Orthostatic Intolerance Following Laparoscopic Sleeve Gastrectomy for Morbid Obesity

| July 10, 2014 | 0 Comments

by Wasef Abu-Jaish, MD, FACS; Reshma Patel, MD; and Mohammad Jafferji, MS IV

Dr. Abu-Jaish is Ass. Professor of Surgery, University of Vermont College of Medicine; Co-Director of Bariatric Surgery Program, Fletcher Allen Health Care, Minimally Invasive And Bariatric Surgery, Burlington,Vermont. Dr. Reshma Patel is a surgical resident, Fletcher Allen Health Care, University of Vermont College of Medicine. Mohammad Jafferji is a 4th year medical student, University of Vermont College of Medicine.

Bariatric Times. 2014;11(7):8–10.

Incidence of patients presenting with autonomic dysfunction, characterized as orthostatic intolerance, following bariatric surgery has been increasing. The etiology of this condition following bariatric surgery is unknown. We present three case reports of patients who underwent laparoscopic sleeve gastrectomy with substantial postoperative weight loss and development of symptomatic orthostatic intolerance.

Obesity, laparoscopic sleeve gastrectomy, Roux-en-Y gastric bypass, complications, excess weight loss, hypertension, orthostatic intolerance

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We present three case reports of patients who underwent laparoscopic sleeve gastrectomy (LSG) with substantial postoperative weight loss and development of symptomatic orthostatic intolerance.

Case 1
A 34-year-old man with morbid obesity (body mass index [BMI] 42kg/m2 and weight 309lbs) presented to our clinic with the following: type 2 diabetes mellitus (T2DM), end stage renal disease (ESRD), hypertension, and depression. He was on insulin therapy, hemodialysis, and the following: amlodipine 10mg daily and furosemide 40mg daily. He underwent uneventful laparoscopic sleeve gastrectomy in preparation for potential kidney and pancreas transplant. His postoperative course was uncomplicated, requiring routine dialysis, and he was discharged home on Postoperative Day 5. At his initial follow-up visit, he was doing well and his diet was advanced as per our bariatric surgery nutritional protocol. Two months later, his BMI was 36kg/m2 (275lbs), and he began having episodes of dizziness and dry heaving with early satiety. His vitals were stable at that time, and he was instructed to increase his oral intake. He continued to have significant weight loss with progressively worsening symptoms. After a 70-lb weight loss, he began experiencing more frequent episodes and ultimately sustained head trauma that brought him to the emergency department. Upon arrival, he was found to have orthostatic hypotension with postural tachycardia—60 beats per minute (bpm) while supine to 110 to 130bpm while standing—which did not improve with fluid resuscitation. His physical examination was unremarkable with no signs of dehydration. He underwent an extensive workup, including a computed tomography (CT) scan of the head, electroencephalography (EEG), cardiac evaluation, and labs, including electrolytes, hemogram, vitamins, and trace elements. All labs were within normal limits. His home medication regimen was modified with discontinuation of the antihypertensive and the antidepressant drugs. He started fludrocortisone and a beta-blocker with continuation upon discharge. He followed up in clinic two weeks later with normal vital signs and with complete resolution of his symptoms. At this time, he is on the list for combined kidney and pancreas transplant.

Case 2
A 62-year-old woman with morbid obesity (BMI 58.3kg/m2 and 337.6lbs) presented to our clinic with the following: T2DM, hypertension, hypothyroid, obstructive sleep apnea (OSA), and spinal stenosis. She was on the following: insulin therapy, furosemide 20mg twice daily, and fosinopril 20mg daily. Her past surgical history included an open cholecystectomy for complicated acute cholecystitis. The patient underwent an uneventful laparoscopic extensive lysis of adhesions and sleeve gastrectomy. She was discharged home on Postoperative Day 1, and her diet was advanced per our bariatric surgery nutritional protocol. Two months after surgery, she presented for regular follow up and reported falling from a standing position with mild head trauma. Her physical exam was unremarkable without signs of dehydration and a total weight loss of 75lbs. Her systolic blood pressure was low, heart rate was elevated, and blood glucose was normal. Her laboratory values were all within normal limits, including trace elements, vitamins, electrolytes, and hemogram. Because her recent preoperative cardiac workup had been negative, no further evaluation was conducted. Her antihypertensive and insulin therapies were discontinued, and her primary care provider was contacted to maintain close follow up. All of her comorbid conditions and orthostatic symptoms had completely resolved at the 3-, 6-, and 9-month follow-up visits with a recorded weight of 198lbs and BMI 35.1kg/m2.

