Airway Management Algorithm
- Birnbaumer, D., MD. (2016, July 21). Airway Management Algorithms. Lecture presented at Harbor-UCLA Department of Emergency Medicine Core Conference in Harbor-UCLA Medical Center, Torrance, CA.
Young male with no significant medical history presenting with progressively worsening right lower quadrant abdominal pain with marked tenderness to palpation and involuntary guarding.
34F with no reported medical history BIBA with severe burns after house fire with estimated 70% TBSA involvement. On arrival, the patient was hypoxic, striderous, and unable to provide history. She was intubated for airway protection with some difficulty. Examination revealed deep partial and full-thickness burns to 70% of total body surface area including circumferential burns to bilateral upper extremities and extensive neck and anterior chest involvement. Initial fluid resuscitation and warming measures were instituted. Emergent bedside bronchoscopy revealed copious carbonaceous material throughout with attempts at lavage. Urine output was minimal despite aggressive resuscitation. Critical care transport to local burn facility was arranged where the patient ultimately expired.
|Superficial||UV exposure||Dry, red
|Superficial partial-thickness||Scald (splash)
|Blisters, moist, red
|Painful to temperature/air|
|Deep partial-thickness||Scald (spill)
Flame, oil, grease
|Blisters, waxy dry, white/red
Flame, steam, oil, grease, chemical, electrical
|Waxy white, leathery grey, black
30 year-old male with no significant medical history presenting with 24 hours of progressively worsening throat pain, difficulty swallowing and voice hoarseness. He reports subjective fevers and chills.
Vital signs notable for Tmax 38.4°C. On physical examination, the patient was sitting upright, unable to swallow secretions with faint inspiratory stridor and dysphonia (though he was able to speak in full sentences and without apparent respiratory distress). Oropharyngeal examination showed minimal right parapharyngeal edema without uvular or palatal deviation and there was exquisite right lateral neck tenderness to palpation.
The patient acutely decompensated prior to fiberoptic laryngoscopy and proceeded emergently to the operating room for controlled intubation. The operative report described the following findings: “The patient had diffuse edema of the posterior oropharyngeal wall. The epiglottis was severely thickened, Omega shaped, soft to palpation and with moderate pressure, it appeared to come to a head and pus was expressed from the lingual side of the epiglottis.” The patient was extubated on hospital day three and discharged soon thereafter, he was doing well on follow-up.
34M with no PMH presenting with joint pain and rash. The patient was in his usual state of good health until 1 week prior to presentation, noting bilateral shoulder pain. Diagnosed with musculoskeletal process at outside hospital and discharged with analgesics. Presented with partner due to worsening pain involving multiple joints, a non-painful, non-pruritic rash on bilateral lower extremities, and apparent confusion/hallucinations. Social history was non-contributory, no recent procedures or instrumentation.
Objectively, vital signs were notable for tachycardia and elevated core temperature. The patient was ill-appearing, disoriented and unable to provide detailed history. Skin examination was notable for non-blanching petechial rash with areas of confluence most dense in anterior distal lower extremities, rarer proximally, and otherwise without palm/sole involvement. Mucous membranes were dry, neck was supple. There was tenderness to palpation and manipulation of bilateral shoulders. No back tenderness to palpation or percussion was identified. Neurological examination notable for disorientation, intact cranial nerve function, pain-limited weakness in bilateral upper extremities particularly shoulder abduction, and 4/5 hip flexion, knee flexion/extension in bilateral lower extremities.
Severe sepsis with end-organ dysfunction, unclear source (urinary tract involvement unlikely to account for severity of illness). Covered empirically with broad-spectrum anti-microbials including CNS infection given component of encephalitis. Admitted to the intensive care unit.
On hospital day 1, the patient underwent non-contrast MRI of the entire neuraxis with findings concerning for L4-L5 and L5-S1 epidural and paraspinal infection resulting in moderate-severe spinal canal stenosis. Blood and urine cultures grew gram-positive cocci in clusters.
