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CASE REPORT Table of Contents   
Year : 2007  |  Volume : 10  |  Issue : 1  |  Page : 54-57
Off-pump coronary artery bypass grafting in a polycythaemic patient - case report and review of literature

1 Department of Anaesthesiology and Critical Care, Department of Cardiac Surgery, Escorts Heart Institute and Research Centre, New Delhi., India
2 Department of Haematology, Batra Hospital, New Delhi, India

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How to cite this article:
Arora D, Juneja R, Pendarkar D, Mehta Y, Tehran N. Off-pump coronary artery bypass grafting in a polycythaemic patient - case report and review of literature. Ann Card Anaesth 2007;10:54-7

How to cite this URL:
Arora D, Juneja R, Pendarkar D, Mehta Y, Tehran N. Off-pump coronary artery bypass grafting in a polycythaemic patient - case report and review of literature. Ann Card Anaesth [serial online] 2007 [cited 2022 Dec 6];10:54-7. Available from:

Polycythaemia, an increase in circulating red blood cells (RBC) may be associated with hyperviscosity of the blood, which can lead to thromboembolism resulting in cerebrovascular accidents, myocardial infarction, abdominal emergencies and peripheral vascular events. [1] Patients requiring coronary artery bypass grafting (CABG) or emergency coronary angioplasty due to thrombosis of coronary arteries secondary to polycythemia vera (PV) have been reported. [2],[3]

Cardiac surgery, particularly CABG in untreated patients with PV may be associated with serious perioperative morbidity. [4] We report the anaesthetic management of a patient with suspected PV who presented for emergency CABG.

   Case report Top

A fifty-two year old male weighing 65 kg with body mass index of 29 presented in the emergency room with complaints of chest pain at rest. He was a chronic smoker, known case of hypertension and diabetes mellitus on regular medication. He did not have any history of sleep apnoea syndrome and vertigo, tinnitus, dizziness or pruritis. His examination revealed heart rate of 90 beats per minute and blood pressure of 130/ 80 mm Hg. Systemic examination was unremarkable, all peripheral pulses were palpable, and no bruising or haematoma were present.

Routine haematological and biochemical investigations including serum uric acid were within normal limits, except for haemoglobin of 20.1g/dL and haematocrit of 60.3%. Coagulation parameters including bleeding time, clotting time, prothrombin time and activated partial thromboplastin time, total and differential leukocyte counts and platelet count were within normal limits. Electrocardiogram (ECG) revealed ST-T depression in the chest leads. Echocardiography showed left ventricular ejection fraction of 60% without regional wall motion abnormality. He was diagnosed as a case of acute coronary syndrome. Coronary angiography was performed, which revealed triple vessel disease with critical stenosis of the left anterior descending artery [thrombolysis in myocardial infaction (TIMI) flow grade II]. Abdominal sonography revealed hepatomegaly with fatty infiltration without evidence of splenomegaly. Haematologist's opinion was sought in view of high haematocrit, who made a provisional diagnosis of PV and advised preoperative phlebotomy to decrease the haematocrit. He was scheduled for CABG on an urgent basis without further investigations for PV, as he developed recurrent angina (Canadian Cardiovascular Society Angina classification IV). He was managed initially with nitrates, metoprolol, ramipril and heparin.

The patient was premedicated with oral lorazepam 2 mg and ranitidine hydrochloride 150 mg on the night before surgery, and morphine sulphate 0.1mg/kg intramuscularly one hour before surgery. On arrival in the operating room, pulse oximetry revealed an oxygen saturation of 96% on air. After securing peripheral venous access, radial artery catheter was inserted. Internal jugular cannulation was performed with 8.5F venous sheath. Anaesthesia was induced with sodium thiopentone (3 mg/Kg) and fentanyl citrate (5 µg/Kg), tracheal intubation was facilitated with vecuronium bromide (0.15 mg/Kg). Anaesthesia was maintained with intermittent doses of fentanyl citrate, vecuronium bromide, and isoflurane in 50% oxygen in air. Following induction of anaesthesia, acute normovolaemic haemodilution (ANH) was performed through the venous sheath. Two units of autologous blood (resulting in a haemoglobin of 16 gm %) were stored in the blood bank. During ANH 700 ml of 6% hydroxylethyl starch was used as replacement fluid and significant haemodynamic changes were not observed. After ANH a pulmonary artery catheter was floated through the same sheath.