Case 3
A 59-year-old man with morbid obesity (386lbs, BMI 51kg/m2) presented to our clinic with a history of hypertension, insulin-dependent diabetes mellitus, asthma, osteoarthritis, OSA, and congenital absence of the right kidney. He was on lisinopril 40mg daily, verapamil 180mg daily, and hydrochlorothiazide 25mg daily. The patient underwent an uncomplicated laparoscopic sleeve gastrectomy. He presented for the first postoperative visit two weeks later with a 55-lb weight loss and complaints of lightheadedness upon standing. His physical examination was unremarkable; however, he was noted to have orthostatic hypotension. His weight was 331 lbs with a BMI 43kg/m2. He was instructed to discontinue his blood pressure medications, which included an angiotensin-converting enzyme (ACE) inhibitor, thiazide diuretic, and a calcium channel blocker. He returned one month later for follow up with improvement in his symptoms and no evidence of orthostatic hypotension. His weight was 315lbs with BMI 41kg/m2.
The patients in Cases 2 and 3 were also instructed to take measures to maintain adequate fluid and salt intake as well as exercise in the horizontal position. They were further instructed to avoid sudden changes in posture, standing still, hot showers, excessive heat, and straining during micturition and defecation.
Adjustments in medication for the patient in Case 1 were unknown because he was followed by his primary care provider in the nearby state for his scheduled dialysis. The dosages of antihypertensive medications were adjusted/ discontinued following surgery in Cases 2 and 3 in collaboration with their primary care physicians.

