Invest Clin 61(3): 242- 264, 2020 https://doi.org/10.22209/IC.v61n3a05


Wilkie’s syndrome. Analysis of 150 cases of the Iberian and Ibero-American medical literature.


Ezequiel Trejo Scorza1, Oscar Luis Colina Cedeño1, Edgar José Brito Arreaza1 and Carlos José Trejo Scorza2


1Centro Médico de Caracas, and Escuela de Medicina “Luis Razetti”, Facultad de Medicina, Universidad Central de Venezuela, Caracas, Venezuela.

2Clínica “La Floresta”, Caracas, Venezuela.


Key words: Wilkie’s syndrome; vascular compression of the duodenum; obstruction duodenal; superior mesenteric artery syndrome.


Abstract. Willkie’s syndrome or superior mesenteric artery (SMA) syndrome is a rare cause of gastrointestinal obstruction, due to exterior compression of the horizontal part of the duodenum by the SMA. For the study of the clinical, diagnostic and therapeutic characteristics of Wilkie’s syndrome in the Iberian and Ibero-American population, we compiled the reports of 150 cases by Iberican and Ibero-American authors, and we found a predominance of cases in females over males in a ratio of 2.57: 1. Fifty percent of the cases were in patients under 20-years of age, with the highest number of cases in schoolchildren and adoles- cents. The most frequent symptoms were abdominal pain, vomiting and weight loss. The disease had two forms of presentation: acute with signs of high intesti- nal obstruction (16.47%), and chronic (83.53%). Diagnostic radiographic studies showed in of the upper gastrointestinal tract narrowing of the horizontal portion of the duodenum and delay in the transit of contrast through the gastroduodenal region, with or without gastroduodenal dilation in 85% of cases. In computed tomographic studies it was observed decreased mesenteric-aortic angle and dis- tance. Upper endoscopic studies showed narrowing of the horizontal part of the duodenum, with or without gastroduodenal dilation in 61.90% of cases. Of the 144 patients that received treatment, 94 cases received medical treatment, with a success rate of 62.77%; and 84 cases required surgical treatment, 59.52% of these, upon admission. The most practiced surgical procedure was laterolateral duodenojejunostomy in 70.24% of cases. We concluded that Wilkie’s syndrome is an entity that results from the reduction of the mesenteric-aortic angle and dis- tance, with two forms of presentation: acute and chronic, that required surgical treatment in 58.33% of cases.


image


Corresponding author: Ezequiel Trejo-Scorza. “Centro Médico” of Caracas, and Escuela de Medicina “Luis Razetti”, Facultad de Medicina, Universidad Central de Venezuela, Caracas, Venezuela. E-mail: trejoscorza@gmail.com


image


Síndrome de Wilkie. Análisis de 150 casos de la literatura Ibérica e Ibero-americana.

Invest Clin 2020; 61 (3): 242-264


Palabras clave: Síndrome de Wilkie; compresión vascular del duodeno; obstrucción duodenal; síndrome de la arteria mesentérica superior.


Resumen. El síndrome de Wilkie o síndrome de la arteria mesentérica (AMS) es una causa poco común de obstrucción gastrointestinal, debido a la compresión externa de la parte horizontal del duodeno por la AMS. Para el es- tudio de las características clínicas, diagnósticas y terapéuticas del síndrome de Wilkie en la población ibérica e iberoamericana, analizamos los reportes de 150 casos por autores ibéricos e iberoamericanos, y encontramos un predomi- nio de casos de sexo femenino sobre el masculino en una proporción de 2,57:

1. El 50% de los casos ocurrieron en menores de 20 años, con el mayor número de casos en escolares y adolescentes. Los síntomas más frecuentes fueron do- lor abdominal, vómitos y pérdida de peso. La enfermedad tuvo dos formas de presentación: aguda con signos de obstrucción del intestino superior (16,47%) y crónica (83,53%). Los estudios de diagnóstico radiográfico mostraron en el tracto gastrointestinal superior: estrechamiento de la porción horizontal del duodeno y retraso en el tránsito del contraste a través de la región gastroduo- denal con o sin dilatación gastroduodenal en 85% de los casos; en tomografía computarizada: disminución del ángulo y la distancia aórtica mesentérica; y en endoscopia superior: estrechamiento de la parte horizontal del duodeno, con o sin dilatación gastroduodenal en 61,90%. De los 144 pacientes que recibieron tratamiento, 94 casos recibieron tratamiento médico, con una tasa de éxito del 62,77%; y 84 casos requirieron tratamiento quirúrgico, 59,52% de estos, al ingreso. El procedimiento quirúrgico más practicado fue la duodenoyeyunos- tomía laterolateral en 70,24%. Concluimos que el síndrome de Wilkie es una entidad que resulta de la reducción del ángulo y de la distancia mesentérica aórtica, con dos formas de presentación: aguda y crónica. Se requirió trata- miento quirúrgico en el 58,33% de los casos.


Received: 31-03-2020 Accepted: 15-07-2020


INTRODUCTION


The constriction of the horizontal part of the duodenum by the root of the mesentery or Wilkie’s syndrome, is also known as vascu- lar compression of the duodenum, superior mesenteric artery syndrome, aortomesenter- ic clamp syndrome, cast syndrome, arterio- mesenteric duodenal compression, arterio-

mesenteric ileus, gastro-mesenteric ileus, chronic duodenal ileus, arterio-mesenteric duodenal obstruction and mesenteric-aortic impingement. It results, in partial or total obstruction of the horizontal part of the du- odenum, and its clinical manifestations are abdominal pain, vomiting, weight loss, and sometimes, abdominal distension. It is an uncommon entity and can compromise the


patient’s life. Due to its low frequency, it is little known, and thus is not included among the first diagnostic possibilities, which delays the diagnosis and proper treatment. Most authors point out that Rokitansky, was the first to describe the compression of the hori- zontal part of the duodenum by the superior mesenteric artery, in 1861; but Bermanski et al (1), who presented a complicated case by pancreatitis and performed a very com- plete historical review, indicated that: 1.- the first description of the superior mesenteric artery syndrome was made by Boernerus in 1752; 2.- Rokitansky in 1842, described the acute dilation of the stomach resulting from compression of the duodenum by the root of the mesentery. 3.- Stavely, in 1910 was the first to practice a successful duodenojeju- nostomy in a patient with gastro-mesenteric ileus. Wilkie in 1921 (2), presented four cas- es and concluded that: 1.- the compression of the horizontal part of the duodenum by the root of the mesentery is a true clinical and pathological entity; 2.- the most proper treatment is drainage of the duodenum by duodenojejunostomy. In 1927 (3) he pre- sented a series of 75 cases, where the female sex predominated in a ratio of 2.26: 1 and the youngest patient was a 7-year-old boy. Of these, 64 cases were operated by the author, and 57 with follow-up with significant cure or improvement in about 81% of the cases. After these papers’ publication, this disease is known worldwide as Wilkie’s Syndrome.

We reviewed the papers published on children cases (4-8) and found that: 1.- The compression of the horizontal part of the duodenum by the superior mesenteric artery represents 23% of extrinsic causes and 15% of the total causes of duodenal obstruction. 2.- the surgical treatment that combines the lowest morbidity and the earliest recovery of the gastrointestinal function, consists in the duodenal derotation procedure (mobiliza- tion, and placement of the duodenum in the right paravertebral canal), proposed by Louw in 1957. This surgical technique is similar to

what is done in the Ladd procedure for intes- tinal malrotation, but the mesentery in the region of the ileocecal valve and the lateral unions of the ascending colon, should be left joined to the retroperitoneum to prevent volvulus of the middle intestine.

We reviewed the world medical litera- ture on this syndrome and were able to com- pile and analyze the papers published by Ibe- rian and Ibero-American authors, regardless of the language of publication of the papers (Spanish, Portuguese or English). We found 58 papers in Latin America with reports of 78 cases (9-66), and 44 papers with 72 cases (67-110) in the Iberian Peninsula; for a total of 102 papers with 150 cases. In all these papers, we reviewed and analyzed the epide- miology, etiopathogenesis, clinical, diagnos- tic, therapeutic procedures and the results obtained.


MATERIALS AND METHODS


Through the search engines of medical papers PubMed, Lilacs, Scielo, Medes, Dial- net, Medigraphic, using the search criteria: Wilkie’s Syndrome and Superior Mesenteric Artery Syndrome, we found 106 publica- tions of Iberian and Ibero-American authors and were able to access 102 of them. We reviewed the data of all patients reported with Wilkie’s Syndrome diagnosis in the 102 reviewed publications. The data extracted and analyzed included sex, age, symptoms presented, medical and surgical history, du- ration of symptoms, means of diagnosis and findings, treatment and results. For its anal- ysis, all the information was entered into a spreadsheet of the LibreOffice program (Ver- sion: 6.1.5.2 Build ID: 1:6.1.5-3+deb10u5; OS: Linux 4.19) and divided them into three groups: a) those that responded to medical treatment, b) those who did not responded to medical treatment and needed surgical treatment, and c) those who needed surgical treatment upon admission.


RESULTS


  1. Sex: Of the 150 cases, 108 (72%) were in females and 42 (28%) were in males, with a predominance of females over males in a proportion of 2.57.

  2. Age: The age range was from one day of life to 83 years of age, with an average of 26.093 years. Two cases were in new- borns, both females (40,66). The dis- tribution by age is shown in Fig. 1. We found that 75 cases (50.00%) were di- agnosed before 20 years of age and the highest number of cases (66 cases) in schoolchildren and adolescents that to- gether represent 88% of cases in pediat- ric ages. See Fig. 2. The high incidence in adolescents seems to be due to rapid growth without weight gain (7,8).

  3. Medical-surgical background and asso- ciated pathologies: Of the 150 patients, 53 (35.33%) presented medical-surgical background and associated pathologies which we grouped into four categories:

  4. a. Patients with weight loss were 24 ca- ses and their causes are shown in Table I.

    1. Patients with anatomical causes that decreased the aortomesen- teric distance were 17 cases and their causes are shown in Table II.

      image

    2. Patients with personal or family his- tories were four cases: family history of Wilkie’s Syndrome (1 case); Raynaud’s syndrome history and psychological disor-


      -

      -

      -


      Fig. 1. Shows the distribution for age groups: 50% of the patients were diagnosed before 20 years of age.

      ders manifested by depression and anxi- ety (1 case); personal medical history of Wilkie’s Syndrome and celiac disease (1 case); and family history of adenomatous polyposis, who underwent ileoanal anasto- mosis, which was the cause of the vascular compression of the duodenum (1 case).

