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Superior Mesenteric Artery Syndrome

Overview

• Definition: Superior Mesenteric Artery (SMA) syndrome, also known as Wilkie's syndrome or arteriomesenteric duodenal obstruction, is a rare cause of upper gastrointestinal obstruction where the third portion of the duodenum is compressed between the superior mesenteric artery (SMA) anteriorly and the abdominal aorta (AA) posteriorly. This compression is typically due to a reduction in the aortomesenteric angle and distance, leading to mechanical obstruction.

• Epidemiology: SMA syndrome is rare, with an estimated incidence of 0.002% to 0.78% in the general population, though its true prevalence may be underestimated due to underdiagnosis. It can affect individuals of any age, from pediatric to geriatric populations. It is more commonly reported in young, asthenic females. There is a bimodal age distribution, with peaks in adolescence and young adulthood, and again in the 6th-7th decades, often following precipitating events like significant weight loss.

• Classification: SMA syndrome is primarily defined by its anatomical compression. It is not formally classified into subtypes, but can be considered:

  • Acute: Rapid onset, often following acute, significant weight loss (e.g., trauma, burns, prolonged bed rest, rapid post-surgical weight loss).
  • Chronic: Gradual onset, often with a history of recurrent, less severe symptoms and potentially less dramatic weight loss. May be associated with chronic underlying conditions like eating disorders or pre-existing anatomical predispositions.

Pathophysiology

• Mechanism: The SMA typically originates from the aorta at an angle of 45-60 degrees. The third part of the duodenum passes between the SMA and the aorta, cushioned by the mesenteric fat pad and lymphatic tissue. In SMA syndrome, there is a reduction or loss of this protective fat pad, causing the aortomesenteric angle to narrow (typically < 25 degrees, often < 15 degrees) and the aortomesenteric distance to decrease (typically < 8 mm, often < 2 mm, compared to normal 10-28 mm). This anatomical change leads to mechanical compression and obstruction of the duodenum. The ligament of Treitz, which fixes the duodenojejunal flexure, also plays a role by suspending the duodenum and potentially exacerbating the compression.

• Risk Factors:

  • Rapid and significant weight loss: The most common and critical factor. Conditions include:
    • Anorexia nervosa, bulimia
    • Malignancy (e.g., cachexia)
    • Major burns or trauma
    • Bariatric surgery (e.g., gastric bypass, sleeve gastrectomy)
    • Severe illnesses or chronic infections (e.g., tuberculosis, AIDS)
    • Prolonged bed rest or immobilization (e.g., "cast syndrome" after spinal surgery for scoliosis, where a body cast or brace can exacerbate lordosis and abdominal compression).
  • Anatomical factors:
    • Asthenic body habitus (low body mass index, reduced abdominal fat).
    • Congenital high insertion of the duodenum at the ligament of Treitz.
    • Spinal deformities (e.g., severe lordosis, scoliosis) that alter abdominal anatomy and increase aortomesenteric angle.
    • Rapid linear growth in adolescents without proportional weight gain.
    • Abdominal surgery that alters anatomical relationships (e.g., extensive adhesiolysis).

• Protective Factors:

  • Adequate intra-abdominal and retroperitoneal fat tissue.
  • Healthy body mass index (BMI).
  • Absence of spinal deformities or conditions requiring prolonged immobilization in hyperextension.
  • Prone or left lateral decubitus positioning (e.g., post-prandial) which can increase the aortomesenteric angle and relieve pressure on the duodenum.

Clinical Presentation

Signs and Symptoms

• Cardinal Features: Symptoms are typically postprandial and exacerbated by eating due to increased duodenal distension.

  • Epigastric pain: Often crampy, burning, or aching, worse after meals.
  • Nausea: Frequent, often leading to reluctance to eat.
  • Vomiting: Characteristic feature, often copious and bilious (due to obstruction distal to the ampulla of Vater). May contain undigested food.
  • Early satiety: Feeling full quickly after starting to eat.
  • Bloating and abdominal distension: Especially in the epigastric region.
  • Weight loss: Significant and progressive, often leading to or exacerbating the condition, creating a vicious cycle.
  • Relief with positional changes: Symptoms often improve with prone position, left lateral decubitus position, or knee-chest position (Hayes maneuver), which allows the SMA to shift away from the duodenum.

