Obesity and anaesthesia

Obesity

BMI = mass (kg)/[height (m)]2
BMI>28 obese, BMI >35 morbidly obese
17% of UK population are obese
Associated with BP, IHD, NIDDM, peripheral vascular disease, gallstones, etc…


Pathophysiology

Obesity is associated with

Increase in absolute blood volume, but it’s low relative to body mass
Increase O2 consumption by metabolically active adipose tissue & work of supporting ms.
Reduced FRC in awake pt, and significantly decreased following induction
Rapid desaturation.
OSA
Obesity hypoventilation syndrome, causing loss of CO2 resp drive & hypoxia, polycythemia and pulmonary hypertension
Increase gastric volume, raised intra-abdominal pressure, and a higher incidence of hiatus hernia pose a significant risk of aspiration.
Insulin resistance may cause peri-operative diabetes.
Vd for drugs is altered due to a smaller proportion of TBW, greater proportion of adipose tissue,
Increase lean body mass, and
Increase blood volume and cardiac output.


Conduct of anaesthesia
Difficult intubation
IV access
Operating table
Thromboembolic events.
Premedication.
Ventilation
Positioning
Regional anaesthesia


Post op
Post op mortality is doubled
Mobilize as soon as possible
Pulmonary atalectasis is common
Early physiotherapy.
Nocturnal nasal CPAP
PCA more predictable than IM morphine
HDU care should be available


Obstructive Sleep Apnoea
At least 5% of morbidly obese patients will have OSA particularly if they have associated risk factors such as large collar size (over 16.5 inches), evening alcohol consumption and pharyngeal abnormalities.

The disease is cause by passive collapse of the pharyngeal airway during deeper planes of sleep, resulting in snoring and intermittent airway obstruction.

Resultant hypoxaemia and hypercapnia results in arousal and disruption of quality sleep thus causing the characteristic daytime somnolence.
Cont.

Pulmonary and systemic vasoconstriction, polycythaemia, right ventricular failure and cor pulmonale can all occur.

lIndeed the relative hypoventilation can cause a progressive desensitisation of the respiratory centres to hypercapnia with resultant Type II respiratory failure.

Formal diagnosis is by sleep studies and treatment includes removal of precipitants, weight loss and nocturnal CPAP.