Anesthetic Management of Emergent Laparoscopic Bilateral Adrenalectomy in a Patient with a Life-Threatening Cortisol Crisis Ankur Sharma, MD,* Rajeshwari Subramaniam, MD,* Mahesh Misra, MS,† Bandi Joshiraj, MD,* Gopi Krishnan, MD,* Prerna Varma, MD,‡ and Shyam Kishore, MD§ Cushing syndrome may rarely present with life-threatening hypercortisolism, manifested by hypertension, hypokalemia, hyperglycemia, and edema. If medical treatment proves ineffective in ameliorating the symptoms, emergent rescue adrenalectomy may be the only way to relieve the crisis. We describe the anesthetic management of a patient with an ectopic adrenocorticotropic hormone-secreting tumor, whose condition was rapidly deteriorating due to severe cortisol excess, and emergent adrenalectomy was the only available therapeutic modality. Despite severe metabolic derangement, edema, and incipient respiratory failure, emergent bilateral laparoscopic adrenalectomy was performed and the patient improved sufficiently to undergo surgery for the ectopic lesion without incident. (A&A Case Reports. 2015;4:15–8.)
C
ortisol crisis is a rare clinical condition characterized by florid, life-threatening manifestations of cortisol excess. If unresponsive to medical management, this condition may require urgent rescue adrenalectomy to rapidly reduce cortisol levels. Emergent rescue adrenalectomy is a relatively little-known clinical entity, and only 3 such cases have been published in the literature. We describe the perioperative problems and anesthetic management of a patient with ectopic adrenocorticotropic hormone (ACTH)dependent Cushing syndrome who required emergent adrenalectomy due to the rapid deterioration of his clinical condition. The patient described in the case has given written and verbal consent for the publication of his case in any medical journal.
CASE DESCRIPTION
A 45-year-old male weighing 73 kg presented in the endocrinology outpatient department with a history of progressive proximal muscle weakness, low back pain, and generalized edema for 6 weeks. He had, in addition, easy fatigability, thinning of skin, and progressive weight gain. His physical examination revealed a body habitus consistent with Cushing syndrome including moon face, bruising on the face, abdomen and limbs, and generalized edema. Laboratory values revealed hypoalbuminemia, hypokalemia (2.0 mEq/L), and hyperglycemia both fasting
195 mg/dL as well as postprandial 242 mg/dL. Adrenal hormonal profile revealed ACTH-dependent hypercortisolism, with increased serum cortisol (63.44 μg/dL, normal 10–25 μg/dL) and plasma ACTH (61.91 pg/mL) levels (normal lab values 9–52 pg/mL). Contrast-enhanced computed tomography of the abdomen and chest showed bilateral adrenal hyperplasia and 2 hypoechoic masses close to the renal vein and uncinate process of the pancreas, both of which also showed significant Gallium-68 (Ga-68) DOTA1-NaI3-octreotide (DOTA-NOC) uptake (Fig. 1). Brain magnetic resonance imaging revealed an enlarged sella tursica with intrasellar herniation of cerebrospinal fluid and compression of the thinned anterior pituitary gland. On the basis of clinical features and investigations, he was diagnosed with ectopic ACTH-dependent Cushing syndrome. The medications we started included amlodipine, metoprolol, spironolactone, ketoconazole, and somatostatin analog orally, with insulin for glycemic control. In the week after hospital admission, there was rapid progression of generalized edema, weight gain (9 kg in 2 weeks), dyspnea, decreasing Spo2, persistent hypokalemia,
From the *Departments of Anesthesia, †Surgical Disciplines, ‡Anesthesiology, and §Endocrinology, All India Institute Medical Sciences, New Delhi, India. Accepted for publication June 22, 2014. Funding: None.