• Early Signs:

  • Intermittent postprandial epigastric discomfort.
  • Mild nausea or early satiety.
  • Reluctance to eat full meals.

• Advanced Signs:

  • Severe, intractable postprandial pain and vomiting leading to significant dehydration and electrolyte imbalances (e.g., hypokalemic, hypochloremic metabolic alkalosis due to persistent vomiting of gastric acid).
  • Profound weight loss and malnutrition (cachexia, muscle wasting).
  • Visible gastric peristalsis or succussion splash on examination.

• Atypical Presentations:

  • Chronic abdominal pain without overt vomiting.
  • Symptoms mimicking gastroparesis or functional dyspepsia.
  • Non-bilious vomiting if the obstruction is proximal to the ampulla of Vater (less common in classical SMA syndrome).
  • Symptoms presenting years after a precipitating event (e.g., spinal surgery).

Physical Examination

• Inspection:

  • Emaciation/Cachexia: Lean body habitus, signs of significant weight loss.
  • Abdominal distension: Often localized to the epigastric region.
  • Visible gastric peristalsis: Wavelike movements across the upper abdomen, indicating forceful gastric contractions against an obstruction.
  • Succussion splash: Audible sloshing sound heard over the epigastrium more than 3-4 hours after a meal, indicating retained fluid in a dilated stomach.

• Palpation:

  • Epigastric tenderness: Non-specific, but may be present.
  • No rebound tenderness or guarding unless complications like perforation occur (rare).

• Special Tests:

  • While not a formal "test," observing symptomatic relief with positional changes (prone, left lateral decubitus, or knee-chest position) can support the diagnosis.

Diagnostic Approach

History Taking

• Key Questions:

  • Weight history: Has there been any recent, rapid, or significant weight loss? (Quantify amount and timeframe if possible).
  • Eating patterns: Are symptoms worse after eating? What types of foods exacerbate symptoms? Do small, frequent meals help?
  • Vomiting characteristics: How often? What is the volume? Is it bilious (green/yellow) or non-bilious? Does it contain undigested food?
  • Pain characteristics: Location (epigastric), character (crampy, burning), radiation, severity.
  • Relieving factors: Does lying on the stomach (prone) or left side, or assuming a knee-chest position, improve symptoms?
  • Medical history: History of eating disorders (anorexia nervosa, bulimia)? Prior spinal surgery (especially scoliosis correction)? Major trauma or burns? Chronic debilitating illnesses?
  • Bowel habits: Any changes? (Less prominent in SMA syndrome).

• Red Flags:

  • Signs of severe dehydration (oliguria, orthostasis, dry mucous membranes).
  • Significant electrolyte abnormalities (e.g., severe hypokalemia, metabolic alkalosis).
  • Evidence of acute kidney injury.
  • Rapid clinical deterioration despite supportive care.
  • Peritoneal signs (rare, but suggest perforation, which is an emergency).

Laboratory Tests

• First-Line: Primarily used to assess for consequences of vomiting and malnutrition, and to rule out other causes.

  • Complete Blood Count (CBC): May show anemia (due to malnutrition, chronic disease) or hemoconcentration (dehydration).
  • Electrolyte Panel (Na, K, Cl, HCO3): Common findings include hypokalemia and hypochloremic metabolic alkalosis due to protracted vomiting.
  • Blood Urea Nitrogen (BUN) and Creatinine (Cr): To assess for dehydration and kidney function. Elevated BUN/Cr ratio may indicate pre-renal azotemia.
  • Liver Function Tests (LFTs): May show abnormalities consistent with malnutrition (e.g., hypoalbuminemia).
  • Amylase/Lipase: To rule out pancreatitis, which can cause similar upper abdominal pain and vomiting.

• Confirmatory: No specific laboratory test confirms SMA syndrome directly. Diagnosis relies on imaging.

