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Pituitary Apoplexy After Surgical Treatment of Lung Cancer

2014; Elsevier BV; Volume: 98; Issue: 5 Linguagem: Inglês

10.1016/j.athoracsur.2013.12.056

1552-6259

Mitsuru Yoshino, Yasuo Sekine, Eitetsu Koh, Atsushi Hata, Naotake Hashimoto,

Myasthenia Gravis and Thymoma

Pituitary apoplexy is a rare but potentially life-threatening condition caused by the sudden enlargement of a pituitary adenoma secondary to infarction and hemorrhage. Surgical stress is 1 cause of pituitary apoplexy, but asymptomatic pituitary adenomas are difficult to diagnose preoperatively. Here we report a case of a 78-year-old male who had postoperative pituitary apoplexy after surgery for lung cancer. He underwent right upper and middle lobectomy and lymph node dissection for squamous cell carcinoma with obstructive pneumonia. On the sixth postoperative day he developed sudden-onset fever, respiratory distress, and polyuria. Brain magnetic resonance imaging revealed an enlarged, hemorrhagic pituitary gland. He was treated with steroid hormone replacement. Subsequent endocrine hormone stress tests revealed recovery of his pituitary function. Based on his clinical course, the patient was diagnosed with acute adrenal insufficiency and diabetes insipidus due to pituitary apoplexy. Pituitary apoplexy is a rare but potentially life-threatening condition caused by the sudden enlargement of a pituitary adenoma secondary to infarction and hemorrhage. Surgical stress is 1 cause of pituitary apoplexy, but asymptomatic pituitary adenomas are difficult to diagnose preoperatively. Here we report a case of a 78-year-old male who had postoperative pituitary apoplexy after surgery for lung cancer. He underwent right upper and middle lobectomy and lymph node dissection for squamous cell carcinoma with obstructive pneumonia. On the sixth postoperative day he developed sudden-onset fever, respiratory distress, and polyuria. Brain magnetic resonance imaging revealed an enlarged, hemorrhagic pituitary gland. He was treated with steroid hormone replacement. Subsequent endocrine hormone stress tests revealed recovery of his pituitary function. Based on his clinical course, the patient was diagnosed with acute adrenal insufficiency and diabetes insipidus due to pituitary apoplexy. Pituitary apoplexy (PA) is a rare but potentially life-threatening clinical syndrome caused by the sudden enlargement of a pituitary adenoma secondary to infarction and hemorrhage [1Cardoso E.R. Peterson E.W. Pituitary apoplexy: a review.Neurosurgery. 1984; 14: 363-373Crossref PubMed Scopus (322) Google Scholar, 2Bills D.C. Meyer F.B. Laws Jr., E.R. et al.A retrospective analysis of pituitary apoplexy.Neurosurgery. 1993; 33: 602-608Crossref PubMed Scopus (348) Google Scholar]. Although surgical stress is 1 cause of pituitary apoplexy, this syndrome has never been reported after lung cancer resection. Here, we present the case of a 78-year-old male who had postoperative pituitary apoplexy, presenting as high-grade fever, respiratory insufficiency, and polyuria after surgical resection of lung cancer. A 78-year-old male presented with evidence of a large tumor and atelectasis of the right upper lobe on chest computed tomography (CT). Bronchoscopic examination was performed and cytologic evaluation revealed squamous cell carcinoma. The final clinical stage was c-T3N1M0 stage IIIA. One week before the scheduled resection, the patient was urgently hospitalized due to high-grade fever. Laboratory evaluation indicated a remarkable inflammatory reaction suggested by elevated white blood cell count and C-reactive protein. Chest CT revealed a rapid increase in the size of the tumor shadow and an obstructive pneumonia with pulmonary abscess. Right upper and middle lobectomy and lymph node dissection was urgently performed. The final histologic diagnosis was clear cell squamous cell carcinoma. After resection, the patient's body temperature immediately normalized and his general condition improved. However, on the sixth postoperative day he developed sudden-onset high-grade fever (approximately 40°C) and oxygenation desaturation. Blood cell counts and chemistry showed an excessive inflammatory reaction and accelerated coagulation suggested by decreased thrombin time and activated partial thromboplastin time; hence, disseminated intravascular coagulation was suspected. In addition, he was found to be hyponatremic (serum sodium 120 mEq/L) and hyperkalemic (serum potassium 5.3 mEq/L). At approximately the same time, his urine volume suddenly increased (Fig 1A). Further labs showed low levels of blood and urine cortisol and adrenocorticotropic hormone, and low-normal levels of antidiuretic hormone (arginine vasopressin [AVP]). Despite the low level of AVP, serum osmotic pressure was high. Hence, a defect in AVP secretion was suspected (Fig 1B). Preoperative brain magnetic resonance imaging (MRI) showed a slightly enlarged pituitary gland (11 mm in diameter) with no evidence of adenoma (Fig 2A). A repeat MRI taken after the diagnosis of acute adrenal insufficiency revealed a mass lesion of 13 mm in the pituitary fossa. A high intensity area was seen inside the pituitary gland on the T1 weighted image, and hemorrhage of a pituitary adenoma was suspected due to the enhanced border (Figs 2B, 2C). Together these findings suggested pituitary apoplexy. Acute respiratory distress syndrome and acute adrenal insufficiency with diabetes insipidus due to the acute pituitary gland hemorrhage (pituitary apoplexy) were suspected. Ventilatory support was started and steroid pulse therapy (hydrocortisone 200 mg/day) and Sivelestat (a neutrophil elastase inhibitor; Sigma-Aldrich, St. Louis, MO) were administered. After 3 days, hydrocortisone