Case 37 - super morbid obesity Flashcards
How do you calculate BMI?
BMI = kg / m2
BMI:
- < 18.5 - underweight
- 18.5-24.9 - normal
- 25-29.0 - overweight
- 30-34.9 - class 1 obesity
- 40-50 - morbid obesity
What are the pulmonary changes associated in superobese patients?
Pulmonary Changes:
- OSA
- upper airway obstruction
- pickwickian syndrome
- chronic hypoxemia, retain Co2 - right sided heart changes
- Restrictive lung disease
- 2/2 fat accumulation of abdomen and thorax –> decrease compliance of lungs
- Decrease FRC, TLC, VC
- Small airway closure
- closing capacity unchanged, but FRC decreases and may fall under closing capacity –> small airway closure during normal tidal volumes
- v/q mismatch
- chronic hypoxemia, Co2 retain
what are the cardiac changes associated with superobese patients?
Cardiac changes
- increase total body volume
- additional adipose tissue requires additional blood supply
- increase SV, increase CO
- LVH –> endpoint L sided heart failure
- HTN commonly seen –> can caues LVH (increase afterload)
- LVH eventually undergoes diastolic dysfunction –> left sided CHF
- RVH –> endpoint Right sided heart failure
- chronic hypoxia and hypercarbia secondary to OSA
- v/ q mismatch –> hypoxic vasoconstriciton –> pulm HTN (cor pulmonale) –> RVH –> diastolic dysfunction –> right sided CHF
- accelerated CAD
What comorbidities are associated with superobesity?
CVS
- CAD
- HTN
- CHF
Resp
- Pulm HTN
- OSA
- obesity hypoventiliation syndrome
CNS
- CVA
GI
- GERD
- fatty liver
Endocrine
- DM 2
- PCOS
Heme
- DVT/PE secondary to hypercoagulation and immobility
What is the pathophysiology of OSA?
Mechanism
- A breath is initiated by contraction of diaphragm and intercostal muscles producing negative intrathoracic pressure
- negative pressure transmits to the the pharynx (muscosa and soft tissue) and draws these tissues into the airway lumen
-
at same time, upper airway dilator muscles constrict to offset the inward movement of pharyngeal muscle and maintain upper airway patency.
- tensor palatine -> brings soft palate off nasopharyngeal wall
- genioglossus –> advances tongue off oropharyngeal wall
OSA
- lose compensation by upper airway dilator muscles –> therefore unopposed pharyngeal tissue obstructing airway lumen
Tx for OSA?
given the mechanism of action of OSA (unopposed pharyngeal tissue entering airway lumen due to loss of upper airway constricting muscles):
Positive airway pressure: CPAP, BiPaP
How is OSA diagnosed?
Apnea-Hypopnea Index (AHI)
- Apnea
- total cessation of gas flow through airway for at least 10 s
- Hypopnea
- > 50% reduction of gas flow through airway for at least 10 s
- AHI
- number of apnea and hypopnea events that occur during 1 hour
- AHI 5-14 = Mild
- AHI 15-30 = Mod
- AHI >30 = Severe
What is the STOP-bang score?
STOP-bang
- identifies/screening tool for patients with sleep disordered breathing
- 1 point per positive finding, max is 8 pts
- Score < or = to 2 - low risk
- Score > 3 or = to 3 = high risk
- Snore
- Tired
- Observed (others see you stop breathing)
- Pressure (HTN?)
- BMI ( > 35)
- Age ( > 50 yo)
- Neck Circumference ( > 40 cm)
- Gender (Male)
What is obesity hypoventilation syndrome (OHS)?
AKA Pickwickian syndrome
Characteristics:
- Obesity - BMI > 30
-
daytime hypoventilation (PaCO2 > 45 mmHg)
- *this differentiates OHS from OSA*
- arterial hypoxemia (PaO2 < 70 mmHg)
- absence of other causes of hypoventilation (neuromusclar dz, metabolic abnormalities)
What are causes of daytime hypercarbia in pickwickian syndrome patients?
1) abnormal respiratory mechanics 2/2 obesity
- restrictive airflow 2/2 excessive neck and airway adipose tissue, decrease chest wall compliance, impaired diaphragm mvmt
2) leptin resistance –> central hypoventilation
- leptin stimulates ventilation in the brain
- OHS patients develop leptin resistance –> cannot enhance their ventilation
3) inaequate compensation of acute hypercapnia
- hypercapnia usally compensated by hyperventilation on aroousal and renal excretion of bicarb
- OHS patients diminish thier ability to compensate, resulting in sustained elevation of PaCO2
how to tx OHS?
- positive airway pressure (cpap, bipap)
- supplemental oxygen
- resp stimulants
- weight loss surgery
Is superobesity always an indication for awake intubation?
NO!
- body weight and BMI are NOT indepenent predictors for awake FOB
- pre-op airway assessment for difficult to intubate and ventilate will determine awake vs asleep intubaiton
- super obese patients have large necks that makes it difficult to assess TM or sternomental distance.
What is optimal position for obese patients during intubation?
- RAMP position
- wedge under paitent’s head, shoulder, upper body
- Goal - align external auditory meatus with sternal notch
- This position unloads excessive abdominal weight off the diaphragm
How would you go about managing the airway in a super obese patient?
- preop assessment for difficulty to intubate and difficulty to ventilate
- awake vs asleep intubation
- If asleep intubation, RSI vs. standard induction
- superobese patients increased risk of O2 desaturation (decrease FRC) and unanticipated mask ventilation and/or intubation
- have another anesthesia provider on standby for assistance
- have different blades, LMA, glidescope, FOB in room
- RAMP patient on OR table
- Use induction agents with rapid recovery profile:
- SUX
- Propofol/etomidate
- if difficulty is encountered, patient can be awakened and resume spont vent quickly
- cannot intubate/cannot ventilate: surgical airway
What drugs need to be dosed according to Total Body weight, what drugs need to be dosed according to Ideal Body Weight?
Obese patients - volume of distribution is altered due to increase total body water & adipose tissue (matters for lipophilic drugs)
total body weight
- bzd
- fentanyl
- sux
- cis-at
- propofol (maintenance infusion)
Ideal body weight
- propofol (induction)
- remifentanil
- vec/roc
