Obesity

Airway exam that predicts trouble - Measure neck circumference at the thyroid cartilage, thyromental and sternomental distance, and Mallampati; these are the findings tied to difficult mask ventilation and difficult intubation at this BMI.

Sleep-disordered breathing - The Berlin Questionnaire flags undiagnosed OSA, which is common and frequently missed; ask about home CPAP use. Obesity hypoventilation syndrome is awake alveolar hypoventilation that other lung disease does not explain, driven by a blunted hypercapnic ventilatory response, and it is often unknown at the time of surgery.

Position before you induce - Ramp the patient so the external auditory meatus sits level with the sternum, or use 25-degree reverse Trendelenburg. Do this before laryngoscopy, not after the first failed look.

Apneic oxygenation - 15 L/min of oxygen through a nasopharyngeal airway plus a standard nasal cannula significantly lengthens the safe apneic window during induction.

Laryngoscope choice - Both direct and video laryngoscopy work here; there is no conclusive evidence that video laryngoscopy is superior in patients with obesity. Pick the one you are fastest with and have the other in the room.

Airway collapse under anesthesia - Loss of upper-airway muscle tone collapses the pharynx and can wipe out the landmarks you need for fiberoptic intubation. Positive pressure delivered through an endoscopic mask stents the airway open and restores the anatomy.

Dosing scalars - Propofol and etomidate on lean body weight, titrated to effect, since total body weight dosing causes hemodynamic instability. Nondepolarizing NMB on ideal body weight. Succinylcholine on total body weight.

Ventilator settings - Tidal volumes of 6 to 8 mL/kg ideal body weight, low to moderate PEEP to limit atelectasis, and FiO2 titrated to an SpO2 of 92 to 95%.

Trust the ABG over the capnograph - The expired-to-arterial CO2 gradient is wider than in lean patients and CO2 production is higher, so end-tidal understates PaCO2. Send an arterial blood gas to set the vent on a long case.

Blood pressure cuff placement - Standard NIBP is less accurate at this body habitus. A forearm cuff outperforms upper arm or lower leg, and wrist readings correlate best with a radial arterial line.

Extubate sitting up - Confirm adequate tidal volumes with the patient ramped or in 25-degree reverse Trendelenburg, and have an oral airway or nasal trumpet ready for obstruction. Repeated post-emergence laryngospasm has been reported in this population.

PACU is where they fail - Watch specifically for apnea, bradypnea, pain-sedation mismatch, CO2 retention and desaturation. Postoperative pulmonary complications lengthen PACU and hospital stay and raise mortality; persistent respiratory events justify an inpatient bed.

Regional when it fits - Spinal anesthesia avoids airway manipulation and cardiopulmonary depressant drugs, reduces PONV, and cuts intraoperative and postoperative opioid requirement — the opioids that drive postoperative pulmonary complications.

The vomiting patient decompensates fast - Hypoventilation gives respiratory acidosis while vomiting adds a metabolic alkalosis; the resulting alkalemia removes the acidemic stimulus to breathe and worsens the respiratory failure.

Where the patient sits on the spectrum - Class I is a BMI of 30 to 34.9 and class II is 35 to 39.9. Risk is a gradient, not a threshold: across 30,549 elective surgical cases BMI independently predicted two of three adverse outcomes studied, namely postoperative respiratory failure, perioperative pulmonary embolism or deep vein thrombosis, and postoperative sepsis.

Pick the dosing scalar before you draw up - Ideal body weight is 50 kg + 2.3 x (height in inches - 60) for men and 45.5 kg + 2.3 x (height in inches - 60) for women. Lean body weight is [9270 x TBW] / [6680 + (216 x BMI)] for men and [9270 x TBW] / [8780 + (244 x BMI)] for women. Adjusted body weight is IBW + a correction factor x (TBW - IBW), which exists to correct for the altered volume of distribution. Applying the wrong scalar is the mechanism by which these patients get overdosed or underdosed.

