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Table of Contents
Year : 2020  |  Volume : 6  |  Issue : 3  |  Page : 45-46

Substantial weight loss can precipitate alarming illness

Professor, Department of Nephrology, Sanjay Gandhi Post Fraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Submission28-Feb-2021
Date of Acceptance01-Mar-2021
Date of Web Publication13-Apr-2021

Correspondence Address:
Dr. Anita Saxena
Department of Nephrology, Sanjay Gandhi Post Fraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrnm.jrnm_8_21

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How to cite this article:
Saxena A. Substantial weight loss can precipitate alarming illness. J Renal Nutr Metab 2020;6:45-6

How to cite this URL:
Saxena A. Substantial weight loss can precipitate alarming illness. J Renal Nutr Metab [serial online] 2020 [cited 2021 Jun 13];6:45-6. Available from: http://www.jrnm.in/text.asp?2020/6/3/45/313634

In early Pleistocene, a million years ago, the human ancestral tree finds a mention of a slender bipedal body with heavily built jaws matching his broad face and huge flat molars adapted for heavy chewing of nutritious nuts for brain growth and development, the man named by the archeologists “the Nutcracker Man” Paranthropus boisei, belonging to a branch of hominid family. Incidentally, the latest reports on Nutcracker Man's body reveal that the “Nutcracker Man” was neither a nutcracker nor a slender primate strolling about East Africa's savannah. He was, rather, a powerful arboreal swinger with strong arms and legs to match his robust jaw.

Although the word “nutcracker” has travelled a long way from heavy jaws to slim ones, in modern times, its implication is much serious. In the medical world, Nutcracker Syndrome (NCS) invites special mention, a renal condition caused by entrapment of left renal vein (LRV) between the superior mesenteric artery (SMA) and the aorta without accompanying symptoms. It can present with left side flank pain, usually manifesting with hematuria, and at times accompanied by albuminuria and pelvic congestion (characterized by symptoms of dysmenorrhea, dyspareunia, lower abdominal pain, dysuria, pelvic, vulvar, gluteal or thigh varices, and emotional disturbances).[1],[2],[3]

Compression of the LRV can cause left renal-to-gonadal vein reflux, resulting in lower limb varices and varicoceles in males.[4]

Although primarily a vascular disorder its manifestations are predominantly urological or gynecological, though some are seen by vascular surgeons also if patient has lower limb varices as their main presenting complaint. Therefore, patients presenting with lower limb varices or recurrent flank pain may be investigated for NCS.[5]

The subtle difference between “Nutcracker phenomenon” and “Nutcracker Syndrome (NCS)” is the time of appearance of symptoms. This issue carries a review on this condition, and the reason why this article merits special reference is that, though there is not much that can be done in NCS through nutritional intervention to ameliorate symptoms, a similar condition exists which involves nutritional intervention, though it neither has a renal origin nor may always be present concomitantly with NCS. The condition similar to NCS portrays Hippocrates belief that “illness in general has an internal cause and thus has a biological nature or etiology.” SMA syndrome corroborates the belief. SMA was first described by Rokitansky in 1861, which arises when there is a loss of aortomesenteric fat around the SMA.

SMA and NCS entities share a common etiology, that is, weight loss. The duodenum and the LRV, present in the same anatomical plane between the SMA and the aorta, are both at risk of compression when this plane is reduced (the normal aortomesenteric angle is reported to be between 28 and 65 degrees and the normal aortomesenteric distance is between 10 and 34 mm). One might assume that as an individual loses enough weight to cause one of the syndromes, it should not be uncommon to have the second syndrome developing as well.[6] Hence, Nutritional therapy should be carefully titrated according to the patient's caloric and protein requirements, with gradual commencement of therapy and close monitoring of fluid and electrolyte balance.[7],[8]

Hence, retroperitoneal fat depletion reduces the fat plane between SMA and the aorta vessels, leading to mechanical compression of the duodenum causing duodenum outlet obstruction and which causes further weight loss due to compromised food intake and thus creates a vicious cycle. It manifests with nonspecific symptoms of nausea, bilious vomiting, anorexia and epigastric pain, early satiety, and postprandial bloating, and if left untreated, result in significant electrolyte imbalances and other morbidities associated with malnutrition because of which the diagnosis of SMA syndrome is often delayed and made through a process of exclusion after the consideration of other differential diagnoses including megaduodenum, pancreatitis, and peptic ulcer disease.