Intraoperative monitoring included ECG with ST segment analysis, oxygen saturation, end-tidal carbon dioxide, temperature, urine output, direct arterial pressure, pulmonary artery and central venous pressures, cardiac output and derived parameters, arterial blood gas analysis, and activated coagulation time (ACT). The patient's temperature was maintained with a hot air warming system (Bair Hugger, 505, Augustine Medical, MN, USA) placed over the patient and a heating mattress below. Intravenous fluids were administered through a Ranger fluid warmer system (Bair Hugger, 505, Augustine Medical, MN, USA).

Off-pump coronary artery bypass grafting (OPCAB) was performed through a median sternotomy. The left internal mammary artery (LIMA) to left anterior descending artery and reversed saphaneous vein to posterior descending artery grafts were constructed on a beating heart with the help of a stabilizer (Octopus III, Medtronic Minneapolis, USA). Heparin 2 mg/Kg was administered after dissection of the LIMA and reversed with protamine sulphate in a 1:1 ratio after completion of grafting. ACT after heparin and protamine administration was 342 and 135 seconds respectively.

The intraoperative period remained uneventful and the patient did not require any inotropic support. Intraoperative blood loss of 700 ml was replaced with 2000 ml of Ringers lactate. Total anaesthesia and surgical times were 240 and 210 minutes respectively. Core temperature remained above 36.5° C. The patient was transferred to the recovery room and the trachea was extubated after six hours of ventilation. Postoperative chest tube drainage was 400 ml. Anticoagulation in the form of heparin 5000 units subcutaneously and aspirin 100 mg per oral was started after chest tube removal. Postoperative analgesia was achieved with intermittent doses of tramadol hydrochloride (1.5 mg/Kg). Postoperatively, ECG was recorded, and creatinine phosphokinase, and coagulation parameters were measured daily for three days, which remained within normal limits. Haemoglobin on zero, 1st and 7th postoperative days was 14, 14.8 and 15 gm/dL respectively. The ECG did not reveal evidence of ischaemia. The patient was mobilized on the second postoperative day. Further postoperative course was uneventful. The patient was advised serum vitamin B12 and erythropoietin levels and postoperative follow up with the haematologist. On being contacted telephonically 6 months later, he had still not been investigated for PV but remained in good health.

   Discussion Top

Polycythaemia is defined as an increase in circulating RBC, haematocrit of more than 50% in males and 45% in females. The increase may be real or apparent due to a decrease in plasma volume. Real polycythaemia may be primary or secondary to tissue hypoxia due to lung disease, high altitude, carbon monoxide poisoning, congenital heart disease, sleep apnoea syndrome, haemoglobinopathy, renal diseases, renal tumour or PV . 5

Polycythaemic patients may remain asympto­matic or have symptoms related to underlying disease or increased RBC mass. Hyperviscosity leads to stasis of blood flow leading to vertigo, tinnitus, headache or visual disturbances, systemic and pulmonary hypertension, cerebrovascular accidents, myocardial infarction or peripheral vascular disease. Physical examination usually reveals a ruddy complexion, hepatosplenomegaly favours PV, and cyanosis suggests congenital heart disease. [5]

PV is a myeloproliferative disease of the haemopoietic stem cells characterized by erythro­cytosis, granulocytosis and thrombocytosis. [1] Splenomegaly may be associated in 75% of patients, [2] in the absence of which thrombocytosis (platelet count 400,000/mm 3 ) and leukocytosis (total count > 12000/mm 3 ) are included as criteria for diagnosis. [6] However early stages may show erythrocytosis alone. Occasionally patients may present with haemostatic defects manifested as easy bruisability, epistaxis and gastrointestinal bleeding as may also be observed in cyanotic patients.

The cause of polycythaemia could not be fully investigated in this patient due to the need for emergent surgery. A probable diagnosis of PV in its early stage or primary (idiopathic) polycythaemia was made for this case, as other causes of secondary polycythaemia were not elicited by history, examination and investigations. The patient was managed as one with polycythaemia with the possibility of PV in mind.

Treatment modalities for PV include repeated phlebotomy to achieve a haematocrit of less than 46%. Specific medications include hydroxyurea, a interferon and phosphorus 32. Hydroxyurea, the safest myelosuppressant available has been shown to be effective in 75% of patients with PV, while low molecular weight Dextran has been used to decrease the viscosity of blood. [6] However, none of these was administered to this patient. Preoperative phlebotomy was also not performed due to presence of unstable angina.

