|Year : 2007 | Volume
| Issue : 2 | Page : 143
Laparoscopic Bilateral Adrenalectomy in a patient of Cushing syndrome: A Challenge for the Anaesthesiologist
Uma K Dahanukar1, Kedar S Joshi1, Vishakha Desai1, Usha D Padhye2, Arun D Joshi2, AM Deshpande3
1 D.A., D.N.B. Resident, Department of Anaesthesiology, Maharashtra Medical Foundation, Pune, Maharashtra, India
2 M.D., D.A. Senior Consultant, Department of Anaesthesiology, Maharashtra Medical Foundation, Pune, Maharashtra, India
3 M.D. D.A. Professor and head, Department of Anaesthesiology, Maharashtra Medical Foundation, Pune, Maharashtra, India
|Date of Acceptance||15-Feb-2007|
|Date of Web Publication||20-Mar-2010|
A M Deshpande
"Sammohini" bungalow, 720/4, Navi-Peth, Pune-411030, Maharashtra
We present a case of Cushing syndrome who underwent laparoscopic bilateral adrenalectomy and discuss her intraoperative management and postoperative course in ICU, especially pulmonary oedema, that occurred within 3 hours after resection (half life of cortisol is 80-110 minutes).  She was diagnosed to have bilateral adrenal hyperplasia with no pituitary involvement on CT scan. Preoperative workup revealed hypokalemia, anaemia, hypertension and hyperglycemia. She was posted for laparoscopic bilateral adrenalectomy. She received general anaesthesia; we did not give epidural analgesia as the patient had fracture of body of L1 vertebrae. Her intra-operative course was uneventful. Post-operative concerns included acute adrenal insufficiency, hypoglycaemia, hypotension and hyperkalemia, which were successfully managed in ICU. Patient was then given oral corticosteroids. One month later she was reassessed and was in better health.
Keywords: Cushing syndrome, Laparoscopic adrenalectomy, Pulmonary oedema, Metabolic alkalosis, Hypokalemia
|How to cite this article:|
Dahanukar UK, Joshi KS, Desai V, Padhye UD, Joshi AD, Deshpande A M. Laparoscopic Bilateral Adrenalectomy in a patient of Cushing syndrome: A Challenge for the Anaesthesiologist. Indian J Anaesth 2007;51:143
|How to cite this URL:|
Dahanukar UK, Joshi KS, Desai V, Padhye UD, Joshi AD, Deshpande A M. Laparoscopic Bilateral Adrenalectomy in a patient of Cushing syndrome: A Challenge for the Anaesthesiologist. Indian J Anaesth [serial online] 2007 [cited 2013 May 20];51:143. Available from: http://www.ijaweb.org/text.asp?2007/51/2/143/61132
| Case report|| |
A lady aged 52 year (ASA II) came with history of loose motions, generalised weakness, puffiness of face and feet for 4-5 days. She weighed 65kg and was 145cms tall. (BMI= 30.9). She was known to have hypertension and diabetes mellitus with persistent hypokalemia. She was on tablet glibenclamide 1.25mg 1-0-1, tablet spironolactone 25mg 1-1-0, liquid potassium citrate 2 teaspoon full 1-1-1. On physical examination, she had generalised anasarca, pallor, abdominal striae, hirsuitism, ecchymotic patches and peripheral cyanosis. She had right basal crepitations. Other systemic examination was unremarkable. Airway examination was normal.
Laboratory investigations revealed haemoglobin 7gm%, sodium 141meq/L, potassium 2.81meq/L, fasting blood sugar 160mg% and S. ACTH 107pg/ml (normal range at our lab< 120 pg/ml), CT brain and echocardiography were normal. ECG showed non-specific ST-T changes (V5-V6), chest X-Ray showed cardiomegaly. X-Ray dorsolumbar spine showed fracture of body of L1. CT scan abdomen/pelvis revealed bilateral adrenal gland hyperplasia. S. testosterone = 13 ng/ml (normal range at our lab = 0.1 to 9 ng/ml), 24 hour urinary cortisol = 25 mg per day (normal range at our lab 3 to 10 mg per day) and S. cortisol after dexamethasone suppression test = 10 mcg/dl (normal would be <6 mcg/dl) were high.
Preoperative arterial blood gas on air showed metabolic alkalosis with respiratory compensation, PaO2 was 55 mmHg; SpO2 was 94.9% (shift in oxygen dissociation curve to left due to alkalosis). Two units packed cells; potassium supplementation and injection hydrocortisone 50 mg 8 hrly were given. Fresh investigations revealed haemoglobin 7.7 gm%, sodium 140 meq/L, potassium 3.09 meq/L and fasting blood sugar 113 mg%. The patient was fasting overnight, received cap.omeprazole 20mg HS and IM glycopyrrolate 0.004 mgkg-1 30 minutes before surgery.
ECG, NIBP, pulse-oximetry and EtCO2 monitors were attached. 18G peripheral line was secured and ringer lactate infusion started in OT. Pre-induction saturation was 65% on air. After oxygenation for 1 minute (4L/minute), saturation increased to 100%. We gave IV ondansetron 0.8 mgkg -1 , IV hydrocortisone 2mgkg -1 and IV ketorolac 0.6 mgkg -1 , IV midazolam 0.04mgkg -1 and IV fentanyl 1.5 mcgkg -1 . Single lumen central venous catheter (right IJV) was inserted under all aseptic precautions. CVP was 15 cms water. Foley's catheterisation was done. The patient was induced with propofol 2.5 mgkg -1 and paralysis achieved with suxamethonium 1.5 mgkg -1 . Oral intubation was done with number 7.5 mm ID cuffed PVC endotracheal tube.