The authors declare no conflicts of interest. This case was presented as a poster in the International Symposium on Endocrine Anesthesia held at the All India Institute of Medical Sciences, New Delhi, from November 30 to December 1, 2013. It was judged by Prof J Lenders and Prof MFM James and awarded 1st prize. Address correspondence to Rajeshwari Subramaniam, MD, Department of Anesthesia, All India Institute Medical Sciences, Room No. 5010-D, 5th Floor Teaching Block, New Delhi, India. Address e-mail to [email protected]. Copyright © 2015 International Anesthesia Research Society DOI: 10.1213/XAA.0000000000000110
January 15, 2015 • Volume 4 • Number 2
Figure 1. Gallium-68 (Ga-68) DOTA-1-NaI3-octreotide (DOTA-NOC) image showing primary lesion. cases-anesthesia-analgesia.org
15
decreasing serum albumin, and difficulty controlling his arterial blood pressure despite medical therapy. One episode of respiratory distress and decreased oxyhemoglobin saturation necessitated intensive care unit admission and noninvasive ventilation for 48 hours. His arterial blood gases at this time were Pao2 78 mm Hg, Paco2 58 mm Hg, pH 7.53, HCO3 44 mmol/L. It was felt that the patient would die in less than a week if adrenalectomy was not performed, including surgery to deal with the primary lesion (in the pancreas) after bilateral adrenalectomy.
PREOPERATIVE EVALUATION
Examination revealed an anxious, pale, obese, dyspneic patient unable to lie supine. His vital signs included tachycardia (124 per minute), hypertension (190/90 mm Hg), and tachypnea (28 per minute). His oxyhemoglobin saturation (Spo2) was 94% breathing oxygen by facemask. Pitting edema extending up to his elbows and knees was present. Air entry in both lung bases was reduced, and crepitations were audible. He had hepatomegaly and stria on the abdomen. His airway was modified Mallampati grade IV with restricted neck movements and mouth opening, normal jaw protrusion, and thyromental distance. His chest radiograph showed bilateral pleural effusion with basal consolidation. The electrocardiogram showed normal sinus rhythm. Echocardiography revealed an ejection fraction of 60% with grade I diastolic dysfunction and trace mitral regurgitation. Serum [Na+] was 145 mEq/L and [K+] 2.0 mEq/L.
ANESTHETIC MANAGEMENT
Oral pantoprazole and antihypertensive medications were administered on the morning of surgery. After attaching routine monitors (electrocardiogram, noninvasive arterial blood pressure, and Spo2), an IV cannula was inserted with difficulty on the edematous dorsal surface of the hand. The right radial artery and the right internal jugular vein were cannulated under ultrasound guidance. After thorough prepping of the skin over the lumbar spine with chlorhexidine-povidone solution and sterile draping, subarachnoid block was performed in the sitting patient at the L3–L4 interspace with a 25–G pencil point needle (B-Braun), using 20 μg fentanyl and 150 μg morphine in 1 mL saline with strict asepsis. After oxygen administration, anesthesia was induced with fentanyl and etomidate and tracheal intubation was facilitated with succinylcholine. Despite some markers for a difficult intubation, a good laryngoscopic view was obtained with a “ramped” position. Anesthesia was maintained with oxygen in air and 0.8% to 1.2% end-tidal isoflurane with intermittent boluses of atracurium. Neuromuscular junction monitoring was performed using the train-of-four count with TOF Watch. A glucose-insulin-potassium infusion (10% dextrose, 20 mmol KCl, 10 units insulin at 100mL/h) was started and continued postoperatively. Intraoperative Spo2, end-tidal CO2 and airway pressures remained in the range of 91% to 94%, 41 to 47 mm Hg, and 28 to 35 cm H2O, respectively, with Fio2 0.6 to 0.8 and volume-controlled ventilation with positive end-expiratory pressure. Pneumoperitoneum with CO2 (abdominal pressure 10–12 cm H2O) resulted in a pH of 7.28, Po2 of 78 mm, Pco2 of 87, HCO3 of 40.9, and Na/K of 140/1.9. Bilateral adrenalectomy was performed with the
16 cases-anesthesia-analgesia.org
patient in the lateral decubitus (right, then left) positions, using a transperitoneal approach. During adrenal dissection, hypertension was treated with titrated nitroglycerin infusion (1–5 μg/kg/min). Surgery lasted 5 hours with an approximate blood loss of 800 mL. Postoperatively, pressure support ventilation (PS 15, positive end-expiratory pressure 5, Fio2 0.5) was initiated. Hydrocortisone 50 mg 6 hourly IV and glucose-insulin-potassium solution were administered. There was a brief period of hypotension postoperatively necessitating norepinephrine infusion for 4 hours and 1 extra steroid dose. The patient remained pain-free and did not require any additional opioids in the postoperative period. The trachea was extubated after 12 hours and continuous positive airway pressure maintained for 48 hours with Spo2 92% to 94%. Both hyperglycemia and hypokalemia normalized within 24 hours. He was discharged home after 15 days with an uneventful recovery. He was readmitted (weight 58 kg) after 4 weeks for a distal pancreatectomy to remove the source of exogenous ACTH and was discharged a week later in good health.