• Monitoring:

  • Repeat electrolytes and renal function during acute management.
  • Nutritional markers (e.g., albumin, prealbumin, C-reactive protein for inflammation) to monitor response to nutritional support.

Imaging

• Recommended:

  • Upper Gastrointestinal Series with Small Bowel Follow-Through (UGI-SBFT): Historically the first-line imaging study, now often replaced by CT angiography due to better anatomical detail. Findings include:
    • Dilatation of the second and third portions of the duodenum.
    • Abrupt, vertical, extrinsic compression and "cut-off" of contrast in the third part of the duodenum.
    • Antiperistaltic flow of contrast (duodenogastric reflux).
    • Delayed gastric emptying.
    • Relief of obstruction with prone or left lateral decubitus positioning (demonstrated during fluoroscopy).
  • Computed Tomography Angiography (CTA) of the Abdomen with Oral and IV Contrast: Considered the gold standard for definitive diagnosis. Provides excellent anatomical detail and allows for precise measurements. Key findings:
    • Aortomesenteric angle (AMA): Reduced, typically < 25 degrees (normal 45-60 degrees).
    • Aortomesenteric distance (AMD): Reduced, typically < 8 mm (normal 10-28 mm).
    • Dilated, fluid-filled duodenum proximal to the SMA compression.
    • Abrupt compression of the third portion of the duodenum.
    • Exclusion of other causes of duodenal obstruction (e.g., tumors, adhesions).

• Advanced:

  • Magnetic Resonance Angiography (MRA): An alternative to CTA, especially useful for patients with contraindications to iodinated contrast or for minimizing radiation exposure. Provides similar anatomical information regarding AMA and AMD.
  • Endoscopy (Esophagogastroduodenoscopy - EGD): Crucial to rule out intrinsic causes of upper GI obstruction (e.g., peptic ulcer disease, gastric outlet obstruction due to pyloric stenosis, duodenal strictures, tumors). While EGD can show duodenal dilatation and perhaps extrinsic compression, it is not diagnostic for SMA syndrome itself, as it cannot measure the aortomesenteric angle or distance. It can assess for mucosal damage from chronic stasis (e.g., gastritis, ulcers).
  • Abdominal Ultrasound (Duplex): Can be used in some centers to measure AMA and AMD, but it is operator-dependent and generally less reliable or precise than CTA/MRA, especially in obese patients.

Management

Acute Management

• Immediate:

  • Nothing by Mouth (NPO): To rest the GI tract and prevent further distension/vomiting.
  • Intravenous (IV) Fluid Resuscitation: Essential to correct dehydration and electrolyte imbalances (e.g., normal saline or lactated Ringer's with potassium supplementation for hypokalemia).
  • Antiemetics: To control nausea and vomiting (e.g., ondansetron).

• Stabilization:

  • Nasogastric (NG) Tube Decompression: Placement of an NG tube for gastric decompression to relieve distension, reduce vomiting, and prevent aspiration. Measure output.
  • Electrolyte Correction: Aggressive correction of hypokalemia, hypochloremia, and metabolic alkalosis.
  • Nutritional Assessment: Evaluate the patient's nutritional status and formulate a plan for re-nutrition.

• Emergency:

  • If conservative measures fail to stabilize the patient, or if there are signs of acute gastric outlet obstruction with severe fluid/electrolyte derangements, surgical consultation is warranted for potential urgent intervention (e.g., surgical decompression).

Chronic Management

• Pharmacological:

  • Prokinetics: Medications like metoclopramide (10 mg TID before meals) or erythromycin (250 mg TID) may be tried to improve gastric and duodenal motility, though their efficacy in mechanical obstruction is limited and they are rarely sufficient alone.
  • Pain Management: Analgesics for symptomatic relief, chosen carefully to avoid opioid-induced constipation which can worsen symptoms.
  • Proton Pump Inhibitors (PPIs) or H2-receptor antagonists: To reduce gastric acid production and prevent stress ulcers or complications from chronic gastric stasis.

• Non-pharmacological:

  • Nutritional Support: The cornerstone of conservative management, aiming for weight gain and restoration of the mesenteric fat pad.

