ABSTRACT
Granulomatosis with polyangiitis (GPA) typically presents with upper or lower respiratory tract symptoms and/or with renal involvement. Although it can affect the peripheral nervous system frequently, with mononeuritis multiplex being the most common pattern, the occurrence of peripheral sensory-motor polyneuropathy as a presenting manifestation is distinctly rare. Prevalence of digital gangrene is also extremely rare in GPA. We describe a 46-year-old woman presenting with severe peripheral sensorimotor polyneuropathy affecting bilateral lower limbs preceded by a purpuric skin rash and multiple painful ulcers confined to the lower limbs. She had evidence of digital ischemia affecting multiple toes and dry gangrene of the left 4th toe. Diagnosis of GPA was made based on skin biopsy, positive ANCA serology, and clinical criteria. She made a good recovery following aggressive immunosuppressive treatment with methylprednisolone and cyclophosphamide and was maintained on prednisolone and azathioprine. This case highlights the importance of suspecting GPA in a patient presenting with sensorimotor polyneuropathy and/or digital ischemia even in the absence of more classic presenting features and underlies the necessity of accurate differential diagnosis in evaluating a case of peripheral neuropathy.
ABSTRACT
BACKGROUND: Plate developer is a chemical used in the printing industry and is a corrosive alkaline agent containing sodium metasilicate as the main substance. Plate developer poisoning is rare. Literature search revealed only a single case report of fatal sodium metasilicate poisoning (Z Rechtsmed 94(3):245-250, 1985). There are no reports of acute kidney injury related to ingestion of sodium metasilicate containing substances. CASE REPORT: A 52-year-old Sri Lankan male with a history of hypertension and affective disorder presented following ingestion of about 150 ml of plate developer solution. He developed severe upper airway obstruction due to laryngeal edema and underwent tracheostomy. While in the ward he developed features of acute kidney injury with high serum creatinine levels and persistent hyperkalemia which necessitated temporary haemodialysis. Because of the corrosive effect, he developed severe inflammation of the upper gastro intestinal tract with narrowing of esophagus and pyloric region, requiring feeding jejunostomy. He died while waiting for the surgery for pyloric stenosis. CONCLUSIONS: Acute kidney injury is a potential treatable complication of plate developer poisoning other than its complications related to corrosive effects. Regular monitoring of renal functions in such a patient would be useful for early recognition of acute kidney injury.