On hospital day 2, the patient became increasingly somnolent. Repeat examination by consulting neurology service was concerning for evidence of meningeal irritation. Cultures speciated as methicillin-sensitive staphylococcus aureus and oxacillin was added. MRI was repeated with gadolinium, findings concerning for L4 epidural vs. paraspinal abscess.
On hospital day 3, the patient’s mental status continued to worsen and he was intubated for airway protection. Neurosurgical intervention was deferred due to deteriorating clinical status. Shoulder synovial fluid aspirate culture positive for MSSA, orthopedic surgery consulted for washout/serial arthrocentesis. TTE performed without evidence of valvular vegetation.
On hospital day 4, additional warm joints were aspirated by orthopedic surgery including knee, bilateral ankles, and shoulder each of which ultimately grew MSSA.
On hospital day 6, the patient underwent OR washout of affected joints with intraoperative findings of purulent fluid. TEE performed without evidence of valvular vegetation. The following day, underwent fluoroscopically-guided lumbar puncture, CSF studies inconclusive. Rifampin added for high-grade bacteremia with multiple seeded sites.
The patient was extubated on hospital day 9 and transferred out of the intensive care unit. The following day, he became increasingly tachypneic with evidence of volume overload on examination and was intubated and returned to the intensive care unit. Sustained PEA arrest post-intubation with ROSC, possibly secondary to pneumothorax vs. hypoxia from extensive mucous plugging. Required increasing vasopressor support over the subsequent 12 hours, emergent CVVHD for worsening academia and hypervolemia. The patient sustained another arrest and ultimately expired.
The final impression was that of high-grade bacteremia from unclear source (vague history of proximate hand laceration/infection) with resultant seeding of epidural/paraspinal space, urinary tract, multiple joints, and likely CNS/meninges. Review of abdominal ultrasonography with evidence of cirrhosis, suggesting that some component of initial hepatic synthetic dysfunction may have been chronic and this may have increased the patient’s risk for disseminated infection and SEA. Neurosurgical intervention was not pursued due to unstable clinical status and as the patient’s neurological findings were not consistent with the location of the identified lesion.
|Focal spinal TTP||52-62%|
|Diffuse spinal TTP||63-65%|
|Abnormal rectal tone||5-10%|
Below is a rapid reference for essential information related to the care of pediatric patients including sizing estimates for endotracheal tubes and weight-based dosing for critical/common medications (rapid sequence intubation, pediatric advanced life support, seizure management), compiled by Dr. Kelly Young1.
|1-10yo||70 + (Age x2)|
|Succinylcholine||1mg/kg (x2 infant, x3 neonate)|
|Defibrillation||2, 4, 10J/kg|
|Epinephrine||0.01mg/kg (0.1mL/kg of 1:10,000)|
|Atropine||0.02mg/kg (minimum dose 0.1mg, maximum 0.5mg)|
|Adenosine||0.1mg/kg (max 6mg), 0.2 mg/kg (max 12mg)|
|Calcium gluconate (10%)||1mL/kg|
|Calcium chloride (10%)||0.2mL/kg|
|Normal saline (0.9%)||20cc/kg|
|Maintenance||4cc/kg (first 10kg), 2cc/kg (second 10kg), 1cc/kg thereafter|
|Lorazepam, Midazolam||0.1mg/kg x3|
|Midazolam IN||0.2mg/kg (max 10mg)|
|Amoxicillin||90mg/kg divided BID|
|Azithromycin||10mg/kg day 1, 5mg/kg days 2-5|
|Fentanyl||1.5mcg/kg (max 100mcg)|
|Midazolam||0.5mg/kg (max 10mg)|
64M with a history of HFrEF (LVEF 20-25%), CAD, AICD (unknown indication), COPD, CKD III presenting with gradual onset shortness of breath, progressive bilateral lower extremity edema.
Examination consistent with severe acute decompensated heart failure presumed secondary to left ventricular dysfunction.
Telemetry monitoring with multiple episodes of nonsustained ventricular tachycardia.
