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• W4247395977 abstract "After general anesthesia, the clinical manifestations of polyuria have occasionally observed. However, because of the usual abrupt onset and rapid spontaneous remission, detailed investigations of polyuria have been limited. We present a case of severe polyuria after lung lobectomy and examine the etiology of the polyuria both endocrinologically and radiologically. We discuss the attributes of this polyuric manifestation. Case Report A 60-yr-old woman weighing 41 kg was discovered to have a coin lesion in the left upper lobe of the lung on chest roentgenogram (Figure 1). After transbronchial lung biopsy, she was scheduled for left upper lobectomy of the lung. The preoperative examination of the patient revealed no abnormalities except for the lung tumor. Of those examined preoperatively, electrolytes were as follows: serum sodium 140 mmol/L (normal 136-144 mmol/L), potassium 4.4 mmol/L (normal 3.7-4.9 mmol/L), chloride 103 mmol/L (normal 102-110 mmol/L). The patient was premedicated with hydroxydine 50 mg subcutaneously 1 h before arriving in the operating room, after which an epidural catheter was introduced at T5-6 and 0.125% bupivacaine was administered intraoperatively at a rate of 4.0 to 5.0 mL/h via the catheter. The patient was tracheally intubated with 200 mg thiopental and 6 mg vecuronium, followed by 0.8%-2.0% sevoflurane in 6 L/min O2 using a semiclosed circuit and the epidural infusion. Although arterial blood pressure decreased to 90/40 mm Hg 15 min after the first epidural administration, it recovered immediately with a 4-mg ephedrine injection. Blood pressure (BP) and heart rate (HR) were stable (BP 100/60 to 120/75 mm Hg, HR 60-75 bpm), and the saturated oxygen (SpO2) was kept at 100%. The total operative time was 4 h and 40 min. The patient inhaled sevoflurane for 4 h and 5 min (4.2 minimum alveolar anesthetic concentration [MAC] hours). Fluid balance during anesthesia was as follows: lactated Ringer's solution 1100 mL, acetated Ringer's solution 1000 mL, 5% plasma protein 250 mL, blood loss 230 g, and urine output 1100 mL.Figure 1: Chest roentgenogram. In the left upper lobe, a small coin lesion was found (arrow). Histologically, the resected tumor was diagnosed as a well differentiated adenocarcinoma.The resected tumor was localized to the left upper segment, in the S (1+2) area, and measured 1.7 x 1.5 x 1.5 cm. It did not involve the pleura or the regional lymph nodes. The pathologic findings revealed a highly differentiated lung adenocarcinoma. On Day 1 postoperatively, the patient's daily urine volume was 7500 mL. She complained of polydipsia and severe general fatigue. Because the hourly urine volume was more than 500 mL and central venous pressure was decreased 30-40 mm H (2) O, rapid fluid replacement was administered for the prevention of dehydration. Laboratory values, which were mildly controlled by the fluid replacement, were as follows: red blood cell count 3.46 x 106/micro L (normal 3.7-4.9 x 106/micro L), white blood cell count 9.2 x 103/micro L (normal 3.0-9.4 x 103/micro L), hematocrit 31.4% (normal 35%-44%), hemoglobin 10.9 g/dL (normal 11.5-14.5 g/dL), serum sodium 143 mmol/L, serum potassium 4.2 mmol/L, serum chloride 105 mmol/L, blood urea nitrogen 4.3 mg/dL (normal 8.1-22 mg/dL), serum creatinine 0.43 mg/dL (normal 0.44-1.04 mg/dL), fasting blood glucose 105 mg/dL (normal 65-105 mg/dL); urine N-acetyl-beta-glucosaminidase 1.8 IU/L (normal 1.1-20.3 IU/L), urine beta2-microglobulin 0.07 mg/dL (normal <0.2 mg/dL). Liver function tests were within normal limits. The endocrinologic data under 6-h water deprivation are shown in Table 1. The serum osmolality increased to 300 mOsm/kg. The urine osmolality decreased to 140 mOsm/kg, and the plasma arginine vasopressin (AVP) concentration was 1.1 pg/mL. The serum cortisol concentration was increased at 26.0 micro g/dL, presumably because of the postoperative stressful state. The plasma renin activity and the aldosterone concentration decreased because of the hyperosmolar state. Thyroid hormones, catecholamines, and other pituitary hormones were normal. The patient was treated with desmopressin (DDAVP), and sequential hourly urine volume diminished significantly (before: 600 mL, 4 h after: 40 mL), and the hourly urine osomolality increased (before: 128 mOsm/kg, 4 h after: 724 mOsm/kg) (Figure 2). A loading test of 5% sodium chloride was given, which resulted in a smaller increase in AVP levels in response to the high serum osmolality (Figure 3a). Cranial magnetic resonance imaging (MRI) exhibited a slightly decreased signal in the high-intensity posterior pituitary region on the T1-weighted images (Figure 4A) and showed mild swelling of the pituitary gland and pituitary stalk on the gadolinium enhanced image (Figure 4B). The patient's daily urine volume was maintained at approximately 4000-5000 mL with DDAVP at doses up to 30 micro g for 14 days postoperatively, and then gradual improvement of urine volume and osmolality was spontaneously shown (Figure 5). The 5% sodium chloride loading test was repeated 1, 2, and 10 mo (Figure 3b, c, and d) after the operation, and the AVP secretory response to high serum osmolality gradually increased, particularly 10 mo after the operation. Cranial MRI 2 mo after the operation exhibited diminished volume of the pituitary gland with a slender pituitary stalk in comparison with previous MRI findings (Figure 4C). The patient had a normal urine volume and no complaints 10 mo after the operation without DDAVP treatment.Table 1: Endocrinologic Data at the Onset of PolyuriaFigure 2: Desmopressin (DDAVP) loading test. Intranasal desmopressin effectively changed the urine volume and urine osmolality. Hourly urine volume was decreased from 600 mL to 40 mL for 4 h. Urine osmolality was elevated from 128 mOsm/kg to 724 mOsm/kg after 4 h.Figure 3: 5% sodium chloride loading test. Upon the manifestation of polyuria, the arginine vasopressin (AVP) secretive response to 5% sodium chloride was lowered (a); 1 mo (b), 2 mo (c), and 10 mo