Multiple pathophysiologic mechanisms have been proposed to be responsible for obesity-related HTN with derangements occurring at the level of major organ systems as well as at the molecular level. They include increased activation of the renin-angiotensin-aldosterone system (RAAS), increased sympathetic nervous system activity (SNS), and insulin resistance.[4] In addition, obesity is associated with increased renal sodium reabsorption, impaired pressure natriuresis, and volume expansion.[4] Furthermore, obesity may also cause marked structural changes in the kidneys that will eventually lead to chronic kidney disease and further increases in blood pressure.[4] In addition, alterations in adipokines, adiponectin, leptin, leptin resistance, dysfunctional fat, free fatty acids, resistin, 11 Beta dehydrogenase, endothelial dysfunction, coagulation factors, systemic inflammation, insulin resistance, and sleep apnea promote HTN and CVD.[4] Many of these factors are interrelated.[4]
It has been proposed that the metabolic syndrome of central, or android, obesity leads to the development of HTN through the effects of insulin-induced sodium reabsorption and increased catecholamine sensitivity. However, it is possible that insulin resistance and HTN simply coexist in centrally obese subjects without a specific causal relationship. As an alternative to the insulin hypothesis, an increase in the intra-abdominal pressure, as seen in central obesity, is the cause of systemic HTN through one, or a combination, of three mechanisms.[5] These include increased renal venous pressure leading to activation of the RAAS, with resultant glomerular capillary injury and proteinuria; direct renal compression with activation of the (RAAS); and/or an increased intrathoracic pressure leading to a decreased venous return and cardiac output with further activation of the RAAS.[5] The net effect of these physiologic perturbations is sodium and water retention, increased blood pressure, and the development of proteinuria, as seen in patients with severe obesity. Renal vein constriction to 30mmHg is associated with an increased plasma renin activity and aldosterone, decreased renal blood flow, and glomerular filtration rate and proteinuria.[5] Diabetes and HTN are merely co-conspirators in the metabolic syndrome of obesity and may be secondary to different mechanisms. Prior studies suggest that HTN in the centrally obese may be a result of increased intra-abdominal pressure.[5]
LSG typically results in impressive weight loss. Two recently reported randomized trials6,[7] have compared LSG to other bariatric procedures that are accepted as primary procedures by The American Society for Metabolic and Bariatric Surgery (ASMBS). The first prospective randomized trial compared LSG to laparoscopic adjustable gastric banding (LAGB) (n=16 in each group) and reported greater EWL (66% vs. 48%; (p=0.025) with LSG at three years. The second prospective randomized trial compared LSG to Roux-en-Y-gastric bypass (RYGB) (n= 40 in each group) and reported better weight loss with LSG at one year (EWL 70% vs. 61% and 65% respectively; p= 0.05).[7]
Postoperative nutritional abnormalities are thought to be associated with neurological complications. Somatic neurological conditions, such as encephalopathy, optic neuropathy, myelopathy, polyradiucolneuropathy, and polyneuropathy, have been documented as sequelae of bariatric surgery.[8] In an effort to determine if there are nutritional consequences after resecting 80 percent of the stomach, Abu-Jaish et al9 reported a series of 218 patients that underwent LSG and were followed at three, six, and 12 months, and on a yearly basis. They concluded that even rare and nonsignificant nutritional deficiencies can occur in patients with morbid obesity undergoing LSG.[9]
There has been an increasing incidence of patients presenting with autonomic dysfunction characterized as orthostatic intolerance following bariatric surgery.[10,11] The etiology of orthostatic intolerance following bariatric surgery is unknown; however, it has been suggested that it results from rapid weight loss following surgery.[10,11]
Orthostatic intolerance refers to “a heterogeneous group of disorders of hemodynamic regulation characterized by insufficient cerebral perfusion resulting in symptoms during upright posture relieved by recumbency.”[11] Orthostatic intolerance can be viewed as a broader category that includes disorders of the autonomic nervous system, such as reflex syncope, postural tachycardia syndrome, and autonomic failure.[12]
Symptoms of orthostatic intolerance include syncope, near syncope fatigue, palpitations, exercise intolerance, cognitive impairment, headache, and fatigue.11 Various forms of orthostatic intolerance, including postural orthostatic tachycardia (POT) and sympathotonic orthostatic hypotension (SOH), have been exhibited following bariatric surgery, specifically after RYGB and Vertical Banded Gastroplasty (VBG).[10,11,13]
Postural orthostatic tachycardia can be defined as an increase in heart rate upon standing without orthostatic hypotension.[14] Sympathotonic orthostatic hypotension refers to orthostatic hypotension upon standing with associated tachycardia.[10,13]
Orthostatic intolerance is a disabling neurological condition that has been linked to bariatric surgery. A retrospective study by Billakanty et al11 examined the incidence of orthostatic intolerance in 15 patients with a mean weight loss of 124.22lbs who underwent either RYGB or VBG. They examined autonomic responses using the tilt table test and found that 53 percent had a neurocardiogenic response, 20 percent had a dysautonomic response, and 20 percent had a postural tachycardia response. They did not find any association between the change in BMI and occurrence of orthostatic intolerance.[11]
A case report by Rubestein et al10 also evaluated the occurrence of orthostatic intolerance in a patient who underwent gastric banding with a 126.67lb weight loss over eight months. Her symptoms did not respond to volume expansion and gradually improved with administration of fludrocortisone, erythropoietin, and diet supplementation. Her symptoms only completely resolved following removal of the band with a subsequent weight gain of 17.78 lbs.[10]
It has been postulated that orthostatic intolerance results from weight loss-related reduction of baseline blood pressure and alteration of autonomic responsiveness.[11] A significant amount of weight loss seems to be a common thread among these patients who exhibit symptoms of orthostatic intolerance. In a case report by Hoeldtke et al,13 four patients with orthostatic intolerance were all found to have significant weight loss from various maladies, and therefore, they suggested that radiation therapy-induced anorexia, weight loss, and malnutrition may all have a role in the etiology of orthostatic hypotension.[13]
Moreover, a hypocaloric protein diet is thought to result in a decrease in sympathetic-nervous-system activity and the development of orthostatic hypotension which also supports the idea that rapid weight loss may alter autonomic function.[15] Although Billakanty et al11 displayed autonomic insufficiency among RYGB and VBG patients, the three cases within this report represent the first documented examples of orthostatic intolerance among LSG patients. All of these patients presented with similar symptoms of dizziness upon standing with tachycardia associated with a significant amount of weight loss (70lbs, 75lbs, and 55lbs respectively). Each case represents varying extremes of the same condition with one requiring hospitalization and medical therapy for severe symptoms, while the others required only conservative management. However, the common thread between the three cases is the significant weight loss within a short time interval following LSG with development of symptomatic orthostatic hypotension. Although orthostatic intolerance has been documented as a complication of RYGB and VBG, to our knowledge these are the first observed cases following LSG.
According to the mechanisms of obesity-related HTN, it seems that drugs acting to block the RAAS and target the SNS should be ideal for treatment. There is little evidence in the literature to suggest that one drug is better than another in controlling HTN.[4] Significant reduction in blood pressure can be seen within one month after surgery, with up to 25 percent of patients showing resolution and 36 percent demonstrating improvement of hypertension.1 Diuretic treatments may also be responsible for dehydration, hypotension, and loss of electrolytes.[16]

