Grand Rounds Recap 3.2.22
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MORBIDITY AND MORTALITY CONFERENCE WITH DR. MEAGHAN FREDERICK
Case 1: Complicated Alcohol Withdrawal
Pathophysiology
Alcohol is a GABA agonist → CNS Depressant
Results in increased excitatory neurotransmitter glutamate and NMDA receptor upregulation to maintain relative activation/alertness homeostasis
With alcohol cessation: Abrupt decrease in GABA inhibitory effects and NDMA receptor antagonism → unopposed increased glutamate → excessive excitatory neurotransmission
Symptoms of Alcohol Withdrawal
Tachycardia, hypertension, agitation and anxiety
Insomnia
Vomiting
Seizures
Hallucinations
Timing of Alcohol Withdrawal
Can start as early as 6 hours from highest blood alcohol content, not last drink
Alcohol hallucinations as early as 8-12 hours
Seizures can occur within 12-24 hours
Delirium Tremens, differentiated from alcoholic hallucinations by change in sensorium, occur in 12-24 hours
Can last 5 days for uncomplicated cases, up to 3 weeks with complications
Dangers of Alcohol Withdrawal
Seizures and status epilepticus
Become more severe with repeated withdrawal episodes with lesser stimuli via Kindling Effect
Cardiac dysrhythmias
Hyperadrenergic state predisposes tachydysrhythmias
Hypokalemia caused by K+ wasting during withdrawal
Chronic Hypomagnesemia
Most common dysrhythmias are QTc prolongation and atrial fibrillation
Risk factors for complicated withdrawal
Chronic alcohol use (at least 7wks, increased risk w/ increased duration of use)
Older age
Prior withdrawal seizure or DTs
Hypokalemia
Prediction of Alcohol WIthdrawal Severity Score (PAWSS)
Perform in setting of pts who have either consumed any EtOH in past 30 days or those who had a detectable blood alcohol level on evaluation
Score < 4 = low risk for complicated withdrawal
EtOH withdrawal in Incarcerated patients
High risk patient population
Check your local justice center for individual protocols and available medications
Hamilton County Justice Center
Inmates screened initially for risk of withdrawal and if positive, are checked with CIWA q8hrs.
If high CIWA at any point, get meds and are transitioned to q6h checks
Case 2: Stridor and Sore Throat
Presentation of sore throat in the ED can be largely grouped into 3 categories:
Uncomplicated (viral pharyngitis, bacterial pharyngitis, tonsillitis, postnasal drip, etc)
Affects posterior oropharynx
Usually is of short duration (3-5 days)
Can be associated w/ recent URI symptoms
On physical exam, usually well appearing with oropharyngeal erythema or exudates.
If edema is present, usually mild and symmetric
Deep Space Infections (peritonsillar abscess, retropharyngeal abscess, Lemierre’s Syndrome, Ludwig’s Angina)
Affects neck and submandibular spaces
Course is often longer, progressive in nature
Can have associated systemic symptoms
Have pain with swallowing and fullness
Physical exam findings of deep space infections result from expansion of neck compartments as infection spreads along the facial planes
The contained inflammation results in edema which impairs movement and compresses on adjacent structures, limiting their function
This is why people develop trismus, for example
In addition to trismus, can also have:
Neck tenderness
Visible swelling
Refusal to range the neck
Muffled voice
Upper Airway Obstruction (epiglottitis, bacterial tracheitis, foreign body, vocal fold dysfunction or mass)
Can occasionally occur due to progression of deep space infections
Patients often complain of voice changes or throat tightness
Physical exam:
Stridor
By the time this is present, airway lumen is reduced by at least 50%
Hoarseness
Normal oropharyngeal exam
Drooling (more of a fear of swallowing than inability to)
Tripoding and hypoxia are late signs
Timeline can be acute or chronic
Workup:
For uncomplicated sore throats, a great oropharyngeal visual exam is key
If concerned about deep space infection, get CT neck with IV contrast
If concerned about upper airway obstruction, perform NP scope
Treatment Mainstays
Uncomplicated sore throat: symptomatic control, abx if bacterial
Deep Space Infection: IV abx, I&D
Upper Airway Obstruction: airway management, can try racemic epinephrine and/or decadron, may need operative management
Case 3: High Sensitivity Troponins
What is HsTn?