DISCUSSION
Cushing syndrome is characterized by obesity, hyperglycemia, metabolic alkalosis, hypokalemia, hypertension, and proximal muscle weakness caused by high glucocorticoid levels. Most cases (70%) result from a pituitary ACTHproducing tumor (Cushing disease), 15% due to primary adrenal tumor and the rest (10%–15%) from ectopically released ACTH.1 In our patient, an ectopic ACTH-secreting tumor was located in the peripancreatic area. Lungs, pancreas (8% of all ectopic sites), thymus, and thyroid are common ectopic ACTH sites.2 Extremely high circulating cortisol levels leading to hypertension and hypokalemia, as seen in our patient, occur in Cushing syndrome caused by ectopic ACTH secretion. Severe metabolic alkalosis has been reported as one of the main, and often the first, clinical manifestations of ectopic ACTH-secreting tumors.1,3 When unopposed by other acid-base disorders, metabolic alkalosis causes an increase in plasma bicarbonate. Bicarbonate levels in our patient ranged from 40 to 45 mmol/L. This metabolic alkalosis normally results in depression of ventilation resulting in an increase of Paco2 and buffering of alkalemia. Compensatory hypoventilation can result in significant resting hypoxemia and also contribute to infection and atelectasis in immune-compromised patients.4 This could explain the severe hypoxemia and hypercarbia seen in our patient. The other implications of metabolic alkalosis are depressed myocardial contractility, arrhythmias, reduced cerebral blood flow and mental obtundation, and neuromuscular excitability. Importantly, alkalosis impairs peripheral oxygen unloading by leftward shift of the oxygen dissociation curve.4 Hypoxemia in Cushing syndrome is multifactorial in origin (hypoventilation consequent to alkalosis, pulmonary microatelectasis and increasing ventilation/perfusion mismatch, as alkalosis inhibits hypoxic pulmonary vasoconstriction.4 This hypoxemia responds well to oxygen therapy. Respiratory muscle injury resulting from hypokalemia,
A & A case reports
manifested by elevated creatine phosphokinase, has also been implicated as a cause of hypoxemia.5 Severe hypokalemia in our patient was another cause of concern. Excess cortisol leads to hypokalemia and metabolic alkalosis by 2 pathways. In normal circumstances, cortisol (which has affinity for the aldosterone receptor) is converted to cortisone by 11-hydroxy steroid dehydrogenase present in the renal tubules and is prevented from exerting a mineralocorticoid effect. However, in ectopic ACTH production, the excess cortisol saturates the available enzyme and exerts a “spillover” effect on the aldosterone receptor. The ensuing potassium loss is accompanied by transport of H+ into the cell, causing intracellular acidosis, which enhances proximal tubule bicarbonate reabsorption, leading to the development of metabolic alkalosis. Excess cortisol also mediates metabolic alkalosis by enhancing Na+:3HCO3− cotransporter (NBC) expression and activity in the proximal tubule. This leads to potassium secretion in the distal collecting duct. Potassium loss also enhances NBC activity.6,7 The anesthetic implications of severe hypokalemia include cardiac arrhythmias and enhancement of neuromuscular blockade. Residual muscle weakness can necessitate ventilator support. This patient required a brief period of ventilator assistance due to deranged arterial blood gases and inadequate respiratory effort in spite of a train-of-four ratio of 0.9. Metabolic alkalosis has been reported