Asian Cardiovasc Thorac Ann 2007;15:e52-e54
© 2007 Asia Publishing EXchange Ltd
Leukocytosis Caused by Tropical Splenomegaly During Cardiopulmonary Bypass
Prabhat Tewari, MD,
Pramod Mittal, MCh1,
Shiv B Singh, BSc2
Department of Anaesthesiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow
1 Escorts Heart hospital, Faridabad
2 Perfusion Department, Department of Cardiothoracic and Vascular surgery, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India
For reprint information contact: Prabhat Tewari, MD Tel: 44 115 969 1169 ext 45637 Fax: 44 115 962 7713 Email: ptewari123{at}yahoo.co.in, Department of Anaesthetics, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, United Kingdom.
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ABSTRACT
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We describe two patients undergoing cardiac surgery under cardiopulmonary bypass with concomitant enlarged tropical spleen. Volume overload and leukocytosis occurred during pump management. In the first patient this resulted in acute lung injury, but in the second case methods to reduce the impact of leukocytosis were taken, resulting in a normal postoperative course.
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INTRODUCTION
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Cardiopulmonary bypass (CPB) during heart surgery encompasses the knowledge of the total blood volume of the patient, the desired flow on the circuit, and the hematocrit after dilution of the blood volume in the circuit. These parameters are calculated initially on the basis of body weight, height, and body surface area, and subsequently the measured values are adjusted according to the circumstantial requirement. We describe two consecutive patients with massive tropical splenomegaly who were operated for different cardiac ailments with CPB, and both had problems of overwhelming volume in the circuit. Both patients had marked leukocytosis, and the first patient developed acute lung injury (ALI) in the postoperative period.
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CASE 1
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A 28-year-old, 68 kg male patient with massive tropical splenomegaly underwent aortic valve replacement under cardiopulmonary bypass. He had no other associated problems except raised IgM levels and had been treated with antimalarials. General anesthetics were planned, and routine monitoring included intra-arterial blood pressure, pulmonary artery and capillary wedge pressure, central venous pressure, and cardiac output (thermodilution technique) monitoring. Hypothermic CPB with cold blood cardioplegia was used. The lowest nasopharyngeal temperature attained was 30°C. Once the patient was placed on CPB, an overwhelming volume (4 litres) drained in the reservoir. During CPB, sodium nitroprusside (SNP) infusion was used and the perfusion pressure was maintained in the range of 40–50 mm Hg with the help of a noradrenaline infusion. The values of hemoglobin and the leukocyte levels are shown in Table 1
. At the end of surgery the patient was rewarmed and weaned off CPB. All the extra volume was used in maintaining adequate filling of the heart without any adverse events. In the postoperative period the patient developed ALI with leukocytosis, fever, infiltrates in the lungs, and low blood gases on high-inspired oxygen percentages (PaO2/FiO2 < 240) after 10 hours. The management of this inflammatory response included assisted ventilation with PEEP (170 hours), steroids, inotropes, antibiotics, diuretics, and physiotherapy. The patient remained in the intensive care unit (ICU) for 15 days.
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CASE 2
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A 33-year-old, 62 kg female patient with massive tropical splenomegaly presented for mitral valve replacement. She had been treated with a long course of antimalarials and had raised IgM levels but other parameters were within normal limits. General anesthetics were planned, and routine monitoring included intra-arterial blood pressure, pulmonary artery and capillary wedge pressure, central venous pressure, and cardiac output (thermodilution technique) monitoring. Hypothermic CPB with cold blood cardioplegia was used and the lowest nasopharyngeal temperature attained was 29°C. Once the patient was placed on CPB, it was found that 4.2 litres of volume drained in the reservoir. Her hemoglobin and leukocyte levels at different times are shown in Table 1
. In this case, perfusion management included venovenous filtration from commencement of CPB using a Pall LeukoGuard® arterial line leukocyte depletion filter (LDF) (Pall Biomedical Ltd, Portsmouth, UK) in the circuit. The patient was given 500 mg of methylpredisone in the pump. The perfusionist filtered 2 litres of the fluid from the pump. The perfusion pressure was maintained in the range of 40–50 mm Hg. At the end of surgery the patient was re-warmed and weaned off CPB. All the extra volume in the pump was sent to the blood bank for cell separation and only washed red cells were transfused using LDF. The patient needed extra fluids to maintain filling pressures during the post bypass period. This patient had no postoperative problems, and tracheal extubation was performed within six hours. The postoperative course was uneventful.