Incredibly sensitive → can detect extremely low levels of troponin, around 1/5th of the standard troponin
Must be able to detect measurable concentrations of troponin below the 99th percentile for at least 50% of healthy individuals
Reliable test at very low levels → can distinguish values just above the minimum detectable level and well within normal levels.
Conventional troponin assay was incredibly unreliable at levels within normal, and so these levels were never reported.
Use of HsTn for ACS Evaluation
HsTn is most validated in the evaluation of typical chest pain concerning for ACS
Increased sensitivity allows earlier detection of ACS events
91% sensitivity for AMI at time of presentation vs 77% with conventional assay
An undetectable HsTn has a NPV of 96.4 with <3hrs from symptom onset and 99.5 at >3hrs
HsTn is faster
Conventional troponins required a minimum of testing 6 hours after onset of chest pain with recommendations for up to 12 hours
HsTn requires only 3 hours
Can provide information grading severity of cardiac injury
HsTn > 5x upper limit of normal is >90% predictive for AMI
Patients with AMI using HsTn who were previously negative in conventional assays have similar morbidity and mortality, suggesting this increased disease detection is meaningful
4th Universal Definition of MI has three components:
At least 1 HsTn > 99% upper limit of normal
Significant rise or fall (defined by the test and time between tests)
Being able to use an absolute delta enables detection of cardiac injury on either side of the acute injury event
AND 1 of the following
Symptoms of ACS
New ECG findings
Regional wall motion abnormalities consistent with ischemia
If patient has elevated HsTn without other criteria meeting AMI definition, now defined as having myocardial injury
Elevated HsTn, all comers = Increased 1 yr mortality (HR 2.3)
No significant difference in outcomes between acute and chronic myocardial injury
Across the board, higher in-hospital, 30-day post-discharge and 5 year all cause mortality in pts with myocardial injury compared to Type 2 MI.
Case 4: Neurogenic Shock
Anatomy Refresher
Spinal cord contains sympathetic preganglionic neurons along its entire length
Cardiac stimulation comes from levels T1-T6
Vascular stimulation comes from T1-L2
Neurogenic Shock Pathophysiology
Disruption of the sympathetic NS but intact parasympathetic NS → Unbalanced parasympathetic outflow to the heart + loss of compensatory peripheral vascular tone
Symptoms/Features
Hypotension
The higher the lesion the more profound the hypotension due to more widespread vasoplegia
~50% require pressors within 4 hours
Bradycardia
Seen with lesions at or above T6
Severe in about 70% of SCI
Patients may initially be tachycardic due to peri-injury catecholamine surge and circulating catecholamines
Flaccid paralysis and loss of reflexes
Shock in Trauma
Hemorrhagic > Obstructive > Neurogenic > Cardiogenic
Shock in Trauma WITH spinal cord injuries
Penetrating → Hemorrhagic > Neurogenic
Blunt → Neurogenic >> Hemorrhagic
Treatment of Neurogenic Shock
Volume Resuscitation and euvolemia
Norepinephrine > Phenylephrine
Avoid vasopressin as can increase water retention and lead to increased swelling and hyponatremia
Add atropine as needed
Goal MAP 85-90mmHg for first 7 days
Have low threshold to intubate with injuries above C5
Steroids are no longer recommended
Autonomic Dysreflexia
A collection of signs/symptoms which occur in response to stimuli below the level of neurologic injury in the context of known spinal cord injury
ED providers are poised to catch this (think trauma patients coming to ED from rehab for abnormal vital sign evaluation)
Typically takes weeks to months to develop
Symptoms:
Bradycardia
Hypertension
Headache
Flushing
Sweating
Negative downstream effects = heart attacks, intracranial bleeds, death, etc.