Renal clearance cuts both ways - GFR and renal drug clearance may run high in a younger patient with obesity and no end-organ damage, courtesy of the higher cardiac output, and then drop once obesity-related hypertension and diabetes have produced chronic kidney disease. Dose renally cleared drugs off a measured creatinine clearance rather than an assumed normal, especially once obesity-related comorbidities are on the chart.

Protein binding shifts - Albumin is generally preserved, but alpha-1-acid glycoprotein levels rise, increasing protein binding and lowering the free plasma concentration of drugs that bind AGP.

Fatty liver changes metabolism - Obesity often coexists with hepatic steatosis and functional hepatic degeneration. CYP450 enzymes are variably affected, so metabolism runs faster or slower depending on the drug rather than uniformly slowing.

Screen with STOP-Bang, not a sleep study - Polysomnography is the diagnostic gold standard but is unsuitable for routine preoperative risk assessment on time and resource grounds, and there is insufficient evidence to delay or cancel surgery purely to obtain a formal OSA diagnosis unless there is significant associated systemic disease or a problem with ventilation or gas exchange. STOP-Bang and the Berlin questionnaire are both sensitive preoperative screens. Where a sleep study already exists, the apnea-hypopnea index grades severity: mild is 5 to under 15 events per hour, moderate 15 to 30, severe above 30.

Keep the PAP machine in play - Pull the previous sleep study and the prescribed PAP settings before the day of surgery. Either stock PAP equipment in the facility or tell the patient to bring their own, and keep them on it at the appropriate times both before and after surgery.

Untreated or partially treated OSA - Patients with untreated OSA and otherwise optimized comorbidities can proceed provided mitigation strategies are in place. Push for additional preoperative cardiopulmonary evaluation when there is a hypoventilation syndrome, severe pulmonary hypertension, or resting hypoxemia with no other cardiopulmonary explanation. For the hypoventilation syndrome itself, see Obesity Hypoventilation Syndrome.

Standard fasting intervals were not written for this patient - ASA preoperative fasting is 2 hours for clear liquids, 4 hours for human breast milk, 6 hours for non-human milk, formula, or a light meal, and 8 hours for fried food, fatty food, or meat. Those guidelines give no separate interval for patients at increased risk of delayed gastric emptying or aspiration, and obesity sits on that list alongside diabetes, GERD, pregnancy, and recent opioid use. Fasting to the clock does not establish that the stomach is empty.

Gastric ultrasound answers the question at the bedside - Scan the antrum in the parasagittal plane at the level of the aorta, supine and then in right lateral decubitus. Estimated volume in mL = 27 + (14.6 x antral cross-sectional area in cm2) - (1.28 x age). Under 1.5 mL/kg is baseline secretion and low risk; above 1.5 mL/kg is a full stomach. Solids, thick liquids, or clear fluid over 1.5 mL/kg postpones an elective case. If the case has to proceed, use full aspiration precautions with RSI and an endotracheal tube, and decompress the stomach with an oral or nasogastric tube.

Why the aspirate matters - Chemical pneumonitis is more likely when aspirate pH is below 2.5 and volume is at least 0.3 mL/kg. Obesity sits on the list of factors that raise aspiration risk alongside emergency surgery, GERD, hiatal hernia, concomitant opioids, lithotomy positioning, and difficult intubation.

GLP-1 receptor agonists rewrote the fasting instruction - Semaglutide, liraglutide, and tirzepatide drive weight loss partly by slowing gastric emptying, so these patients can hold solid gastric contents through a textbook fast. Current guidance does not hold the drug: the 2024 multisociety guidance (ASA with the American Gastroenterological Association, ASMBS, ISPCOP, and SAGES) and the 2025 SPAQI consensus continue GLP-1 receptor agonists perioperatively in patients without significant GI symptoms and extend the solid fast to 24 hours on clear liquids instead, with 8 hours for clear liquids at or above 10% glucose and 4 hours below. Highest risk is recent initiation or dose escalation, higher doses, short-acting formulations, and tirzepatide. Severe nausea, vomiting, or inability to tolerate oral intake sends an elective case back to the prescriber rather than to the OR.