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DISCUSSION
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The sequestration of unusually large amounts of blood in the reservoir in these patients could be explained by the spleen contributing to the total blood volume. In man there is no definite evidence of contraction of the normal spleen but pathologically enlarged spleens have been shown to contract with epinephrine to expel blood into the circulation.1 This is not an active, forceful, muscular contraction of very thin muscle fibers of human spleen; instead it is due to marked constriction of the splenic artery and its intra-splenic branches with a resultant passive deflation of the organ. The presence of elastic tissue in the capsule and the trabeculae of the enlarged spleen assist in this passive deflation.2 During initiation of bypass it has been found that there is intense sympathetic discharge in the form of raised epinephrine levels which facilitates expulsion of a large amount of blood in the circulation.3
Giant splenomegaly is a disease of adults in endemic malarial areas and is usually due to an abnormal immune response to repeated attacks of malaria. The condition needs to be differentiated from other etiologies such as parasitemia (kala azar, schistosomiasis), non-tropical idiopathic splenomegaly, and certain malignancies. Raised IgM levels, antimalarial antibodies, and response to treatment with antimalarials ascertain the malarial etiology. The disease runs a benign course but sometimes patients present with anemia and signs of hypersplenism with leukopenia and thrombocytopenia. Neither of our cases showed these signs. These patients are also more prone to secondary bacterial infections of the skin and respiratory tract, and have an increased mortality.
Leukocytosis with an increase in neutrophils and lymphocytes seen in both these patients seems to result from contribution of the spleen. It is well known that activation of the immune system occurs when the patients blood comes in contact with the extracorporeal circuit.4 Activated neutrophils are known to elicit endothelial dysfunction via secretion of proteolytic enzymes, such as elastase, or oxygen radicals, followed by edema and tissue destruction.5 Besides the systemic negative impact of CPB-related neutrophil activity, it is proposed that neutrophils damage cardiac and lung tissue during reperfusion.6 In malarial spleens B cell lymphocytosis is seen as there is suppression of T cells. However, reduction of T cells has also been seen as a normal sequelae of CPB, with trends revealing an antiinflammatory pathway mediating a humoral immune response.
The leukocytes remained in the peripheral circulation in these patients. In the second patient venovenous filtration probably filtered out inflammatory markers, shown as low levels of highly sensitive (hs) C reactive protein and interleukin 8. Significant reduction in leukocyte numbers occurs when LDF is used but it is not clear whether it assists in reducing inflammatory markers or in leukocyte activation. However, several studies have shown that LDF can result in leukocyte activation.7,8 The LDF concept may be more significant in longer bypass and also when their function is optimized.8 In our second patient LDF reduced leukocyte numbers significantly. Secondly, venovenous filtration has been shown to reduce inflammatory markers. Additionally, cell numbers were reduced by cell separation and washing the remaining pump blood which was then transfused to the patient.
We can conclude that in Asian countries patients with tropical large spleen may undergo cardiac surgery. As the enlarged spleens can give rise to leukocytosis, appropriate management is essential to effect leukocyte depletion and reduce the chances of ALI.
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REFERENCES
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- Miller DK, Rhoads GP. The effect of splenic contraction on the formed elements of the blood in a case of anaemia and splenomegaly. J. Clin. Invest. 1933;12:1009–12[Medline]
- Schaffner A, Augustiny N, Otto RC, Fehr J. The hypersplenic spleen. A contractile reservoir of granulocytes and platelets. Arch Intern Med 1985:145:651–4.[Abstract/Free Full Text]
- Tan CK, Glisson SN, EI-Etr AA, Ramakrishnaiah KB. Levels of circulating norepinephrine and epinephrine before, during, and after cardiopulmonary bypass in man. J Thorac Cardiovasc Surg 1976;71:928–31.[Abstract]
- Butler J, Rocker GM, Westaby S. Inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 1993;55:552–9.[Abstract]
- Carden D, Xiao F, Moak C, Willis BH, Robinson-Jackson S, Alexander S. Neutrophil elastase promotes lung microvascular injury and proteolysis of endothelial cadherins. Am J Physiol 1998;275(2 pt 2):H385–92.[Medline]
- Matheis G, Scholz M, Simon A, Henrich D, Wimmer-Greinecker G, Moritz A. Timing of leukocyte filtration during cardiopulmonary bypass. Perfusion 2001;16 Suppl:31–7.[Abstract/Free Full Text]
- Baksaas ST, Flom-Halvorsen HI, Ovrum E, Videm V, Mollnes TE, Brosstad F, et al. Leucocyte filtration during cardiopulmonary reperfusion in coronary artery bypass surgery. Perfusion 1999;14:107–17.[Abstract/Free Full Text]
- Moreno JB, Margraf S, Schuller AM, Simon A, Moritz A, Scholz M. Inhibition of neutrophil activity in cardiac surgery with cardiopulmonary bypass: a novel strategy with the leukocyte inhibition module. Perfusion 2004;19:11–6.[Abstract/Free Full Text]