Grand Rounds Recap 2.7.18

Airway grand rounds : the pediatric airway WITH DR. Carleton

The Case
3 year old in house fire requiring transport to the ED, 40% TBSA, stridulous, intercostal retractions, cough is hoarse and barking, soot in the airway and carbonaceous sputum with edema in the airway
VS: 160, R 36, O2 91% on NRB
Can you bag this patient through transport or does this patient need a definitive airway?  If so what drugs do you use? How do you position the patient? What ETT size do you place to what depth?

Epidemiology of the Pediatric Airway
Emergent pediatric intubation is rare, rate is 1.1-3.3 per 1000 visits
Mean number in a pediatric ED is 64 per year, mean age requiring ETT is ~2.4 years old
Difficulty is usually encountered in infants and small children (3 and under but mostly 2 and younger)

Difficult Pediatric Airways
They are rare
Difficulty is usually predictable based on physical exam although we do not have a validated rule such as LEMON as we do for adults to officially guide us
Multiple studies show that in the setting of difficulty laryngoscopy, BVM is an extremely adequate rescue devices as is an LMA. Pediatric patients often do not have the same ventilatory challenges as adults do

Errors and Cognitive Load
Children are less tolerant of errors and delays due to decreased tolerance of hypoxia and acidemia and less pharmacologic "wiggle room" with dosing of RSI meds
Errors and delays are common in the pediatric airways due to variable anatomy and physiology, size effects on equipment and meds and lack of opportunities to gain proficiency

Approach to the Patient
Does the patient need an airway and if so why?
If so, when and how? Crash or not? Apply the universal airway algorithm always.
Will it be difficult? Have a back-up plan ready.
How do I know if I am failing? 
How do I overcome failure? Apply rescue methods (BVM or bag + laryngeal device)

Increase succinylcholine in infants to 2.0mg/kg
Topical anesthesia: greater potential for toxicity and laryngospasm
Fentanyl: higher incidence of rigid chest syndrome in high doses
Consider atropine in infants if using succinylcholine although the data is not convincing

1. Behavioral issues

2. Anatomic differences

  • Small airway caliber
    • Obstructs easily
    • Flow resistance increases to the fourth degree with any kind of edema
  • Airway/chest compliance
    • From infancy to age 3 especially this can lead to dangerous dynamic obstruction (which can usually overcome with positive pressure)
    • Very responsive and compliant with BVM as opposed to adults
    • FB more likely to move with positive pressure which can be 
  • High anterior airway (C3 in infants) makes for difficult laryngoscopy, nasotracheal intubation and surgical airways
  • Large occiput affects positioning
  • Small mandible and relatively large tongue makes laryngoscopy difficult
  • Large, stiff (the idea that it is "floppy" is a myth), angled epiglottis makes it difficult to see with DL
  • Small cricothyroid membrane makes surgical airways difficult
  • Syndromic patients add a whole other element to anatomic difficulties

Pearls to overcome these differences:
Age specific positioning: Position properly with thorax raised (as opposed to occiputs in adults), especially in infants
Instinct will make you want to be really close to the patients mouth however back away from the patient to maximize your chance of seeing the very anterior airway
Use a straight blade to overcome a large tongue and epiglottis
Floppy airway and ETT: use stylettes except in the neonate but be sure they don't protrude beyond the tip of the ETT

3. Physiologic differences
Infancy to age 5

  • O2 consumption and CO2 generation is twice that of an adult (they will de-sat and become acidotic faster, consider bagging them through induction more than adults)
  • FRC is 1/2 that of adult and they have increased dead space (less reserve after de-nitrogenation during pre-ox)
  • Pediatric patients compensate by breathing faster not deeper however we're limited by how fast we can bag them 
  • Fatigue more easily

4. Assessment for difficulty
LEMON law for pediatrics

  • Look: most important but is still somewhat limited compared to adults limitations 
  • Evaluate: assessment of mouth opening will be valuable
  • Mallampati: Difficult to obtain and not very useful however the ability to displace the tongue may be helpful
  • Obstruction/Obesity: obstruction is the prime reason for intubation and usually evident on H&P
  • Neck mobility: Decreased in trauma or in some syndromes

Quick Tools: mouth opening, evaluate for micrognathia and assess for submental compliance/ability to compress tissues

Predicting Difficult Bagging
MOPS mnemonic
Mask seal
Obstruction: laryngospasm, T&A, foreign bodies, etc
Stiffness: fentanyl or burns

Tips to bag better
Position the patient appropriately
Open airway by displacing mandible forward, create an under bite!
Allow adequate expiratory time (squeeze, release, release cadence)
Two-person, two-handed technique, always
Don't push the mask down on the face, pull their face into the mask using thenar technique

Global health : point of care ultrasuond WITH DR. Lagasse


In a resource limited setting it may be the only imaging modality available
This should fulfill a definitive criteria
Identify the target population, they should have a relatively high incidence of the disease