In the ED, the patient developed worsening respiratory failure despite initiation of therapy, requiring endotracheal intubation. Continuous cardiac monitoring revealed persistent salvos of NSVT, progressing to slow ventricular tachycardia without device intervention.
Device interrogation revealed multiple events, 3 shocks, several ATP’s over the recorded period.
Non-specific IVCD, LAA, VPC
VT initiated by fusion complex
31F with autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), presenting with fever and cough.
Evaluation consistent with sepsis presumed secondary to pulmonary source.
Telemetry monitoring initially with ventricular bigeminy, then nonsustained ventricular tachycardia.
In the ED, the patient developed pulseless ventricular tachycardia – apparently polymorphic. Chest compressions and epinephrine produced return of spontaneous circulation with recovery to baseline neurologic function.
ECG revealed prolonged QTc and chemistry panel notable for critical hypokalemia/hypomagnesemia.
Non-sustained ventricular tachycardia noted on telemetry monitoring
In some patients, NSVT is associated with an increased risk of sustained tachyarrhythmias and sudden cardiac death. In others it is of little prognostic significance.6,7,8
38M, unknown medical history, brought in after being found unresponsive next to an empty bottle of Seroquel. Presenting vital signs notable for blood pressure of 96/43, heart rate 103. Examination reveals tentatively protected airway (GCS E2 M5 V3, SpO2 100%, RR 14), normal pupil diameter and reactivity, dry mucous membranes with thick vomitus in oral cavity.
Laboratory evaluation was unremarkable, and there was no evidence of aspiration on chest radiography. ECG showed sinus tachycardia without QT prolongation. Blood pressure increased to normal range with fluid resuscitation. The patient’s mental status progressively improved and he was discharged after six hours of uneventful continuous cardiac monitoring.
|Class||Vital Signs||Mental Status||Pupils||Skin||Other||Examples|
|Other||HR > 100||1|
30 year-old female with a history of autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), polysubstance use, brought to the emergency department by ambulance with reported chief complaint of fever. On presentation, the patient reported fever for one day, associated with cough. She was lethargic and confused, answering yes/no questions but unable to provide detailed history. She states that she has been taking her home medications as prescribed, which include hydrocortisone, fludrocortisone, synthroid and insulin. No collateral information was immediately available.
Additional history was obtained from chart review upon discharge. The patient was hospitalized two weeks prior with pneumonia and discharged after two days. For 2-3 days prior to presentation, she reported the following symptoms to family members: nausea/vomiting, cough, decreased oral intake, fevers, and palpitations – she did not take her home medications during this time.
|Gen:||Alert, fatigued, slow responses.|
|HEENT:||No meningeal irritation, dry mucous membranes.|
|Pulmonary:||Tachypnea, inspiratory wheezing and faint crackles at left and right inferior lung fields, appreciated anteriorly as well.|
|Neuro:||Alert, oriented to self, situation, not month/year. PERRL, EOMI, facial muscles symmetric, tongue protrudes midline without fasciculation. Peripheral sensation grossly intact to light touch and moves all extremities on command.|
The patient’s evaluation in the emergency department was concerning for severe sepsis secondary to suspected pulmonary source (given association of fever with cough, hypoxia and abnormal chest imaging findings). The patient had persistent alteration in mental status concerning for CNS infection. While preparing for lumbar puncture, cardiac monitoring revealed sustained polymorphic ventricular tachycardia without appreciable pulse. CPR was initiated, amiodarone 150mg IV push administered and at first pulse check a perfusing sinus rhythm was noted with immediate recovery of prior baseline mental status. Amiodarone load was continued and additional potassium sulfate (PO and IV) was administered. Review of telemetry monitoring revealed preceding 30-45 minutes of non-sustained ventricular tachycardia. The patient had two more episodes of sustained ventricular tachycardia requiring defibrillation. The patient was admitted to the medical intensive care unit for continued management.