    3. Patients with histories of many surgi- cal interventions on the abdominal cav- ity were five cases and in all of them, the symptoms persisted and only disappeared when an enteric bypass procedure was practiced: duodenojejunostomy in four cases, and gastrojejunostomy in Y of Roux in one case.

  5. Clinical manifestations: we were able to collect the time of appearance of symptoms in 85 cases, and ranged from 12 hours to 27 years, manifesting in hours one case, in days 13 cases, in months 39 cases and in years 32 cases. In the 150 cases analyzed, we found the symptoms shown in Table III, and as you can see, the most frequent were ab- dominal pain, vomiting and weight loss. Abdominal pain of epigastric location and of postprandial apparition, which was sometimes reported as fullness or postprandial discomfort, which calmed down with vomiting, which could be oc- casional or incoercible. Vomiting was reported as bilious in 41 (36.28%) of the 113 cases with this symptom. The sum of the incidence of the symptoms: food intolerance, nausea and vomiting accounted for 119 patients (79.33%). Weight loss occurred in 48.67% and abdominal distension in 18.00%. Ab- dominal distention when it occurred was a sign of massive gastric dilation as showed the radiological studies. We divided the patients depending on the required treatment, into three groups: a) Those who responded to med- ical treatment: 60 patients, b) those who did not respond to medical treat- ment and needed surgical treatment: 34 patients and c) those who needed


    image


    Fig. 2. Shows the age distributions in pediatric patients. The schoolchildren and adolescents together repre- sent 88% of cases in pediatric ages.


    TABLE I

    WILKIE’S SYNDROME. CAUSES OF WEIGHT LOSS.


    CAUSES

    Number of cases and percentage

    Anorexy

    5 (20.83%)

    Disabling neurological diseases

    5 (20.83%)

    Low-calorie diets

    4 (16.67%)

    Oncological diseases

    3 (12.50%)

    Endocrine diseases (hyperthyroidism)

    2 (8.33%)

    Plastic surgery (patients undergo diets with losing weight before

    plastic surgery) 2 (8.33%)

    Burns 1 (4.17%)

    Debilitating diseases and chronic infections 2 (8.33%) Repetitive episodes of lung infection; hepatitis at age 16;

    chickenpox in childhood; disseminated herpes simplex; 1

    autoimmune hemolytic anemia and bronchiectasis

    Chronic malnutrition exacerbated and family history of

    tuberculosis and abdominal tuberculosis demonstrated by 1

    lymph node biopsy

    image


    TABLE II

    image

    WILKIE’S SYNDROME. ANATOMICAL CAUSES THAT DECREASED THE DISTANCE AORTOMESENTERIC.

    CAUSES Number of cases Percentage

    Diseases of the spine, or orthopedic or surgical procedures on the spine

    10 58.82%

    Peripheral vascular diseases 5 (Abdominal aortic aneurysms 4)

    29.41%


    Previous surgical interventions (ileoanal anastomosis) 1 5.88%


    A large mass located in the hepatic angle of the colon (colon adenocarcinoma) The tumor that pulled and tensed from the transverse mesocolon causing the duodenal compression.


    1 5.88%



    TABLE III

    image

    WILKIE’S SYNDROME. CLINICAL MANIFESTATIONS.

    groups studied, to predict what symp- toms could establish the need for sur- gical treatment, the Chi-square values

    Clinical manifestations

    Number of cases

    Percentage

    obtained were: for pain 1,105824541,

    for vomiting 11,051156656 and for

    Abdominal pain 114 76%

    weight loss 18,78133536. As the value

    of the degrees of freedom was 2 and the

    Vomiting


    Bilious vomiting

    113


    41 (36.28%)

    of the 113 cases with vomiting

    75.33%

    reliability of 99%, the critical value cor- responded to 18,4662 and the only val- ue of the Chi-square test that exceeded the critical value, was the value of Chi-

    Nausea 5 3.33%

    Food intolerance 1 0.67%

    Weight loss 73 48.67%

    Abdominal

    distension 27 18.00%

    image


    surgical treatment upon admission: 50 patients. We excluded six patients, five in which the treatment received was not specified and one that died before being able to receive the treatment. The clinical manifestations of each of these groups are shown in Table IV. The incidence of vomiting and weight loss were more frequent in patients who re- quired surgical treatment as you can see in Table V. Bilious vomiting was more frequent in patients who need sur- gical treatment upon admission. When we applied the Chi-square test to each of the clinical manifestations (pain, vomiting, and weight loss) in the three

    square test for weight loss.

  6. The diagnostic studies performed were simple standing X-ray of abdomen (24 cas- es), upper gastrointestinal tract radiogra- phy (100 cases), upper gastrointestinal tract endoscopy (42 cases), computed to- mography (CT) (74 cases), magnetic res- onance imaging (MRI) (3 cases), arteriog- raphy (2 cases), abdominal ultrasound (29 cases), diagnostic laparoscopy (1 case). The results of the radiologi- cal and endoscopic studies are shown in Tables VI, VII and VIII. Belowareshownthemostfrequentfindings ineachofthediagnosticstudiesperformed:

    a. - Standing X-ray of the abdomen showed gastric dilation, accompanied or not by duodenal dilation, in 62.50% of cases. b.- Upper gastrointestinal tract radiogra- phy showed the narrowing of the hori- zontal part of the duodenum and delay in contrast transit through the gastroduo- denal region accompanied or not by gas-


    TABLE IV

    image

    WILKIE’S SYNDROME.CLINICAL MANIFESTATIONS BY GROUPS.


    Abdominal pain

    Vomiting

    Weight loss

    Total Patients

    Patients responded to medical treatment


    47 (42.34%)


    39 (34.51%)


    17 (23.94%)


    60 (41.67%)

    Patients did not respond to medical treatment and needed surgical treatment


    24 (21.62%)


    30 (26.55%)


    20 (28.16%)


    34 (23.61%)

    Patients needed surgical treatment upon admission


    40 (36.03%)


    44 (38.93%)


    34 (47.89%)


    50 (34.72%)

    Total

    111

    113

    71

    144


    TABLE V

    WILKIE’S SYNDROME. CLINICAL MANIFESTATIONS IN PATIENTS THAT RESPONDED TO MEDICAL TREATMENT VS CLINICAL MANIFESTATIONS IN PATIENTS THAT NEEDED SURGICAL TREATMENT.


    Abdominal pain

    Vomiting

    Weight loss

    Total Patients

    Patients responded to medical treatment


    47 (42.34%)


    39 (34.51%)


    17 (23.94%)


    60 (41.67%)

    Patients needed surgical treatment


    64 (57.66%)


    74 (65.49%)


    54 (76.06%)


    84 (58.33%)

    Total

    111

    113

    71

    144


    TABLE VI

    image

    WILKIE’S SYNDROME. RADIOLOGICAL FINDINGS IN THE X-RAYS OF THE STANDING ABDOMEN IN 24 CASES.


    Radiological findings found Number of cases Percentage

    Gastric dilatation 13 (two cases with

    significant gastric dilatations)

    54.17%

    Gastric and duodenal dilatation 2 8.33% Air-fluid level in upper abdomen and gastric chamber distension 2 8.33% Air-fluid level in right iliac fossa 1 4.17%

    Double bubble image 1 4.17%

    Dilatation loop small intestine 1 4.17%

    Intestinal pneumatosis 1 4.17%

    Study reported without alterations or inconclusive 3 12.50%

    Total 24 100%

    image


    TABLE VII

    image

    WILKIE’S SYNDROME. RADIOLOGICAL FINDINGS IN THE UPPER GASTROINTESTINAL TRACT RADIOGRAPHS IN 101 CASES.

    Radiological findings Number of cases Percentage

    Gastroduodenal dilatation with duodenal constriction and delay in contrast transit

    50 50%

    Duodenal constriction and delay in contrast transit 35 35%

    Gastroduodenal dilatation 11 11%

    Study reported as normal 02 2%

    Radiological findings suggestive of Wilkie’s syndrome 01 1%

    Duodenal ulcer with delay in contrast transit 01 1%

    Total 100 100%


    TABLE VIII

    WILKIE’S SYNDROME. FINDINGS FOUND IN UPPER DIGESTIVE TRACT ENDOSCOPY IN 42 CASES.


    Findings

    Number of cases

    Percentage

    Gastroduodenal dilatation with narrowing of the horizontal part of the duodenum


    13


    30.95%

    Narrowing of the horizontal part of the duodenum

    13

    30.95%

    Gastroduodenal dilatation

    03

    7.14%

    Stomach operated Billroth I

    01

    2.38%

    Gastric cancer

    01

    2.38%

    Gastritis and gastroduodenitis

    04

    9.52%

    Bile inside the stomach

    01

    2.38%

    Gastric stasis

    03

    7.14%

    Phytobezoar in the duodenum

    01

    2.38%

    Study reported as normal

    02

    4.76%

    Total

    42

    100%


    troduodenal dilation in the 85% of cases. c.- Computed tomography showed: the aortomesenteric angle was reported di- minished, without indicating its valor in 9 cases. In 37 cases the valor of the aortomesenteric angle was reported with precision, varying between 6º to 40º and with an average of 16.1º. In the rest of the 11 cases, the valor of the aortomesenteric angle was reported as follows: less than 13º (one case), less than 15º (one case), less than 20º (six cases) and less than 25º (three cases). The aortomesenteric distance was reported diminished, without indicating its valor in 14 cases, one of them with an aneurysm. The valor of the aortomesenteric distance was reported in 22 cases. In 19 cases the valor of aortomesenteric distance was re- ported with precision, varying between from 0.53 mm to 10.5 mm with an aver- age of 4.38 mm. In three cases the valor of the aortomesenteric distance was report- ed as follows: less than 5 mm, between 4 and 5 mm, and between 6 and 8 mm. d.- Upper gastrointestinal tract endoscopy showed the narrowing of the horizontal part of the duodenum, accompanied or not

    by gastroduodenal dilation in the 61.90%. e.- Magnetic resonance imaging was prac- ticed in three cases, reporting the value of the aortomesenteric angle in two cases (10º and 17º) and in the remaining case, they reported extrinsic compression of the horizontal part of the duodenum. f.- Arteriography in two cases, the aor- tomesenteric angle was reported di- minished, without indicating its valor.

    g. - Abdominal ultrasound was performed in 29 cases, showing bowel dilation in

    13 cases, decreased aortomesenteric angle in three cases, decreased aorto- mesenteric distance two cases in both of 3 mm, compression of the horizon- tal part of the duodenum one case and pneumobilia and fluid in pelvis one case. h.- Diagnostic laparoscopy in one case revealed extrinsic compression of the duodenum by the mesenteric vessels at the level of the birth of the middle colic artery.