Major surgery in PV patients revealed significant mortality and morbidity attributed mainly to thrombosis and haemorrhage in an uncontrolled group versus controlled group (36% and 79% versus 5% and 28% respectively). [4] The authors advised myelosuppressants to achieve normal blood counts prior to surgery, avoidance of heat loss and circulatory stasis during surgery and rapid haemodilution with phlebotomy in emergent cases. [6],[7] In patients with uncontrolled PV undergoing above knee amputation, a multi­disciplinary approach and special assessment of coagulation and platelet function prior to surgery were suggested. [8] Prevention of deep vein thrombosis by preoperative phlebotomy, elastic stockings, intermittent pneumatic compression intraoperatively and early extubation has been suggested in a geriatric patient with PV who underwent transthoracic oesophagectomy, [9] as also in a patient who underwent prostatic surgery. [10]

There is lack of literature for anaesthetic management in patients with PV undergoing cardiac surgery. The only case reported is one who underwent CABG on cardiopulmonary bypass (CPB) following von Willebrand's disease complicated by PV and coronary thrombosis. The authors suggested prior control of the disease and use of factor VIII concentrate to prevent bleeding after CPB. [11]

Elective surgery should not be performed in uncontrolled PV in view of haemorrhagic and thrombotic complications, till the disease has been brought under control with hydroxyurea for six to eight weeks. In emergency conditions, as in the present case, isovolaemic phlebotomy should be performed prior to surgery. [6]

This is the first report of a patient with suspected PV undergoing OPCAB surgery. Literature has been reviewed as there is a paucity of such reports in the English literature. Phlebotomy after induction of anaesthesia, liberal perioperative fluid administration, maintenance of core temperature, early extubation, monitoring of myocardial ischaemia, infarction and vascular events, intense chest physiotherapy and early mobilization postoperatively formed the essential modes of care.

Cardiac surgery in patients with PV increases perioperative complications. A multimodal approach involving various specialities to confirm the diagnosis and control of the disease process prior to surgery and in the perioperative period is recommended.

   References Top

1.Berk PD, Goldberg JD, Donovan PS, et al. Therapeutic recommendations in polycythaemia vera based on polycythaemia vera study group protocols. Semin Hematol 1986; 23: 132-43.  Back to cited text no. 1    
2.Beutler E. Polycythaemia. In: Beutler E, Lichtmann MA, Coller BS, Kips TJ, Setibsohn U, eds. William Haematology. 6ed, New York: Mc GrawHill, 2001: 689­-701.  Back to cited text no. 2    
3.Polycythaemia and the heart: A review. Tex Heart Inst J 1994; 21: 198-201.  Back to cited text no. 3    
4.Wassermann LR, Gilbert HS. Surgical bleeding in polycythaemia vera. Ann New York Acad Sci 1964; 115: 122-38.  Back to cited text no. 4    
5.Adamson JW, Longo DL. Anaemia and polycythaemia. In: Braunwald E, Fauci AS, Kasper DL, eds. Harrison's principles of internal medicine, 15 th edition, New York; McGraw-Hill; 2001: 348-54.  Back to cited text no. 5    
6.Spivak JL. Polycythaemia vera and other myeloproliferative diseases. In: Braunwald E, Fauci AS, Kas per DL, eds. Harrison's principles of internal medicine, 15edition, New York; McGraw-Hill; 2001: 701-706  Back to cited text no. 6    
7.Cance. In: Stoelting RK, Dierdorf SF, eds. Anesthesia and coexisting diseases. 3rd ed, New York: Churchill Livingstone; 1993: 485-500.  Back to cited text no. 7    
8.Ahmad A, Shah AK. Perioperative management of a patient with uncontrolled polycythaemia vera for above knee amputation. J Pak Med Assoc 2004; 54: 34-36.  Back to cited text no. 8    
9.Katayama S, Kita T, Mammoto T, et al. Perioperative management for radical esophagectomy in a patient with polycythaemia vera. Masui 2001; 50 : 1345-47  Back to cited text no. 9  [PUBMED]  
10.Sois MB. Anaesthesia for polycythaemia vera. J Clin Anesth 1990; 2: 31-34.  Back to cited text no. 10    
11.Tsuruta Y, Uemura S, Fukuchi S, et al. A case of CABG in a patient complicated with von Willebrand's disease secondary to polycythaemia vera. Kyobu Geka 1995; 48: 329-31.  Back to cited text no. 11  [PUBMED]  

Correspondence Address:
Rajiv Juneja
Senior Consultant Anaesthesiologist, Escorts Heart Institute and Research Centre, Okhla Road, New Delhi 110025.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.37926

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