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• W4253922795 abstract "EDITOR: Neutropenia and/or pancytopenia developing during operation, or soon afterwards, may pose a diagnostic challenge to anaesthesiologists. Interventions, such as blood transfusion (transfusion associated graft vs. host disease) or drugs, such as anaesthetics (nitrous oxide) or antibiotics (cephalosporins) as well as patient factors, such as paroxysmal nocturnal haemoglobinuria or aplastic anaemia, can cause neutropenia or pancytopenia [1-7]. A 31-yr-old female was admitted to the Anaesthesiology Intensive Care Unit (ICU) after maxillary reconstruction with flap operation. Adenocarcinoma had been diagnosed in 1997. She was not receiving any medication before operation; her preoperative laboratory tests were normal, including total white blood cell count of 5600 cells mm−3, haemoglobin 10.7 gm dL−1, platelets 239 000 dL−1. The patient's trachea was intubated using a fibrescope after propofol 200 mg, succinylcholine 50 mg, cefazolin 1 g and fentanyl 50 μg had been given intravenously (i.v.). General anaesthesia was maintained with sevoflurane 2-3% in O2 and 2 L min−1 and N2O 4 L min−1; vecuronium was used for further muscle paralysis. Cefazolin 1 g was repeated twice intraoperatively and was continued postoperatively 1 g three times per day. The intraoperative course during 7 h of surgery was especially notable for blood loss (estimated to be approximately 1800 mL) which necessitated the administration of 4 U of non-irradiated packed red blood cells, fresh frozen plasma 2 U, crystalloids 5 L, hydroxyethylstarch 500 mL. Intraoperatively, multiple complete blood counts were ordered (Table 1). The patient arrived in the Anaesthesiology ICU awake, well oxygenated and with a stable cardiovascular system. During the first postoperative day, her white cell count and haemoglobin concentration progressively declined and reached a nadir on the third postoperative day. Serum lactate dehydrogenase (peaked at 1975 U L−1) and bilirubin concentration (peak total bilirubin 24.5 mg dL−1, peak direct bilirubin 19.38 mg dL−1) progressively increased together with dark urine, strongly positive for bilirubin. A peripheral smear revealed hypochromic, micrositic anisocytosis with 40% polymorph nuclear leucocytes, 52% atypical lymphocytes and 0.8% monocytes. Fine needle bone marrow aspiration showed fibrosis and aplastic bone marrow. Four units of antibody and subgroup cross-matched irradiated packed red blood cells were given. Prothrombin time, International Normalized Ratio, activated prothrombin time, serum haptoglobulin concentrations, serum folic acid and vitamin B12 concentrations were normal. Serum fibrinogen 747 (normal 144-430 mg dL−1) and D-dimer concentrations 6.4 (0.0-0.5 ng dL−1) were elevated, whereas thrombin time 14.2 (15-22 s) and antithrombin III activity 72 (80-120%) were low. Direct and indirect Coombs tests were negative. Other laboratory findings included the following: alanine aminotransferase 18 U L−1, aspartate aminotransferase 59 U L−1 and alkaline phosphatase 140 U L−1.Table 1: Perioperative complete blood count changes.On the third postoperative day spiked fever developed with a maximum body temperature of 38.8°C and neutropenic fever was diagnosed. Results of blood, sputum, wound, stool and urine cultures were negative. Serums for viral titres (cytomegalovirus, Epstein-Barr virus and hepatitis B virus) were not indicative of acute or past infection. The haematology department was consulted and bone marrow biopsy showed fatty tissue with rare mature bone marrow elements. Granulocyte colony-stimulating factor (30 mU day−1) was administered i.v. together with amikacin (1 g day−1) and cefepime (2 × 2 g). Serum bilirubin and lactate dehydrogenase concentrations progressively decreased to normal while her white cell count and haemoglobin concentration increased. Antibiotics were discontinued and she was transferred to the plastic surgery ward on the eighth postoperative day and from the hospital on the eighteenth postoperative day. In our patient, the decrease in haemoglobin concentration and white cell and platelet counts, and the peripheral smear findings and aplastic bone marrow all suggested the diagnosis of acute acquired aplastic anaemia. Acquired aplastic anaemia can be idiopathic or secondary to radiation, paroxysmal nocturnal haemoglobinuria, pregnancy, many classes of pharmaceutical agents, viruses or immune diseases [1]. Transfusion associated graft vs. host disease, paroxysmal nocturnal haemoglobinuria and drugs (nitrous oxide, antibiotic therapy) were probably the cause of the acquired aplastic anaemia. Paroxysmal nocturnal haemoglobinuria is a rare acquired disorder of bone marrow stem cells resulting in the production red cells, granulocytes and platelets with both membrane and enzyme defects causing abnormal sensitivity to complement fixation [2]. These patients are particularly at risk for haemolysis and thrombosis as a result of surgery and anaesthesia [2,3]. We first entertained the diagnosis of paroxysmal nocturnal haemoglobinuria when our patient developed Coombs negative haemolysis and pancytopenia with a hypoplastic bone marrow but then had to exclude it because of the normal Ham's (acidified serum) and sucrose haemolysis tests. Transfusion associated graft vs. host disease may occur in presumed immunocompetent patients (patients after cardiac surgery) receiving non-irradiated blood products [4]. Clinical features include pancytopenia, fever, pruritus, rash, abnormal results of liver function tests, dyspnoea and gastrointestinal symptoms such as nausea, vomiting, anorexia and diarrhoea [4]. Our patient complained of nausea, vomiting and abdominal discomfort that we thought were common postoperative problems. We suspected the diagnosis of acute graft vs. host disease after considering the chronology of events (blood transfusion, elevated aspartate aminotransferase, bilirubin concentration, pancytopenia with aplastic bone marrow) and so we gave only irradiated blood products after operation as irradiation of blood products is recommended for the prevention of this disease. But there was no rash or pruritus, and, fortunately, our patient improved after granulocyte colony-stimulating therapy and survived; therefore, we thought diagnosis of acute graft vs. host disease in our patient was unlikely. The possibility of nitrous oxide induced bone marrow suppression cannot be entirely excluded [7]; however, it is extremely unlikely that this could have occurred only 1 h after nitrous oxide administration. In fit patients undergoing elective surgery, a period of at least 5-6 h exposure to 50% nitrous oxide in 50% oxygen is required before megaloblastic changes in bone marrow occur [7]. The white cell count did not return to normal after cessation of nitrous oxide, vitamin B12 and folic acid concentrations were normal and the bone marrow did not show any megaloblastic changes [7]. Neutropenia seems to be related to the use of cefazolin sodium in our patient. Neutropenia secondary to antibiotic administration is thought to result primarily from an immunological reaction with latent period of 7-14 days after the first exposure or immediately after re-exposure [5,6]. The precipitous fall in white cell count within 2 h of cefazolin administration suggested prior exposure; and old medical records documented the use of cefazolin for prophylaxis in the previous operation. But, our patient did not have the rash, pruritus or eosinophilia that is common in antibiotic associated neutropenia. As a result, we would like to point out that anaesthesiologists should be aware that cefazolin can cause perioperative neutropenia. Not only haemoglobin and platelets but also haematological indices, such as white blood cell counts, should be monitored when cefazolin is given for surgical prophylaxis in patients undergoing major surgery. S. B. Akinci T. Aykut A. Gozacan M. Kanbak S. Ozgen Ü. Aypar Department of Anesthesiology and Reanimation Hacettepe University, Ankara, Turkey" @default.
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• W4253922795 title "Perioperative neutropenia" @default.
• W4253922795 doi "https://doi.org/10.1017/s026502150423112x" @default.
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