Multidisciplinary Challenges in the Diagnosis and Management of Treatment Induced Diabetic Neuropathy

Presentation Number: SAT 618
Date of Presentation: April 1st, 2017

Paul A Riordan* and Afreen Shariff
Duke University


A 39-year-old cachectic appearing female with a history of major depressive disorder, generalized anxiety disorder and opioid dependence presented to the medical intensive care unit on ventilatory support secondary to DKA. Patient had no prior history of diabetes.

She was identified as a new diagnosis of ketosis prone T2DM supported by negative GAD, ZnT-8, insulin antibodies, HbA1c of 17.2%, and an unintentional weight loss of 20-30 pounds. At admission she was appropriately managed with an intravenous insulin infusion. Endocrinology assisted with transition from 2.4units/kg/day to a subcutaneous insulin regimen. Shortly afterwards she reported acute achy back and thigh pain and opioid withdrawal was suspected given mild pupil dilation, tachycardia, and diarrhea. Additionally, extensive workup for alternate causes of acute pain showed elevated erythrocyte sedimentation (110 mm/hr), mildly elevated C reactive protein (0.79 mg/dL) and an MRI of her thigh negative for myonecrosis and osteomyelitis. Despite symptomatic treatment she reported no improvement and started to report severely worsening burning and tingling in her hands and feet. Neurology was consulted to perform an EMG which showed subacute to chronic sensorimotor polyneuropathy with both demyelinating and axonal features- consistent with “insulin neuritis” or “treatment induced diabetic polyneuropathy”.

Treatment induced neuropathy is a rare reversible complication linked to rapid glycemic control It is characterized by acute and severe neuropathic pain secondary to peripheral nerve destruction. The true incidence of this disease is unknown since it has mainly been described by case reports. Proposed mechanisms include endoneural ischemia, apoptosis due to sudden glucose deprivation and hypoglycemia induced neurovascular damage. Treatment response is often poor requiring up to 18 months of euglycemia. About 69% patients also have autonomic dysfunction which was noted in our patient (1).

In our patient assessing response to treatment was particularly challenging due to premorbid anxiety, maladaptive coping skills and history of substance abuse, requiring a multidisciplinary approach with medicine, psychiatry, neurology, pain management and endocrinology. Her pain was managed with both medications (methadone, amitriptyline, and pregablin) and CBT skills (guided imagery and relaxation techniques). At discharge, she noted about a 50% overall improvement in function, which she felt was sufficient for her to cope in the outpatient setting.


Nothing to Disclose: PAR, AS