Common triggers:
Bladder distension
Fecal impaction
Tight clothing
Pressure sores
Sexual activity
Treatment:
Sit patient upright
Remove tight clothing
Find and correct noxious stimuli
If needed, correct HTN with pharmacotherapy
Case 5: Gonococcal Septic Arthritis
Epidemiology
Occurs in 0.5-0.9% of pts with Neisseria gonorrhoeae infection
Is responsible for only ~1.5% of all cases of septic arthritis
Predominately occurs in women under 45yo who are sexually active
Comparing Gonococcal vs Nongonococcal arthritis
Gonococcal
Polyarticular
More common in healthy pts without comorbidities
Female >> males (3:1)
Affects young to middle aged adults
Nongonococcal
Monoarticular in vast majority of cases
Occurs in pts with multiple comorbid conditions (DM, RA, OA)
Affects children and elderly patients
Males >> females
Clinical Presentation
Migratory tenosynovitis, dermatitis and polyarthralgia type
More common
Skin lesions can be pustular of vesiculopustular and are typically painless
Usually located on distal extremities
Last 3-4 days even without treatment
Purulent arthritis type presents as a more classic septic arthritis picture
Workup
Gram stain is markedly less sensitive for detection of N. gonorrhoeae
Synovial culture often negative as gonorrhea is difficult to grow
Gold standard is to send NAAT from synovial fluid
Treatment of Gonococcal Arthritis
Tenosynovitis type = Ceftriaxone x7 days
Purulent arthritis type - I&D and Ceftriaxone x14 days
Co-testing for other STIs
AIR CARE GRAND ROUNDS: TRANSPORT OF IABP AND IMPELLA WITH DR. KATE CONNELLY
Intra Aortic Balloon Pump
Inflation: Increases supply of oxygen to the myocardium
Balloon inflates at onset of diastole (when aortic valve closes) → displaces blood from the aorta into both the systemic circulation and coronary arteries
Benefits include increasing coronary artery perfusion
Deflation: Decreases LV workload and therefore myocardial oxygen demand
Balloon deflates just prior to systolic ejection (before aortic valve opens) → Rapid ⇊ in aortic pressure (decreased afterload) → ⇊ ejection pressure (pressure required to open aortic valve) → ⇊ LV workload + reduces time LV spends in isovolumetric contraction [the major determinant of myocardial O2 demand]
TL;DR: Basically, if the aortic valve is a door and the LV is pushing to open it, the deflating balloon helps pull it open from the other side
Benefits
Decreases cardiac workload
Increases cardiac output
Triggers
Multiple modes but we care about only a few:
ECG = Trigger event is the R-Wave
Trigger of choice when an adequate R-Wave is present
Pacer spikes are automatically rejected
Pressure = Trigger event is the systolic upstroke
Trigger of choice in patients with a regular rhythm when an adequate R-Wave is not present
Errors with Trigger Timing
Pearls
Always safer to have later inflation, earlier deflation (fiddle to the middle)
Choose auto for timing
Early inflation of balloon is a deadly problem
Evaluation of the patient on an AIBP
Pulse ox on L hand only
Document and follow UOP
CXR is great if possible
Check access site for bleeding, hematoma and device depth
Check and document DP pulses
Blood in catheter tubing → indicates balloon rupture
IABP troubleshooting
Alarm: IAB Catheter restriction (ie. kinked)
Normal IAB waveform should look like a chair and have a baseline of ~10-15 mmHg
A rounded waveform (no back on the chair) or elevated baseline suggest the catheter may be kinked
Can occur w/ HOB elevation, obese patients
Try lowering head of bed <30 degrees, carefully repositioning leg
Press START if needed to restart pump
Alarm: Gas loss in IAB circuit (i.e. helium leak)
Will see as a baseline below the expected 10-15 mmHg, especially if occurring as a sudden drop from a previously-normal baseline
First step is to check for blood in tubing - this include flecks that look like betadine (if they don’t wipe off, need to assume they’re blood)
Yes, there’s blood = the balloon has ruptured.
TURN THE PUMP OFF and call ahead to notify. IAB needs to be removed within 30 minutes.
