Acute kidney injury, hyperbilirubinemia, and ischemic skin necrosis due to massive sulindac overdose.

Sulindac is a long-acting nonsteroidal anti-inflammatory drug (NSAID) widely used for the management of osteoarthritis, rheumatoid arthritis, ankylosing sponydlitis, and acute gouty arthritis. Reports of sulindac toxicity in the literature are rare. We report the case of a 22-year old male with a history of bipolar disorder who was brought to the emergency department after ingesting approximately 15 g of sulindac in a suicide attempt. He was found to have acute kidney injury and hyperbilirubinemia. Despite aggressive fluid resuscitation, his renal function progressively worsened requiring the initiation of hemodialysis. Ten days following ingestion of sulindac, he began to develop ischemic skin changes with a gangrenous appearance in his hands and feet. He continued to receive supportive treatment, and his acute kidney injury, hyperbillirubinemia, and ischemic skin necrosis eventually resolved. Clinicians should be aware of this long-acting NSAID and its ability to cause prolonged multisystem organ dysfunction.

An overdose fatality in a child involving disopyramide and sulindac.

The results of an accidental overdose fatality in a child involving disopyramide and sulindac are reported in this paper. Quantitation of disopyramide was performed by gas chromatography using codeine as the internal standard. Sulindac was assayed by high- performance liquid chromatography using ketoprofen as the internal standard. The postmortem blood concentrations of disopyramide and sulindac were 41.3 and 12.2 mg/L, respectively. The concentrations of disopyramide and sulindac were also quantitated in the liver, in bile, and in urine.

Renal impairment after acute diclofenac, naproxen, and sulindac overdoses.

Acute renal dysfunction has been described as a feature of acute overdoses of the nonsteroidal anti-inflammatory drugs benoxaprofen, fenoprofen, ibuprofen, mefenamic acid, piroxicam, suprofen, and zomepirac. The cases reported here include renal impairment after acute overdoses of another three nonsteroidal anti-inflammatory drugs: diclofenac (one case), naproxen (two cases), and sulindac (five cases). The eight patients presented with lumbar pain and oliguria and had protein and erythrocytes in the urine. Serum creatinine was increased to a maximum of 190-932 mumol/L. Renal impairment was generally transient but in one case was treated by hemodialysis and one by continuous arterio-venous hemofiltration dialysis. In all cases of significant acute overdose of nonsteroidal anti-inflammatory drugs, the risk of acute renal dysfunction must be considered.

Intoxication with sulindac, tiaramide hydrochloride and diclofenac sodium.

Overdosage intoxication of sulindac, tiaramide and diclofenac caused excitability of central nervous system, followed by unconsciousness. The case was treated with ordinary therapies and direct hemoperfusion (DHP). Serum concentrations of these drugs and their metabolites were correlated well with the clinical symptoms. DHP may be effective to eliminate these drugs and their metabolites.

A fatal case of sulindac-induced Lyell syndrome (toxic epidermal necrolysis).

A 37-year-old woman died after 18 days from her starting to take sulindac for low back pain. Based on her clinical course and the autopsy findings, the cause of her death was Lyell syndrome (toxic epidermal necrolysis) induced by sulindac. This case is described together with the legal aspects of medical malpractice to which it gave rise.