was gradually tapered to 25 mg/day. Intranasal dDAVP (1-deamino-8-D-arginine vasopressin) was administered for the treatment of central diabetes insipidus. Subsequently, the patient's urine volume decreased and his serum electrolyte balance improved (Fig 1). After the patient's signs and symptoms improved, 4 endocrine hormone stress tests were performed. Adrenocorticotropic hormone, prolactin, cortisol, thyroid-stimulating hormone, gonadotropin (luteinizing hormone and follicle-stimulating hormone) and growth hormone were measured after corticotropin-releasing hormone, growth hormone releasing hormone, luteinizing hormone-releasing hormone and thyrotropin-releasing hormone loading. Results revealed a recovery of pituitary gland function. Four months after the operation, a follow-up brain MRI showed resolution of the intrapituitary hemorrhage. Although different predisposing events have been implicated in PA, the pathogenesis remains unclear [1Cardoso E.R. Peterson E.W. Pituitary apoplexy: a review.Neurosurgery. 1984; 14: 363-373Crossref PubMed Scopus (322) Google Scholar]. Bailey first described the syndrome in a 50-year-old acromegalic male in 1898, and PA was discovered during autopsy [3Bailey P. Pathological report of a case of acromegaly, with special reference to the hypophysis cerebri and in the thyroid gland; a case of haemorrhage into the pituitary.Philadelphia Med J. 1898; 1: 789-792Google Scholar]. Pituitary apoplexy was first named by Brougham and colleagues in 1950 [4Brougham M. Heusner A.P. Adams R.D. Acute degenerative changes in adenomas of the pituitary body—with special reference to pituitary apoplexy.J Neurosurg. 1950; 7: 421-439Crossref PubMed Scopus (204) Google Scholar]. In addition to pituitary insufficiency, the pathologic syndrome is characterized by headache (76%), visual field defect (62%), ocular palsy (40%), nausea and vomiting (21%), altered mental status (19%), and hemiparesis (4.3%) [5Nichols B.D. Romanchuk K.G. Pituitary apoplexy presenting with light-near dissociation of pupils.J Clin Neuroophthalmol. 1987; 7: 139-144Crossref PubMed Google Scholar]. During an acute episode, the expanding pituitary mass may compress surrounding structures such as the cavernous sinus and neurovascular bundle, resulting in cranial nerve palsies and ophthalmoplegia. Causes of PA include radiation therapy, head injury, estrogen replacement, cerebrovascular imaging, anticoagulant therapy, pregnancy, lumbar puncture, myelography, infection, hypertension, diabetes, and hormone load examination. In addition, PA can be precipitated by various types of surgical stress including cardiac surgery [6Hidiroglu M. Kucuker A. Ucaroglu E. Kucuker S.A. Sener E. Pituitary apoplexy after cardiac surgery.Ann Thorac Surg. 2010; 89: 1635-1637Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar], abdominal surgery, thyroidectomy [7Kato K. Nobori M. Miyauchi Y. et al.Pituitary apoplexy after subtotal thyroidectomy.Int Med. 1996; 35: 472-477Crossref PubMed Scopus (10) Google Scholar], and laparoscopic lumbar spinal fusion. To our knowledge, this is the first reported case of pituitary apoplexy after lung cancer resection. Generally, patients have no history of pituitary disease prior to developing acute onset PA. A recent study suggests that 20% of patients with PA become symptomatic, and no precipitating cause can be identified in 9.5% of patients with PA [1Cardoso E.R. Peterson E.W. Pituitary apoplexy: a review.Neurosurgery. 1984; 14: 363-373Crossref PubMed Scopus (322) Google Scholar]. It has been suggested that pituitary adenomas have a relatively compromised blood supply. Hence, constriction of any abnormal vessels in the pituitary gland might lead to ischemia, necrosis, and hemorrhage. History of cerebral vascular damage, disordered coagulation, and intracardiac thrombi can predispose patients to PA. Cardoso and Peterson [1Cardoso E.R. Peterson E.W. Pituitary apoplexy: a review.Neurosurgery. 1984; 14: 363-373Crossref PubMed Scopus (322) Google Scholar] have postulated that an intrinsic vasculopathy of pituitary adenomas renders them more susceptible to infarction or hemorrhage. In our case, preoperative brain MRI revealed a minor enlargement of the pituitary gland, suggesting the presence of a small adenoma. In such cases, it remains difficult to assess the risk of PA preoperatively. Standard treatment of PA includes removal of the hemorrhagic pituitary gland and induction of hormone replacement therapy. However, many patients recover naturally so surgical treatment is not always necessary. In our case, the patient developed signs of hypopituitarism, such as diabetes insipidus and adrenal insufficiency, but did not develop visual field defects or headache. Therefore, the pressure by the hematoma was thought to be mild and the hemorrhagic gland was not removed. The diagnosis of PA may be delayed due to its nonspecific neurologic features. However, CT and MRI are effective means of radiologic diagnosis. By demonstrating an increased T1 signal intensity, MRI is superior to CT in identifying the hemorrhagic nature of the tumor [2Bills D.C. Meyer F.B. Laws Jr., E.R. et al.A retrospective analysis of pituitary apoplexy.Neurosurgery. 1993; 33: 602-608Crossref PubMed Scopus (348) Google Scholar]. Although a clear cause for the precipitation of PA may be elusive, early recognition and treatment is of paramount importance. Pituitary apoplexy is a rare but potentially life-threatening clinical syndrome. Surgical stress is one of the causes of pituitary apoplexy, but this syndrome has never been reported after lung cancer resection. The possibility of PA should be kept in mind. The diagnosis of PA may be delayed due to its nonspecific neurologic features but in such a case MRI is useful.