  7. Treatment: Of the 144 patients in whom the treatment received was registered,

    94 (65.27%) received medical treat- ment and of these, 59 patients (62.77%) presented a satisfactory response. One


    62-year-old male patient, with the diag- nosis of well-differentiated gastric ade- nocarcinoma classified as Borrmann II, died for bronchoaspiration with sepsis of respiratory origin, while waiting for a laparoscopic approach to gastric can- cer and Wilkie syndrome. Of the 84 pa- tients who required surgical treatment, 50 patients (59.52%) required it upon

    admission, and 34 patients (40.48%) af- ter receiving medical treatment with an unfavorable response. Table IX shows the surgical procedures performed. Lat- erolateral duodenojejunostomy alone or in combination with other surgical

    procedures was the surgical interven- tion most used and was performed in 59 cases (70.24%).

  8. Postoperative results, complications, and mortality: Of the 84 patients who received surgical treatment, 79 cases (94.05%) had satisfactory results, the- re were four deaths (4.76%) and one case (1.19%) did not report results. Intra and postoperative complications occurred in seven patients and are shown in Table X.

  9. The causes of death are shown in Table XI.


TABLE IX

SURGICAL PROCEDURES IN WILKIE’S SYNDROME.


Surgical procedures

Nº of Cases

Percentaje

A. Duodenal derotation (1)

2

2.38%

    1. Treitz ligament section with duodenal descent (Strong technique)

      as a unique surgical procedure (2) 11 13.10%

    2. Treitz ligament section with duodenal descent (Strong technique) combined with another surgical procedure in an only surgical intervention

with laterolateral duodenojejunostomy

10

11.91%

with superior mesenteric vessel reimplantation in the infrarenal aorta

1

1.19%

3. Enteric bypass by

3.1.

Gastrojejunals anastomosis

gastrojejunostomy due to significant gastric dilatation

3

3.57%

terminoterminal gastrojejunostomy en Roux Y by previous Billroth I.

1

1.19%

3.2.

Duodenoduodenostomy

1

1.19%

3.3.

Duodenojejunostomy as a unique surgical procedure

laterolateral duodenojejunostomy

47

55.95%

Roux-en-Y duodenojejunostomy

3

3.57%

Duodenojejunostomy ahead of the superior mesenteric vessels with

segmental resection of the duodenum 1 1.19%

  1. Total gastrectomy due to gastric necrosis 2 2.38%

  2. Other surgical procedures

jejunostomy for enteral feeding 1 1.19% resection of a large colon tumor that pulled and tensed the

transverse mesocolon causing the duodenal compression. 1 1.19%

image

  1. one case presented perforated ulcer at the level of the horizontal part of the duodenum that required resection of third and fourth part of the duodenum and terminoterminal anastomosis of the second part of the duodenum to jejunum.

  2. two cases required a second intervention (laterolateral duodenojejunostomy) in one accompanied by a gastrec- tomy partial.


TABLE X

SURGICAL COMPLICATIONS IN WILKIE’S SYNDROME.


Surgical complications

Nº of Cases

Percentaje

1. Need for surgical reinterventions

5

71.42%

Obstruction of the efferent loop by adhesions

1

Anastomosis leak

1

A patient undergoing duodenal derotation that required two reoperations: one by a bowel obstruction by adhesions, and another by an ulcer perforated in the horizontal part of the duodenum that required resection of the horizontal and ascended parts of the duodenum with a terminoterminal duodenumjejunal anastomosis


1

Unsuccessful response to Strong’s technique

2

2. Pancreatic injury with fistula that responded to medical treatment

1

14.29%

3. Postoperative shock in a patient with large colon tumor that it pulled and tensed the transverse mesocolon causing a duodenal compression


1


14.29%


TABLE XI

image

CAUSES OF DEATH IN WILKIE’S SYNDROME.

Causes of death Nº of Cases Percentaje

Cardiovascular complications in a female patient of 83 years 1 16.67%

Multiple organ dysfunction syndrome three months after the operation in

a 56-year-old male patient with a history of hypertension, alcoholism and chronic renal failure with aortic stent due to aneurysm

Respiratory symptoms five days after the operation in a 19-year-old female patient with a history of repetitive episodes of lung infection; hepatitis at age 16; chickenpox in childhood; disseminated herpes simplex; autoimmune hemolytic anemia and bronchiectasis

Postoperative shock in a 77-year-old female patient with colon cancer when resecting a tumor. The tumor pulled and tensed the transverse mesocolon causing the duodenal compression

Bronchoaspiration with sepsis of respiratory origin in 62-year-old male patient with the diagnosis of well-differentiated gastric adenocarcinoma classified as Borrmann III who was waiting for a laparoscopic approach to gastric cancer and Wilkie syndrome

Rupture of an aortic aneurysm before being able to receive treatment in a

1 16.67%


1 16.67%


1 16.67%


1 16.67%

66-year-old male patient 1 16.67%

image


DISCUSSION


Wilkie syndrome or vascular compres- sion of the duodenum is the constriction of the horizontal part of the duodenum by the root of the mesentery with partial or total duodenal obstruction. It is a rare and little known entity with an incidence between

0.0024% and 0.53% (111), not included in the initial diagnostic possibilities, which de- lays the diagnosis (38) and treatment.

Its embryological and anatomical bases are well known (111,112): in humans, the superior mesenteric artery under normal conditions arises from the abdominal aorta at the level of the first lumbar vertebra at an


angle that averages 42.4 degrees, with a wide range of variation from 18 to 70 degrees.

The extrinsic compression of the duo- denum by the superior mesenteric artery occurs when the aortomesenteric angle de- creases to values between 1 to 40 degrees with an average of 15.2 degrees (Fig. 3). The left renal vein and the uncinate process of the pancreas, located over the horizontal part of the duodenum, occupy the narrowest part of the aortomesenteric angle (Fig. 3). When the amplitude of the angle decreases, the left renal vein is pressed by the superior mesenteric artery, causing the nutcracker syndrome, which can occur alone (113) or in combination with the vascular compres- sion syndrome of the duodenum (105,114).

In the etiopathogenesis of this disease are distinguished predisposing and precipi- tating factors. The predisposing factors that contribute to the development of the compression of the duodenum by the supe- rior mesenteric artery are (111,115): 1.- The crossing of the horizontal part of the duode- num at the level of the fourth lumbar vertebra where the lumbar curvature reaches its most anterior position and is more pronounced. Under normal conditions, the horizontal part of the duodenum crosses the abdomen at the level of the third lumbar vertebra; oc- casionally, in women, the crossing is at the

level of the fourth lumbar vertebra. 2.- ex- aggerated lumbar lordosis, or orthopedic or surgical procedures on the spine: normally, the aortomesenteric distance is from 10 to 28 mm and an exaggerated lumbar lordosis decreases it to 2 to 8 mm. 3.- A shortened or hypertrophied of the suspensory muscle of the duodenum causes an upward movement of the duodenum at the angle between the superior mesenteric artery and the aorta. 4.- An abnormally low origin of the superior mesenteric artery. The precipitating factors are the significant weight loss or rapid growth without weight gain (8,115) associated with an extensive loss of retroperitoneal and mes- enteric fat that contribute to a decrease in the aortomesenteric angle and distance (8).

We found a predominance of the female sex over the male in a proportion of 2.57, and the 50% of cases occurred in patients under 20 years of age, with the highest inci- dence in schoolchildren and adolescents, as it has been reported in the literature (111). The age range was from one day of life to 83 years of age, with an average of 26.093 years. Medical-surgical background and associated pathologies were present in 53 patients, with weight loss being present in 24 patients (45.28%) (Table I) and anatomical causes that decreased aortomesenteric distance in 17 patients (32.07%) (Table II).


image


Fig. 3. Shows in the left side a normal angle aortomesenteric, and in the right side the constriction of the horizontal part of the duodenum by a decrease of the angle aortomesenteric.


The clinical manifestations of this syn- drome are abdominal pain, vomiting, weight loss (Table III), and sometimes, abdominal distention. The disease has two forms of pre- senting: acute, with signs of high small bow- el obstruction (115-117), and chronic, with an insidious medical history of intermittent abdominal pain associated with vomiting, early satiety, and anorexia, many times for many years. In the chronic presentation, the symptoms are less specific and compatible with those of peptic ulcer disease, pancreati- tis, biliary colic, and patients who are mis- diagnosed and mistreated for many years, (116,118) delaying diagnosis and proper treatment. In our analysis, we could compile the time of apparition of symptoms in 85 cases that ranged from 12 hours to 27 years. The disease manifested in an acute form in 14 cases (16.47%) (in hours in one case and days in 13 cases) and in a chronic form in 71 cases (in months in 39 cases and years in 32 cases) (83.53%). In our review, the most frequent symptoms were abdominal pain, vomiting, and weight loss. The abdominal distention, when it was present was a sign of gastric dilation (79,81,100,119,120) and could be complicated with gastric necrosis (81,100).

To make the diagnosis is necessary a high index of clinical suspicion and the meticulous evaluation of the radiological studies.

The acute presentation form manifests with signs of high partial obstruction of the small intestine. Simple X-ray of abdomen shows a gastric air bubble with few amounts of gas in the intestine distal to the site of ob- struction (5,7,66) See Fig. 4. In the chronic presentation form, the symptoms often do not have the intensity that in the acute pre- sentation form, the vomiting may not have bile, and the clinical picture can be confused with anorexia nervosa and bulimia delaying the diagnosis by months and years.

The upper gastrointestinal tract ra- diography shows (66): 1.- gastroduodenal dilatation with delay in contrast transit through the gastroduodenal region, accom-

panied or not by gastroduodenal dilation, and fight sign of the stomach. Under normal conditions, the descending part of the duo- denum empties the barium so quickly, that it is difficult to get a radiograph that shows this part of the duodenum well-distended; while in patients with vascular compression of the duodenum, the descending part of the duodenum remains distended (7); 2.- the narrowing of the horizontal part of the duo- denum, as a vertical abrupt cut-off over or to the right of the spine and 3.- few amounts of contrast and gas, in the intestine distal to the site of obstruction; 4.- the relief of ob- struction with postural changes (121,122).

