Acute cholecystitis in a patient on dual antiplatelet therapy

This is moderate (grade II) acute cholecystitis by Tokyo Guidelines criteria: symptoms for more than 72 hours, white cell count above 18 × 10^9/L, and marked local inflammation, but no organ dysfunction. He is not in septic shock; the creatinine is only mildly elevated and the lactate is 2.8 mmol/L. The key issue is not the grade alone but the high operative risk: recent drug-eluting stent, dual antiplatelet therapy, obesity, diabetes, and mild renal impairment.

In the next 6 hours I would:

• Keep him nil by mouth, give IV crystalloid, analgesia, and antiemetics.
• Take blood cultures and start broad-spectrum antibiotics covering Gram-negative and anaerobic organisms, for example piperacillin-tazobactam, adjusted for renal function.
• Involve cardiology early about antiplatelet management.
• Arrange percutaneous cholecystostomy under local anaesthesia if it can be done promptly, rather than waiting for tomorrow’s theatre slot. This achieves source control with far less bleeding and anaesthetic risk than laparoscopic cholecystectomy on dual antiplatelet therapy.
• If percutaneous drainage is unavailable and he develops generalised peritonitis, worsening sepsis, or organ dysfunction, proceed to emergency cholecystectomy with cardiology input and meticulous haemostasis.

A tomorrow-morning slot is acceptable only if he remains stable and drainage has been performed or is planned; it should not be used as an excuse to delay source control in a septic patient.

Stopping clopidogrel reduces surgical bleeding, but in a patient with a drug-eluting stent inserted only 10 weeks ago it risks stent thrombosis and myocardial infarction. Current practice is to continue aspirin in most non-cardiac surgery, while clopidogrel is often withheld for 5–7 days before major elective operations. That rule is not safely applied to a recent stent without cardiology agreement; premature cessation of dual antiplatelet therapy is a recognised cause of catastrophic stent thrombosis.

The recent stent therefore pushes the balance strongly toward a non-operative or minimally invasive source-control strategy. Percutaneous cholecystostomy can usually be performed without stopping either antiplatelet agent, because the bleeding risk is low and controllable. If laparoscopy becomes unavoidable for worsening sepsis, I would operate on dual antiplatelet therapy with careful dissection and haemostasis rather than stop both drugs. Platelet transfusion would be reserved for active bleeding, not given routinely. The decision should be documented with cardiology input, and the patient should be told that the drain is a temporary measure while the stent matures and the infection settles.

I would explain that the gallbladder is infected and swollen, and that removing it is the definitive treatment. However, he has a recently placed heart stent and is on two blood-thinning medicines. An operation now carries a higher risk of serious bleeding and cardiac complications. The safer first step is to place a small drain through the skin into the gallbladder under local anaesthetic, drain the infected bile, and treat the infection with antibiotics. This usually settles the attack within a few days.

The drain can then stay for several weeks while the heart stent matures and cardiology adjusts the blood thinners. Later, when the risks are lower, he can have a planned laparoscopic cholecystectomy. I would be honest about the risks of the drain: bleeding, infection, dislodgement, blockage, and recurrence of symptoms in a minority of patients. I would also explain the risks if surgery becomes urgent: bleeding, bile duct injury, conversion to open operation, retained stones, and cardiac events. He should return immediately with worsening pain, fever, jaundice, or vomiting. This shared plan respects both the infection and the cardiac risk.