after (d), the AVP response was gradually improved. The dotted area shows the normal range for the ratio of AVP concentration to serum osmolality [8].Figure 4: The sequential cranial magnetic resonance imaging findings. At the onset of polyuria, the pituitary gland exhibited a decreased high-intensity signal (arrow) on the T1-weighted image (A) and slight swelling of the pituitary gland (small arrow) and stalk (large arrow) on the gadolinium-enhanced image (B). Two months later, the pituitary gland (small arrow) was diminished with a slender stalk (large arrow) on the gadolinium-enhanced image (C).Figure 5: The clinical course. One day after the surgery, the patient abruptly manifested polyuria, 7500 mL/day. She received fluid replacement to prevent dehydration. Desmopressin (DDAVP) was administered intranasally for the control of urine volume. Approximately 2 wk after the onset of polyuria, her urine volume was decreased without desmopressin, and 1 mo after that, it was completely normalized. Daily urine volume (UV) is shown as closed column, and daily fluid replacement volume (DIV) is shown as open column.Discussion After general anesthesia, the manifestation of polyuria is sometimes observed. The onset is abrupt and within several days after the operation. In cases of brain surgery involving the pituitary gland or hypothalamus, the postoperative central diabetes insipidus (DI) is easily recognizable; however, anesthetic and operatic procedures, except for cranial surgery, rarely affect water balance. In this procedure, among the factors affecting water balance were blood and fluid loss, excessive fluid transfusion, anesthetics, unexpected brain damage, and previously undetected DI. In the present case, as in the preceding description, blood loss, excessive transfusion, and brain metastasis within one year after the operation were negative, but we could not exclude the manifestation of an unexpected DI. Although operative stress and damage, particularly in thoracic surgery, affects the baroreceptor and AVP inhibitory vagal nerve in thorax [1], the symptomatic feature is usually a syndrome of inappropriate secretion of antidiuretic hormone rather than polyuria. This is also in agreement with cases with hormone producing neoplasm, e.g., antidiuretic hormone secreting oat cell carcinoma in lung. In this patient, sevoflurane was used for general anesthesia. Sevoflurane is one of the inhaled fluorinated anesthetics that rarely causes polyuria [2]. However, the pathogenesis of polyuria has not been clarified, and sevoflurane has not been shown to produce renal impairment, despite its administration to approximately 2 million patients in Japan. Biotransformation of the fluorinated volatile anesthetics results in the production of fluoride metabolites, which may be associated with hepatic or renal toxicity [3,4]. Sevoflurane undergoes hepatic biotransformation in humans, producing peak plasma inorganic fluoride concentrations similar to those associated with renal impairment after methoxyflurane anesthesia [5,6]. In the case of methoxyflurane, biotransformation by the renal cytochrome P450 is believed to be closely associated with renal damage [4-6]. In the case of enflurane, which is also a fluorinated anesthetic, the mechanism of polyuric renal impairment is controversial [7]. Previous investigations suggest that renal tubular damage is due to a direct toxic effect of these drugs rather than to the inorganic fluoride ion produced when they are metabolized. The patient's renal function tests (serum creatinine, blood urine nitrogen, and urinary N-acetyl-beta-glucosaminidase and beta2-microglobulin both) at the onset of polyuria and at two months showed no abnormalities. The polyuria was diagnosed as partial central DI because of the blunted AVP-secretory response to hyperosmolality [8] and to the adequate renal concentrating response to exogenous vasopressin. In a study by Murakawa et al. [9] of 24 patients who underwent sevoflurane anesthesia, no significant pre- or postoperative changes in plasma AVP or human atrial natriuretic peptide levels were reported. Although the present case also showed a normalranged AVP concentration at the onset of polyuria, a precise examination of the correlation with osmolality using the sodium loading test proved an impaired AVP-secretory capacity. On the other hand, the remarkable improvement of AVP response on sodium loading tests in 10 months obscures a presumable preoperative impairment of AVP secretion. A pituitary MRI finding at the onset of polyuria showed a slight decrease of high intensity in the posterior lobe on T1-weighted images, which indicates the diminished AVP-neurosecretory granules [10]. It also showed a mild swelling of the pituitary gland and stalk on the gadolinium-enhanced images. Moreover, two months of postoperative images exhibited diminished volume of the pituitary gland and stalk. The sequential change in the pituitary MRI findings strongly suggests that the central DI in this case was closely associated with infundibulo-neurohypophysitis, which is a known cause of idiopathic [11] or autoimmune-associated central DI [12]. Although postoperative polyuria tends to be underestimated because of its reversibility and the lack of apparent renal damage, further examination of both pituitary function and AVP responsiveness is necessary to clarify the pathogenesis. Fortunately, we could examine a patient with postanesthetic polyuria, which was diagnosed as attributable to partial central DI; however, we cannot completely determine what caused the central DI. To exclude the unexpected factors, inducing water imbalance, other than sevoflurane anesthesia, and to determine this pathogenesis, further studies including the AVP-secretory response toward high osmolality or water deprivation on cases of postoperative and postanesthetic polyuria are necessary." @default.
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• W4247395977 title "Postanesthetic Polyuria Attributable to Central Diabetes Insipidus" @default.
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