Peripheral Neuropathy (PN)

Document the deficit first - Map the existing sensory and motor loss and write it down: stocking-glove distribution, ankle reflexes, 10 g Semmes-Weinstein monofilament, and the 128 Hz tuning fork at the hallux IP joint. Do it before any block and before positioning, because after the case a new deficit and an old one look identical.

Positioning - The limb is insensate and the skin is vulnerable to pressure injury, so the patient cannot tell you a position hurts and will not shift off a pressure point. Pad every bony prominence, respect the reduced joint mobility that comes with long-standing diabetes, and recheck after every table position change.

Regional anesthesia - Pre-existing PN is not an automatic reason to skip a block, but it is the reason the documented baseline has to exist first. Charted deficit, charted plan, charted discussion.

Autonomic involvement — hemodynamics - Resting tachycardia and reduced heart rate variability are among the earliest signs of autonomic neuropathy, followed by orthostatic hypotension and impaired baroreceptor function. These patients are prone to labile hemodynamics under general anesthesia. Get a resting HR and orthostatic vitals preop — a fixed, unvarying rate is the tell.

Autonomic involvement — aspiration - Gastroparesis is part of the autonomic picture, and it means the stomach may not be empty when you induce. Documented delayed gastric emptying, autonomic signs on exam, or the classic GI symptoms all argue for treating them as a full stomach and doing an RSI.

Thermoregulation - Autonomic damage causes anhidrosis and impaired vasoconstriction, so they neither shed heat well when awake nor hold it under anesthesia. Forced-air warming from the start and monitor core temperature.

Silent ischemia - Myocardial ischemia in autonomic neuropathy can present without the usual anginal warning, so a baseline ECG and a look at exercise tolerance carry more weight here than the patient's symptom history does.

Urinary retention - They are prone to retention under general anesthesia. Bladder scan before discharge from PACU on any case where a catheter was not placed.

Neuropathic pain - Small-fiber neuropathic pain does not respond to simple analgesics. Continue the home membrane stabilizer, gabapentinoid, or tricyclic through the perioperative period rather than starting from zero with opioids, and build a multimodal plan.

Glycemic control - Perioperative glucose control matters, but it will not undo established autonomic and sensory neuropathy. Manage the glucose and plan around the neuropathy as a fixed condition on the day.

Wound and skin - Wound healing is delayed and infection risk elevated in the neuropathic limb. Tape, adhesives, tourniquets, and prolonged pressure all leave marks that turn into ulcers.

Peripheral neuropathy (PN) is damage to peripheral nerve cells and fibers — motor, sensory, and autonomic — from metabolic, toxic, nutritional, inflammatory, infectious, or hereditary causes. Diabetes is the most common; around half of patients with chronic diabetes eventually develop it, and about 2.4% of the general population is affected, rising to 8% in the elderly.

Whatever the cause, nerve injury follows a few common patterns: segmental demyelination, Wallerian degeneration, and axonal degeneration. Demyelinating injury remyelinates and recovers reasonably well; axonal injury has to regrow and reinnervate, so it recovers poorly or not at all. The clinical picture runs from stocking-glove numbness and burning paresthesias to weakness, muscle wasting, and absent deep tendon reflexes. Perioperatively the issue is threefold: an already-injured nerve tolerates stretch, pressure, and ischemia badly; autonomic fibers are frequently involved; and any new postoperative deficit lands on the anesthetic.