Overview-Anesthetic Implications

• Anesthetic implications in the Diabetic patient with autonomic dysfunction

  • Increased risk for general anesthesia -- associated with more cardiovascular morbidity

  • Gastroparesis (secondary to vagal degeneration) may require awake/rapid-sequence intubation

Diabetes mellitus: most common cause of autonomic neuropathy

•  Anatomical Characteristics:

  •  Early small-fiber damage

    1. Reduced sweating

    2. Reduced peripheral sympathetic tone (increase in local blood flow)

    3. Heart rate variability secondary to abnormal vagal tone

  •  Diabetic neuropathic foot is initially associated with reduced temperature/pain sensation followed by reduced sensitivity to touch/vibration

    • Sympathetic denervation results in increased blood flow (arteriovenous shunting) due to dilated, stiff peripheral arteries (calcification)

    • Despite increased total  blood flow, capillary flow may decrease with distal ischemia.

    • Reduced precapillary vasoconstriction in the foot alters systemic blood distribution, e.g. for healthy individuals about 700 ml of blood volume pools in the  legs/splanchnic vascular beds upon standing (with a decrease of about 20% in cardiac output)  

      • Baroreceptor-mediated compensation is effected by increased sympathetic tone to the vasculature and heart. In diabetes:

        1. Baroreceptor function in diabetic patients, however, is associated with:

           1. Reduced compensatory (sympathetic nervous system mediated) vasoconstriction in the periphery

           2. Reduced or absent cardioacceleration to compensate for diminish cardiac output

Cardiovascular Effects of Aging:

• Increased cardiovascular lability and responsiveness secondary to reduced α₂ and  β-receptor-mediated systems

• Increased vascular reactivity (hypertension and orthostatic hypotension (frequency for orthostatic hypotension = 20%))

  •  Increased incidence of Orthostatic hypotension in the elderly: reduced baroreceptor sensitivity

  •  Reduced responsiveness to:

    • Valsalva maneuver

    • Blood-pressure changes

• Reduced vagal tone

• Reduced norepinephrine reuptake-- primary autonomic defect in aging

  •   Causes:

    • β₁-receptor down-regulation

    • β₂-receptor uncoupling, secondary to diminished G_s activity

• Increased  norepinephrine release, secondary to blunted a₂ adrenergic receptor-mediated presynaptic inhibition

• Reduced postsynaptic α₂ receptor activity causes reduced vasoconstrictor tone.

Anesthesia-management in patients with Spinal Cord Transaction

• In the presence of autonomic dysreflexia:

  •  Despite  absence of sensory/motor functions, visceral reflexes may be induced-- Anesthetic approaches to reduce this reflex (even in the absence of pain):

    •  Spinal anesthesia

    •  General anesthesia

    •  Vasodilation using nitroprusside sodium (Nipride) or nitroglycerin or clonidine (Catapres)

• Reduced control of body temperature (thermogenesis) requires careful monitoring of patients during anesthesia

  • Hypothermia, secondary to cutaneous vasodilation in the absence of the ability to shiver

  • Hyperthermia-absence of normal sweating mechanism

• Physiological changes associated with autonomic dysreflexia-- stimulation below the level of the spinal cord lesion

  • Bladder/bowel distention causes"mass reflex"

    •  Significant increase in BP

    •  Reduced blood flow to the periphery

    •  Sweating/flushing above the lesion level

    •  Reduced heart rate

Other cardiovascular abnormalities in patients with spinal cord transaction

• Profound bradycardia secondary to unopposed vagal tone.

  • Vagal tone may be further enhanced during hypoxemia associated with tracheal suctioning.

• Dysfunctional sympathetic nervous system state leads to increased reliance on the renin-angiotensin-aldosterone axis which results in:

  • Exaggerated sensitivity to angiotensin converting enzyme inhibitors

Plasma catecholamine levels as an indication of autonomic state:

• Most anesthetic protocols, e.g. inhalational, regional, and opiate reduce stress response

• Certain anesthetic protocols (using high-dose opiates) which diminish perioperative stress levels may improve outcome.

• Reduction of perioperative catecholamines (often associated with general anesthesia) reduces the incidence of:

  • Ischemic complications

  • Thrombotic events

• Significant increases in catecholamine levels (> 1000 pg/ml, relative to a normal range of 100-400 pg/ml) suggest significant sympathetic nervous system activation and may influence hemodynamic status

 Autonomic Dysfunction:Clinical Manifestations:

• ANS disorders: are due to both

  • Central nervous system (CNS) causes and

  • Peripheral nervous system (PNS) causes.

• Signs/Symptoms: due to interruption of reflex arc

  • Site of interruption:

    • Afferent limb

    • CNS processing center

    • Efferent limb

  • Examples:

    •  Posterior fossa tumors: medullary lesions may cause --

      • Pmpaired blood-pressure responses to postural change (orthostatic hypotension)

    • Lesions of vasomotor nerve fibers to blood vessels (e.g. diabetes or spinal cord disease)

    • Lesions to afferent connections (e.g. Guillain-Barre syndrome)

    •  Segmental disorders (focal deficits):

      • In spinal cord disease

      • Reflex sympathetic dystrophy

      • Horner's syndrome

• Horner's Syndrome

  • Oculosympathetic Palsy or Horner Syndrome

    Neuro-opthalmology:  Horner Syndrome (Oculosympathetic Palsy, "Horner Syndrome") https://www.youtube.com/watch?v=-neXQ6iFSQg Custom Clinical Education:  https://www.youtube.com/channel/UCTlpGP51J9ych9-mrs6iyog

  •  

    "Left-sided Horner's Syndrome"

    Note miosis. Attribution:  Waster / CC BY (https://creativecommons.org/licenses/by/2.5) Nautiyal A Singh S DiSalle M O'Sullivan J (2005) Painful Horner Syndrome as a Harbinger of Silent Carotid Dissection.  PLos Med 2(1): e19 doi:  10.1271/hournal.pmed 0020019 https://commons.wikimedia.org/wiki/File:Miosis.jpg https://en.wikipedia.org/wiki/Horner's_syndrome

• Horner's syndrome is due to an interruption of the oculosympathetic nerve pathway between the hypothalamus and the eye.

