A 24-year-old man, with underlying type 1 diabetes diagnosed in 2018, developed diabetic ketoacidosis (DKA) with an HbA1C of 17.5% on admission. Following rigorous treatment for DKA, he was discharged with both short-acting (Actrapid® 14 units TDS) and long-acting (Insulatard® 18 units ON) subcutaneous insulin injection.
One month later, he began to experience pain in his feet that affected his daily activities and sleep. The pain was described as persistent pricking in nature with a pain score of 9 out of 10. It originated from the toes and radiated to the medial side of thigh regions. He also developed a few episodes of postural giddiness which led to unsteady gait. Besides that, he also had a loss of appetite and significant weight loss about 15kg over two months, that led to a drop in his BMI to 17.6 kg/m2. However, unlike in diabetic neuropathy cachexic, his mood was not affected.
The physical examination revealed a significant drop in blood pressure from sitting to standing. His blood pressure was 141/110 mmHg lying and 113/67 mmHg standing. Heart rate was 140 beats per minute when lying, but it dropped to 92 beats per minute when standing. His neurological examination of bilateral lower limb showed that hyporeflexia for ankle reflex and hyperaesthesia in dermatome L2 and below with absence of proprioception of big toes for bilateral lower limbs. Other neurological and organ system examination were normal.
Short synacthen test showed an adequate response, excluding the diagnosis of adrenal insufficiency. The thyroid function test, folate and vitamin B12 were within the normal range. Chest x-ray finding was unremarkable. Nerve conduction test indicated that length-dependent sensorimotor axonal polyneuropathy, which is most likely due to the underlying diabetes mellitus. With that, the patient was initially diagnosed with diabetic neuropathy and started on tablet gabapentin and mecobalamin. Fludrocortisone 0.1 mg OD was also prescribed for postural hypotension.
His neuropathic pain initially improved with gabapentin; however, the pain subsequently became worse despite the high dosage of gabapentin given. The pain was so severe that he had difficulty to bear weight or walk. The postural giddiness also persisted despite taking Fludrocortisone 0.1 mg OD. In the meantime, we noticed that his HbA1C reduced from 17.5–7.4% over the past two months. Coupling the rapid reduction in HbA1c with his clinical presentations of pain and autonomic dysfunction that were not improving with the treatment plan for diabetic neuropathy, the diagnosis of TIDN was made.
Considering TIDN as the diagnosis, the patient’s insulin dosage was reduced with a relaxing glycaemic target. As for postural hypotension, fludrocortisone was increased to 0.2 mg. Two weeks after the adjustment of medications, his condition improved tremendously. He had fewer episodes of postural giddiness. The pain was very much reduced and he could bear weight and walk. His latest sitting blood pressure was 130/92 mmHg with a sitting heart rate of 110 beats per minute, and the standing blood pressure was 120/87 mmHg with a standing heart rate of 130 beats per minute. His medication was then maintained with subcutaneous Actrapid® 6 units TDS, Insulatard® 6 unit ON, Tablet mecobalamin 500mcg TDS, Capsule pregabalin 75 mg BD and Fludrocortisone 0.2mg OD.