A Case of Septic Shock and Disseminated Intravascular Coagulation Complicated by Acute Myocardial Infarction Following Amniocentesis
A 40-year-old female patient presented to us with dyspnea, fever, chills and hematuria. She was at the 17th week of gestation and amniocentesis had been done 2 days previously for the prenatal evaluation of fetal anomalies at a private clinic. After amniocentesis, she complained of fever, chills, progressive dyspnea, hematuria and abdominal pain. Her systolic blood pressure was less than 80 mmHg. Ultrasonographic examination demonstrated that the fetus had died. Intravenous antibiotics were started and a therapeutic abortion was performed. After this, the patient was transferred to our hospital for the management of her septic complications.\nOn admission, her blood pressure was 80/50 mmHg, the pulse rate was 105/min, the body temperature was 38.6℃ and the respiration rate was 30/min. Chest auscultation revealed basal rales in both lower lung fields. Vaginal spotting and oliguria were observed.\nThe complete blood cell count showed leukocytosis (white blood cell count: 28,300/mm3) and thrombocytopenia (platelet count: 13,000/mm3). The blood chemistry revealed elevated liver enzymes (aspartate aminotransferase: 645 IU/L, alanine aminotransferase: 170 IU/L), azotemia (blood urea nitrogen: 41.7 mg/dL, creatinine: 3.1 mg/dL) and an increased level of inflammatory markers (C-reactive protein 10.1: mg/dL, erythrocyte sedimentation rate: 67 mm/hour). The coagulation profiles showed a prolongation of the prothrombin time (international normalized ratio: 2.63) and the activated partial thrombin time (87 seconds), a low level of fibrinogen level (83 mg/mL), a decreased level of anti-thrombin III (2.81 mg/dL) and increased levels of fibrin degradation products (105.2 µg/mL) and d-dimer (9.65 mg/L). Escherichia coli was isolated from the culture of the amniotic fluid and blood. Therefore, we concluded that the patient had septic shock and disseminated intravascular coagulation (DIC) following her intrauterine infection, and this was possibly complicated by the amniocentesis.\nIntravenous antibiotics, diuretics and inotropic agents, including dopamine and norepinephrine, were infused continuously. Four units of fresh frozen plasma and 12 units of platelet concentrates per day were infused. Five thousands units of anti-thrombin III per 6 hours were also administered.\nSeveral hours later after the admission, she complained of continuous substernal and epigastric pain that was associated with cold sweating. Electrocardiography (ECG) showed sinus tachycardia with non-specific ST segment changes (), and the cardiac enzymes were markedly elevated (creatinine kinase: 326 U/L, MB fraction of creatine kinase: 256 U/L, cardiac specific troponin T: 2.17 ng/mL, cardiac specific troponin I: 9.19 ng/mL, myoglobin: 190.2 ng/mL). Trans-thoracic echocardiography (TTE) showed the dilated left ventricle (LV) with a chamber size of 60 mm for the end-diastolic dimension; akinesia of the anterior and, septal wall motion and LV systolic dysfunction (ejection fraction: 38%) were also observed (). We could not perform immediate coronary angiography (CAG) due to the oliguria and renal dysfunction, and the patient was treated conservatively for AMI.\nAfter treatment, the patient's vital signs were stabilized and the subjective symptoms of the patient were improved. However, the thrombocytopenia was not improved for several days despite the replacement of the platelet concentrates, and the renal function progressively deteriorated despite the normalized urine output. On the fourth hospital day, myocardial single photon emission computed tomography (M-SPECT) was performed and the M-SPECT revealed a large, partly reversible perfusion defect in the anterior wall on stress, and the resting image suggesting anterior wall myocardial infarction ().\nThe coagulation profiles and thrombocytopenia were normalized on the eighth hospital day. Follow-up TTE was done on the eighth hospital day, and it revealed normalized LV wall motion (). The blood urea nitrogen (BUN) and creatinine reached their peak levels on the ninth hospital day (blood urea nitrogen: 110.9 mg/dL, creatinine: 8.0 mg/dL) and then they progressively declined. On the thirteenth hospital day, the patient was discharged.\nDuring clinical follow-up at the outpatient clinic, the renal function was normalized at 3 weeks after discharge. The patient was readmitted for diagnostic CAG. The CAG revealed no significant stenosis in both the coronary arteries (). Follow-up M-SPECT revealed markedly improved perfusion in the territory of the left anterior descending coronary artery with the remaining perfusion defect ().