Clinical Syndromes
Surgical Stress Response
Surgical stress, particularly associated with major operations,
results in profound metabolic and endocrine responses. The combination of autonomic,
hormonal, and catabolic changes that accompany surgery has been called the surgical
stress response.[466]
Despite the widespread
clinical intuition that attenuation of the stress response is beneficial, there has
been a long-standing debate about whether such a strategy does affect outcome. Three
separate lines of evidence suggest that attenuation of the surgical stress response
can lead to improved outcomes. In a series of studies, interruption of the sympathetic
response to surgery markedly reduced surgical stress intraoperatively and postoperatively.
[467]
The use of continuous thoracic epidural infusions
of local anesthetics minimized the rise in plasma catecholamines, cortisol, and glucagon
and improved outcome. Improved outcome was independent of the patient's level of
pain because metabolic and endocrine responses to surgery were not similarly reduced
in patients receiving other methods of pain relief, including nonsteroidal anti-inflammatory
drugs and opioids.[467]
Continuation of epidural
infusions well into the postoperative period was regarded as essential to improving
outcome. Inflammatory and immunologic responses, which are necessary for infection
control and wound healing, appear to be unaffected. Using similar techniques and
other stress-reducing maneuvers, faster and more complete recoveries were achieved
in elderly patients undergoing colon resections.[468]
A separate line of evidence supporting the hypothesis that long-term
attenuation of the stress response alters outcome comes from the pediatric literature.
When neonates with complex congenital heart disease underwent cardiac surgery, those
who received high-dose sufentanil infusions intraoperatively and for the first 24
hours postoperatively to reduce the stress response had lower β-endorphin, norepinephrine,
epinephrine, glucagon, aldosterone, and cortisol levels compared with controls.[459]
The mortality rate in the opiate group was significantly lower than in the study
or historical controls. Anesthetic techniques can have profound effects on the metabolic
and endocrine responses to surgery, and effective management of these reflexes can
alter outcomes.
A third line of evidence involves the results from the multicenter
study of the perioperative ischemia research group (see "Perioperative β-Blockade").
[334]
The ability to alter overall survival at
2
years by a perioperative regimen of β-blockade has been validated by several
other studies,[335]
[336]
[338]
has provided compelling evidence of the benefit
of attenuating the stress response, and has altered clinical practice for patients
at risk for cardiac morbidities.
Diabetes Mellitus
Diabetic autonomic neuropathy is the most common form of autonomic
neuropathy and the most extensively
investigated (see Chapter 27
).
It occurs in 20% to 40% of all insulin-dependent diabetic patients. The symptoms
associated with diabetic autonomic neuropathy confer an increased risk during anesthesia
and surgery by direct and secondary mechanisms. Common manifestations of diabetic
autonomic neuropathy include impotence, postural hypotension, gastroparesis, diarrhea,
and sweating abnormalities.[469]
Early small-fiber
damage is revealed by loss or impairment of vagally controlled normal heart rate
variability, decreased peripheral sympathetic tone with subsequent increase in blood
flow, and diminished sweating. In the diabetic neuropathic foot, the senses of pain
and temperature are lost before loss of touch or vibration. With sympathetic denervation,
sympathetic nerves normally found supplying small arterioles are entirely absent
or are abnormally distant from their effector sites. When impotence or diarrhea
is the sole manifestation, there is little effect on survival; however, with postural
hypotension or gastroparesis, 5-year mortality rates are greater than 50%.
Most clinicians recognize that diabetic patients with autonomic
neuropathy may be at additional risk in general anesthesia.[470]
Gastroparesis is probably caused by vagal degeneration and is of clinical relevance
because awake or rapid-sequence intubation may be required. Systemic injury to the
vasa vasorum in patients with postural hypotension increases the risk of hemodynamic
instability and cardiovascular collapse in the perioperative period. Mechanisms
that maintain normal standing blood pressure are altered, and normal precapillary
vasoconstriction in the foot on standing may be diminished. When healthy people
stand, roughly 700 mL of the blood volume may pool in the legs and splanchnic circulation,
with an associated 20% decrease in cardiac output. Baroreceptors in the carotid
sinus and aortic arch, which normally detect the decrease and mediate sympathetic
impulses to the heart and blood vessels, are compromised by diabetic neuropathy.
Diabetic patients with orthostatic hypotension usually have lower norepinephrine
levels.
Even in seemingly minor surgery, diabetic autonomic neuropathy
can lead to significant complications. In a series of ophthalmologic procedures
requiring general anesthesia, diabetics with autonomic neuropathy had a significantly
greater decline in blood pressure with induction and a greater need for vasopressors
than did diabetic patients without autonomic dysfunction.[470]
Page and Watkins[471]
reported five cases of unexpected
cardiorespiratory arrest in young diabetic patients, all of whom had symptoms of
autonomic neuropathy. In a large, prospective study of diabetic autonomic neuropathy
using the five evocative clinical tests discussed earlier, parasympathetic dysfunction
preceded sympathetic failure in 96% of the patients.[472]
This battery of autonomic tests identifies patients with autonomic neuropathy and
is highly predictive of mortality[469]
and perioperative
risk.[448]