to respond to correction of hypokalemia; we replaced K+ at 20 mmol/h in a glucose-insulin solution throughout surgery. Medical management with steroidogenesis inhibitors such as ketoconazole, metyrapone, and mitotane may be used to suppress cortisol production. Kamenický et al. have reported a rapid decrease in cortisol levels with mitotane, metyrapone, and ketoconazole. Mitotane can take several months for adrenolytic action and careful monitoring of plasma levels is needed. Metyrapone and ketoconazole have a rapid onset of action, but regulation of hypercortisolism is usually lost with oversecretion of corticotropin.8 In this case, the patient’s condition was rapidly deteriorating and there was no response to medical management. Metyrapone is presently not available in India. Bilateral adrenalectomy appeared to be the only option to rapidly reduce cortisol levels.9 Han et al.10 have recently reported a similar case; however, no perioperative management details are available. Laparoscopic adrenalectomy results in reduced morbidity postoperatively compared with an open approach by reducing postoperative pain, permitting earlier oral intake and ambulation compared with open surgery. The incision used for posterior adrenalectomy, with its associated 12th rib resection and subcostal (T12) nerve retraction, can cause incisional and musculoskeletal problems that may persist postoperatively. Incisional problems, including flank pain, numbness, and loss of muscle tone, are especially pronounced and severe in patients with Cushing syndrome because of poor wound healing, laxity of the abdominal wall, obesity, and musculoskeletal complaints associated with the condition. Compared with the open approach, bilateral laparoscopic adrenal surgery is associated with much less tissue injury in patients who are immunocompromised and/or are predisposed to delayed wound
January 15, 2015 • Volume 4 • Number 2
healing.11–13 The potential advantages of laparoscopy were appealing because we planned to use a small dose of intrathecal morphine to effectively manage the pain of multiple port incisions, avoid further opioid use, and fast-track the patient from ventilator support. Most reviews on laparoscopic adrenalectomy agree that this procedure is more time-consuming than open adrenalectomy. Our concerns were that this would translate into worsening of CO2 retention, increased airway pressures, and problems with oxygenation. As expected, pneumoperitoneum, lateral decubitus position, and central obesity aggravated the preexisting hypoxia and hypercarbia. Intraabdominal pressures restricted to 10 to 12 cm H2O, Fio2 0.6–0.8 and repeated alveolar recruitment maneuvers were used to keep the Spo2 at 93% to 95%. Maintaining peak airway pressures
C
ortisol crisis is a rare clinical condition characterized by florid, life-threatening manifestations of cortisol excess. If unresponsive to medical management, this condition may require urgent rescue adrenalectomy to rapidly reduce cortisol levels. Emergent rescue adrenalectomy is a relatively little-known clinical entity, and only 3 such cases have been published in the literature. We describe the perioperative problems and anesthetic management of a patient with ectopic adrenocorticotropic hormone (ACTH)dependent Cushing syndrome who required emergent adrenalectomy due to the rapid deterioration of his clinical condition. The patient described in the case has given written and verbal consent for the publication of his case in any medical journal.
