What is the treatment for an aceclofenac (diclofenac derivative nonsteroidal anti-inflammatory drug (NSAID)) overdose in a patient, particularly one with a history of kidney or liver disease?

Aceclofenac Overdose Treatment

Treat aceclofenac overdose with supportive care only—there is no specific antidote, and management focuses on gastrointestinal decontamination (if presenting early), symptomatic treatment, and monitoring for complications, particularly in patients with pre-existing kidney or liver disease who are at substantially higher risk for organ toxicity. 1

Immediate Management

Gastrointestinal Decontamination

• Administer activated charcoal (1 g/kg orally) if the patient presents within 1-2 hours of ingestion, as this is the most effective window for preventing absorption of NSAIDs like aceclofenac 2, 1
• Gastric lavage followed by activated charcoal may be considered if presentation occurs within the first hour, though current trends favor charcoal alone for most cases 1
• Do not induce emesis with syrup of ipecac in the emergency department setting, as this delays more effective interventions 1

Supportive Care Protocol

• Provide entirely supportive treatment focusing on symptom management, as no specific antidote exists for NSAID overdose 1
• Monitor vital signs continuously and establish IV access for fluid resuscitation if needed 1
• Treat nausea and vomiting with antiemetics as needed 1
• Address metabolic acidosis with IV sodium bicarbonate if severe (pH <7.1) 1

Expected Clinical Presentation

Typical Symptoms (Most Common)

• Nausea, vomiting, headache, drowsiness, blurred vision, and dizziness are the most frequently reported symptoms across all NSAID overdoses 1
• Most NSAID overdoses result in benign outcomes, with serious toxicity occurring primarily after massive ingestions in suicide attempts 1

Serious Complications (Rare but Critical)

• Seizures, hypotension, apnea, coma, and acute renal failure can occur with substantial ingestions, though these are uncommon 1
• Metabolic acidosis, respiratory depression, and CNS depression may develop in severe cases 1

High-Risk Populations Requiring Intensive Monitoring

Patients with Pre-existing Kidney Disease

• Even a single oral dose of diclofenac (aceclofenac's parent compound) can cause transition from subclinical acute kidney injury to chronic kidney disease 3
• Aceclofenac has been documented to cause acute tubulointerstitial nephritis, which can rapidly deteriorate renal function 4
• Monitor serum creatinine, BUN, and urine output closely in any patient with baseline renal impairment 5
• Consider early nephrology consultation if creatinine rises or oliguria develops, as hemodialysis may be required for oliguric renal failure (though it does not enhance drug elimination) 1

Patients with Pre-existing Liver Disease

• Diclofenac derivatives commonly cause aminotransferase elevations (3.1% develop ALT/AST >3x ULN), with clinical liver events occurring in approximately 23 per 100,000 patients 6
• Hepatotoxicity can develop early (within days) or late (up to 21 months), though most occurs within the first 4-6 months of chronic therapy 6
• In overdose settings with pre-existing liver disease, monitor AST, ALT, bilirubin, INR, and PT closely 6
• If aminotransferases exceed 1000 IU/L or coagulopathy develops, consider early hepatology consultation and ICU-level care 2

Chronic Alcohol Users

• Patients with chronic alcohol consumption have increased susceptibility to NSAID-induced hepatotoxicity and should be monitored more intensively 5
• Lower thresholds for organ toxicity exist in this population 5

Monitoring Parameters

Essential Laboratory Studies

• Obtain baseline and serial measurements of:
  • Serum creatinine and BUN to assess renal function 4
  • AST, ALT, alkaline phosphatase, and total bilirubin to monitor hepatotoxicity 6
  • Complete blood count to detect gastrointestinal bleeding 5
  • Coagulation studies (PT/INR) if liver injury is suspected 6
  • Electrolytes and arterial blood gas if metabolic acidosis is suspected 1

Timing of Monitoring

• Initial laboratory assessment upon presentation 1
• Repeat studies at 4-6 hours and 12-24 hours post-ingestion, particularly in high-risk patients 6
• Continue monitoring until clinical improvement and laboratory normalization 4

Interventions That Are NOT Effective

Do Not Attempt Enhanced Elimination

• Urine alkalinization and forced diuresis are not beneficial despite aceclofenac having a pKa in the acidic range, because NSAIDs are highly protein-bound with minimal unchanged renal excretion 1
• Hemodialysis does not enhance elimination of aceclofenac due to high protein binding, though it may be required for management of oliguric renal failure as a complication 1
• Multiple-dose activated charcoal is unlikely to be beneficial for aceclofenac (unlike longer half-life NSAIDs such as piroxicam) 1

Critical Pitfalls to Avoid

• Do not assume a benign course in patients with pre-existing kidney or liver disease—these patients can develop serious organ toxicity even with therapeutic doses, making overdose particularly dangerous 3, 4, 6
• Do not delay supportive care while attempting unproven elimination techniques 1
• Do not discharge patients with pre-existing organ dysfunction without adequate observation period (minimum 12-24 hours) and repeat laboratory studies 4, 6
• Consider gastrointestinal prophylaxis with proton pump inhibitors in all overdose patients, as NSAIDs increase risk of upper GI bleeding, particularly in those with risk factors (age ≥60, male gender, concurrent corticosteroids or anticoagulants) 5