    • Oral Feeding: If tolerated, small, frequent (e.g., 6-8 meals/day), high-calorie, easily digestible meals and liquid supplements.
    • Positional Therapy: Encouraging the patient to lie in the prone position or left lateral decubitus position for 20-30 minutes after meals (Hayes maneuver) to facilitate duodenal emptying.
    • Enteral Nutrition: If oral intake is insufficient or poorly tolerated, consider post-pyloric feeding via a nasojejunal tube or percutaneous jejunostomy tube. This bypasses the obstructed duodenum.
    • Total Parenteral Nutrition (TPN): Reserved for severe cases where enteral nutrition is not feasible or tolerated, providing complete nutritional support via IV access.

  • Psychological Support: Essential for patients with underlying eating disorders or chronic conditions leading to cachexia. A multidisciplinary approach involving nutritionists, psychologists/psychiatrists, and gastroenterologists is critical.

• Monitoring:

  • Weight monitoring: Weekly or bi-weekly weight checks to ensure adequate weight gain.
  • Nutritional status: Regular assessment of clinical signs of improvement, and monitoring of nutritional markers (albumin, prealbumin).
  • Symptom assessment: Frequent evaluation of pain, nausea, vomiting frequency and severity.
  • Electrolyte and renal function: Periodic checks to ensure stability.

Treatment Algorithms

• First-Line (Conservative Management): Initial management is always conservative, focused on aggressive nutritional rehabilitation and weight gain.

  1. NPO with NG decompression for acute severe symptoms.
  2. IV fluid and electrolyte correction.
  3. Gradual reintroduction of small, frequent, high-calorie, easily digestible oral meals.
  4. Implement positional therapy after meals.
  5. If oral intake is insufficient, advance to enteral nutrition (nasojejunal or jejunostomy tube feeds).
  6. Consider TPN if enteral nutrition fails or is contraindicated.
  7. Monitor weight, nutritional markers, and symptoms closely. Conservative management typically continues for 4-6 weeks.

• Second-Line (Surgical Management): Indicated if conservative management fails after an adequate trial (e.g., 4-6 weeks) or if severe complications develop (e.g., intractable symptoms, severe malnutrition unresponsive to conservative measures, or signs of impending bowel compromise).

  • Laparoscopic Duodenojejunostomy: The procedure of choice. It involves creating an anastomosis between the dilated proximal duodenum and a loop of jejunum, bypassing the compressed segment. This is highly effective, with success rates typically >90%.
  • Laparoscopic Lysis of Ligament of Treitz (Strong's Procedure): Involves dividing the ligament of Treitz to mobilize the duodenum and increase the aortomesenteric angle. It is a less invasive anatomical correction, but its success rate is lower than duodenojejunostomy and it may not be sufficient in all cases, particularly if the angle/distance remains critically narrow. Reserved for select cases without significant duodenal dilatation.
  • Gastrojejunostomy: Historically performed but less common now. Creates an anastomosis between the stomach and jejunum, bypassing the duodenum entirely. It can lead to complications such as blind loop syndrome, marginal ulcers, and dumping syndrome.

• Refractory Cases:

  • Re-evaluate for alternative diagnoses or persistent underlying risk factors (e.g., ongoing eating disorder, unaddressed psychological issues).
  • If previous surgery failed, re-imaging (CTA) to assess for persistent compression or new anatomical issues. Revision surgery or alternative bypass procedures may be considered.
  • Long-term TPN may be necessary for patients who cannot maintain adequate nutrition through other means.
  • Comprehensive multidisciplinary team involvement (surgery, gastroenterology, nutrition, psychology).

Complications

• Common:

  • Severe weight loss and malnutrition.
  • Dehydration.
  • Electrolyte imbalances (hypokalemia, hypochloremic metabolic alkalosis).
  • Chronic gastric outlet obstruction symptoms (nausea, vomiting, abdominal pain).
  • Gastritis and duodenitis due to chronic stasis and reflux.

