

If no MI, consider placing a Cordis, especially if after hours or at an OSH

AHA: High degree AV block and/or new BBB (especially left) or bifasicular block in patients with anterior/lateral MI (unlikely to resolve because it affects the conduction system)

Inferior/posterior MI - transient vagal simulation and likely to resolve 

Where to do it?

Right IJ or left subclavian (try to avoid this because this is where EP is going to want to put box there)

While waiting

TC pacing???

Push Dose Epi (10mcg/ml)

“Diry Epi Drip”

  • 1mg into 1L saline bag (1mcg/ml)
  • Wide open 18g = 20-30mcg/min (similar to push dose epi)

Dopamine if you have it

Isoproterenol (pure beta): inotropy and chronotropy and dromotropy, (20mcg q 2-3 minutes)

When it doesn’t work?

  • Hyperkalemia, CCB, Beta-blocker, digoxin
  • Conduction system itself is messed up

Style Points

If they are being TC paced set that rate to 60 and the TV pacer to 90 so you know when you’re getting TV capture over the TC capture

How to do it?

  • Start with 6F Cordis (works like a trauma cath with dilator already in place)
  • Don’t think bigger is better because the wire will have too much wiggle room
    • Harder to control and more blood loss
  • Place swan-dom
  • Test balloon with air only!
  • Put wire through swandom to 15-20cc, at this point balloon is well past tip of sheath
  • Turn on pacer (mA 20, HR 80 or above the patient’s, sensitivity all the way down/asynchronous)
  • Short, proximal, positive, red!!!
  • Push to 30 with balloon up
  • Take down balloon and recheck for capture 

Is it in the right spot?

  • Use the ultrasound with a subxiphoid view for both floating and mechanical capture?
  • ECG monitor is great for electrical capture but SpO2 pulse can show you mechanical capture
  • Can put negative (distal) to V1 
  • Feel a pulse…

What do I do with pacer now?

  • Can’t leave them in “honey badger mode”
  • Over time the heart responds less and less to pacing
  • Start to bring down mA until you lose capture

UCEM PGY-1 Central Line Primer

Disclaimer: this is just one way of doing things and NOT an official departmental mandate

  1. Setup site & equipment
      1. scrub site with chlorhexidine
      2. place mayo stand near dominant hand
      3. if using US, place it so line of sight will be parallel to vessel
  2. Wash hands
  3. Instrument prep #1
      1. open sterile bundle on mayo
      2. open central line kit and dump onto sterile area
  4. Full-body precautions
      1. cap
      2. mask (remove eye shield if comfortable and want to avoid fogging)
      3. gown (secure neck velcro straps first; then insert hands)
      4. gloves (apply using cuffs of gown without exposing hands)
      5. full-body drape (apply with head of stick figure toward patient’s head)
      6. US probe cover (gel inside of cover —> insert probe —> gel atop cover)
  5. Trendelenburg patient + time out (if non-crash line)
  6. Lidocaine: if awake & stable: 5 cc to area around vessel (under US guidance)
  7. Instrument prep #2 
      1. needle: align numbers with bevel (loosens connection and indicates bevel position)
      2. wire: prime guidewire for insertion
      3. dilator: place near wire and scalpel
      4. catheter: uncap TLC brown port & prime all three ports with saline*

    *the necessity of this step is debated by various practitioners

  1. Needle insertion (with aspiration)
  2. Establish line
    1. micro-skill 1: disconnect syringe while holding needle firmly in place
      1. confirmation method A: if no US, attach tubing to needle (if artery blood pulsates to top)
    2. micro-skill 2: feed wire (holdup early: remove & re-aspirate; holdup late: remove & redirect)
      1. confirmation method B: if US, visualize wire in vein on both lateral & longitudinal views
    3. micro-skill 3: incise (with needle still in place, blade away from wire, 1/2-3/4 blade depth)
    4. micro-skill 4: dilate (push and twist dilator close to skin entry site + hold wire taut)
    5. micro-skill 5: thread TLC over wire until hubbed or ectopy (can stop earlier for R IJs / SCs)
    6. micro-skill 6: aspirate & flush all ports (using proper technique to prevent emboli)
  1. Secure line: 
    1. scrub site with chlorhexidine (to remove blood)
    2. apply Biopatch (if available)
    3. suture TLC hub to skin (and, if needed, also suture clip to skin)
    4. apply Tegaderm