Complications of Cardiac Catheterization & PCI

Access-site complications

Radial versus femoral. Most catheterization complications occur at the arterial access site. Femoral access causes more bleeding and vascular injury than radial access, which is now preferred at most centers. The usual radial complication, radial artery occlusion, is typically silent because the ulnar artery and palmar arches keep supplying the hand. Bleeding risk rises with large sheaths, intense anticoagulation, older age, female sex, and low body weight.

Puncture height matters. A femoral puncture above the inguinal ligament cannot be compressed against the femoral head and bleeds into the retroperitoneum; a puncture below the femoral bifurcation favors pseudoaneurysm and arteriovenous fistula. A simple groin hematoma, the most common problem, responds to manual compression.

Retroperitoneal hematoma. Within hours of femoral access: hypotension, tachycardia, ipsilateral back, flank, or lower-quadrant pain, and a falling hemoglobin — often with a normal-looking groin, because blood tracks upward out of sight. Femoral nerve compression can cause thigh numbness or quadriceps weakness. Resuscitate with fluids and blood, stop heparin (protamine reverses it), and once the patient is stable confirm with noncontrast CT of the abdomen and pelvis. Most bleeds stop with conservative care; persistent instability calls for endovascular repair (covered stent or balloon tamponade) or surgery.

Pseudoaneurysm. A contained hematoma that communicates with the artery through a neck and lacks the three wall layers of a true aneurysm. It appears days after the procedure as a tender, pulsatile groin mass with a systolic bruit. Duplex ultrasound shows swirling "yin-yang" flow in the sac and to-and-fro flow in the neck. Small (under about 2 cm), asymptomatic lesions often thrombose on their own and are followed with repeat duplex; larger or symptomatic ones receive ultrasound-guided thrombin injection (first-line, high success) or ultrasound-guided compression. Surgery is reserved for rapid expansion, infection, skin necrosis, limb ischemia, or nerve compression.

Arteriovenous fistula. When the needle traverses both the femoral artery and an adjacent vein, a fistula forms with a continuous "machinery" bruit or thrill, often without a mass. Duplex confirms it. Most are small and close or remain benign, so observation is standard; repair is indicated for enlargement, limb swelling or ischemia, or high-output heart failure.

Hypotension with bradycardia, nausea, pallor, and sweating — often during sheath removal — is a vasovagal reaction: atropine, IV fluids, and leg elevation. Tachycardia with a falling hemoglobin points to bleeding.

Cholesterol embolization syndrome

Mechanism and timing. Catheter manipulation in an atherosclerotic aorta — less often anticoagulation or thrombolysis — releases cholesterol crystals that lodge in small arterioles and provoke a foreign-body inflammatory reaction. Unlike contrast injury, findings appear days to weeks after the procedure.

Findings. Livedo reticularis, painful blue toes with palpable pedal pulses, digital gangrene; subacute, stepwise AKI; abdominal pain or GI bleeding; and retinal Hollenhorst plaques — bright, refractile yellow emboli at arteriolar bifurcations. Labs show transient eosinophilia, eosinophiluria, low C3/C4, and a high ESR. Biopsy of skin, muscle, or kidney reveals biconvex, needle-shaped clefts where the crystals dissolved during tissue processing. Eosinophiluria also occurs in acute interstitial nephritis, but livedo, blue toes, and low complement point to emboli.

Management. There is no specific therapy: supportive care (dialysis if needed, wound care), a high-intensity statin and aspirin to stabilize plaque, and blood pressure control. Renal recovery is often incomplete.

Avoid anticoagulants, thrombolytics, and further catheter procedures when possible — they can provoke more embolization.

Contrast-associated AKI

Risk and mechanism. Highest risk: eGFR <30 (especially with diabetes), intra-arterial contrast as in cardiac catheterization, large contrast volume, volume depletion, heart failure, NSAID use, multiple myeloma, and older age. Contrast causes renal vasoconstriction with medullary hypoxia plus direct tubular toxicity; unusually for tubular injury, the FENa can be below 1%.

Metformin is not nephrotoxic; it is held because contrast AKI would let it accumulate and cause lactic acidosis.

Contrast reactions

Mechanism. Most immediate reactions to iodinated contrast are anaphylactoid — direct, non-IgE mast-cell degranulation — ranging from hives to bronchospasm and shock. The strongest predictor is a prior reaction to iodinated contrast. Shellfish or povidone-iodine allergy is not a contraindication; shellfish allergy is directed at tropomyosin, not iodine.

Premedication. After a prior contrast reaction: prednisone 50 mg orally 13, 7, and 1 hour before plus diphenhydramine 50 mg 1 hour before, and a different low-osmolar agent. Breakthrough reactions still happen, so be ready to treat anaphylaxis with IM epinephrine.

Coronary and procedural complications

Acute stent thrombosis. Abrupt chest pain with ST elevation in the stented territory, acute (<24 h) or subacute (up to 30 days). Causes include stent underexpansion or malapposition, edge dissection, missed antiplatelet doses, and clopidogrel nonresponse. Treat with emergent repeat angiography and PCI. In-stent restenosis, by contrast, returns gradually as exertional angina months later.

Coronary perforation and tamponade. Guidewire perforation can bleed into the pericardium during or hours after PCI: hypotension, tachycardia, JVD, muffled heart sounds, and pulsus paradoxus. Obtain a bedside echo, perform emergent pericardiocentesis, reverse heparin, and seal the leak, for example with a covered stent.

Other events. Periprocedural (type 4a) MI, arrhythmias, stroke, and acute limb ischemia from access-site dissection or thrombosis — a cold, pulseless leg needs emergent vascular evaluation.