#Sustained Ventricular Tachycardia
Initially attributed to critical hypokalemia and hypomagnesemia. However, after appropriate repletion serial ECG’s continued to demonstrate prolonged QT interval (possibly acquired secondary to medications, later review revealed multiple promotility agents for treatment of gastroparesis which could contribute to QT-prolongation including erythromycin and metoclopramide, also associated with endocrinopathies). Early echocardiography demonstrated global hypokinesis with estimated EF 30-35%. This was initially attributed to severe sepsis, as well as recurrent defibrillation. However, cardiac CT after resolution of acute illness showed persistent depressed ejection fraction, no evidence of coronary atherosclerosis. The presence of non-ischemic cardiomyopathy (may be attributable to chronic endocrine dysfunction or prior history of methamphetamine abuse) associated with malignant dysrhythmias warranted ICD placement for secondary prevention which the patient was scheduled to receive.
Attributed to pulmonary source given CT findings, healthcare associated and covered broadly. Mental status gradually improved and returned to baseline. CT head was negative, lumbar puncture deferred.
Unclear etiology. Adrenal insufficiency commonly associated with hyperkalemia and no history of surreptitious fludrocortisone use. Possibly secondary to GI losses. Improved with repletion.
#Autoimmune Polyglandular Syndrome
Started on stress-dose steroids in emergency department. Transiently developed DKA which was reversed appropriately and hydrocortisone was tapered to home regimen. Home levothyroxine was resumed.
|Constitutional||Weight loss, heat intolerance, perspiration|
|Cardiopulmonary||Palpitations, chest pain, dyspnea|
|Neuropsychiatric||Tremor, anxiety, double vision, muscle weakness|
|Neck||Fullness, dysphagia, dysphonia|
|Reproductive||Irregular menses, decreased libido, gynecomastia|
|Vital signs||Tachycardia, widened pulse pressure, fever|
|Cardiovascular||Hyperdynamic precordium, CHF, atrial fibrillation, systolic flow murmur|
|Ophthalmologic||Widened palpebral fissure, periorbital edema, proptosis, diplopia, restricted superior gaze|
|Neurologic||Tremor, hyperreflexia, proximal muscle weakness|
|Dermatologic||Palmar erythema, hyperpigmented plaques or non-pitting edema of tibia|
|Neck||Enlarged or nodular thyroid|
Essentially an exaggeration of thyrotoxicosis featuring marked hyperthermia (104-106°F), tachycardia (HR > 140bpm), and altered mental status (agitation, delirium, coma).
|Moderate (rales, atrial fibrillation)||10|
|Nausea/vomiting, abdominal pain||10|
|Constitutional||Weight gain, cold intolerance, fatigue|
|Cardiopulmonary||Dyspnea, decreased exercise capacity|
|Neuropsychiatric||Impaired concentration and attention|
|Reproductive||Irregular menses, erectile dysfunction, decreased libido|
|Integumentary||Coarse hair, dry skin, alopecia, thin nails|
|Vital signs||Bradycardia, hypothermia|
|Cardiovascular||Prolonged QT, increased ventricular arrhythmia, accelerated CAD, diastolic heart failure, peripheral edema|
|Neurologic||Lethargy, slowed speech, agitation, seizures, ataxia/dysmetria, mononeuropathy, delayed relaxation of reflexes|
|Musculoskeletal||Proximal myopathy, pseudohypertrophy, polyarthralgia|
Either primary due to adrenal gland failure (often secondary to autoimmune destruction), or secondary most often due to exogenous glucocorticoid administration (usually requiring more than 30mg/day for > 3wks).
|Gastrointestinal||Anorexia, nausea, cramping|
|Reproductive||Amenorrhea, decreased libido|
|General||Hyponatremia, orthostatic hypotension, low-grade fever|
|Primary||Hyperpigmentation, hyperkalemia, hyperchloremia, acidosis|
Unfortunately, this patient’s comprehensive clinical picture does not fit neatly into a particular category of endocrinologic pathology. Her underlying autoimmune disorder manifests both primary adrenal and thyroid dysfunction. Components of the patient’s presentation are suggestive of critical hypothyroidism (myxedema coma) including alteration in mental status, QT-prolongation and hyponatremia as well as possible precipitant of pneumonia. However, despite elevated TSH, the patient’s free T4 level was within normal range. Also absent was hypoventilation (the patient was appropriately tachypneic for degree of hypoxia and with resultant respiratory alkalosis) or bradycardia/hypothermia.