Acquired factors for this syndrome are numerous, and the syndrome has also been described following cancer, burns, other surgeries, and psychological disorders associated with weight loss, such as bariatric surgery. In younger patients, it most commonly occurs after corrective spinal surgery for scoliosis. Some patients may have genetic predisposition too. Congenital factors include an abnormally high origin of the ligament of Treitz which pulls the duodenum toward the root of the mesentery. A short aortomesenteric distance or a narrow aortomesenteric take-off angle is a hallmark of SMA, with duodenal obstruction, leading to postprandial abdominal pain relieved by vomiting and nasogastric decompression and proper positioning after eating (such as lying in the left side or standing or sitting with a knee-to-chest position) may be recommended to alleviate symptoms.[9]

In severe cases, intravenous, parenteral[10] nutritional support, and/or a feeding tube may be needed to provide enough calories. The nutritional impact of SMA Syndrome may vary between patients. Some individuals may be able to tolerate small, frequent meals, or a liquid or soft diet. In contrast, other individuals may not be able to tolerate oral or gastric enteral feeding at all, in which case, nasojejunal feeding or parenteral nutrition may be needed.[11]

Symptomatic patients are usually started on oral enriched liquids which will relieve fatigue by increasing energy levels, followed by slow and gradual introduction of small and frequent soft (mashed) meals and reintroduction of normal diet as tolerated.[7]

Regular solid foods are later introduced as per patient's tolerance. Antiemetics treatment to prevent vomiting can benefit. The absence from food since the patient is unable to tolerate per orally intake though suppresses symptoms but escalates malnutrition.[12]

Therefore, nutritional therapy should be carefully titrated according to the patient's caloric and protein requirements, with gradual commencement of therapy and close monitoring of fluid and electrolyte balance to prevent refeeding syndrome.[13]

Needless to say that underfeeding can lead to delays in the correction of SMA syndrome, poor wound healing, respiratory muscle weakness, immunosuppression, and loss of lean body mass.[14],[15]

Hence, the management of nut cracker targets nutritional support that would ensure weight regain as a cure for most of the cases.

This issue also addresses gut microbiota dysbiosis, modulator of immune function, and Licorice plant extract, a probable immunity booster with targeted anti-inflammatory activity, and a, protective complimentary remedy as an antiviral. Article on implementation of nutrition care process in nephrology practice and a clinical case accompanying it on application of Medical Nutrition Therapy in chronic renal disease is of immense relevance for introducing and implementing it in Indian clinical practice.

  References Top

Ahmed K, Sampath R, Khan MS. Current trends in the diagnosis and management of renal nutcracker syndrome: A review. Eur J Vasc Endovasc Surg 2006;31:410-6.  Back to cited text no. 1
d'Archambeau O, Maes M, De Schepper AM. The pelvic congestion syndrome: The role of nutcracker phenomenon and results of endovascular stent. JBR-BTR 2004;87:1-8.  Back to cited text no. 2
Scultetus AH, Villavicencio JL, Gillespie DL. The nutcracker syndrome: Its role in the pelvic venous disorders. J Vasc Surg 2001;34:812-9.  Back to cited text no. 3
Little AF, Lavoipierre AM. Unusual clinical manifestations of the nutcracker syndrome. Australas Radiol 2002;46:197-200.  Back to cited text no. 4
Takemura T, Iwasa H, Yamamoto S, Fukushima K, Isokawa S, Okada M, et al. Clinical and radiological features in four adolescents with nutcracker syndrome. Paediatr Nephrol 2000;14:1002-5.  Back to cited text no. 5
Inal M, Unal Daphan B, Karadeniz Bilgili MY. Superior mesenteric artery syndrome accompanying with nutcracker syndrome: A case report. Iran Red Crescent Med J 2014;16:e14755.  Back to cited text no. 6
Chan DK, Mak KS, Cheah YL. Successful nutritional therapy for superior mesenteric artery syndrome. Singapore Med J 2012;53:e233-6.  Back to cited text no. 7
Vulliamy P, Hariharan V, Gutmann J, Mukherjee D. Superior mesenteric artery syndrome and the 'nutcracker phenomenon'. BMJ Case Rep 2013;2013:bcr2013008734.  Back to cited text no. 8
Karrer FM. Superior Mesenteric Artery Syndrome. Medscape Reference; 6 January 2017. Available from: http://emedicine.medscape.com/article/932220-overview.  Back to cited text no. 9
Bohanon FJ, Nunez Lopez O, Graham BM, Griffin LW, Radhakrishnan RS. A case series of laparoscopic duodenojejunostomy for the treatment of pediatric superior mesenteric artery syndrome. Int J Surg Res 2016;2016:1-5.  Back to cited text no. 10
Diab S, Hayek F. Combined superior mesenteric artery syndrome and nutcracker syndrome in a young patient: A case report and review of the literature. Am J Case Rep 2020;21: e922619-1–e922619-5.  Back to cited text no. 11
Felton BM, White JM, Racine MA. An uncommon case of abdominal pain: Superior mesenteric artery syndrome. West J Emerg Med 2012;13:501-2.  Back to cited text no. 12
Covelli HD, Black JW, Olsen MS, Beekman JF. Respiratory failure precipitated by high carbohydrate loads. Ann Intern Med 1981;95:579-81.  Back to cited text no. 13
Khan LU, Ahmed J, Khan S, Macfie J. Refeeding syndrome: A literature review. Gastroenterol Res Pract 2011;2011:410971.  Back to cited text no. 14
Allison SP. Effect of insulin on metabolic response to injury. JPEN J Parenter Enteral Nutr 1980;4:175-9.  Back to cited text no. 15


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