SUN-629 - The Perils of Speed: Acute Worsening Neuropathy Triggered by Rapid Hyperglycemia Correction

BACKGROUND
Treatment-Induced Neuropathy of Diabetes (TIND) is an uncommon complication that occurs after rapid improvement in glycemic control, with reported incidence around 10–20%.Although not often discussed in routine clinical practice, it is important to recognize because symptoms typically begin within days to weeks of abrupt glucose lowering, and early recognition may prevent further progression. Understanding the timing of symptom onset in relation to glycemic change is the key factor in diagnosis and management.
CASE
A 37-year-old woman with long-standing type 1 diabetes and baseline neuropathy presented with rapidly progressive paresthesia of bilateral hands, spreading to her arms, face, and legs over 48 hours complicated by a new right upper-extremity weakness. She had been non-compliant with insulin before receiving a large corrective insulin dose, raising concern for sudden glycemic change. Her initial evaluation showed hyperglycemia. CT head, MRI brain, and cervical spine imaging revealed no acute abnormalities. Neurologic exam showed absent lower-extremity reflexes and asymmetric right arm weakness.
With an HbA1c of 15.5% and the close temporal relationship between glucose correction and symptom onset, TIND was most consistent with diagnosis. TIND has been well described in patients with chronic hyperglycemia who experience rapid reductions in glucose or HbA1c.We then pursued a gradual glycemic control, consistent with published guidance to avoid further nerve injury. Her respiratory status remained stable, and no acute interventions were required.
DISCUSSION
This case highlights the importance of linking acute neuropathic symptoms to timing after swift glycemic correction. TIND is believed to result from microvascular changes affecting small nerve fibers during abrupt metabolic shifts.
A similar principle is seen in osmotic demyelination syndrome (ODS), a condition caused by rapid correction of osmotically active substances, most commonly sodium in hyponatremia but also described with other osmotic gradients, including glucose. Although the mechanisms differ, both TIND and ODS reinforce the concept that the nervous system is vulnerable to injury when metabolic or osmotic parameters change expeditiously. This amplifies the recommendation that glycemic improvements in chronically uncontrolled diabetes be approached gradually to avoid complications.
CONCLUSION
TIND should be considered in patients with significantly uncontrolled diabetes who develop acute neuropathic symptoms shortly after a sudden decrease in glucose levels. Recognizing the timing of symptom onset in relation to glycemic changes is crucial for early identification and effective management.

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