• Serious:

  • Acute kidney injury (due to severe dehydration).
  • Aspiration pneumonia (due to intractable vomiting).
  • Esophagitis, stricture, or Barrett's esophagus (from chronic reflux).
  • Gastric or duodenal ulceration (from chronic stasis and acid exposure).
  • Acute pancreatitis (rare, potentially due to duodenal obstruction impacting bile/pancreatic duct outflow).
  • Severe, life-threatening malnutrition and cachexia, leading to multi-organ dysfunction.

• Long-term:

  • Chronic pain and discomfort, impacting quality of life.
  • Persistent nutritional deficiencies if not adequately managed.
  • Psychological distress, anxiety, depression (especially if associated with eating disorders or chronic illness).
  • Complications of surgical interventions (e.g., anastomotic leak, stricture, internal hernia, dumping syndrome, blind loop syndrome).

Prognosis

• Factors: The prognosis for SMA syndrome is generally good with prompt diagnosis and appropriate management. Factors influencing outcome include:

  • Severity of initial compression: More severe anatomical compression may be less responsive to conservative measures.
  • Duration of symptoms: Delayed diagnosis can lead to more severe malnutrition and complications, making recovery more challenging.
  • Underlying cause: Patients with self-limiting precipitating factors (e.g., trauma, cast syndrome) often respond well to conservative therapy. Those with chronic conditions like anorexia nervosa require long-term, multidisciplinary management.
  • Response to conservative management: Successful weight gain often resolves the condition without surgery.
  • Success of surgical intervention: Surgical bypass has high success rates in resolving obstruction.
  • Patient compliance: Adherence to dietary recommendations and positional therapy.

• Survival: Mortality specifically attributable to SMA syndrome is rare but can occur in severe, untreated cases due to profound malnutrition, electrolyte derangements, and complications. Overall survival is excellent with appropriate intervention.

• Quality of Life: Can be significantly impaired by chronic pain, nausea, vomiting, dietary restrictions, and weight loss. Successful treatment (conservative or surgical) typically leads to marked improvement in symptoms, nutritional status, and quality of life.

Prevention

• Primary:

  • Gradual weight loss: For individuals undergoing weight reduction, especially in high-risk groups (e.g., very low BMI, spinal deformities), encourage gradual weight loss rather than rapid, extreme methods.
  • Awareness in high-risk settings: Clinicians should be aware of the risk of SMA syndrome in patients undergoing major spinal surgery (e.g., scoliosis correction) or bariatric surgery, and implement prophylactic measures if appropriate (e.g., early mobilization, nutritional support).

• Secondary:

  • Early detection: Maintain a high index of suspicion for SMA syndrome in patients presenting with postprandial upper abdominal pain, nausea, vomiting, and weight loss, especially if they have risk factors.
  • Prompt diagnosis: Utilize appropriate imaging (CTA) to confirm diagnosis quickly once suspected.
  • Early nutritional intervention: Initiate nutritional support (oral, enteral, or parenteral) as soon as symptoms suggest obstruction to prevent severe malnutrition.

• Tertiary:

  • Preventing complications: Aggressive management of malnutrition and electrolyte imbalances.
  • Timely surgical intervention: When conservative management fails, prompt surgical consultation and intervention are crucial to prevent progression of malnutrition and other severe complications.
  • Long-term follow-up: For patients managed conservatively or surgically, monitor for recurrence of symptoms or complications.

Special Populations

• Pediatric:

  • More commonly associated with rapid growth spurts without adequate weight gain, spinal surgery (e.g., corrective surgery for scoliosis, where prolonged immobilization or casting can induce "cast syndrome" by increasing lumbar lordosis), or conditions causing rapid weight loss.
  • Management principles are similar, with strong emphasis on ensuring adequate caloric intake for growth and development. Nutritional support often requires a multidisciplinary team.

• Geriatric:

  • Less common, but can occur in frail elderly individuals with underlying chronic illnesses, malignancy, or prolonged bed rest leading to significant weight loss and sarcopenia.
  • Diagnosis may be challenging due to non-specific symptoms and multiple comorbidities.
  • Conservative management may be prolonged due to slower recovery from malnutrition. Surgical risk assessment is crucial.

