Case Report
 

CABG in a patient recovering from Dengue fever

S.K. S. Rawat, MD; Yatin Mehta, MD, MNAMS, FRCA, FAMS; Taha Yaseen,MD, MRCP;
Jeetender Sharma,MD, IDCC; Vijay Kohli, MS; Naresh Trehan, MD


Dept. of Anaesthesia and Cardiac Surgery
Indraprastha Apollo Hospitals, New Delhi

Abstract

Dengue fever (DF) is the most common and widespread arbovirus infection worldwide. It is endemic in the tropical and sub-tropical areas of the world especially in southeast Asia, the Pacific, East and West Africa, the Caribbean and South America with cyclical epidemics. Major epidemics of DF have occurred in India and southeast Asia in the last two decades. We have outlined the anaesthetic management of a 64 year old man with dengue fever who needed urgent CABG.

Keywords: Dengue fever, anaesthetic management, CABG.

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.

Coronary artery bypass graft surgery (CABG) specially left main coronary artery stenosis in a patient recovering from dengue fever becomes a surgical and anaesthetic challenge.

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
A 64 years old male was admitted to hospital with complaint of angina on exertion class III. He had been treated conservatively for biliary Pancreatitis with multiple gall bladder stones one and half months back and recovered uneventfully. He was normotensive, nondiabetic, nonsmoker and had no family history of coronary artery disease (CAD).

At the time of admission his platelet count was 2.6 x 109 /cu mm and total leukocyte count was 11500 /cu mm, liver functions were normal, serum amylase was 59 IU/L and serum lipase was 184 IU/L. His other laboratory tests are Hb 12.4 g, TLC 12100, urea 29, creatinine 0.1 , SGOT 45, SGPT 32, PT 13.0sec, PTTK 33 sec.

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.

Correspondence: Dr.Yatin Mehta, Sr. Consultant Anaesthesiologist Indraprastha Apollo Hospitals, New Delhi
Email: yatinmehta@hotmail.com

Indian Heart J. 2009; 61:386-388
 
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CABG in a patient recovering from Dengue fever
 
 

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.

Serological test for dengue was performed which detected IgM antibodies for dengue quantitative assay up to 11.5 Panbio units which was significant.

A provisional diagnosis of dengue fever was made. He was managed conservatively and he improved uneventfully.

Patient was planned for CABG immediately after recovery in convalescent phase of dengue because of significant LMCA disease.

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.

Left internal mammary artery (LIMA) was harvested. After harvesting the artery unfractionated intravenous heparin 2mg per kg was administered to achieve activated clotting time (ACT) 300 seconds. On beating heart coronary grafting was performed with LIMA to LAD and reverse saphenous vein grafts to circumflex using intracoronary shunt and octopus stabiliser (Medtronics Inc, Minneapolis, USA). During grafting his ABG  remained within normal limits. ABP 125/67/87 mmHg; PA 23/14/18; CO 4.86, CI 3.1, SVR 1174, PVR 124. After complete grafting heparin was reversed with protamine sulphate in dose of 2 mg per kg.  Patient was shifted to recovery room with stable haemodynamics. Post operative his ABG pH 7.42 PCO2 37.2 mmHg PO2 152.6 mmHg HCO3 25.2, BE -2.1, ABP 129/65/86 mmHg, PA 26/13/16, CO 4.92, CI 3.27, SVR 1261, PVR 121. On post operative day 2 trachea was extubated and patient was shifted to the ward on post operative day 4.  His total chest / mediastinal tube drainage was 320 ml and no blood or blood products were administered perioperatively. His post opertive echocardiography was normal. He was discharged from the hospital on 7th postoperative day.

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.
Serological testing is generally of little value because most severe infections are in previously infected patients.
Classical dengue fever manifests as fever lasting 2-5 days. The fever is usually between 39-40oC and may be biphasic, occasionally can be associated with frontal or retro–orbital headache, muscle and joint pain, nausea, vomiting and rashes. Diffuse flushing or fleeting pinpoint eruption or maculopapular rash may be observed during the initial febrile illness over the face, chest and neck.
Since the main clinical description of the LMCA disease by Herrick in 19123, numerous studies have shown that LMCA stenosis is of critical prognostic importance. LMCA disease  poses special management problems due to extensive myocardial territory  at risk during revascularisation procedure. Histological differences including the increased elastic tissue within the LMCA also make their management special.

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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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.

The danger of operating for CABG during recovery of DF are the possibility of haemodynamic instability and increased surgical bleeding due to thromocytopenia.  Although this patient’s platelet count was normal still the platelet dysfunction related to cardiopulmonary bypass (CPB) can worsen the perioperative bleeding.  Therefore performing CABG without CPB would certainly reduce this risk.  Many previous study have shown reduced morbidity i.e. renal pulmonary and neurological after OPCAB, along with reduced bleeding and blood requirement15.
In conclusion we would like to highlight that careful and vigilant perioperative haemodynamic monitoring and observation is essential to ensure a favourable outcome in patient with DF undergoing CABG, preferably as OPCAB.

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