Anaesthesia was maintained using O2, N2O, sevoflurane 0.8-1.2% and atracurium with IPPV using Bain's circuit. Intra-operatively, the patient was haemodynamically stable. Approach was transabdominal  (3 left-sided and 4 right-sided ports) with patient in supine position. At the end of procedure (duration 150 min.), the patient was reversed with injection glycopyrrolate 0.01mgkg-1 and injection neostigmine 0.05mgkg-1. We gave 1 unit whole blood, 500ml 5% dextrose-normal saline + 5U insulin + 10meq KCL and 500 ml RL + 10 ml calcium gluconate. Total blood loss was 200ml. Urine output was 700ml. She was kept in ICU on O2 (4 L/minute) via endotracheal tube with T-piece, until wide-awake. Saturation was 94%. Respiratory efforts and tidal volume were adequate.
Three hours postoperatively, the patient became tachypnoeic, tachycardic, desaturated and had bilateral crepitations. Pinkish froth appeared in endotracheal tube, chest x-ray revealed pulmonary oedema. ABG showed respiratory and metabolic alkalosis with severe hypoxia, SpO2 82.1%. CVP=30cms of water. IV frusemide 1mgkg-1 was given. The patient was put on IPPV (FiO2 100%). Once ABG showed acceptable oxygenation, FiO2 60% was continued overnight. IV hydrocortisone 50 mg thrice daily was continued.
Next morning, she became hypotensive and hypoglycaemic (systolic BP 70 mmHg, CVP 12 cms water, random sugar between 31 to 120mg%). IV dopamine 5 mcgkg-1min-1, IV 25% dextrose were started. She required ventilation for 6 days plus potassium supplementation for persistent hypokalemia, proximal muscle weakness and easy fatigability. Gradually, her ionotropic support was tapered off. On the 6th postoperative day, she was extubated. On the 7th postoperative day, her serum potassium was 6.5meqL-1 for which she was treated. Over the next 2 days, oral steroids (tab. prednisolone 10 mg thrice a day) were started and discharged on 14th postoperative day.
One month later in a review visit her body weight was 52 kg. She had reduction in facial puffiness, anasarca, pallor, peripheral cyanosis and hirsuitism. She was normotensive and euglycaemic on maintenance steroids.
| Discussion|| |
The most common cause of Cushing's syndrome is long-term administration of exogenous glucocorticoids for arthritis, asthma or allergies.  60-70% of cases are associated with pituitary micro-adenoma or non-endocrine ACTH production, 10-20% with an ACTH-independent process (adrenal adenoma/carcinoma).
Features suggestive of glucocorticoid excess are moon-faced plethoric individual, truncal obesity, skinny extremities, buffalo-hump, thin skin, easy bruising, and striae. In women, adrenal androgen excess causes acne, hirsuitism, oligomenorrhea/ amenorrhoea  etc. These patients may have osteopenia, fluid retention, hypertension, hyperglycemia, diabetes mellitus, emotional changes (irritability to frank psychosis)  . Hypokalemia, hypochloremia and metabolic alkalosis owing to activation of renin-angiotensin system in kidneys by supranormal (>30 mg/ day) cortisol production  .
They need extra care during positioning, as they are more vulnerable to pressure induced nerve injuries and fractures. Intra-operative handling of the adrenal gland leads to surges in vasoactive amines and blood pressure.
Likely postoperative complications are acute adrenal insufficiency requiring steroid supplementation, pneumothorax, bleeding, post-operative hyperkalemia and hypoglycaemia.
Our patient received general anaesthesia only. We did not give epidural analgesia as the patient had fracture of body of L1. Injection ketorolac was given for pre-emptive analgesia. We used Ringer's lactate as the patient's sugar was controlled and she did not have acidosis. Sevoflurane 0.8% to 1.2% was used, titrated as per need. Sevoflurane produces less hemodynamic changes and is not known to cause steal phenomenon. Atracurium was chosen for its shorter duration of action, and its effectiveness to eliminate the possibility of residual postoperative muscle weakness as was expected to occur in this case. There are several reports claiming upper hand for laparoscopy; in a review of 30 cases J. Pujol et. al. found a shorter hospital stay, faster postoperative recuperation and more rapid resumption of normal activity. There is less post-operative pain and risk of intestinal adhesions. Thus our surgeon chose to do this case laparoscopically.
The duration of carboperitoneum was 105 minutes, intraperitoneal pressure was maintained between 10 to 12 mmHg. Total volume of carbon dioxide required was 100 litres. End tidal carbon dioxide, ECG, NIBP and SpO2 were measured, they remained within acceptable range. 
| References|| |
|1.||Text book of Anaesthesia. Edited by Ronald D. Miller. 5th ed. Philadelphia, Churchill livingstone. 2000: 918-19. |
|2.||Wylie& Churchill-Davidsons. "A practice of Anaesthesia" 6th ed. London: Edward Arnold 1995: 395. |
|3.||Mishra MC; Hemal AK. Laparoscopic Adrenalectomy for a large phaeochromocytoma Indian Journal of Urology. 1998 Mar; 14(2): 131-32. |
|4.||J. Pujol, M. Viladrich, A. Rafecas, L. Llado, A. Garcia-Barrasa, J. Figueras, E. Jaurrieta. Laparoscopic adrenalectomy a review of 30 initial cases. Surg Endosc 1999; 13: 488-92. |