Case Presentation: A 52 year old man with a PMHx of IVDU and HLD presents with a CC of “Cold Leg”. This was preceded by sudden onset numbness and weakness of his right foot and leg, inability to ambulate and severe pain in his thigh. He reported prodromal fevers, sweats and arthralgias. His last IVDU was approximately 2 weeks ago. Patient is sexually active. Initial vitals demonstrated tachycardia. On exam, he appeared in no distress. A grade III/VI systolic murmur was auscultated at the mitral area. Vascular exam revealed a cool right lower extremity with absent popliteal and dorsalis pedis pulses. Laboratory studies were notable for a leukocytosis to 41. CTA revealed occlusion of the right common femoral artery and distal superficial femoral artery. Intraoperative trans-esophageal echo revealed a 1.6cm mitral valve vegetation. He was treated with heparin and underwent embolectomy. Blood cultures finalized without growth. Ultimately, the diagnosis was confirmed after the thrombus tissue culture grew Neisseria gonorrhea. Patient was started on Ceftriaxone and is awaiting surgical mitral valve repair.
Discussion: Our patient presented with acute limb ischemia (ALI), secondary to septic embolization from Neisseria gonorrhea infective endocarditis (IE). Etiologies of ALI include atherothrombotic, atheroembolic, and cardioembolic etiologies – with nearly 30% of ALI having an embolic source. Clinical clues for an embolic source of ALI include rapid symptom onset, multiple sites of occlusion on CTA, and prior history of atrial fibrillation. When an embolic source is suspected, echocardiography is needed to confirm origin. Septic embolization increases mortality, morbidity, and complicates patient care, as management often requires surgical interventions.While surgical interventions are necessary, tissue cultures of the embolus may establish the diagnosis. As in our patient, fastidious organisms such as Neisseria gonorrhea are notoriously hard to culture, leaving the hospitalist to pursue treatment of culture negative endocarditis. When disseminated gonococcal infection (DGI) is diagnosed, gonococcal endocarditis (GE) only occurs in 1-2% of these cases. The clinical features of DGI or GE include subacute symptoms of fever, chills, malaise, tenosynovitis, arthritis, or symptoms of heart failure. Risk factors include unprotected sexual encounters and diagnostic delays can results from previous exposure to antibiotics for subacute symptoms. Treatment typically includes Ceftriaxone for at least 4 weeks however, antibiotics alone are often ineffective and 50-70% of the time patients require valve repair or replacement.
Conclusions: Gonococcal endocarditis is a rare and often life threatening complication of DGI due to valvular destruction and diagnostic difficulty. Embolic cultures are a valuable tool in establishing a diagnosis for GE. Gonococcal endocarditis should be considered in culture negative endocarditis with septic embolization.
