Case: A 27-year-old female with a seven-year history of type 1 diabetes mellitus (T1DM) was hospitalised and successfully managed for diabetic ketoacidosis (DKA) secondary to persistent nausea, vomiting and poor sick day management. On specific questioning, her vomiting was induced by oxycodone and pregabalin which were being trialled as treatment for a three-month history of worsening, lower back pain and severe distal lower limb, nocturnal neuropathic pain, associated with paraesthesia. Trials of oxycodone, meloxicam and pregabalin were ineffective.
Since her diagnosis, her glycaemic control was poor resulting in multiple episodes of DKA. However, recent lifestyle modifications and better family support resulted in rapid improvement in glycaemic control, evidenced by a reduction in HbA1c from 13.3% to 6.4% within four months.
Examination was consistent with a lower limb sensory neuropathy with reduced sensation to monofilament testing up to the ankles bilaterally. There was no lower limb weakness. There was no focal spinal tenderness and her lumbar flexion was normal.
Investigations for autoimmune, thyroid and nutritional causes of neuropathy were unremarkable. A MRI of the spine did not reveal a cause for the symptoms.
Her symptoms were strongly suggestive of treatment-induced neuropathy of diabetes (TIND). Given pain refractory to pre-existing therapy, duloxetine was commenced and an assessment for consideration of local nerve decompression was arranged.
Discussion: TIND is an under-recognised iatrogenic complication of diabetes management with unclear incidence, however may be up to 90% amongst those with a > 5% change in HbA1c over 3 months.1,2,3 The pain is often severe and difficult to manage with analgesics but usually improves gradually in the long-term.1 It is also associated with faster progression of retinopathy and microalbuminuria.3 Awareness of this iatrogenic complication of rapid improvement in glycaemic control is important to reduce the risk of morbidity amongst those with long term poor glycaemic control.