The computed tomography as a diag- nostic study replaced the hypotonic duode- nography and the aortic and superior mes-


image


Fig. 4. Shows a Simple X-ray of abdomen standing where we can see a gastric air bubble with few amounts of gas in the intestine distal to the site of obstruction, a characteristic image of a high partial obstruction of the small intestine.


enteric artery angiography, because it is: 1. a fast, reliable, non-invasive method, 2. shows the exact anatomic position of the duode- num in the aortomesenteric angle, 3. allows to calculate the values of the aortomesenter- ic angle and the distance aortomesenteric, and 4. excludes other causes of obstruction (111,122).

In the papers reviewed (121-128), the normal value of the aortomesenteric angle varied between 28º to 65º and the of the aor- tomesenteric distance between 10 and 34 mm. The values of the aortomesenteric angle and distance are considered abnormal when these are less than 22º to 25º and of 8 to 10 mm respectively (66,121-128). In our review, the value of the aortomesenteric angle varied from 6º to 40º with an average of 16.1º, and the of the aortomesenteric distance varied from 0.53 to 10.5 mm with an average of 4.38 mm; and these values coincide with those re- ported in the literature (111,112).

The upper gastrointestinal tract en- doscopy allows: to show the presence of the narrowing of the horizontal part of the duodenum sometimes reported as pulsatile compression, accompanied or not by gas- troduodenal dilation, also rule out associ- ated pathologies such as bezoars (97) and peptic ulcers (107,129-131) and, allows the placement of nasojejunal tubes beyond the obstruction site to provide enteral nutrition support (118). When it is performed with curvilinear array endoscopy ultrasound, the value of the aortomesenteric angle (132) can be determined.

In the differential diagnosis, it is con- venient to keep in mind the diagnosis of inverse duodenum, which is a duodenal anomaly that has also been associated with obstructive symptoms and that simulate the clinical manifestations of Wilkie’s syndrome and its upper gastrointestinal tract radiogra- phy has been interpreted as compatible with the superior mesenteric artery syndrome (133-135).

In the absence of pathological condi- tions that need immediate surgical explora-

tion, for example, an aneurysm, the treat- ment of the Wilkie’s syndrome is initially medical and consists of gastric decompres- sion, correction and maintenance of the hydro-electrolytic balance, antibiotic thera- py and enteral nutritional support through of nasogastric (110) or nasojejunal tube (136-137), which causes weight gain with an increase in the peripheral fat to the superior mesenteric artery that augmentation the angle and the distance between the superior mesenteric artery and the aorta, with the disappearance of the symptomatology. Sur- gical treatment is necessary when medical treatment fails, or when there are clinical manifestations of intestinal obstruction (51, 66,118,137-139).

There are three types of surgical inter- ventions:

  1. Enteric bypass procedure. Of the three surgical procedures included in this section, the laterolateral duodenojeju- nostomy, proposed by Bloodgood (140), first performed successfully by Stavely

    (141) and popularized by Wilkie (2-3), is the most frequently performed surgi- cal procedure with satisfactory results and with a very low complication rate. Gastrojejunostomy has been performed when there is a significant gastric dila- tion but it is not recommended because the duodenal content before the site of obstruction must pass to the stomach to drain to the jejunum (137,139). Sometimes, during the surgical inter- vention, the inframesocolic duodenum does not look dilated and the diagnosis of vascular compression of the duode- num could be missed (4). There is an intraoperative maneuver that consists of the injection of 150 to 300 cc of air through a nasogastric tube, observing after the air injection, dilatation of the duodenum from 4 to 5 cm, when there is a vascular compression of the duode- num (139).

  2. Section of the suspensory muscle of the duodenum with the descent of


the duodenal-jejunal angle: In 1958,

malrotation. The mesentery should be

Strong described one case of arteriome-

left attached to the retroperitoneum

senteric duodenal obstruction in which

in the region of the ileocecal valve, and

he practiced the section of the sus-

the lateral attachments of the ascend-

pensory muscle of the duodenum with

ing colon should also be preserved to

surgical mobilization of the ascending

prevent midgut volvulus (8). It has been

part of the duodenum and relocation of

practiced successfully and has the ad-

the duodenojejunal angle from the level

vantage that it does not need the use of

of the second to the third lumbar ver-

anastomosis (4-8,143-147).

tebral body, with complete remission

When analyzing the medical treatment

of the symptomatology (142). In our

vs. surgical treatment of 150 patients, six pa-

analysis, we found this surgical techni-

tients were excluded: five in whom the treat-

que was performed as an only surgical

ment received was not specified, and one that

procedure in 11 patients with a success

died before being able to receive the treat-

rate of 81.82%. Two of these cases re-

ment. Of the remaining 144 patients, 94 re-

quired a second intervention (laterola-

ceived medical treatment, with a satisfactory

teral duodenojejunostomy). In eleven

response in 62.77% of cases, and one death

cases, it was performed with another

for bronchoaspiration with sepsis of respira-

surgical procedure in a single surgical

tory origin, in a 62-year-old male patient with

intervention; in 10 cases with duodeno-

the diagnosis of well-differentiated gastric

jejunostomy and in one case with reim-

adenocarcinoma, classified as Borrmann III,

plant of the superior mesenteric artery.

who expected by a therapeutic laparoscopic

3.

Duodenal derotation: described by

approach to gastric cancer and Wilkie syn-

Louw and recommended by Wayne

drome. Of the 84 patients who required sur-

and Burrington for the treatment of

gical treatment, 59.52% of the cases required

children with this pathology (6-8),

it upon admission and 40.48% had received

in our analysis, it was only performed

medical treatment with an unfavorable re-

in 2 cases and one of them required

sponse. Intra or postoperative complications

a second intervention by had perfo-

occurred in seven cases (8.235%), and of

rated ulcer in the horizontal part of

these, five cases (5.88%) required surgical re-

the duodenum that required resec-

intervention. The causes of surgical reinter-

tion of horizontal and ascending part

ventions are shown in Table X. Once the surgi-

of the duodenum and terminotermi-

cal complications were overcome, all patients

nal anastomosis of the descending

undergoing surgical treatment responded

part of the duodenum to the jejunum.

satisfactorily, and the symptoms disappeared.

The duodenal derotation also is known

Causes of death. As can be seen in Table

as Ladd’s procedure (143-144), consist-

XI, the causes of death found are related to

ing of lysing the suspensory muscle of

pathologies concomitant with the duodenal

the duodenum with of mobilizing the

vascular compression syndrome (aneurysms,

entire duodenum and the proximal je-

malignant tumors, senility, immunological

june. The opening at the root of the

alterations).

mesentery is enlarged to at least 10

From this review, we can conclude that

cm in length, and the entire jejunum is

vascular compression of the duodenum is a

passed to the right through this open-

pathological entity that results from the de-

ing. The entire duodenum and proximal

crease in angle and distance aortomesenteric,

part of the jejunum now lie in the right

whose highest incidence is in patients under

paravertebral gutter, much as they do

20 years of age, predominating in schoolchil-

after the Ladd procedure for intestinal

dren and adolescents. This syndrome has two


ways of manifesting clinically: 1. an acute clin- ic form, with a high partial intestinal obstruc- tion; and 2. a chronic, insidious presentation, which is often confused with anorexia nervo- sa. It is diagnosed by upper gastrointestinal tract radiography, computed tomography, and upper gastrointestinal tract endoscopy. The diagnostic radiological criteria are: 1. abrupt vertical and oblique compression of the mucosal folds, produced by the constric- tion of the horizontal part of the duodenum by the superior mesenteric artery; 2. delay in contrast transit through the gastroduodenal region; 3. dilatation of the first and second portions of the duodenum, with or without gastric dilatation; 4. an antiperistaltic flow of barium proximal to the obstruction pro- ducing to-and-fro movements; 5. relief of obstruction when the patient is placed in a position that diminishes the drag of the small bowel mesentery (the left later decubitus, prone, or the knee-chest position) (148). The tomographic criteria are: 1. abrupt obstruc- tion in the third portion of the duodenum, with active peristalsis, 2. an aortomesenteric angle less than 25º and an aortomesenteric equal to or less than 8 mm 3. high fixation of the duodenum by the suspensory muscle of the duodenum or anatomical variants of the superior mesenteric artery (46,149). The up- per gastrointestinal tract endoscopy allows:

  1. to show the presence of the narrowing of the horizontal part of the duodenum, some- times reported as pulsatile compression, ac- companied or not by gastroduodenal dilation,

  2. rule out associated pathologies such as be- zoars and peptic ulcers and, 3. the placement of nasojejunal tubes beyond the obstruction site for providing enteral nutrition support.

The treatment is initially medical (110) and consists of gastric decompression, fluid electrolytes imbalance correction, antibi- otic therapy, and nutritional support either through total parenteral nutrition or nasoje- junal tube feeding (46,150). The nutritional support is aimed at the gain of weight, to the restoration of retroperitoneal fat, with increase in retroperitoneal and mesenteric

fat that contributes to increasing the values of the aortomesenteric angle and distance. Posturing maneuvers during meals and pro- kinetic medications may be helpful in some patients with nutritional support. If medi- cal treatment fails there are three surgical treatment options (137): 1- Section of the suspensory muscle of the duodenum with the descent of the duodenal-jejunal angle;

  1. laterolateral duodenojejunostomy, and

  2. duodenal derotation. Of these, the most practiced is the laterolateral duodenojeju- nostomy with satisfactory results.


ACKNOWLEDGMENTS


We would like to thank the staff of the “Dr. Francisco Baquero González” Library for the search for medical research papers; Drs. Hilda Martorelli and Jorge Barba Flores, who reviewed the paper and for its transla- tion into the English language.


REFERENCES


  1. Bermanski P, Golden Richard L, Ricca Richard J. Superior mesenteric artery syn- drome complicated by pancreatitis. A case presentation and historical background. Vasc Surg 1995; 29(3):217-223. Available from: http://journals.sagepub.com/doi/pdf

    /10.1177/153857449502900308.

  2. Wilkie DPD. Chronic duodenal ileus.

    Br J Surg 1921;9:204-214. https://doi. org/10.1002/bjs.1800093405.

  3. Wilkie DPD. Chronic duodenal ileus. Am J Med Sci 1927;173:643-649.

  4. Wayne ER, Burrington JD. Extrinsic duo- denal obstruction in children. Surg Gynecol Obstet. 1973;136(1):87-91.

  5. Wayne ER, Burrington JD. Management of 97children with duodenal obstruction. Arch Surg 1973; 107(6):857–860. Availa- ble from: https://Doi:10.1001/archsurg. 1973.01350240027009.