CASE DESCRIPTION
A 45-year-old male weighing 73 kg presented in the endocrinology outpatient department with a history of progressive proximal muscle weakness, low back pain, and generalized edema for 6 weeks. He had, in addition, easy fatigability, thinning of skin, and progressive weight gain. His physical examination revealed a body habitus consistent with Cushing syndrome including moon face, bruising on the face, abdomen and limbs, and generalized edema. Laboratory values revealed hypoalbuminemia, hypokalemia (2.0 mEq/L), and hyperglycemia both fasting
195 mg/dL as well as postprandial 242 mg/dL. Adrenal hormonal profile revealed ACTH-dependent hypercortisolism, with increased serum cortisol (63.44 μg/dL, normal 10–25 μg/dL) and plasma ACTH (61.91 pg/mL) levels (normal lab values 9–52 pg/mL). Contrast-enhanced computed tomography of the abdomen and chest showed bilateral adrenal hyperplasia and 2 hypoechoic masses close to the renal vein and uncinate process of the pancreas, both of which also showed significant Gallium-68 (Ga-68) DOTA1-NaI3-octreotide (DOTA-NOC) uptake (Fig. 1). Brain magnetic resonance imaging revealed an enlarged sella tursica with intrasellar herniation of cerebrospinal fluid and compression of the thinned anterior pituitary gland. On the basis of clinical features and investigations, he was diagnosed with ectopic ACTH-dependent Cushing syndrome. The medications we started included amlodipine, metoprolol, spironolactone, ketoconazole, and somatostatin analog orally, with insulin for glycemic control. In the week after hospital admission, there was rapid progression of generalized edema, weight gain (9 kg in 2 weeks), dyspnea, decreasing Spo2, persistent hypokalemia,
From the *Departments of Anesthesia, †Surgical Disciplines, ‡Anesthesiology, and §Endocrinology, All India Institute Medical Sciences, New Delhi, India. Accepted for publication June 22, 2014. Funding: None.
The authors declare no conflicts of interest. This case was presented as a poster in the International Symposium on Endocrine Anesthesia held at the All India Institute of Medical Sciences, New Delhi, from November 30 to December 1, 2013. It was judged by Prof J Lenders and Prof MFM James and awarded 1st prize. Address correspondence to Rajeshwari Subramaniam, MD, Department of Anesthesia, All India Institute Medical Sciences, Room No. 5010-D, 5th Floor Teaching Block, New Delhi, India. Address e-mail to [email protected]. Copyright © 2015 International Anesthesia Research Society DOI: 10.1213/XAA.0000000000000110
January 15, 2015 • Volume 4 • Number 2
Figure 1. Gallium-68 (Ga-68) DOTA-1-NaI3-octreotide (DOTA-NOC) image showing primary lesion. cases-anesthesia-analgesia.org
15
decreasing serum albumin, and difficulty controlling his arterial blood pressure despite medical therapy. One episode of respiratory distress and decreased oxyhemoglobin saturation necessitated intensive care unit admission and noninvasive ventilation for 48 hours. His arterial blood gases at this time were Pao2 78 mm Hg, Paco2 58 mm Hg, pH 7.53, HCO3 44 mmol/L. It was felt that the patient would die in less than a week if adrenalectomy was not performed, including surgery to deal with the primary lesion (in the pancreas) after bilateral adrenalectomy.
PREOPERATIVE EVALUATION
Examination revealed an anxious, pale, obese, dyspneic patient unable to lie supine. His vital signs included tachycardia (124 per minute), hypertension (190/90 mm Hg), and tachypnea (28 per minute). His oxyhemoglobin saturation (Spo2) was 94% breathing oxygen by facemask. Pitting edema extending up to his elbows and knees was present. Air entry in both lung bases was reduced, and crepitations were audible. He had hepatomegaly and stria on the abdomen. His airway was modified Mallampati grade IV with restricted neck movements and mouth opening, normal jaw protrusion, and thyromental distance. His chest radiograph showed bilateral pleural effusion with basal consolidation. The electrocardiogram showed normal sinus rhythm. Echocardiography revealed an ejection fraction of 60% with grade I diastolic dysfunction and trace mitral regurgitation. Serum [Na+] was 145 mEq/L and [K+] 2.0 mEq/L.