There is clear consensus in the management of pre-existing medical conditions to make adjustments to concomitant drug treatment. In those patients without complete resolution of their T2DM, hyperlipidemia, or HTN, continued surveillance and management should be guided by currently accepted practice guidelines for those conditions.[2] In those patients in whom T2DM, hyperlipidemia, and HTN have resolved, continued surveillance should be guided by recommended screening guidelines for the specific age group.[2]
Blood pressure increases again over the course of 10 years following weight reducing surgical procedures, despite ongoing weight loss.[17] Antihypertensive differential therapy should be focused on pathophysiology and concomitant and target organ disease. Thus, ACE inhibitors, in combination with low dose diuretics, should be preferentially administered, followed by calcium antagonists.[17] Beta blockers should be used if definite cardiac indications are present.[17]
Appropriate medical management of the hypertensive patients during surgical weight loss involves close follow up with frequent blood pressure assessments and timely down regulation of medications and doses to compensate for the diuresis and spontaneous blood pressure lowering. The role of the general practitioner has to be emphasized: clinical visits and follow ups should be monitored and coordinated with the bariatric team, including the surgeon, the obesity specialist, the dietitian, and mental health professionals.
Some patients may develop significant orthostatic intolerance due to autonomic insufficiency following bariatric surgery. Awareness of the potential association between LSG and a new orthostatic intolerance is important for providing timely care.

1.    Hinojosa M, Varela J, Smith B, et al. Resolution of systemic hypertension after laparoscopic gastric bypass. J Gastrointest Surg. 2009;13(4):793–797.
2.    Mechanick JI, Kushner RF, Sugerman HJ, et al. American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery medical guidelines for clinical practice for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient. Obesity. 2009; 17:1–70.
3.    Abu-Jaish, W, Rosenthal, W. Sleeve Gastrectomy: A new surgical approach for morbid obesity. Expert Rev. Gastroenterol. Hepatol. 2010;4(1):101–119.
4.    Kurukulasuriya LR, Stas S, Lastra G, et al. Hypertension in obesity. Med Clin North Am. 2011;95(5):903–917.
5.    Sugerman H, Wolfe L, Sica D, et al. Diabetes and hypertension in severe obesity and effects of gastric bypass induced weight loss. Ann Surg. 2003;237:751–758.
6.    Himpens J, Dapri G, Cadiere GB. A prospective randomized study between laparoscopic gastric banding and laparoscopic isolated sleeve gastrectomy: results after 1 and 3 years. Obes Surg. 2006;16(11):1450–1456.
7.    Karamanakos SN, Vagenas K, Kalfarentzos F, et al. Weight loss, appetite suppression, and changes in fasting and postprandial ghrelin and peptide-YY levels after Roux-en-Y gastric bypass and sleeve gastrectomy: a prospective, double blind study. Ann Surg. 2008;247(3):401–407.
8.    Juhasz-Pocine K, Rudinicki S, Archer R, Harik S. Neurologic complications of gastric bypass surgery for morbid obesity. Neurology. 2007;68:1843–1850.
9.    Abu-Jaish W, Ramirez A, Patel S, et al. Prevalence of nutritional deficiencies after laparoscopic sleeve gastrectomy as a final step in morbidly obese patients. Presented at: The ASMBS 26th Annual Meeting. Grapevine, TX, USA, 21–26 June, 2009.
10.    Rubinstein R, Ciubortaru M, Elad H, Bitterman H. Severe orthostatic hypotension following weight reduction surgery. Arch Intern Med. 2001;161:2145–2147.
11.    Billakanty S, Klingman M, Kanjwal Y, Kosinski D, et al. New-onset orthostatic intolerance following bariatric surgery. Pacing Clin Electrophysiol. 2008;31(7):884–888.
12.    Grub B. Neurocardiogenic syncope and related disorders of orthostatic intolerance. Circulation. 2005;111:2997–3006.
13.    Hoeldtke R, Dworkin G, Gaspar S, Israel B. Sympathotonic orthostatic hypotension. A report of four cases. Neurology. 1989;38:34–40.
14.    Jacob G, Costa F, Shannon J, Robertson R, et al. The neuropathic postural tachycardia syndrome. N Eng J Med. 2000;343:1008–1014.
15.    Dehaven J, Sherwin R, Hendlerm R, Felig P. Nitrogen and sodium balance and sympathetic nervous system activity in obese subjects treated with low-calorie protein or mixed diet. N Engl J Med. 1980;302:477–482.
16.    Poitou Bernert C, Ciangura C, Coupaye M, Czernichow S, Bouillot JL, Basdevant A. Nutritional deficiency after gastric bypass: diagnosis, prevention and treatment Diabetes Metab. 2007;33:13–24.
17.    Scholze J1, Patschan S, Dörffel Y, Hansen A. Therapy of obesity-associated hypertension. Dtsch Med Wochenschr. 2005;130(46):2645–2650.

Funding: No funding was provided.

Disclosures: The authors report no conflicts of interest relevant to the content of this article.

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