Spleen Ultrasound

Why ultrasound the spleen?
Increased ability to detect splenomegaly more than physical exam
Splenomegaly is a finding in many tropical diseases
Views needed: 10th & 11th intercostal line, posterior axillary line, measured in three planes
Definition of splenomegaly:
Greater than 12 cm longitudinally
Inferior pole of the spleen extends beyond the inferior pole of the kidney
Splenomegaly + portal hypertension = schistosomiasis
Accessory spleen: normal anatomic variant in 20-25% of people, usually less than 25mm in diameter, round, and extra-splenic

  • Ways to help differentiate it from an abscess/cyst: extrasplenic not intrasplenic, same echogenicity as spleen, same color flow as spleen


Looks for extra-pulmonary TB (EPTB) in population with high HIV prevalence
EPTB more difficult to diagnose and is more commonly seen in immunosuppressed patients
Definitive diagnosis of the underlying etiology of abnormalities found in a FASH exam are not possible by ultrasound alone
In a high prevalence resource limited setting this can provide you with valuable information
Why its important: can help guide decision, may alter treatment of TB dependent on what organ system is involved, mortality rates are high in those co-infected with TB and HIV
1. Pericardial effusion: subxiphoid cardiac or parasternal long
        Treatment with steroids is useful in addition to treatment for EPTB
2. Pleural effusion:
        Most common form of EPTB in HIV positive patients, often unilateral
3. Abdominal effusion (ascites) using classic FAST views
        Associated with TB peritonitis, often affects the terminal ileum or cecum
FASH Plus Exam:
1. Upper abdominal lymph nodes: pathological when >1.5cm
2. Focal splenic lesions: multiple, small hyperechoic lesions and splenomegaly

Most common form of EPTB in the US is in the cervical lymph nodes (scrofula)


Ultrasound of the liver to aid in diagnosis echinococcosis

  • Parasitic tapeworm infection, whose definitive host is dogs and intermediate host is commonly livestock, common in poor communities that raise livestock using dogs as herding animals or guard dogs

Most commonly affects the liver
Ultrasound screening for hepatic CE diagnosis, staging and management is common


Waterborne blood fluke that affects the GI or GU tracts
Snails are host and praziquantel is your treatment of choice
Chronic infections affects a significant proportion of the population
Early stages = periportal fibrosis
Late stages = portal fibrosis
Enlarged portal vein diameter and presence of advanced fibrosis are associated with a >70% increased risk of variceal bleed

Pediatric Pneumonia

#1 cause of mortality in children under five, 90% occur in low and middle income countries
WHO Classifications

  1. Non-pneumonia (URI symptoms +/- wheezing)
  2. Pneumonia (tachypnea)
  3. Severe pneumonia (retractions)
  4. Very severe pneumonia (altered mental status, cyanosis, lethargy)

Criteria are 77-94% sensitive and 39-98% specific

6 sonographic views (3 on each hemithorax)

  • Anterior (mid-clavicular)
  • Lateral (mid-axillary)
  • Posterior (between spine and scapula)

Start cephalic and move caudal until you see diaphragm move in
Lung consolidation is echo poor or has tissue like look/"hepatitization" of the lung
Can also see air bronchogram (branching echogenic structures that create a dirty shadow behind them, move with breathing), fluid bronchograms (fluid filled bronchi, anechoic structures with hyperechoic wall), or B lines (due to subpleural fluid)

R1 clinical diagnostics : Pulmonary function testing WITH DR. Gleimer

Primer Here

Case 1

57 y/o female presents to the ED with shortness of breath, dyspnea on exertion and occasional lightheadedness. She states that over the past several months she has had worsening dyspnea on exertion, and now doing household chores like laundry are causing her to become extremely out of breath. Today she got out of her car to walk into work and got so dyspneic that she thought she was going to pass out, so she called 911. She is currently on no medications. She reports a remote history of “a clot in my lungs” in her mid-20s when she was on birth control. She smokes one pack of cigarettes daily. She works in a sheet concrete factory. She tells you that she recently got health insurance and did go see a primary care doctor about her symptoms last week. They did a chest xray and some “breathing tests,” but she hasn’t gotten the results back
Vitals: HR 115 BP 137/80 RR 22 SpO2 93% on RA Temp 97.7
On exam, she is tachypneic but has an otherwise unremarkable pulmonary exam without wheezes or rales. You think you might hear an early diastolic murmur but aren’t sure. She has mild +1 pitting edema in the lower extremities bilaterally.