ANESTHETIC MANAGEMENT
Oral pantoprazole and antihypertensive medications were administered on the morning of surgery. After attaching routine monitors (electrocardiogram, noninvasive arterial blood pressure, and Spo2), an IV cannula was inserted with difficulty on the edematous dorsal surface of the hand. The right radial artery and the right internal jugular vein were cannulated under ultrasound guidance. After thorough prepping of the skin over the lumbar spine with chlorhexidine-povidone solution and sterile draping, subarachnoid block was performed in the sitting patient at the L3–L4 interspace with a 25–G pencil point needle (B-Braun), using 20 μg fentanyl and 150 μg morphine in 1 mL saline with strict asepsis. After oxygen administration, anesthesia was induced with fentanyl and etomidate and tracheal intubation was facilitated with succinylcholine. Despite some markers for a difficult intubation, a good laryngoscopic view was obtained with a “ramped” position. Anesthesia was maintained with oxygen in air and 0.8% to 1.2% end-tidal isoflurane with intermittent boluses of atracurium. Neuromuscular junction monitoring was performed using the train-of-four count with TOF Watch. A glucose-insulin-potassium infusion (10% dextrose, 20 mmol KCl, 10 units insulin at 100mL/h) was started and continued postoperatively. Intraoperative Spo2, end-tidal CO2 and airway pressures remained in the range of 91% to 94%, 41 to 47 mm Hg, and 28 to 35 cm H2O, respectively, with Fio2 0.6 to 0.8 and volume-controlled ventilation with positive end-expiratory pressure. Pneumoperitoneum with CO2 (abdominal pressure 10–12 cm H2O) resulted in a pH of 7.28, Po2 of 78 mm, Pco2 of 87, HCO3 of 40.9, and Na/K of 140/1.9. Bilateral adrenalectomy was performed with the
16 cases-anesthesia-analgesia.org
patient in the lateral decubitus (right, then left) positions, using a transperitoneal approach. During adrenal dissection, hypertension was treated with titrated nitroglycerin infusion (1–5 μg/kg/min). Surgery lasted 5 hours with an approximate blood loss of 800 mL. Postoperatively, pressure support ventilation (PS 15, positive end-expiratory pressure 5, Fio2 0.5) was initiated. Hydrocortisone 50 mg 6 hourly IV and glucose-insulin-potassium solution were administered. There was a brief period of hypotension postoperatively necessitating norepinephrine infusion for 4 hours and 1 extra steroid dose. The patient remained pain-free and did not require any additional opioids in the postoperative period. The trachea was extubated after 12 hours and continuous positive airway pressure maintained for 48 hours with Spo2 92% to 94%. Both hyperglycemia and hypokalemia normalized within 24 hours. He was discharged home after 15 days with an uneventful recovery. He was readmitted (weight 58 kg) after 4 weeks for a distal pancreatectomy to remove the source of exogenous ACTH and was discharged a week later in good health.
DISCUSSION
Cushing syndrome is characterized by obesity, hyperglycemia, metabolic alkalosis, hypokalemia, hypertension, and proximal muscle weakness caused by high glucocorticoid levels. Most cases (70%) result from a pituitary ACTHproducing tumor (Cushing disease), 15% due to primary adrenal tumor and the rest (10%–15%) from ectopically released ACTH.1 In our patient, an ectopic ACTH-secreting tumor was located in the peripancreatic area. Lungs, pancreas (8% of all ectopic sites), thymus, and thyroid are common ectopic ACTH sites.2 Extremely high circulating cortisol levels leading to hypertension and hypokalemia, as seen in our patient, occur in Cushing syndrome caused by ectopic ACTH secretion. Severe metabolic alkalosis has been reported as one of the main, and often the first, clinical manifestations of ectopic ACTH-secreting tumors.1,3 When unopposed by other acid-base disorders, metabolic alkalosis causes an increase in plasma bicarbonate. Bicarbonate levels in our patient ranged from 40 to 45 mmol/L. This metabolic alkalosis normally results in depression of ventilation resulting in an increase of Paco2 and buffering of alkalemia. Compensatory hypoventilation can result in significant resting hypoxemia and also contribute to infection and atelectasis in immune-compromised patients.4 This could explain the severe hypoxemia and hypercarbia seen in our patient. The other implications of metabolic alkalosis are depressed myocardial contractility, arrhythmias, reduced cerebral blood flow and mental obtundation, and neuromuscular excitability. Importantly, alkalosis impairs peripheral oxygen unloading by leftward shift of the oxygen dissociation curve.4 Hypoxemia in Cushing syndrome is multifactorial in origin (hypoventilation consequent to alkalosis, pulmonary microatelectasis and increasing ventilation/perfusion mismatch, as alkalosis inhibits hypoxic pulmonary vasoconstriction.4 This hypoxemia responds well to oxygen therapy. Respiratory muscle injury resulting from hypokalemia,