  6. Wayne ER, Burrington JD. Duodenal Obs- truction by the superior mesenteric artery in children. Surg 1972;72(5):782-768.

  7. Burrington JD, Wayne ER. Obstruction of the duodenum by the superior mesenteric


    artery — Does it exist in children? J Pediatr Surg 1974;9(5):733-741. Doi: https://doi. org/10.1016/0022-3468(74)90112-2.

  8. Burrington JD. Superior mesenteric artery syndrome in children. Am J Dis Child 1976; 130(12):1367-1370. Doi: 10.1001/archpe- di.1976.02120130073015.

  9. Rodríguez A, Romero Vidomlansky SI, Fe- rrarotti C, Larrañaga N, Gallo JC, Kozi- ma S. Síndrome de la arteria mesentérica superior. Presentación de un caso. Rev Ar- gent Radiol 2014;78(2):96-98. Https://doi. org/10.1016/j.rard.2014.06.007.

  10. Naveiro JJ, Jimenez A, Kury M, Abate M, Amor H. Síndrome de compresión vascular del duodeno. Rev Argent Cir 1991;61:146- 149.

  11. Fiorini S, Sáenz Tejeira MM, Tennina C, Tomezzoli S, Requejo N. Síndrome de la arteria mesentérica superior (síndrome de Wilkie). Caso clínico. Arch Argent Pe- diatr 2008;106(6):533-551. https://www. sap.org.ar/docs/archivos/2008/arch08_6/ v106n6a15.pdf

  12. Arrieta Yánez L, Aycardi Valverde F, Quin- tana C. Síndrome de la arteria mesentérica superior en adolescente de 15 años de edad. Reporte de un caso. Rev Pediatr Elizalde 2015;6(1-2):31-33. Available from: https:// apelizalde.org/revistas/2015-1-2-ARTICU- LOS/RE_2015_1-2_RC_4.pdf

  13. Manfrin L, Scrigni A. Adolescente con dolor abdominal y vómitos. Med Infant 2013;20(1):58-61. Available from: http:// www.medicinainfantil.org.ar/images/sto- ries/volumen/2013/xx_1_058.pdf

  14. Herbella FAM, Varela CE, Miranda Jr. F, Del Grande JC, Beaton HL. Superior me- senteric artery syndrome and aortic aneu- rism. Arq Bras Cir Dig 2005;18(1):25-27.

  15. Barchi LC, Alves AM, Jacob CE, Caldas Bres- ciani CJ, Yagi OK, Nogueira TG, Cecconello I, Zilberstein B. Favorable minimal invasi- ve surgery in the treatment of superior me- senteric artery syndrome: Case report. Int J Surg Case Rep 2016;29:223-226. https://doi. org/10.1016/j.ijscr.2016.09. 016.

  16. Takano C, Oliveira F, Okawa M. Síndrome do pincamento aorto-mesenterico – Relato de caso. Rev Med Paraná 2004;62(1):24-26.

  17. Barros DH de, Arguello MEF, Hoyo MBD, Ramos SRTS. Síndrome da artéria mesen-

    térica superior: relato de um caso. Pediatria (São Paulo) 2003;25(3):134-137.

  18. Lima HS, Maia AM, Castro Neto AKP de.

    Síndrome da artéria mesentérica superior. Rev Col Bras Cir 2000;27(2):128-130.

  19. Alvarez GC, Dal Bosco MH, Streher LA, Alvarez SJ, Ritzel RA. Síndrome da arté- ria mesentérica superior. Rev Col Bras Cir 1994;21(4):225-226.

  20. Cavichini QN, Tinoco ECA, Brum AV, An- derson PAV, Gomes LR. Obstruçäo duode- nal por compressäo vascular: síndrome da artéria mesentérica superior. Rev Col Bras Cir 1994;21(4):229-232.

  21. Almeida Jr. N de. Estase duodenal crônica por oclusäo aortomesentérica Rev Bras Med 1987;44(4):94-97.

  22. França Neto PR, Paiva RdeA, Lacerda Filho A, Queiroz FL de, Noronha T. Su- perior mesenteric artery compression syn- drome - case report. J Coloproctol (Rio J.) 2011;31(4), 401–404. Doi: 10.1590/s2237-

    9363201100040001.

  23. Matheus Claudio de Oliveira, Wais- berg J, Zewew MH de Toledo, Godoy AC de. Syndrome of duodenal compression by the mesenteric artery following res- torative proctocolectomy: a case report and review of literature. Sao Paulo Med J 2005;123(3):151-153. Available from: http://www.scielo.br/pdf/spmj/v123n3/ a13v123n3.pdf.

  24. Cesconetto DM, Mattosinho TJ, Gestic MA, Chaim EA. Superior mesenteric artery syn- drome: case report. GED 2012;31(4):138-

    141. Available from: http://files.bvs.br/ upload/S/0101-7772/2012/v31n4/a3929. pdf.

  25. Martín Torres OJ, Soares Costa V da C, Noleto Araujo RA, Lima e Lima CN, Cos- ta de Castro IT. Síndrome da artéria me- sentérica superior: relado de caso. GED 2013;32(2):50-52.

  26. Zorrón R, Milcent M, Contreras M, Lukas- hok H, Marquez R, Madureira Filho D. La- paroscopic repair of superior mesenteric artery syndrome: sutured Handsewn duode- nojejunostomy technique. Rev Bras Video Cir 2003;1(3):87-91. https://www.sobracil.org. br/revista/rv010103/rbvc010103_087.pdf.

  27. De Oliveira Martins RG. Síndrome de Wi- lkie secundária a volumoso aneurisma da


    aorta abdominal: relato de caso. Available from: http://iradtelerradiologia.com.br/ wp-content/uploads/2017/12/RELATO- DE-CASO-SAMS.pdf.

  28. Pastén González A, Muñoz Araneda A, Peirano Bastías A, Rojas Castro S, Hen- ríquez Alessandrini V. Síndrome de la ar- teria mesentérica superior. Presentación de un caso y revisión de la literatura. Cir Pediatr 2016;29:180-183. Available from: https://www.secipe.org/coldata/upload/re- vista/2016_29-4_180_183.pdf

  29. Ríos M G, Thumler U J, Toro A C. Sín- drome de la arteria mesentérica superior. Presentación de dos casos. Rev Chil Pe- diatr 1986;57(4):355-358. Available from: https://scielo.conicyt.cl/pdf/rcp/v57n4/ art10.pdf.

  30. Ibarra-I FJ, Arriagada-M D. Síndrome de la arteria mesentérica superior: caso clínico y revisión. Bol Esc Med UC de Chile 2006;31(1):42-46 Available from: http://publicacionesmedicina.uc.cl/Bole- tin/20061/SindromeArteria.pdf

  31. Tapia-V A, Sharp-P A, Llanos-L O, Rahmer- O A, Zúñiga Díaz A. Síndrome de compre- sión vascular del duodeno. Comunicación de 2 casos. Rev Med Chile 1993; 121: 425-

    429.

  32. Castaño Llano R, Chams Anturi A, Aran- go Vargas P, García Valencia Á. Síndrome de la arteria mesentérica superior o sín- drome de Wilkie. Rev Colomb Gastroente- rol 2009;24(2):200-209. Available from: http://www.scielo.org.co/pdf/rcg/v24n2/ v24n2a14.pdf.

  33. Jiménez-Castro L, Aguirre HD, Posada- López AF. Síndrome de arteria mesentérica superior secundario a quemadura severa. CES Medicina 2014;28(1):139-146. Avai-

    lable from: http://www.scielo.org.co/pdf/ cesm/v28n1/v28n1a12.pdf

  34. Vásquez-Arango JN, Durán-Meléndez MA, Vásquez-Maya C. Tratamiento mí- nimamente invasivo del síndrome de Wi- lkie. Rev Colomb Cir 2018; 33:299-306. Available from: http://www.revistacirugia. org/media/k2/attachments/sindrome- de-Wilkie-vasquez.pdf. https://doi.org/10. 30944/20117582.75.

  35. Poblete-Otero F, Álvarez-Pertuz H, Arana- Sáenz A. Síndrome de Wilkie . Acta Méd Cos-

    tarric 2015;57(3):145-148. Available from: http://actamedica.medicos.cr/index.php/ Acta_Medica/article/download/893/811

  36. Delgado Alonso A, Morales Díaz I, Pita Armenteros L. Síndrome de la arteria me- sentérica superior: presentación de un caso y revisión de la literatura. Rev Cubana Cir 2008;47(2) Available from: http://scielo. sld.cu/pdf/cir/v47n2/cir08208.pdf.

  37. Larrea Fabra ME. Compresión vascular del duodeno: presentación del caso. Rev Cuba- na Cir 1986;25(1):35-40.

  38. Molina Proaño GA, Cobo Andrade MM, Guadalupe Rodríguez RA, Gálvez Salazar PF, Cadena Aguirre DP, González Poma GV, Gutierrez Granja BM. Wilkie’s syndro- me, a missed opportunity. J Surg Case Rep 2018;9:1–3. Doi: 10.1093/jscr/rjy246.

  39. Castillo León J, Pacheco Barzallo F, Ordo- ñez M del Cisne, Pacheco Granda F. Sín- drome de Wilkie. Rev Cir 2017;14(1):49-54. Available from: http://www.scgp.org/revis- ta-cirujano/pdf/2017-REVISTA-CIRUJANO. pdf.

  40. Alvarado-García R, Ponce-Rosas A, García- Sánchez D, Gallego-Grijalva JE. Compre- sión vascular del duodeno en un neonato. Acta Pediatr Méx 2007;28(2):69-73. Avai- lable from: https://www.medigraphic.com/ pdfs/actpedmex/apm-2007/apm072e.pdf.

  41. Calderon Elvir C, Tapia Garibay JI, Ismael Cuzmar M. Síndrome de la arteria mesen- térica superior: un diagnóstico infrecuente en el cual se debe pensar. Acta Pediatr Méx 1994;15(1):37-40.

  42. García Álvarez J, Pérez Islas A, Sánchez Conde RM, Luna Ortíz K. Síndrome de la arteria mesentérica superior. Informe de una paciente. Cir Gen 2000;22(4):347-350. Available from: https://www.medigraphic. com/pdfs/cirgen/cg-2000/cg004h.pdf.

