Ludwig's angina and acute myocardial infarction: A case report

Abstract

Ludwig's angina was first described in 1839 by German physician, Wilhelm Frederick Von Ludwig as a rapidly and fatal progressive gangrenous cellulitis and edema of the soft tissues of the neck and floor of the mouth with rapid spread to other places like anterior mediastinum. However, Type 2 acute myocardial infarction (MI) due to Ludwig's angina has not been documented. A 62‐year‐old male presented to the emergency department with visible anterior neck swelling for 1 week, which was preceded by a tooth arch 1 week prior, the patient presented with a high grade fevers, dysphonia, dysphagia, and facial swelling. No history of trauma. He reported in the past 24 h prior to evaluation, a steady progression of pain intensity with rapid progression and anterior neck skin erythema and swelling. The pain was exacerbated by rotation of the neck, tongue protrusion, and speaking. On examination, there was a visible anterior neck swelling measuring 10.0 × 3.0 cm in widest dimensions, exquisitely tender to palpation with a positive temperature gradient, skin hyperpigmentation and firm in consistency, no crepitus, fluctuance, or induration. Tongue appeared elevated with sublingual edema and pooling of secretions. No stridor. A chest and neck ultrasound scan revealed an extensive abscisic mass from the submandibular, neck, sternal notch, and right clavicular region with the largest pockets measuring 2.11 × 0.8 cm, 2.03 × 0.62 cm, 1.50 × 1.1 cm, with noted submandibular, subclavicular and deep and superficial cervical lymph nodes, the largest measuring 1.23 × 1.63 cm in dimensions. A neck‐CT scan with contrast revealed a pronounced subcutaneous tissue localized collection extending to both submandibular spaces measuring about 5.5 × 12.5 × 9.5 cm with mural enhancement. The upper chest cuts showed moderate pleural effusions and a paracardial hypodense well‐defined lesion measuring 7.5 × 2.5 cm with mild pericardial effusion. The patient was referred to the ear, neck and throat, ENT surgeon for urgent drainage of the abscess, which was done successfully and about 300 mL of hemorrhagic pus was drained. Then transferred to highly dependent unit, (HDU) for IV antibiotic administration and vital observations, prior to that electrocardiogram, ECG showed a normal sinus rhythm. The following day in HDU, the patient started experiencing a chest pain of sudden onset radiating to the upper jaws, left forearm and throbbing in nature, palpitations and started becoming diaphoretic. Blood pressure was 150/70 mmgh and pulse of 120 bpm. ECG readings demonstrated ST‐elevation, at lead 11, V2, and V3, cardiac Troponin I and CK‐MB were elevated 10.0 ng/mL, (<0.4 ng/mL) and 150.0 IU/L, (5‐25 IU/L) respectively. The patient was started on medications to relief acute ischemic pain these included, sublingual nitroglycerin 0.6 mg, morphine 5 mg intravenous slowly, antithrombotic, and beta‐adrenergic blockade. He was kept in HDU later with heparin 80 U/kg bolus and 8 U/kg continuous infusion and was taken for coronary angiogram which demonstrated no any coronary artery occlusion. The patient later on started to register improvement and later discharged on medications for follow‐up. On follow‐up, the subsequent ECG showed persistent atrial fibrillation and patient was discharged on P2Y12 inhibitor, clopidogrel, 75 mg, and beta‐blocker, metoprolol 50 mg. Over the past three decades, mortality rates for acute MI have increased significantly, One common subtype, type 2 MI is noted and driven by a myocardial oxygen supply and demand mismatch in the absence of coronary thrombosis. T2MI can occur with or without obstructive coronary disease like in this patients with angiographically normal coronary arteries. T2MI is increasingly recognized because of various septic pathophyisologies that cause increased myocardia oxygen demand. Evidence of myocardial ischemia especially those with sepsis are likely to develop myocardial injury. T2MI is frequent and explains a significant increase in clinical practice. A consensus is needed about how the diagnosis is established, to facilitate evidence‐based therapies geared toward improving outcomes.