Similarly, adrenal insufficiency is typically associated with hyperkalemia, whereas our patient had critical hypokalemia that was determined to be at least a contributory factor to her ventricular dysrhythmia. The etiology of the patient’s hypokalemia remained unexplained.
|Anaphylaxis||Exposure to allergen||Abrupt onset, facial swelling||Stridor, wheezing, hives|
|PE||Immobilization, malignancy, prior DVT/PE, surgery, OCP||Abrupt onset, pleuritic chest pain||Tachycardia, hypoxia||ECG (RV strain)
CT PA, D-dimer
LE US (DVT)
|Pneumonia||Exposure, tobacco use||Fever, productive cough||Focal rales||CXR
|Pneumothorax||Trauma, thin male||Abrupt onset, chest pain||Decreased BS, subQ emphysema, JVD and tracheal deviation if tension||CXR
|Fluid overload||Dietary indiscretion, medication non-adherence||Orthopnea, PND||JVD, S3/S4, peripheral edema||CXR
|COPD/Asthma||Tobacco use, personal/family history||Progressive||Retractions, accessory muscle use, wheezing||CXR
US (distinguish from fluid overload)
|Malignancy||Tobacco use, weight loss||Hemoptysis||CXR
58 year-old female with no known past medical history, brought to emergency department by husband due to fatigue and weakness. The patient does not speak and cannot provide history. Her husband describes a progressive decline from normal baseline two weeks ago, noting lethargy/fatigue. Noted decreased speech and attention one week ago, and absent speech and requiring assistance with ambulation for the past two days. Thorough review of systems unremarkable excepting vomiting with decreased oral intake (tolerating fluids) and prior headache which resolved.
On examination, vital signs were normal, the patient was lying in bed and in no acute distress. The patient was non-verbal and did not follow commands (GCS E4-M5-V2). She was unable to comply with a thorough neurological examination, however pupils were equal and reactive, eyes tracked without nystagmus, no facial asymmetry noted, reflexes 1+ and symmetric in UE/LE, cannot participate in strength/sensory testing. Abdominal examination notable for infraumbilical and left-sided mass which elicits groans with palpation, though no rigidity or guarding. Mucous membranes moist, no skin tenting.
The patient was admitted to the medical intensive care unit. The following problem list details findings from the extensive inpatient evaluation.
#Altered Mental Status: The patient’s dramatically depressed level of consciousness improved gradually with correction of hyponatremia and the patient was alert, oriented and at baseline at the time of discharge. Evaluation included MRI brain which showed only chronic microvascular changes. A lumbar puncture was notable for isolated elevation of CSF protein. The patient was treated empirically for HSV encephalitis until CSF HSV PCR resulted negative. Neurology was consulted and identified increased CSF oligoclonal bands of unclear significance.
#Hyponatremia: Nephrology consulted, presumed SIADH based on urine studies (secondary to infection or malignancy). Corrected upon discharge.
#Pelvic Mass: Initially thought to arise from small bowel on CT abdomen/pelvis, after bladder decompression and transvaginal ultrasound, thought to arise from adnexa. Gynecology consulted, cyst characteristics (homogenous, fluid-filled) suggest benign process and tumor markers within normal limits. No acute intervention, drainage or biopsy warranted.
#Bladder distension: Unclear etiology, associated with mild/moderate hydronephrosis. Thought to be secondary to bladder outlet obstruction secondary to pelvic mass. Indwelling catheter placed, discontinued prior to discharge with successful spontaneous voiding trial and normal post-void residual.