Ddx for reduced DLCO: alveolar wall pathology (fibrosis), decreased lung volume (restrictive disease), anemia, emphysema, PE, CHF, pulmonary htn
Final diagnosis: pulmonary artery hypertension in the setting of chronic PE
Quick Tips:

  • If obstructive think emphysema
  • If restrictive think ILD
  • If neither think CHF/pump failure

Case 2

A 35 y/o female with a history of asthma presents with shortness of breath, cough and audible wheezing. She reports that she’s been feeling ill for the past three days with low grade fevers, increasing shortness of breath and a little chest pain, all of which got worse today. She has been using her rescue inhaler every two hours without improvement
Vitals: HR 104 BP 117/78 RR 35 SpO2 95% RA Temp 99.4 Height: 165 cm
On exam, she appears uncomfortable in mild to moderate respiratory distress with inspiratory and expiratory wheezing, diminished lung sounds at the base, and can only speak in 4-5 word sentences
RT tells you her peak flow is 320 L/min
After treatment and monitoring, her peak flow is now 415 L/min. She is still complaining of SOB and has inspiratory wheezing

Peak expiratory flow in the ED asthma patient has not been shown to improve outcomes, admission, morbidity or mortality
No recommendation to measure PEF universally

Case 3

The patient is a 45 y/o male with a history of schizophrenia, bipolar disorder and myasthenia gravis who presents with agitation and shortness of breath. History is difficult due to the patient’s agitation, but a family member with him states he was diagnosed with the flu several days ago. Since then, they think he hasn’t been taking his schizophrenia medication and has been complaining of feeling short of breath with a cough for the past several days
Vitals: HR 130 BP 113/50 RR 20 SpO2 93% RA Temp 100.5 Weight 100 kg
On exam, the patient is agitated and not cooperative. You note bilateral ptosis that the family member confirms is worse than baseline. On exam, he is not tachypneic but is taking somewhat shallow breaths. You note a weak cough and the use of some accessory muscles
His NIF is -20 cmH20

NIF and FVC in MSK Respiratory Failure
FVC decrease of 10% upright to supine is the best indicator of diaphragmatic weakness
FVC < 20ml/kg or NIF >-30mm H20 are indicators for intubation
Count test: 50 seconds indicates normal VC, 15 indicates severe impairment of VC

clinical pathologic case presentation : Altered mental status WITH DRs. ham & wright

The Case:
Middle aged female with schizophrenia from a group home with AMS. No paperwork or personnel. EMS report says she's been altered for an unknown period of time with no known baseline
BP 114/95 P 121 R 20 O2 Sat 96% on RA Temp 103.4
Exam: Tachycardic with weak pulses, awake but nonverbal, does not follow commands, moves all extremities but has pronounced tremor rigidity of bilateral uppers

Initial Attending Thoughts:
1. Address Life Threats (ABCs)
2. Eval and treat for time dependent entities
3. Complete a broad laboratory workup including EKG, CXR and HCT
4. Search for more information (call group home) 
1. SIRS: infection, tox, endocrine (thyrotoxicosis, adrenal insufficency), primary neuro (SCE)
2: CNS compromise: infection, tox, primary neuro (SCE, parkinsonism), endocrine (thyrotoxicosis, pheochromocytoma)
Resuscitation with crystalloid, broad sepctrum abx (it is time to treatment not time to diagnosis that improves this patient outcomes), benzodiazepines, antipyretics, consider LP but do not delay for treatment

WBC 22,000
CPK 10,767
Lactate elvated, respiratory alkalosis, hypokalemia, LFTs mildly elevatedwith AST >ALT, normal TFTs
HCT: Normal

Revisiting the DDx:
Primary neuro causes, infection, endocrine (thyroid now less likely)

Collateral Info: 
Patient usually conversant, ambulatory and does many of her ADLs
Notable Meds: Amantadine, haldol IM (monthly), benztropine, clopidogrel, furosemide, lorazepam, mirtazapine
What's unusual or levelable? What can cause lab abnormalities (ie furosemide and potassium)

DDx Again:
Unlikely to be primary neuro given lab abnormalities and medication list
1. Infectious etiology

  • Meningo-encephalitis: bacterial vs viral (West Nile depending on season)

2. Tox

  • NMS: dopamine going away (haldol dose boosted or amantadine being withdrawn abruptly)
    • Hyporeflexic with lead pipe rigidity
  • Seratonin Syndrome: too much seratonin floating around 
    • Hyperreflexic with clonus, increased tone and cog-wheel rigity 

Diagnostic Test of Choice: CSF studies showing strep pneumo meningitis

Bacterial Meningitis
Rare but carries a high rate of morbidity and mortality
Classic Triad: Fever, headache and nuchal rigidity

  • This is rarely present in its entirety, but most patients will have at least two of the "three. Hypotension, altered mental status, and seizures all portend a poor prognosis. Leukoc

CSF lactate is rarely ordered, but evidence suggests it may actually out-perform the standard CSF labs (cell count/culture, protein, glucose) and can function as a "differentiator" from aseptic meningitis, likely more to come in the future

Contraindication to LP without CT: immune-compromise, CNS disease, papilledema, age >65, AMS

  • Some recent data may suggest removing AMS as a contraindication to improve door-to-antibiotic time and decrease mortality.

Benefits of dexamethasone are often debated and results of studies are inconsistent, but most recent data has shown reduced mortality and lower rates of hearing loss in Pneumococcal meningitis
Consider adding rifampin to your empiric regimen when you use dexamethasone. Steroids reduce CNS penetration of common empiric agents, but rifampin will help ensure adequate coverage