MEDREH · EP 14 · ENDOCRINE
Before You Listen
Episode Setup
- Topic in one line: Part 1 builds the diabetes-rehabilitation framework (pre-exercise glucose thresholds, the length-dependent axonal sensorimotor pattern of diabetic distal symmetric polyneuropathy, monofilament screening, the Wagner classification of diabetic foot ulcers, total contact casting as the off-loading gold standard, and Charcot neuroarthropathy with its erythema-warmth-swelling-without-pain presentation), then contrasts hypothyroid myopathy (elevated creatine kinase (CK), “hung-up” delayed-relaxation deep tendon reflexes, carpal tunnel from myxedematous deposition) against hyperthyroid myopathy (normal CK, brisk reflexes, postural tremor), maps post-traumatic brain injury (TBI) anterior pituitary dysfunction (25 to 50 percent of moderate-severe TBI; growth hormone deficiency most common), and explains why secondary adrenal insufficiency presents with hyponatremia but no hyperkalemia and why steroid myopathy is the proximal weakness with normal CK that distinguishes it from inflammatory myopathy.
- Prerequisites: the intensive care unit acquired weakness (ICU-AW) and critical illness polyneuropathy versus critical illness myopathy framework from MEDREH-12; the standard pressure-injury and immobilization complication framework from REHAB-07 and REHAB-09.
- Runtime: approximately 35 minutes for Part 1.
- Scope boundary: Part 1 covers diabetes, the diabetic foot, thyroid, pituitary, and adrenal/steroid topics. Part 2 covers immobilization hypercalcemia and the saline-loop-bisphosphonate sequence with the thiazide contraindication; vitamin D screening with the enzyme-inducing anticonvulsant trap; spinal cord injury (SCI) body composition and the adapted body mass index (BMI) cutoffs; Paget disease, HIV polyneuropathy and myopathy; and Ehlers-Danlos syndrome (EDS) rehabilitation.
Vignette. A 58-year-old man with type 2 diabetes mellitus for 18 years (most recent hemoglobin A1c 9.2 percent), hypertension, and a remote stroke is admitted to inpatient rehabilitation following a left fifth-metatarsal partial amputation for an infected diabetic foot ulcer. On day 3 of rehabilitation, the therapy team reports that his right foot has become “red and swollen and warm” overnight; he is afebrile with vital signs at baseline. Skin temperature of the right foot is 4.8°C above the contralateral side. The foot is dramatically erythematous and edematous but the patient rates pain only 2 of 10. Plain radiographs show midfoot fragmentation at the tarsometatarsal joints without periosteal reaction. White blood cell count is 7.8 × 10⁹/L. Pre-therapy fingerstick glucose is 287 mg/dL with negative urine ketones; he had been allowed to participate in therapy that morning.
What is the most likely diagnosis of his right foot finding and what is the immediate weight-bearing status; was the team correct to allow him to participate in therapy at a glucose of 287; how should management proceed if osteomyelitis cannot be excluded clinically; and what is the long-term off-loading strategy after the acute phase resolves?
(Answer at the end of this chapter)
Section 1: Diabetes — Exercise Thresholds, Distal Symmetric Polyneuropathy, and the Diabetic Foot
Bottom line: diabetes affects 25 to 30 percent of inpatient rehabilitation patients and impairs every domain that matters in rehab (wound healing, infection, neuropathy, perfusion, retinopathy). Exercise increases insulin sensitivity through insulin-independent glucose transporter type 4 (GLUT4) translocation in skeletal muscle, with glucose-lowering effects persisting up to 24 hours, creating a prolonged hypoglycemia window; bolus insulin should be reduced 20 to 50 percent before planned exercise. The three pre-exercise glucose thresholds (avoid exercise above 250 mg/dL with ketones, above 300 mg/dL without ketones, or below 100 mg/dL without carbohydrate supplementation) and the rule of fifteen for hypoglycemia treatment are the most heavily tested numbers. Diabetic distal symmetric polyneuropathy is a length-dependent axonal sensorimotor polyneuropathy in a stocking-glove distribution; the sural nerve is affected earliest and most severely on nerve conduction studies (NCS) and the intrinsic foot muscles earliest on needle electromyography (EMG). The 5.07 Semmes-Weinstein monofilament (10 g force) is the standard screen for loss of protective sensation.
Diabetes mellitus affects approximately 25 to 30 percent of inpatient rehabilitation patients. It worsens virtually every rehabilitation domain: wound healing (hyperglycemia inhibits neutrophil function, collagen synthesis, and angiogenesis), infection risk (surgical site, urinary tract, pneumonia), peripheral neuropathy (mobility and balance), peripheral arterial disease (PAD) (exercise tolerance, perfusion), and retinopathy (therapy participation, fall risk). A diabetes diagnosis on the admission problem list reshapes every other rehabilitation prescription.
Exercise increases insulin sensitivity through insulin-independent GLUT4 translocation in skeletal muscle, lowering blood glucose with effects persisting up to 24 hours. That long tail creates a prolonged hypoglycemia window after a single therapy session. Bolus insulin should be reduced by 20 to 50 percent before planned exercise. For insulin pump users, temporary basal rate reduction starting 30 to 60 minutes before exercise is effective. Hypoglycemia risk is highest in patients on insulin or insulin secretagogues (sulfonylureas such as glyburide and glipizide). Patients should carry a fast-acting glucose source during exercise.
Pre-exercise glucose thresholds are board content the numbers must be exact.