  43. García-Frade-Ruiz LF, Mundo-Gallardo LF, Solís-Ayala E. Síndrome de Wilkie. Med Int Méx 2017;33(2):254-258. Available from: http://www.scielo.org.mx/pdf/mim/ v33n2/0186-4866-mim-33-02-00254.pdf.

  44. Garteiz Martínez D, Carbó Romano R, Bravo Torreblanca C, López Acosta ME, Vega Rivera F, Weber Sánchez A. Aborda- je laparoscópico para la liberación del liga- mento de Treitz en paciente con síndrome de arteria mesentérica superior. Rev Méx


    Cir Endoscop 2009;10(1):49-53. Available from: https://www.medigraphic.com/pdfs/ endosco/ce-2009/ce091j.pdf.

  45. González Camarena V. Síndrome de com- presión duodenal por los vasos mesentéri- cos. Cir Cir 1984;52(3):203-206.

  46. González Hermosillo-Cornejo D, Díaz Girón-Gidi A, Vélez-Pérez FM, Lemus- Ramírez RI, Andrade Martínez-Garza P. Síndrome de Wilkie. Reporte de un caso. Cir Cir 2015; 85(1):54–59. Https://doi. org/10.1016/j.circir.2015.08.009.

  47. González Mondragón MB, Granados Na- vas FJ, Herrera Garcia W. Síndrome de la arteria mesentérica superior en un pa- ciente con tuberculosis abdominal. Acta Pediatric Méx 2010;31(5):244-247. Avai- lable from: http://www.redalyc.org/pdf/ 4236/423640325011.pdf.

  48. Loera-Torres MA, García-Núñez LM, Cabe- llo-Pasini R, Morales Arias S, Núñez Can- tú O, Rivera-Cruz JM. Síndrome de Wilkie: Reporte de dos casos. Rev Sanid Milit Méx. 2010;64(1):41-46. Available from: https:// www.medigraphic.com/pdfs/sanmil/sm- 2010/sm101g.pdf.

  49. Navarrete-Arellano M, Soto-Fernández AE. Síndrome de arteria mesentérica superior: Dos casos clínicos en pacientes pediátri- cos. Rev Méx Cir Pediatr 2009;16(3):119-

    125. Available from: https://www.medigra- phic.com/pdfs/revmexcirped/mcp-2009/ mcp093c.pdf.

  50. Ochoa-Nava R, Guadarrama-Vallejo AC, García-Carrizosa S, Herrera-Víctor FJ. Sín- drome de la arteria mesentérica superior: una causa inusual de obstrucción intestinal incompleta en un paciente pediátrico. Rev Méx Pediatr 2017;84(2):61-65. Available from: https://www.medigraphic.com/pdfs/ pediat/sp-2017/sp172d.pdf.

  51. Osegueda de Rodríguez EJ, Hernández- Villegas AC, Serralde-Zúñiga AE, Reyes- Ramírez ALdelC. The two sides of superior mesenteric artery syndrome treatment: conservative or surgical management? Nutr Hosp 2017;34(4):997-1000. Available from: http://scielo.isciii.es/pdf/nh/v34n4/33_ nota.pdf.

  52. Ovalle-Chao C, Hinojosa-Martinez LM, Gutierrez-Castillo A, Velazco-De La Garza JH, Flores-Villalba E, Diaz-Elizondo JA,

    Garza-Serna U. Acute-onset of superior mesenteric artery syndrome following sur- gical correction of scoliosis: Case report and review of literature. J Pediatr Surg Case Rep 19 (2017) 31e33. https://doi. org/10.1016/j.epsc.2017.02.008.

  53. Sánchez-Lozada R, Acosta-Rosero AV, Ba- las-Salame C, Chapa-Azuela O, Hurtado- López LM. Síndrome de la arteria mesen- térica superior como causa de intolerancia parcial crónica a la alimentación oral. Re- porte de un caso y revisión del tema. Rev Gastroenterol Méx 2002;67(1):38-42.

  54. Suárez Gutiérrez R, Jiménez Urueta PS, Castañeda Ortiz RA, Sánchez Mi- chaca VJ, García Galavís JL. Megagas- tria y megaduodeno asociado con sín- drome de arteria mesentérica superior y síndrome de cascanueces. Rev Esp Méd Quir 2011;16(1):51-55. Available from: http://www.redalyc.org/service/redalyc/ downloadPdf/473/47317815010/1.

  55. Valdes A, Cárdenas O, Espinosa A, Villazón O, Valdes V. Superior mesenteric artery syn- drome. J Am Coll Surg 2005;201(5):808. https://doi.org/10.1016/j.jamcollsurg. 2005.04.033.

  56. Ruíz-Mar G, Cárdenas Serrano OE, Álva- rez Correa LA, Morán Sierra OT, Sánchez Navarro López AL, Sánchez-Delgado, Pé- rez Escobedo SU. Manejo quirúrgico de urgencia en el síndrome de Wilkie. A pro- pósito de un caso. Cir Gen 2018;40(4):279-

    281. Available from: https://www.medigra- phic.com/pdfs/cirgen/cg-2018/cg184j.pdf.

  57. Loja Oropeza D, Alvizuri Escobedo J, Vilva Vazquez M, Sánchez Mercado M. Síndrome de Wilkie: Compresión vascu- lar del duodeno. Rev Gastroenterol Perú 2002;22(3):248-252. Available from: http:// www.scielo.org.pe/scielo.php?pid=S1022- 51292002000300009&script=sci_arttext.

  58. Varela Vega M, Durán F, Larrosa G, Re- yes S, Cabillón J, Simonet F. Síndrome de Wilkie: un caso de oclusión duodenal por pinza aortomesentérica. Salud Militar 2017;36(1):51-54.

  59. Czarnevicz Canavesi D, Secondo G, Ra- dio A, Odriozola M, Rossi I, Iacopino J. Oclusión duodenal por pinza aortomesen- térica. Un nuevo caso clínico. Cir Uruguay 1994;64:225-227.


  60. Acosta-M B, Guachalla G, Martínez C, Fel- ce S, Ledezma G. Compresión vascular del duodeno. GEN 1991;45(1):61-64.

  61. Sánchez Ismayel A, Cohén D, D’Amelio C, Daly K, Sánchez R, Salas J. Síndrome de arteria mesenterica superior: causa inusual de obstruccion duodenal. Vitae 2007;32. Available from: http://vitae.ucv.ve/index_ pdf.php?module=articulo_pdf&n=1136.

  62. Bandres D, Ortiz A, Dib Jr. J. Superior mesenteric artery syndrome. Gastrointest Endosc 2008;68(1):152–156: https://doi. org/10.1016/j.gie.2007.09.033.

  63. Mota M, Abusaid S, Muñoz C. Síndrome de Wilkie: a propósito de un caso. CIMEL. 2014;19(2):91-95. Available from: https:// www.cimel.felsocem.net/index.php/CI- MEL/article/download/491/297.

  64. Vassallo M, Marín J, Hernández Y, Cha- parro ML, Malave H. Síndrome de la ar- teria mesentérica superior. Reporte de un caso y revisión de la literatura. Rev Fac Med 2010;33(2):159-163. Available from: http://190.169.30.98/ojs/index.php/rev_ fmed/article/download/4909/4720.

  65. Trejo Padilla E. Cirugía del tubo digestivo en el niño. Tribuna Médica 1976;45(5):41-48.

  66. Trejo Scorza E, Brito Arreaza EJ, Colina Cedeño OL, Lander Gonzalez BJ, Trejo Scorza CJ. Vascular compression of the duodenum or Wilkie’s syndrome. Presenta- tion of a case and review of world medical literature. Rev Cent Med 2019;58(148):43-

    48. Available from: https://www.revistacen- tromedico.org/ediciones/2019/2/art-3/

  67. Rosa-Jiménez F, Rodríguez González FJ, Puente Gutiérrez JJ, Muñoz Sánchez R, Adarraga Cansino MD, Zambrana García JJ. Compresión duodenal por la arteria me- sentérica superior: análisis de 10 pacientes. Rev Esp Enferm Dig 2003;95(7):480-484.

  68. Gutiérrez Junquera C, Gonzálvez Piñera J, Pérez Martínez A, Marco Macián A. Sín- drome de arteria mesentérica superior: Una causa infrecuente de obstrucción duodenal en la infancia. An Esp Pediatr 1996;45:289-

    290. http://www.aeped.es/sites/default/ files/anales/45-3-14.pdf.

  69. Morán Penco JM, Cardenal Murillo J, De La Calle Pato U, Masjoan D. Un posible caso de origen congénito de síndrome de la arteria mesentérica superior (SAMS). Cir

    Pediatr 2008;21:228-231. Available from: https://www.secipe.org/coldata/upload/re- vista/2008;21.228-31.pdf

  70. Fernández López MT, López Otero MJ, Bardasco Alonso ML, Álvarez Vázquez P, Rivero Luis MT, López Barros G. Síndro- me de Wilkie: a propósito de un caso. Nutr Hosp 2011;26(3):646-649. Available from: http://scielo.isciii.es/pdf/nh/v26n3/31_ caso_clinico_01.pdf.

  71. Ruíz Padilla FJ, Mostazo Torres J, Vílchez Jaimez M. Significant gastric distension caused by superior mesenteric artery syn- drome or Wilkie’s syndrome. Gastroente- rol Hepatol 2017;40:581-583. https://doi. org/10.1016/j.gastre.2017.08.002.

  72. Beltrà Picó R, Hernández Castelló C, Sanchis Solera L, Guindos Rúa S, Mol A, Germani M. Laparoscopia en cirugía pe- diátrica. Utilidad en enfermedades poco frecuentes. Canar Pediátr 2013;37(3):172-

    178. Available from: http://portal.scptfe. com/wp-content/uploads/2013/12/2013- 2.a.pdf

  73. Castañeda Heredia A, Gálvez García C, Rivero Falero M, Abreu Yanes I, Martín Fumero L. Síndrome de arteria mesenté- rica superior en una niña de 11 años con escoliosis tratada con un corsé corrector. Canar Pediátr 2013;37(3): 179-181. Availa- ble from: http://portal.scptfe.com/wp-con- tent/uploads/2013/12/2013-2.b.pdf.

  74. Farré R, Blanco JA, Isnard RM, Alastrue A, Castellví A. Pinça aortomesentèrica, sín- drome de l’artèria mesentèrica superior o síndrome de Wilkie. A propòsit d’un cas. Pe- diatr Catalana 2008;68:205-207. Available from: http://webs.academia.cat/revistes_ elect/view_document.php?tpd=2&i=2127.