  • Primary clinical findings are:

    • Ptosis,

    • Pupillary miosis and

    • Facial anhidrosis.

• Pathophysiology:

  • Sympathetic innervation to the eye is composed of a three neuron arc.

    •  First order neurons cell bodies are found in the hypothalamus. Their axons descends and travels between the levels of the eighth cervical and forth thoracic vertebrae (C8-T4) of the spinal cord. 

    • These axonal terminals synapses with second order neurons whose preganglionic cell bodies give rise to axons. 

      • These axons pass over the apex of the lung and enter the sympathetic chain in the neck, synapsing in the superior cervical ganglion. 

    • In the superior cervical gangion, cell bodies of third order neurons produce postganglionic axons that course to the eye via the cavernous sinus. 

      • These sympathetic nerve fibers travel anteriorly through the uveal tract joining long posterior ciliary nerves fibers to innervate the dilator of the iris. 

      • Postganglionic sympathetic fibers also innervate the muscle of Mueller within the eyelid, which is responsible for the initiation of eyelid retraction during eyelid opening. 

      • Postganglionic sympathetic fibers, responsible for facial sweating, follow the external carotid artery to the sweat glands of the face. 

      • Interruption at any location along this pathway (preganglionic or postganglionic) will induce an ipsilateral Horner's syndrome.

• Causes: 

  1. Common causes of acquired preganglionic Horner's syndrome include trauma, aortic dissection, carotid dissection, and tuberculosis.

  2. Common causes of post-ganglionic Horner's syndrome include trauma, cluster migraine headache and neck or thyroid surgery.
     

• The diagnosis and the localization of a Horner's syndrome is accomplished with pharmacological testing. 

  • Ten percent liquid topically applied cocaine,  an indirect acting sympathomimetic agent due to norepinephrine reuptake inhibition results in poor pupillary dilation.

    • A patient with Horner's disease will exhibit subnormal pupillary dilation due to reduced (absence) of  endogenous norepinephrine at the nerve ending.

    • The test is usually evaluated thirty minutes after the drop instillation .

      • The cocaine test is used to confirm or deny the presence of a Horner's syndrome. Subsequent steps are required to localize the lesion.

• To localize the lesion as either preganglionic or postganglionic, Paradrine 1% (hydroxyamphetamine) or Pholedrine 5% (n-methyl derivative of hydroxyamphetamine) can be instilled two days later. 

  • Pholedrine and Paradrine promote endogenous norepinephrine  release from adrenergic presynaptic vesicles. 

  • If the third neuron is damaged, there will be no endogenous norepinephrine and the pupil will not dilate, thus indicating a postganglionic lesion. 

  • Dilation indicates first or second order neuron lesion;however, topical testing approaches are not available to distinguish a first order preganglionic lesion from a second order preganglionic lesion. 

• *"Horner's Syndrome: Handbook of Ocular Disease Management

Autonomic Dysfunction: symptoms are organ dependent

• Impotence:  first sign of autonomic failure in men, often appearing well in advance (perhaps 10 years) before other mainifestations.

  1.  Sequence:

     1. Lost of spontaneous early morning erection

     2.  Loss of nocturnal penile tumescence

     3.  Total impotence

• Bladder dysfunction:

  •  Occurs early both in men and women (especially with CNS involvement)

  •  Brain/spinal cord disease: above the level of the lumbar spine(upper motor neuron) disease:

    1.  Urinary frequency/small bladder volumes

    2.  Incontinence

  •  Autonomic fiber disease to the bladder (lower motor neuron disease) or sensory denervation:

    • Large bladder volumes

    • Urinary frequency

    • Overflow incontinence

• Gastrointestinal Dysfunction:

  •  Severe constipation typically

    • Exception:  diabetes diarrhea causing

      1. Rapid transit of contents

      2. Uncoordinated small bowel activity

    • Osmotic diarrhea

  • Decreased salvation (glandular effects)

• Eye irritation:  reduced lacrimation

•  Orthostatic Hypotension: most disabling feature of autonomic dysfunction

  • Definition: postural decrease of at least 20 mm Hg in systolic or 10 mm Hg in diastolic blood pressure sustained for least 3 minutes (to differentiate between autonomic dysfunction and sluggish baroreceptor reflex response (common in the elderly))

  •  Symptoms of postural hypotension:

    • Dimming or loss of vision

    • Light headedness

    • Diaphoresis

    • Impaired hearing

    • Pallor/weakness

    • Syncope

Primary Reference: Engstrom, J, and Martin, J.B. Disorders of the Autonomic Nervous System, In Harrison's Principles of Internal Medicine 14th edition, (Isselbacher, K.J., Braunwald, E., Wilson, J.D., Martin, J.B., Fauci, A.S. and Kasper, D.L., eds) McGraw-Hill, Inc (Health Professions Division), 1998, pp 2372-2377.

Primary Reference: Moss, J. and Renz, C. The Autonomic Nervous System in Anesthesia, Fifth Edition (Ronald D. Miller, editor; consulting editors: Roy F. Cucchiara, Edward D. Miller, Jr., J. Gerald Reves, Michael F. Roizen and John J. Savarese) volume I, Churchill Livingstone (Hartcourt Brace and Company) Philadelphia, 2000, pp. 566-569.