- Avoid exercise if glucose >250 mg/dL with ketones present (risk of diabetic ketoacidosis).
- Avoid exercise if glucose >300 mg/dL even without ketones (risk of worsening hyperglycemia through counterregulatory hormone release).
- Avoid exercise if glucose <100 mg/dL without pre-exercise carbohydrate supplementation (hypoglycemia risk).
The board distractor flips ketones on or off. A glucose of 270 mg/dL without ketones is below the 300 threshold and the patient may participate. The same 270 mg/dL with positive ketones crosses the 250-with-ketones threshold and therapy is held until ketones clear and glucose drops below 250.
Hypoglycemia treatment uses the rule of fifteen: administer 15 g of fast-acting carbohydrate (glucose tablets, four ounces of fruit juice, regular soda), recheck blood glucose in 15 minutes, and repeat the same 15 g if glucose remains below 70 mg/dL. Patients on beta blockers may lose adrenergic warning signs (tremor, tachycardia) and present with neuroglycopenic symptoms only (confusion, behavior change), so a fingerstick must be checked at the first sign of altered behavior.
The American Diabetes Association (ADA) exercise prescription is a minimum of 150 minutes per week of moderate-intensity aerobic exercise at 50 to 70 percent of maximum heart rate, spread over at least three non-consecutive days with no more than two consecutive days without exercise, plus resistance training at least two days per week targeting all major muscle groups. The split structure matters because the GLUT4 effect decays over roughly 48 hours; longer gaps surrender the insulin-sensitivity gain.
Distal symmetric polyneuropathy (DSP) is the most common diabetic neuropathy, affecting up to 50 percent of patients with long-standing diabetes. Clinical presentation follows a stocking-glove distribution: numbness, tingling, burning pain, and eventual loss of protective sensation beginning in the toes and progressing proximally. Upper-extremity involvement appears once lower-extremity sensory loss has reached the mid-calf, reflecting the length-dependent rule that the longest axons fail first.
The electrodiagnostic findings are a length-dependent axonal sensorimotor polyneuropathy.
- Sensory nerve action potential (SNAP) amplitudes reduced distally; the sural nerve is affected earliest and most severely.
- Compound muscle action potential (CMAP) amplitudes reduced distally (peroneal, tibial motor nerves).
- Conduction velocities mildly to moderately reduced but not in the demyelinating range, because slowing reflects loss of the fastest large-diameter axons rather than segmental demyelination.
- Needle EMG shows fibrillation potentials and positive sharp waves in distal muscles (intrinsic foot muscles earliest), with reduced recruitment and neurogenic motor unit action potential (MUAP) changes.
Figure 14.2 — Stocking-glove distribution of diabetic distal symmetric polyneuropathy: shaded sensory loss starting in toes and feet, progressing proximally up the legs to mid-calf, with later upper-extremity involvement starting in the fingers and hands as a glove pattern. Length-dependent labeling shows that the longest sensory axons (sural to lateral foot) fail first. Annotation panel: sural nerve earliest affected on NCS; intrinsic foot muscles earliest affected on needle EMG; monofilament testing site map (first, third, fifth metatarsal heads and plantar surface). Open-source anatomy pending.
Autonomic neuropathy is a distinct but commonly co-occurring entity. It produces orthostatic hypotension, resting tachycardia from loss of vagal tone, gastroparesis (delayed gastric emptying with postprandial nausea and unpredictable glucose excursions), neurogenic bladder, erectile dysfunction, and sudomotor dysfunction with anhidrosis in the feet and compensatory hyperhidrosis in the upper body. The dry insensate foot is the perfect storm: cracked skin offers an entry point, lost sensation hides the developing wound, and impaired sweating prevents the normal humectant film.
Monofilament testing with the 5.07 Semmes-Weinstein monofilament (which exerts 10 g of force) is the standard screen for loss of protective sensation in the diabetic foot. Inability to detect the monofilament at any of the standardized plantar test sites indicates elevated ulceration risk, requires therapeutic footwear, comprehensive foot care education, and regular podiatric surveillance. Feet should be inspected before and after every exercise session because neuropathic patients may not detect blisters, wounds, or foreign bodies in shoes. The classic teaching example is a pebble that an able-bodied person would feel and remove in seconds; the neuropathic patient walks miles on it and produces a deep ulcer down to bone.
High Yield — Diabetes exercise and neuropathy
- Exercise glucose thresholds: avoid if >250 with ketones, >300 without ketones, or <100 without carb supplementation.
- Exercise → insulin-independent GLUT4 translocation; glucose-lowering effect persists up to 24 hours; reduce bolus insulin 20 to 50 percent before planned exercise.
- Rule of fifteen: 15 g fast-acting carbohydrate, recheck at 15 minutes, repeat if <70 mg/dL.
- ADA prescription: ≥150 min/week aerobic at 50 to 70 percent max heart rate; resistance training ≥2 days/week.
- Diabetic DSP: length-dependent axonal sensorimotor; sural nerve earliest on NCS; intrinsic foot muscles earliest on EMG.
- Monofilament: 5.07 Semmes-Weinstein = 10 g force; inability to detect = elevated ulceration risk.
- Autonomic neuropathy: orthostatic hypotension, resting tachycardia, gastroparesis, neurogenic bladder, erectile dysfunction, sudomotor.
Mnemonic — “250 with, 300 without, 100 below”
The three exercise glucose thresholds in one line: above 250 with ketones, above 300 without ketones, or below 100 without a carbohydrate snack all hold therapy. Anything else proceeds.