  75. Calero-García P, Jurado-Román M, Martín- Scortechini M, Flores-Garnica LM, Sagre- do P, Valiente-Carrillo J. Duodenal vascular compression syndrome: Cause to be consi- dered in cases of intestinal obstruction. Rev Esp Enferm Dig 2012;104(10):559-560.

  76. Pérez-Flecha González M, Rioja Conde P, Caso Maestro Ó, García Aroz S, Marcacuz- co Quinto AA, Bermello Meza CF, Pérez Torres JB, Jiménez Romero LC. Síndro- me de arteria mesentérica superior como causa de dolor abdominal crónico. Cir Esp 2015;93 (Espec Congr):390.


  77. Velazquez Kennedy K, Yela R, Achalan- dabaso MdelM, Martín-Pérez E. Superior mesenteric artery syndrome: Diagnostic and therapeutic considerations. Rev Esp Enferm Dig 2013;105(4):236-238.

  78. Sihuay-Diburga DJ, Accarino-Garaventa A, Vilaseca-Montplet J, Azpiroz-Vidaur F. Acute pancreatitis and superior mesente- ric artery syndrome. Rev Esp Enferm Dig 2013;105(10):626-628.

  79. Barquín-Yagüez J, Abadía-Barno P, García- Pérez JC. Superior mesenteric artery syndro- me: an uncommon cause of intestinal obstruc- tion. Rev Esp Enferm Dig 2017; 109(1):60.

  80. Castillo Wisman MA, Alvarez Galán MdelC, Rodriguez-Bobada Aguirre R, Are- nas Mosqueda J. Dolor abdominal recu- rrente psicológico o anatómico secundario a síndrome de Wilkie. Rev Clín Med Fam 2014;7(2):130-133. Available from: http:// www.revclinmedfam.com/PDFs/0c74b7f78 409a4022a2c4c5a5ca3ee19.pdf.

  81. Bázquez Lautre L, Soriano Gil P, Merck Navarro B, Vicente García F, Herrera Ca- bezón J, Lera Tricas JM. Necrosis gástrica por distensión aguda del estómago y sín- drome de la pinza mesentérica. Rev Esp En- ferm Digest 1995;87(1):56-57.

  82. Fuentes J, Sebastián JJ, Martín ML, Mane- ro S, Uribarrena R. Técnicas de imagen en la pinza aorto-mesentérica. Rev Esp Enferm Dig 1997;89(12):934.

  83. Molina Rodríguez JL, Martí Obiol R, López Mozo, F, Ortega Serrano J. Sín- drome de la pinza aortomesentérica. Cir Esp 2012;90(1):53 http://dx.doi. org/10.1016/j.ciresp.2010.06.018.

  84. Etxebarria Beitia E, Díez del Val I, Lou- reiro González C, González Serrano C, Bilbao Axpe JE. Duodenoyeyunostomía laparoscópica como tratamiento del sín- drome de la arteria mesentérica superior. Cir Esp 2014;92(2):127–141. http://dx.doi. org/10.1016/j.ciresp.2013.06.020.

  85. Martínez-Pérez A, Trullenque-Juan R, Santarrufina-Martínez S, Armañanzas- Villena E. Massive gastrointestinal pneu- matosis in a patient with celiac disease and superior mesenteric artery syndrome. Rev Esp Enferm Dig 2015;107(11):709-710.

  86. García Espinoza J, Martínez Matínez A, Tomás Muñoz P, Ruiz Carazo E. Superior

    mesenteric artery syndrome: a rare cause of intestinal obstruction due to the lack of fat. Sapd online 2017;40(4):193-195. Available from: https://www.sapd.es/revis- ta/2017/40/4/06/pdf.

  87. Aneiros Castro B, Cano Novillo I, García Vázquez A, Martín Alelu R, Gómez Fraile

    1. Wilkie’s syndrome in monozygotic twins treated by 3-D laparoscopic duodenojejunos- tomy. Asian J Endosc Surg 2019;12(1):125-

      127. Available from: https://onlinelibrary. wiley.com/doi/epdf/10.1111/ases.12489.

  88. Valle Hernández E del, Goyanes Martí- nez A, Muñiz González J. Compresión vascular del duodeno. Rev Esp Enferm Dig 1984;65(1):41-48.

  89. Oliva Fonte C, Fernández Rey CL, Pere- da Rodríguez J, González Fernández AM. Wilkie’s syndrome. Rev Esp Enferm Dig 2017;109(1):62-63.

  90. Alsina Seguí E, Moreno Flores A, Llo- rens Salvador R. Síndrome de la arteria mesentérica superior en edad pediátrica:

    ¿Infrecuente o infradiagnosticado? Rev Esp Pediatr 2014;70(4):183-188. Availa- ble from: https://www.seinap.es/wp-con- tent/uploads/Revista-de-Pediatria/2014/ REP%2070-4.pdf#page=6

  91. Fernández Fernández L, Vicente Colomer JM, Vicente Guillén V, Luengo R. de Le- desma, L. Compresión vascular duodenal. Rev Esp Enferm Dig 1988;73(3):322-323.

  92. Sánchez Blanco JM, Figueroa Andollo JM, Moreno Azcoita M, Sieira Pérez A, Moreno González E. Obstrucción duodenal aguda por pinzamiento aorto-mesentérico. Rev Esp Enferm Dig 1979;56(4):353-360.

  93. Rodríguez Caraballo L, Carazo Palacios ME, Ibáñez Pradas V, Rodríguez Iglesias P. Wilkie syndrome: A differential diagnosis of abdomi- nal pain. An Pediatr 2015;82(6):445-6. Avai- lable from: https://www.sciencedirect.com/ science/article/pii/S1695403314005694/ pdfft?md5=d01b1007ad520caa 17221ede53957508&pid=1-s2.0-S1

    695403314005694-main.pdf.

  94. Octavio de Toledo JM, Gómez Lorenzo F, Domínguez J, Cimadevila J, Bermú- dez J, Fernández P. Comprensión vascular del duodeno relacionada con un corsé de yeso (cast syndrome) Rev Esp Enferm Dig 1993;83(1):38-41.


  95. Gómez Beltrán OD, Valverde Martínez A, Pé- rez Manrique M del C, Sánchez Rodríguez J, Lizárraga Febres E, Rufián Peña S. Superior mesenteric artery syndrome in a patient with Charcot Marie Tooth disease. World J Gas- trointest Surg 2011;3(12):197–200.

  96. Villalba Ferrer F, Vázquez Prado A, Arti- gues Sánchez de Rojas E, Garay Burdeos M, Martínez Sanjuán V, García Moneó P, Tru- llenque Peris R. Diagnóstico de la compre- sión duodenal aorto-mesentérica mediante angiografía por resonancia magnética. Rev Esp Enferm Dig 1985;87(5):389-392.

  97. Hernández-Gea V, García-Alba C, Soria- no G, Pernas JC, Farré A. Coexistence of superior mesenteric artery syndrome and phytobezoar. J Gastrohep 2008;32(2):132-

    134. https://doi.org/10.1016/j.gastrohep.

    2008.09.012.

  98. Sánchez Abuin J, Fernández Fernández JC, Rodríguez Sáenz de Buruaga V, Egaña Barrenechea JM. Tratamiento de la compresión vascular del duodeno mediante reimplante de la arteria mesentérica supe- rior. Cir Esp 2010;87(2):114–126.

  99. Escartí Carbonell E, Cervera Delgado M. Dispepsia y síndrome de Wilkie, una causa poco frecuente, pero a menudo olvidada. J Gastrohep 2018;41(7),472–473. Https:// doi.org/10.1016/j.gastrohep.2018.02.005.

  100. Núñez Gaviño P, Vázquez Ferro D, Bazarra Carou R, Deza Garrote T. Síndrome de la arteria mesentérica superior o síndrome de Wilkie. FMC 2013;20(2):114-115. Https:// doi.org/10.1016/S1134-2072(13)70536-X.

  101. Irastorza-Terradillos I, Álvarez-Abad I, Santidrián-Martínez JI, Vitoria-Cormen- zana JC. Dolor abdominal recurrente por síndrome de la arteria mesentérica supe- rior. An Pediatr (Barc). 2010;73(3):150-1. https//doi/10.1016/j.anpedi.2010.05.023.

  102. Alvarenga A, Espinheira C, Guerra P, Gar- cia M, Abreu M, Campos M. Superior me- senteric artery syndrome: weight loss can be a problem, weight gain can be a solution. GE Port J Gastroenterol 2017;24:43–46. Available from: https://www.karger.com/ Article/Pdf/450898.

  103. Carvalho Lourenço L, Martins A, Oliveira AM, Valadas Horta D, Reis J. Wilkie Syn- drome behind Crohn Disease? Superior me- senteric artery syndrome mimicking and

    complicating Crohn disease of the upper gas- trointestinal tract. GE Port J Gastroenterol 2017;24:50–52. Doi: 10.1159/000450873.

    Available from: https://www.karger.com/ Article/Pdf/450873.

  104. Catarino Santos S, Loureiro AR, Simão R, Pereira J, Pinheiro LF, Casimiro C. Wilkie’s syndrome: a case report of favora- ble minimally invasive surgery. J Surg Case Rep 2018(2):1–4. https://doi.org/10.1093/ jscr/rjy027.

  105. Pereira IJ, Tavares C. Apertando o cinto: Síndrome de Wilkie e Síndrome de Nutcrac- ker. Galicia Clin 2014; 75 (2): 82. Available from: https://dialnet.unirioja.es/descarga/ articulo/4794395.pdf.

  106. Pires S, Veloso N, Dinis-Silva J. A Rare cau- se of proximal intestinal obstruction. GE Port J Gastroenterol 2016;23(3):175-176.

  107. Rocha V, Lebre R, Ferreira P, Cardoso A, Augusto A. Síndroma da artéria mesen- térica superior. A propósito de dois casos clínicos. Act Med Port 1993;6(1):47-50. Available from: https://www.actamedica- portuguesa.com/revista/index.php/amp/ article/download/3045/2387.

  108. Silva E, Ribeiro C, Guerreiro S, Domín- gues A. Síndrome de Wilkie – a propósito de um caso clínico. Rev Port Cir 2016;37:25-

    28. Available from: http://www.scielo.mec. pt/pdf/rpc/n37/n37a05.pdf.

  109. Silva G, Moreira Silva H, Tavares M. Iatrogenic superior mesenteric ar- tery syndrome. Rev Esp Enferm Dig 2018; 110(11):742-743. Available from: https://online.reed.es/downMaquetaArt. aspx?fcd=x550.222872Js.