Esophageal manometry for PEEP titration - PEEP titration is genuinely hard at this body habitus. Esophageal manometry stands in for pleural pressure and lets you track transpulmonary pressure, keeping alveoli open as long as transpulmonary pressure exceeds atmospheric.

Get the IV before you need it - Obesity is a recognized cause of difficult peripheral IV access. Ultrasound reaches vessels too deep to palpate; target veins over 4 mm, and consider the basilic vein in the upper arm, which is usually deep enough to still be available when the superficial forearm veins are gone.

Venous thromboembolism is one of the outcomes - Perioperative pulmonary embolism and deep vein thrombosis tracked with rising BMI in the 30,549-case elective surgical series, and bariatric surgery is classified as high VTE risk with prophylaxis indicated. Check the interval since the last dose against the ASRA guidelines (fifth edition, 2025, which reclassified agents as low dose and high dose rather than prophylactic and therapeutic) before any neuraxial technique.

Check an HbA1c across the whole spectrum - Lifetime diabetes risk climbs from 7% to 70% in men and from 12% to 74% in women as BMI moves from under 18.5 to over 35 kg/m2, which is why diabetes screening belongs in the workup at class I and class II rather than only at the top of the range.

Work the comorbidity list systematically - The preoperative workup runs by system, looking for coronary artery disease, heart failure, hypertension, hyperlipidemia, diabetes, GERD, non-alcoholic fatty liver disease, OSA, obesity hypoventilation syndrome, and paroxysmal nocturnal dyspnea, supported by an ECG, a basic metabolic panel, and an arterial blood gas where gas exchange is in question.

Name the class, not just the number - Overweight starts at a BMI of 25 kg/m2 and obesity at 30. Obesity then divides into class I at 30 to 34.9, class II at 35 to 39.9, and class III at 40 or more — or 35 or more with an obesity-related comorbidity such as hypertension or diabetes, which is the patient older sources call morbidly obese. Put the class in the record: it is the shorthand that tells the next provider how thin the oxygen reserve is and how far to go with ramping, apneic oxygenation, and postoperative monitoring.

Class III obesity — a BMI of 40 kg/m2 or more, or 35 or more with an obesity-related comorbidity such as hypertension or diabetes — pushes respiratory mechanics into frank restrictive disease. Fat loading of the thorax and abdomen drops chest wall and lung compliance, cutting FRC (mostly through a lower ERV), VC and TLC while the FEV1/FVC ratio stays normal. Once FRC falls below closing capacity, small airways close during tidal breathing and produce V/Q mismatch, right-to-left shunt and arterial hypoxemia.

Under anesthesia FRC drops about 50% versus about 20% in a lean patient, so the oxygen reserve after induction is thin. Metabolic demand runs high: oxygen consumption and CO2 production both rise, and normocapnia holds only through increased minute ventilation. Chronic hypoxemia drives pulmonary hypertension and cor pulmonale. Fat mass also grows faster than lean mass as BMI climbs, which is why weight-based dosing scalars diverge.

Obesity is a spectrum, and anesthetic risk rises along it rather than switching on at a single number. A BMI of 30 kg/m2 or more defines obesity, subdivided into class I at 30 to 34.9 and class II at 35 to 39.9 before class III begins. More than 40% of American adults now fall somewhere in that range. In a series of 30,549 elective surgical cases, BMI was an independent positive predictor of two of the three adverse outcomes tracked — postoperative respiratory failure, perioperative pulmonary embolism or deep vein thrombosis, and postoperative sepsis — so a class I or class II patient is not a normal-weight patient who needs a bigger cuff.

The pharmacokinetic changes that drive dosing start well below class III. Volume of distribution and cardiac output both rise; cardiac output climbs roughly 20 to 30 mL/kg of excess fat while the share of that output reaching fat falls from about 5% to 2%. Serum albumin usually stays normal, but alpha-1-acid glycoprotein rises, so drugs that bind it circulate at a lower free concentration. Hepatic steatosis frequently coexists and alters metabolism, with individual CYP450 enzymes pushed in different directions. Glomerular filtration rate may actually run high in a younger patient with obesity and no end-organ damage, then fall as obesity-driven hypertension and diabetes produce chronic kidney disease.