Grand Rounds Recap 8.21.19

Airway - R4 Case Follow Up - SCUBA & Dysbarism - R4 Simulation

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AIRWAY GRAND ROUNDS WITH DR. CARLETON

The Physiologically Difficult Airway

• Using the standard airway algorithm, we tend to focus on anatomically difficulties - we should expand this category to include the physiologically difficult airway

  • Causes of peri-intubation hypotension

    • Underlying disease process

    • Under-resuscitation

    • Induction agents for intubation

      • All induction agents are cardio-depressant, including ketamine in catechol depleted states

    • Acidemia

      • Acidemia leads to decreased inotropy, arrhythmias, and decreases the effectiveness of catecholamines

    • Hypoxia

  • Avoiding the HOp Killers

    • Hemodynamic instability

    • Oxygenation deficits

    • Low pH

      • Sodium bicarbonate will not help if the patient also has hypercarbic respiratory failure, as they will be unable blow off the excess carbon dioxide

      • Apnea causes a rise in PaCO2 by 12 mmHg in the first minute in healthy patients - this is multiplied in patients with an increased minute ventilation from acidemia

    • Not addressing these factors prior to intubation can cause a viscous cycle and ultimately cardiac arrest

    • Ways to address this prior to intubation:

      • Volume resuscitate and use vasopressors as needed

      • Choose your induction agent wisely and reduce your doses (even with ketamine)

      • Avoid hypoxia

      • Prevent and treat acidemia

  • Matching the Minute Ventilation

    • Patients who have maximal respiratory compensation from a profound metabolic acidosis often worsen after intubation - this is often because we do not match their pre-intubation minute ventilation on the ventilator

    • We can quantify the patient’s minute ventilation using NIPPV or a ventilator on non-invasive mode (either pressure support or CPAP)

    • Pseudo-NIPPV Intubation

      • Supplies needed: NIPPV Mask, ventilator, ETCO2/O2 sat monitors, RSI drugs, intubation gear

      • The goal is to maintain pre-intubation MV during and after intubation

      • Apply the NIPPV mask with ventilator in pressure support mode to quantify the patient’s minute ventilation

      • Once RSI medications are pushed, change the vent to VC and set the TV and RR to what the patient was pulling on PS mode

      • Once intubated, try to match the minute ventilation as closely as possible without causing barotrauma (consider doubling the flow rate to deliver breaths faster)

      • In a 70 kg person, in order to maintain the patient’s current PaCO2, we need a minute ventilation of 60 mL/kg/min (4.2 L/min)

      • The relationship between PaCO2 reduction and minute ventilation is exponential, and we will quickly run out of room increasing their minute ventilation using the ventilator alone (i.e., don’t paralyze these patients and take control of their respiratory mechanics - you are not smarter than the patient’s hypothalamus)

  • DASHHH-1A Intubation

    • Definitive airway sans hypoxia/hydrogen ions/HOp killers on the 1st attempt

    • This should be our goal for every intubation, every time

Blind Methods for Intubation

• Intubation through an extra glottic device

  • Blind intubation through an I-gel is successful about 2/3 of the time

• Blind nasotracheal intubation

  • This is contraindicated in facial trauma

• Surgical cricothyrotomy

• Digital/Tactile oral intubation

  • When do we do this?

    • When equipment is unavailable or has failed due to patient position (e.g., entrapped in a motor vehicle), oropharyngeal trauma, anatomic variations, or immense blood/secretions

  • A small study showed that digital intubation was 98% successful in the OR when the patient was sedated and paralyzed

  • Another study in the pre-hospital setting showed that digital intubation was successful 89% of the time

  • Technique

    • Place the patient in semi-Fowler’s position

    • Stand facing the patient with your dominant hand forward

    • Insert the index and long fingers of the non-dominant hand into the mouth and push the epiglottis anteriorly with the long finger and drop the index finger into the hypopharynx

    • Insert the ETT with your dominant hand until you can feel the ETT tube and displace it anteriorly until the tube is felt passing through the glottis

  • Tips

    • An ETT with a stylet has the greatest success rates

      • Shape the tube similar to a bicycle handlebar - this allows you to place the ETT with more rotational force to direct the ETT anteriorly

    • Don’t forget your other methods to bring the larynx closer to the tip of the ETT such as external laryngeal manipulation

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R4 CASE FOLLOW UP  WITH DR. OWENS

Salicylate Toxicity

• Overview

  • The most common source of salicylates is aspirin. Oil of wintergreen and pepto bismol also contain salicylates

  • Aspirin is rapidly metabolized to salicylic acid which decouples oxidative phosphorylation

  • Salicylism classically presents with respiratory alkalosis prior to an anion gap metabolic acidosis

  • Salicylic acid crosses the blood brain barrier and causes a relative neuroglucopenia, leading to altered mental status

  • There is significant overlap in symptomatology with sepsis, and it is often impossible to differentiate without laboratory studies

• Workup

  • VBG - you can use Winter’s formula to determine if there is appropriate respiratory compensation or if there is a second acid base disorder. Salicylic acid directly stimulates the medullary respiratory center and causes a primary respiratory alkalosis

  • A renal panel will show an anion gap metabolic acidosis, hypokalemia, elevated creatinine, as well as a falsely elevated chloride level

  • Salicylate level: therapeutic levels are 15-30 mL/dL

    • Salicylates have a large volume of distribution and levels can be lower in chronic toxicity