  110. Albano MN, Costa Almeida C, Louro JM, Martinez G. Increase body weight to treat superior mesenteric artery syndrome. BMJ Case Rep 2017; Doi: 10.1136/bcr-2017- 219378.

  111. Townsend Jr. CM, Naoum JJ. Chapter 83.

    Vascular Compression of the Duodenum. In Fischer JE. Editors. Mastery of Surgery. 5th Edition Lippincott Williams & Wilkins 2007. p. 955-961.

  112. Akin JT Jr, Skandalakis JE, Gray SW. The anatomic basis of vascular compres- sion of the duodenum. Surg Clin Nor- th Am 1974;54(6):1361-70. Https://doi. org/10.1016/S 0039-6109(16)40491-3.


  113. Velásquez-Jones L, Medeiros M, Patiño- Ortega M, Guerrero-Kanan R, Valadez-Re- yes MT, Valverde-Rosas S, Moral-Espinosa I del, Franco-Alvarez I, Romo-Vázquez JC. Síndrome de cascanueces: causa de hema- turia y proteinuria masiva no glomerular. Bol Med Hosp Infant Mex 2014;71(5):298-

    302. Available from: http://www.scielo.org. mx/pdf/bmim/v71n5/v71n5a7.pdf.

  114. Barsoum MK, Shepherd RF, Welch TJ. Pa- tient with both Wilkie syndrome and nutcrac- ker syndrome Vasc Med 2008;13(3):247-50. Doi: 10.1177/1358863X08092272. Availa-

    ble from: https://journals.sagepub.com/ doi/pdf/10.1177/1358863X08092272.

  115. Ahmed AR, Taylor I. Superior mesen- teric artery syndrome. Postgrad Med J 1997;73(866):776-778. Doi: 10.1136/pg mj.73.866.776.

  116. Guthrie Jr RH. Wilkie’s Syndrome. Ann Surg 1971;173(2):290-293. Doi: 10.1097

    /00000658-197102000-00017.

  117. Paul JG, Eggleston FC, Singh CM. Acute intestinal obstruction secondary to vascu- lar compression of the duodenum. Am J Surg 1973;126(5):658–660. Doi:10.1016/ s0002-9610(73)80016-9

  118. Mathenge N, Osiro S, Rodriguen II, Salib C, Tubbs RS, Loukas M. Superior mesente- ric artery syndrome and its associated gas- trointestinal implications. Clin Anat 2014; 27(8):1244-1252. Doi: 10.1002/ca.22249.

  119. Veysi VT, Humphrey G, Stringer MD. Su- perior mesenteric artery syndrome presen- ting with acute massive gastric dilatation. J Pediatr Surg 1997;32(12):1801–1803. Doi: 10.1016/s0022-3468(97)90541-8.

  120. Lim JE, Duke GL, Eachempati SR. Supe- rior mesenteric artery syndrome presen- ting with acute massive gastric dilatation, gastric wall pneumatosis, and portal venous gas. Surgery 2003;134(5):840–843. Doi: 10.1016/s0039-6060(02)21677-3.

  121. Agrawal GA, Johnson PT, Fishman EK. Multidetector row CT of superior mesen- teric artery syndrome. J Clin Gastroente- rol 2007;41(1):62–65. Doi: 10.1097/MCG. 0b013e31802dee64.

  122. Lamba R, Tanner DT, Sekhon S, McGahan JP, Corwin MT, Lall CG. Multidetector CT of vascular compression syndromes in the abdomen and pelvis [published correction

    appears in Radiographics 2015 ;35(3):973].

    Radiographics 2014;34(1):93–115. Doi: 10. 1148/rg.341125010.

  123. Gould R, Sandstrom CK, Strote J. Identi- fication of superior mesenteric artery syn- drome from vascular angle measurements. J Emerg Med 2015;49(1):e35–e36. Doi: 10.1016/j.jemermed.2014.12.087.

  124. Kothari TH, Machnicki S, Kurtz L. Su- perior mesenteric artery syndrome. Can J Gastroenterol 2011;25(11):599–600. Doi: 10.1155/2011/617201.

  125. Raman SP, Neyman EG, Horton KM, Ec- khauser FE, Fishman EK. Superior me- senteric artery syndrome: spectrum of CT findings with multiplanar reconstruc- tions and 3-D imaging. Abdom Imaging 2012;37(6):1079–1088. Doi: 10.1007/s00

    261-012-9852-z

  126. Makary MS, Rajan A, Aquino AM, Chamar- thi SK. Clinical and radiologic considera- tions for idiopathic superior mesenteric ar- tery syndrome. Cureus 2017;9(11):e1822. Doi: 10.7759/cureus.1822. Available from: https://www.ncbi.nlm.nih.gov/pmc/arti- cles/PMC5755943/

  127. Narkiewicz-Jodko AS, Delaney VG, Bra- verman SE, Chow B. SMA Syndrome: A diagnostic dilemma. J Surg Radiol 2012; 3(1):16-19.

  128. Konen E, Amitai M, Apter S, Garniek A, Gayer G, Nass S, Itzchak Y. CT angiogra- phy of superior mesenteric artery syndro- me. Am J Roentgenol 1998;171(5):1279– 1281. DOI:10.2214/ajr.171.5.9798861.

  129. Thompson NW, Stanley JC. Vascu- lar Compression of the duodenum and peptic ulcer disease. Arch Surg 1974; 108(5): 674–679. Doi: 10.1001/archsurg.

    1974.01350290038005.

  130. Dalal S, Sahu R, Garg P, Nityasha. SMA Syndrome with peptic ulcer perforation: A rare co-existence. The Internet J Gas- troenterol 2007;7(1):1-3. Available from: https://print.ispub.com/api/0/ispub-arti- cle/11403.

  131. Giles RC. Chronic duodenal ileus. Am J Sur 1957;93(5):824-828. Doi: 10.1016/0002-

    9610(57)90557-3.

  132. Bandres D, Brewer O, Roman O, Fernan- dez S. Wilkie’s syndrome diagnosed by curvilinear array endoscopy ultrasound: an


    unsuspected entity. J Gastrointest Endos- cop 2009; 69(2):S234. Doi: 10.1016/j.gie. 2008.12.097.

  133. Long FR, Mutabagani KH, Caniano DA, Dumont RC. Duodenum inversum mimic- king mesenteric artery syndrome. Pediatr Radiol 1999;29(8):602–604. Doi: 10.1007/ s002470050658.

  134. Chandan S, Choudhry Chandan O, Hewlett AT. Duodenum inversum: a rare cause of chronic nausea and vomiting. Case Rep Gastrointest Med 2018;2018:7538601. Doi: 10.1155/2018/7538601.

  135. Kim ME, Fallon, SC, Bisset GS, Mazziotti MV, Brandt ML. Duodenum inversum: A re- port and review of the literature. J Pediatr Surg 2013;48(1):e47–e49. Doi: 10.1016/j.

    jpedsurg.2012.10.066.

  136. Welsch T, Büchler MW, Kienle P. Reca- lling superior mesenteric artery syndro- me. Dig Surg 2007;24(3):149–156. Doi: 10.1159/000102097.

  137. Colina-Cedeño OL, Trejo-Scorza E, Brito- Arreaza EJ. La compresión vascular del duodeno ó Síndrome de Wilkie en imáge- nes. Rev Cent Med 2019; 58(147): 17-21. Available from: https://www.revistacentro- medico.org/ediciones/2019/1/art-3/

  138. Lee TH, Lee JS, Jo Y. Superior mesenteric artery syndrome: where do we stand today? J Gastrointest Surg 2012;16(12):2203– 2211. Doi: 10.1007/s11605-012-2049-5

  139. Jones SA, Carter R, Smith LL, Joergenson EJ. Arteriomesenteric duodenal compres- sion. Am J Surg 1960; 100:262–277. Doi: 10.1016/0002-9610(60)90300-7.

  140. Bloodgood JC. Acute dilatation of the stomach-gastromesenteric ileus. Ann Surg 1907;46(5):736-762.

  141. Stavely AL. Chronic gastro-mesenteric ileus. Surg Gynecol 1910;11:288.

  142. Strong EK. Mechanics of arteriomesen- teric duodenal obstruction and direct surgical attack upon etiology. Ann Surg 1958;148(5):725-730.

  143. Alsulaimy M, Tashiro J, Perez EA, Sola JE. Laparoscopic Ladd’s procedure for superior mesenteric artery syndrome. J Pediatr Surg 2014;49(10):1533–1535. Doi: 10.1016/j.

    jpedsurg.2014.07.008.

  144. Bing L, Shun-Lin X, Ji-Hua O, Wei-Bing C, Ye-Bo W. Laparascopic Ladd’s procedure as treatment alternative, when parenteral or prolonged hospital nutrition is not an option for superior mesenteric artery syndrome J Pediatr Surg 2017;S0022-3468(17)30416-

    5. Doi: 10.1016/j.jpedsurg.2017.07.004.

  145. Marchant EA, Alvear DT, Fagelman KM. True clinical entity of vascular compression of the duodenum in adolescence. Surg Gy- necol Obstet 1989;168(5):381–386.

  146. Ha CD, Alvear DT, Leber DC. Duode- nal derotation as an effective treatment of superior mesenteric artery syndrome: a thirty-three year experience. Am Surg 2008;74(7):644–653.

  147. Pillay Y. Superior mesenteric artery syndro- me: A case report of two surgical options, duo- denal derotation and duodenojejunostomy. Case Rep Vasc Med 2016;2016:8301025. Doi: 10.1155/2016/8301025.

  148. Hines JR, Gore RM, Ballantyne GH. Su- perior mesenteric artery syndrome. Diag- nostic criteria and therapeutic approaches. Am J Surg 1984;148(5):630–632. Doi: 10.1016/0002-9610(84)90339-8.

  149. Merrett ND, Wilson RB, Cosman P, Bian- kin AV. Superior mesenteric artery syndro- me: diagnosis and treatment strategies. J Gastrointest Surg 2009;13(2):287–292. Doi: 10.1007/s11605-008-0695-4.

  150. Salem A, Al Ozaibi L, Nassif SMM, Osman RAGS, Al Abed NM, Badri FM. Superior mesenteric artery syndrome: A diagnosis to be kept in mind (Case report and literature review). Int J Surg Case Rep 2017;34:84– 86. Doi: 10.1016/j.ijscr.2017.03.018.