A & A case reports
manifested by elevated creatine phosphokinase, has also been implicated as a cause of hypoxemia.5 Severe hypokalemia in our patient was another cause of concern. Excess cortisol leads to hypokalemia and metabolic alkalosis by 2 pathways. In normal circumstances, cortisol (which has affinity for the aldosterone receptor) is converted to cortisone by 11-hydroxy steroid dehydrogenase present in the renal tubules and is prevented from exerting a mineralocorticoid effect. However, in ectopic ACTH production, the excess cortisol saturates the available enzyme and exerts a “spillover” effect on the aldosterone receptor. The ensuing potassium loss is accompanied by transport of H+ into the cell, causing intracellular acidosis, which enhances proximal tubule bicarbonate reabsorption, leading to the development of metabolic alkalosis. Excess cortisol also mediates metabolic alkalosis by enhancing Na+:3HCO3− cotransporter (NBC) expression and activity in the proximal tubule. This leads to potassium secretion in the distal collecting duct. Potassium loss also enhances NBC activity.6,7 The anesthetic implications of severe hypokalemia include cardiac arrhythmias and enhancement of neuromuscular blockade. Residual muscle weakness can necessitate ventilator support. This patient required a brief period of ventilator assistance due to deranged arterial blood gases and inadequate respiratory effort in spite of a train-of-four ratio of 0.9. Metabolic alkalosis has been reported to respond to correction of hypokalemia; we replaced K+ at 20 mmol/h in a glucose-insulin solution throughout surgery. Medical management with steroidogenesis inhibitors such as ketoconazole, metyrapone, and mitotane may be used to suppress cortisol production. Kamenický et al. have reported a rapid decrease in cortisol levels with mitotane, metyrapone, and ketoconazole. Mitotane can take several months for adrenolytic action and careful monitoring of plasma levels is needed. Metyrapone and ketoconazole have a rapid onset of action, but regulation of hypercortisolism is usually lost with oversecretion of corticotropin.8 In this case, the patient’s condition was rapidly deteriorating and there was no response to medical management. Metyrapone is presently not available in India. Bilateral adrenalectomy appeared to be the only option to rapidly reduce cortisol levels.9 Han et al.10 have recently reported a similar case; however, no perioperative management details are available. Laparoscopic adrenalectomy results in reduced morbidity postoperatively compared with an open approach by reducing postoperative pain, permitting earlier oral intake and ambulation compared with open surgery. The incision used for posterior adrenalectomy, with its associated 12th rib resection and subcostal (T12) nerve retraction, can cause incisional and musculoskeletal problems that may persist postoperatively. Incisional problems, including flank pain, numbness, and loss of muscle tone, are especially pronounced and severe in patients with Cushing syndrome because of poor wound healing, laxity of the abdominal wall, obesity, and musculoskeletal complaints associated with the condition. Compared with the open approach, bilateral laparoscopic adrenal surgery is associated with much less tissue injury in patients who are immunocompromised and/or are predisposed to delayed wound
January 15, 2015 • Volume 4 • Number 2
healing.11–13 The potential advantages of laparoscopy were appealing because we planned to use a small dose of intrathecal morphine to effectively manage the pain of multiple port incisions, avoid further opioid use, and fast-track the patient from ventilator support. Most reviews on laparoscopic adrenalectomy agree that this procedure is more time-consuming than open adrenalectomy. Our concerns were that this would translate into worsening of CO2 retention, increased airway pressures, and problems with oxygenation. As expected, pneumoperitoneum, lateral decubitus position, and central obesity aggravated the preexisting hypoxia and hypercarbia. Intraabdominal pressures restricted to 10 to 12 cm H2O, Fio2 0.6–0.8 and repeated alveolar recruitment maneuvers were used to keep the Spo2 at 93% to 95%. Maintaining peak airway pressures