No blood = verify connections are tight and restart the pump
Alarm: Pump Failure
Manage your patient (pressors, inotropes)
Try to prevent clot formation
Disconnect helium extension tubing from IABP
Insert stopcock into tubing and attach 60 cc syringe (both of these are in the pump bag)
ASPIRATE FIRST - if you withdraw blood then STOP - the balloon has ruptured
If there’s no blood, rapidly inflate the balloon w/ 40-50 cc air then deflate every 5 minutes
Does not provide any cardiac support, just keeps clots from forming
Cardiac Arrest in Patients with IABP
OK to do closed chest compressions
Safe to defibrillate
Give meds/treat reversible causes as needed
If rhythm is asystole, VT or VF, change trigger from EKG to pressure (or honestly just rip the ECG leads off and reconnect with ROSC)
Impella
What is it? A microaxial pump that augments forward flow across the aortic valve by aspirating blood from the LV and ejecting it into the aorta
Increased cardiac output
Improved coronary and systemic perfusion
Offloads LV resulting in reduced myocardial oxygen demand
See this awesome Taming The SRU post here for more details on how it works!
Placement signal CANNOT be used as a MAP surrogate
Performance level → Increased P level = increased motor RPM = increased impella flow
Keep at P-2 or higher
Patient assessment
Check access site for hematoma, ecchymosis, bleeding
Check device depth
Pulses in all extremities
Device Assessment
Note initial setting
Make sure Tuohy-Borst valve is locked for transport
Transport concerns
Battery life lasts 60 mins at full charge – must plug into AC power if able
Purge bag system must remain upright to prevent air getting into circuit
consider taping bag to the impella console
Troubleshooting
Purge Alarm
De-air purge system: Device walks you through the fix
Purge pressure high:
check device for kinkings (straighten tubing, slear sidearm or catheter
Is purge fluid too concentrated? It must be D5W +/- heparin
Check motor current → if too high may indicate impending pump failure
Purge pressure low:
Tighten connections, replace purge cassette if leaking
Is purge fluid too dilute? Must be D5W +/- heparin
Check motor current → if too high may indicate impending pump failure
Suction Alarm
Caused by drop in LV preload → either from hypovolemia or RV failure
Regardless of etiology, drop P-level until suction breaks (but never go below P-2, will get retrograde flow)
Consider blood/fluid if volume down
Consider vasopressors/inotropes (norepi, vaso, dobutamine are reasonable – avoid phenylephrine in RV failure!)
Return to initial P-level once resuscitated
Wrong Position Alarm
If still at the referring facility
request an echo to confirm position and request cardiologist evaluation and reposition device
Do not load-and-go with a malpositioned Impella - is providing no circulatory support and has potential for harm
If you get a malposition alarm in flight
Immediately drop P-level to P-2
DO NOT ATTEMPT TO REPOSITION THE IMPELLA YOURSELF
Call ahead to the receiving facility
Medically manage the patient – will no longer be receiving circulatory support from device, anticipate need for vasopressors/inotropes
Unknown Position Alarm
Assess cardiac function → Your patient’s heart is no longer beating effectively enough for the Impella to sense a pressure difference across the aortic valve – this is an extremely low or no flow state.
Reasonable chance you need to start compressions if you get this alarm
Cardiac arrest w/ impella
Decreased P level to P-2
Do CPR, meds and defibrillation as normal
AIR CARE GRAND ROUNDS: LIFE LESSONS WITH DR. BILL HINCKLEY
Use checklists during high stakes performances to cognitively off load
Resuscitate before you intubate
Products/fluids/push dose pressors
Maximally pre-oxygenate and de-nitrogenate
Apneic oxygenation
Impact Brain Apnea is a real thing
Rarely witnessed
Typically occurs with blunt trauma
The higher energy mechanism, the longer apneaic time
Distinct from airway obstruction, is true central apnea
Likely a frequent etiology of TBI deaths within 10 mins of injury
Implications for clinical practice:
Increased awareness in high risk arenas (sports med, military)
Is an asterix for the mantra of “isolated head injury does not cause shock” → apnea leads to hypoxia leads to cardiovascular collapse
Ways to improve performance in times of high stress
Beforehand: smile (even if fake or forced), listen to music if you can or sing in your head, tactical “box” breathing, have a mantra, visualize success
Practice!