• Management

  • Alkalinization - this traps salicylic acid in the plasma and urine to be renally excreted

    • Alkalinization will drive potassium into the intracellular space and quickly cause hypokalemia

      • Target a potassium level of 5.5 prior to administering sodium bicarbonate

    • Give 1-2 mEq of sodium bicarbonate as a bolus (about 2-3 amps in most adults) and start a sodium bicarbonate drip at 1.5-2 times maintenance rate

      • A bicarbonate drip can be quickly mixed by injecting 3 amps of sodium bicarbonate into 1 liter of D5W

      • The goal serum pH is 7.55 and a urine pH of 8.0

  • Dialysis

    • There are no hard and fast indications

      • It is generally accepted that patients with a salicylate level > 100 mg/dL should be dialyzed

      • A small study showed that patients with levels > 50-80 had improved mortality with dialysis

      • CKD patients with levels > 90 should be dialyzed

    • Other relative indications

      • Evidence of end organ dysfunction - altered mental status, acute kidney injury

      • Volume overload such as pulmonary edema

      • If the patient’s clinical status is refractory to maximal medical therapy

  • Intubation

    • Tachypnea is not an indicator for intubation

    • Indications - new onset pulmonary edema, hypoxia, hypercarbic respiratory failure, worsening acidemia despite medical treatment

    • Matching the minute ventilation post intubation is key. See above.

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SCUBA EMERGENCIES AND DYSBARISM WITH DR. COMISKEY

Barotrauma

• Ear

  • Outer ear - due to air trapping within the external canal and causes significant pain

  • Middle ear - this is the most commonly affected area and is prevented with equalization during descent

    • Facial baroparesis - air within the middle ear can cause a facial nerve palsy through CNVII compression

  • Inner ear - typically occurs during ascent and causes vertigo, hearing loss, and tinnitus

• Sinuses

  • Occurs most commonly during descent and ascent

  • Presents with pressure, dental pain, and mucous expulsion/tearing

• Pulmonary

  • This is caused by a rapid ascent with a closed glottis and causes a pneumothorax

Decompression Illness

• Decompression sickness

  • This is caused by nitrogen bubbles precipitating within the vasculature from a rapid ascent

  • Divers can prevent this with a controlled ascent based on total dive time and depth

  • Type 1 - The bends

    • Symptoms include muscle aches and pain upon ascent

    • This more commonly occurs following a long, deep dive of if flying in an airplane < 12-24 hours after diving

  • Type 2

    • Symptoms include CNS and cardiovascular abnormalities

    • There is a fairly high morbidity and mortality associated with this type of decompression sickness

• Arterial gas embolism

  • This is an acute occlusion of any arterial bed due to nitrogen gas precipitation

  • Symptoms depend on what organ system is affected

    • Can present with stroke symptoms, myocardial ischemia, or shortness of breath due to a pulmonary embolism

• Treatment

  • 100% FiO2 is first line therapy

  • Re-compression therapy is indicated for severe or debilitating symptoms

  • Position the patient in trendelenberg to prevent embolism to the pulmonary/cardiovascular/cerebrovascular arterial system

Gas Toxicities

• Nitrogen narcosis

  • Seen at deeper depths (greater than 100 feet)

  • CNS dysfunction mimics ethanol intoxication

  • Usually resolves upon ascent

• Carbon dioxide toxicity

  • Usually caused by hypoventilation during a dive

  • Treat with 100% FiO2

• Oxygen toxicity

  • This is rare, but typically occurs at depths > 120 feet and with oxygen enriched diving (Nitrox)

  • Symptoms include visual disturbances, ear ringing, cough, and pulmonary irritation

  • This will usually resolve upon ascent

Take Home Points

• History is the most important aspect to identify SCUBA emergencies

• Morbidity and mortality is relatively low in most cases

• Most SCUBA emergencies resolve with non-invasive management

• When in doubt, treat the patient with 100% FiO2

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R4 SIMULATION WITH DRS. BANNING, MURPHY-CREWS, AND SCANLON

Calcium Channel Blocker (CCB) Overdose

• Dihydropyridine CCB

  • Primarily affects peripheral vascular calcium channels and causes profound hypotension

• Non-dihydropyridine CCB

  • Primarily affects cardiac calcium channels resulting in bradycardia

  • The selectivity of both type of CCBs is lost at high doses typically taken in an intentional overdose

• Hyperglycemia is associated with higher mortality

• Treatments

  • Calcium

    • Unlikely to be effective, and if the patient responds it will usually only be transient

  • Glucagon

    • Needs to be given at extremely high doses and several repeat doses are necessary

    • Glucagon is also not as effective in CCB overdose compared to beta blocker overdose

  • Vasopressors

    • Be aggressive early - start at a high dose and rapidly up titrate

    • Norepinephrine is the recommended first line treatment

    • Add epinephrine early if the patient continues to be hypotensive and/or bradycardic

  • High dose insulin euglycemic therapy

    • This is a recommended first line treatment and should be started early

    • The mechanism of action is unknown but is believed to cause increased inotropy

    • The starting dose is 1 unit/kg/hr and should be rapidly uptitrated until a hemodynamic response is seen

  • VA ECMO, lipid emulsion therapy, plasmapheresis

    • Use of these agents is controversial and it is unclear if there is any benefit

    • These can be considered on a case to case basis, especially in refractory cases