Case Report |
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CABG in a patient recovering from Dengue fever |
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INTRODUCTION Dengue fever is a mosquito borne viral disease caused by the dengue virus and is endemic in large areas of Asia. Typically dengue fever is an acute febrile illness characterized by frontal headache, retrocular pain, muscle and joint pain, nausea, vomiting and rashes. Atypical presentation is infrequent and may lead to catastrophic illness like dengue haemorrhagic fever progressing to shock. We report a case of a 64 years male with unstable angina with left main coronary artery disease and recovering from dengue fever. Case Report |
Transthoraic 2D echocardiography showed no regional wall motion abnormality, left ventricular ejection fraction 60%, mild concentric left ventricular hypertrophy, other cardiac chamber dimensions were normal, mild mitral regurgitation and normal other valves. No intracardiac clot, vegetations or pericardial effusion, Diastolic relaxation abnormality was present. Doppler study of carotid and peripheral arteries were normal. His coronary angiography revealed left main coronary artery (LMCA) 95% stenosed with 100 % ostial stenosis of left anterior descending artery (LAD) and left circumflex artery (LCx). Magnetic retrograde cholangiopancreatography (MRCP) showed pancreatitis small calculi in the lower end of cystic bile duct but common bileduct (CBD) was not dilated. Gall bladder was full of calculi and no intrahepatic biliary radicles (IHBR) After MRCP, endoscopic retrograde cholangiopancreatography (ERCP) was performed which revealed normal papilla, juxta papillary diverticulum. CBD was cannulated selectively endoscopic papilectomy (EPT) was performed and CBD was normal in size. A small stone was seen in the lower part of CBD and was extracted with the help of basket. Balloon wire used to clear the CBD. Balloon cholangiogram done after the procedure showed no stone. There was no complication of the procedure. Patient was posted for CABG but later was postponed due to presence of high-grade fever. On evaluation his general condition was fair with no icterus. Clinical examination of respiratory, cardiovascular, abdomen and central nervous system were unremarkable. He was investigated for causes of fever. |
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Correspondence: Dr.Yatin Mehta,
Sr. Consultant Anaesthesiologist
Indraprastha Apollo Hospitals, New Delhi |
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Indian Heart J. 2009; 61:386-388 |
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CABG in a patient recovering from Dengue fever |
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Laboratory investigations were, hemoglobin 10.6 gm/dl, total leukocyte counts were 12200 per cubic mm, neutrophils 73%, lymphocytes 18%, monocytes 4% and eosinophils were 5%. Platelets count were 226000 per cubic mm. His peripheral blood film was negative for malarial parasite. Chest X ray was normal. Bacterial culture for blood and urine were sterile. A provisional diagnosis of dengue fever was made. He was managed conservatively and he improved uneventfully. Patient was premedicated with lorazepam 2mg per oral and morphine sulphate 5 mg intramuscular. Under local anaesthesia peripheral venous cannula and 20 gauge left radial artery catheter were inserted. A 7.5 Fr pulmonary artery catheter was floated through introducer sheath in right internal jugular vein. The mean pulmonary artery pressure was 23 mm Hg. Noninvasive monitoring included ECG, pulse oximetry, blood temperature, end tidal carbon dioxide and urine output. Anesthesia was induced with intravenous, thiopentone sodium 250 mg, fentanyl citrate 250 microgram and midazolam 2 mg. Vecuronium bromide 8mg intravenously, was administered and trachea was intubated with 8.5 mm orotracheal tube. Anaesthesia was maintained with inhalation of isoflurane, oxygen and air, and incremental doses of fentanyl and mechanical ventilation. |
Discussion Dengue infection is transmitted by Aedes aegypti mosquito and is caused by flaviviruse. In about half of the cases fever is associated with rashes. Other symptoms and signs are headache, musculoskeletal pain and leukopenia1. The clinical infection can vary from mild self limited febrile syndrome(classical dengue) to dengue haemorrhagic fever characterized by thrombocytopenia, hemorrhagic manifestation and increased vascular permeability, to dengue shock syndrome characterized by cardiovascular instability.2 Dengue viruse infection is diagnosed on the basis of clinical presentation and detection of viral RNA by PT-PCR. The virus responsible for dengue infection is a single stranded envelope RNA virus with four distinct subtype (DEN 1 to 4). Infection with one serotype provides life long immunity to that virus, although there is only transient weak cross infection protection from one infection to other. Angiographically significant LMCA stenosis has been defined as diameter stenosis greater then 50%. Prevalence of significant LMCA disease in patients with CAD varies from 2.5 to 10% in previous published studies. 4,5 The mortality and morbidity of this condition depends on various factors including the severity of the LMCA stenosis, associated disease in other coronaries including the RCA, left dominance and LV function. There are various controversies in medical vs surgical treatment. Patients with LMCA stenosis who are managed medically have a poor prognosis. Elliot6 in an analysis of patients with LMCA stenosis awaiting surgery, found a one year mortality of 21% and an event free survival at one year of only 46%. In the earlier landmark studies that looked at medical vs. surgical treatment of LMCA stenosis, the three year survival of for medical treatment was 60% in the VACSS, 7 69% in CASS, 8 and 82% in ECASS, 9 where the patients are younger and with better LV function. The comparative surgical survival was 82%, 91% and 91 respectively. This benefit has been shown in the CASS10 study to persist in the long term with a median survival in the surgical group being 13.3 years against 6.6% years in the medical group. |
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Indian Heart J. 2009; 61:386-388 |
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SKS Rawat et al |
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Most of these studies which were carried out in an earlier era, had an operative mortality, which ranged from 3.5 to 12%. Majority of these patients received vein grafts rather than mammary arteries. With the improvement in operative techniques, the current operative mortality rates are below 3%. Furthermore with the use of mammary artery even in these high-risk patients, the long term results should be even better. According to World Health Organization (WHO) guidelines, mild to moderate dengue fever needs to be managed with intravenous fluid therapy for 24-48 hrs and careful observation of the patient for progression of the disease process.11 Although, no separate guidelines are available for surgical patients, those who continue to demonstrate thrombocytopenia and petechiae should be hospitalised and observed carefully for impending circulatory shock. Anticipatory platelets transfusion is not warranted in all surgical patients, as low platelets do not necessarily predict a high chance of bleeding in dengue fever.12 Our patient did not have significant bleeding postoperatively and low normal platelet counts preoperatively. Dengue fever is an acute disease process in which marked thrombocytopenia is associated with capillary leakage resulting in haemoconcentration, pleural effusion and ascites, Patients with severe plasma loss may develop dengue shock syndrome. (DF grade III and IV). However in patients with DF grade I and II, even with severe thrombocytopenia, circulatory failure is not common. Although the exact pathophysiology is not known, mild albuminuria and deranged liver enzymes indicative of transient liver cell injury has been documented in DF13. Central nervous system involvement is rare and renal function is normal. Thrombocytopenia may be caused by compliment activation due to platelets binding to virus antigens. In addition bone marrow depression may occur during DF contributing to the thrombocytopenia. Platelet that escape compliment- mediated destruction may also have diminished function; several studies have reported impaired platelet aggregation due the acute phase of DF. 14 The platelet may start regenerating from the marrow once the disease process starts regressing. |
References
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Indian Heart J. 2009; 61:386-388 |