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Diseases » Diabetic Peripheral Neuropathy » Diagnosis

Diagnosis of Diabetic Peripheral Neuropathy

Diabetic Peripheral Neuropathy Diagnosis: Book Excerpts

Diagnostic Tests for Diabetic Peripheral Neuropathy: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Diabetic Peripheral Neuropathy.

Peripheral Edema: Differential Diagnosis
(In a Page: Signs and Symptoms)

Venous insufficiency
–Caused by incompetent venous valves
–Skin characteristically has superficial varicose veins associated with a reddish-brown pretibial discoloration (“venous stasis skin changes”)
–Swelling is typically worse after legs are held in a dependent position and is least noticeable after a night's sleep
Congestive heart failure
–Associated with pitting peripheral edema
–Other signs of heart failure include a third heart sound, cardiomegaly, and hepatomegaly
Cellulitis
–Usually unilateral
–Edematous legs are typically red, warm, and inflamed
–The patient may exhibit signs of systemic toxicity with fever and leukocytosis
- Deep venous thrombosis
  –Typically unilateral swelling
  –May exhibit a palpable cord representing a thrombosed vein
  –Homan's sign (pain in the calf with passive dorsiflexion of the foot)
  –Virchow's triad (hypercoagulable states, venous stasis, and vessel injury) are risk factors
- Cirrhosis
  –Advanced liver disease results in hypoalbuminemia and poor venous return through cirrhotic liver tissue
  –Other stigmata of chronic liver disease include caput medusae, ascites, and spider angiomata
- Nephrotic syndrome
  –Glomerular damage results in protein loss and decreased oncotic pressure
- Less common etiologies (“zebras”) include filariasis (lymphatic infection by Wuchereria bancrofti worm), myxedema (seen in patients with severe hypothyroidism), Milroy's disease (congenital lymphedema), chronic lymphedema (e.g., lymphatic damage due to surgery, such as vein harvesting for CABG), and gout
Workup and Diagnosis
- History and physical examination should focus on time course, associated symptoms (e.g., dyspnea, urinary changes, fever), unilateral versus bilateral involvement, pitting versus nonpitting edema, and risk factors for DVT
- Initial labs may include CBC, electrolytes, BUN/creatinine, urinalysis, coagulation studies, LFTs, serum albumin, and thyroid function tests
- Chest X-ray may reveal signs of pulmonary edema or cardiomegaly
- Duplex ultrasound of the legs is useful in diagnosing deep venous thrombosis
- Echocardiography may reveal a depressed ejection fraction in cases of congestive heart failure
- Blood cultures are often indicated in immunocompromised or systemically ill patients
- Renal or liver biopsy may be necessary to diagnose cirrhosis or renal pathology leading to nephrotic syndrome

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Source: In a Page: Signs and Symptoms, 2004

Peripheral Neuropathy: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Diabetes

❑ Alcohol

❑ Vitamin B₁₂ deficiency

❑ Drugs

❑ Carcinomatous

❑ Lead

❑ Guillain-Barré

❑ Tabes dorsalis

❑ Syringomyelia

❑ Polyarteritis nodosa

❑ Amyloidosis

❑ Polymyositis

❑ Pellagra

❑ Arsenic

❑ Porphyria

❑ Wallenberg syndrome

❑ Thalamic lesion

❑ Brown-Sequard syndrome

Diagnostic Approach

Sensory neuropathy symptoms include positive phenomena such as tingling; pins/needles; and burning, cold, or lancinating pain. Physical findings include weakness, fasciculations, atrophy, ataxia, wide-based gait, abnormal sweating, decreased or absent deep tendon reflexes, orthostatic hypotension, hypesthesia surrounded by a zone of hyperesthesia, and vibration or position sense affected before pinprick or temperature sense.

Autonomic neuropathy symptoms include impotence, retrograde ejaculation, diaphoresis, incontinence, urinary retention, constipation, diarrhea, orthostatic dizziness, and flushing. Physical findings include delayed pupillary light response, resting tachycardia, sinus arrhythmia, and orthostatic hypotension.

Sensory loss confined to part of a limb suggests injury to a peripheral nerve, plexus, or spinal root, resulting from trauma, entrapment, or vascular insufficiency. Mononeuropathy multiplex affects multiple nerves over time (e.g., due to diabetes or vasculitis). Polyneuropathy occurs in a stocking-glove distribution starting with the longest nerves, and is due to axonal neuropathy, with a toxic or metabolic origin. Bilaterally symmetrical symptoms are found in polyneuropathy or spinal cord lesions, while unilateral involvement is seen in contralateral disease of the brainstem, thalamus, or cortex.

Injury to large myelinated nerves produces decreased light touch and proprioception with a sensation of “walking on a thick carpet” or imbalance. Injury to medium fibers causes decreased light touch and vibration sense. Injury to small unmyelinated fibers, as occurs in diabetes or amyloidosis, decreases pain and temperature sensation and produces dysesthesias. Disproportionate loss of vibration sense and proprioception compared with pain and temperature sensation occurs with diseases of the dorsal column of the spinal cord (e.g., neurosyphilis, vitamin B ₁₂ deficiency, or multiple sclerosis) and demyelinating polyneuropathy.

Transverse cord lesions produce loss of all modalities below the level of the lesion and a band of hyperalgesia at the level of the lesion. Lateral cord compression is heralded by early sensory changes. Dorsal cord compression affects proprioception and tactile discrimination without pain or temperature loss. Pernicious anemia and tabes dorsalis preferentially affect the dorsal columns.

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Source: Field Guide to Bedside Diagnosis, 2007