• Pregnancy:

  • Extremely rare. Any rapid weight loss in pregnancy could potentially trigger it, though usually, weight gain is expected.
  • Management involves careful consideration of maternal and fetal well-being. Nutritional support is paramount. Surgical intervention during pregnancy carries higher risks and would only be considered in severe, refractory cases after extensive multidisciplinary discussion.

• Comorbidities:

  • Eating Disorders (e.g., Anorexia Nervosa): A significant comorbidity. Requires a highly integrated multidisciplinary team approach including gastroenterologists, dietitians, psychiatrists/psychologists, and surgeons. Psychological therapy is essential for long-term success. Surgical intervention is often a last resort, as primary focus is on addressing the underlying eating disorder and achieving weight gain.
  • Spinal Deformities/Surgery: Patients undergoing scoliosis correction or other spinal procedures need careful monitoring for symptoms of SMA syndrome post-operatively. Early mobilization, positional changes, and nutritional support are critical.

Clinical Pearls

• Diagnostic:

  • Think SMA syndrome in "the 6 D's": Duodenal obstruction, Due to Distal third duodenal compression, Due to Decreased aortomesenteric Distance/angle.
  • Always consider SMA syndrome in an asthenic patient with postprandial bilious vomiting, early satiety, and significant weight loss, especially with a history of rapid weight loss or spinal surgery.
  • Don't rely solely on endoscopy for diagnosis; it primarily rules out intrinsic pathology. CTA is the diagnostic imaging of choice.
  • Remember the Hayes maneuver: Positional relief (prone or left lateral decubitus) is a key historical clue.

• Treatment:

  • Conservative management with aggressive nutritional support is the first-line treatment. Prioritize weight gain.
  • Nasogastric decompression and IV fluid/electrolyte repletion are crucial acute interventions.
  • Surgical intervention (Laparoscopic Duodenojejunostomy) is reserved for patients who fail conservative management after an adequate trial (typically 4-6 weeks) or who develop severe complications.
  • A multidisciplinary approach is vital, especially for patients with underlying eating disorders.

• Pitfalls:

  • Misdiagnosis: Often initially misdiagnosed as functional dyspepsia, gastroparesis, psychological illness, or other non-obstructive GI disorders, leading to diagnostic delay.
  • Underestimation of severity: Failure to appreciate the severity of malnutrition and electrolyte derangements can lead to serious complications.
  • Premature surgical intervention: Operating before an adequate trial of conservative management may be unnecessary, increasing risks.
  • Inadequate nutritional support: Lack of aggressive and sustained nutritional repletion is a common reason for conservative management failure.

Recent Updates

• Guidelines: No single, universally adopted international guideline exists for SMA syndrome due to its rarity. However, clinical consensus increasingly favors:

  • Improved diagnostic imaging: Widespread availability and improved resolution of CTA/MRA have allowed for earlier and more definitive diagnosis.
  • Emphasis on multidisciplinary care: Recognition of the complex interplay of nutritional, psychological, and anatomical factors, especially in chronic cases.
  • Shift in surgical approach: Laparoscopic duodenojejunostomy has become the preferred surgical technique due to its minimally invasive nature and high success rates compared to older open procedures or less effective techniques like Strong's procedure for most cases.

• Evidence:

  • Recent case series and systematic reviews continue to support the effectiveness of surgical bypass (duodenojejunostomy) for patients refractory to conservative therapy, with favorable long-term outcomes.
  • Growing literature highlights the importance of meticulous nutritional support as the cornerstone of conservative treatment, emphasizing enteral feeding over TPN when feasible.

• Controversies:

  • Optimal duration of conservative management: While 4-6 weeks is a common recommendation, the exact timeframe for transitioning to surgical management can vary based on patient factors, severity of symptoms, and rate of clinical deterioration.
  • Role of Strong's procedure: While less invasive, its efficacy compared to duodenojejunostomy remains debated, with most evidence suggesting bypass has higher long-term success rates, especially in cases with significant duodenal dilation. Strong's procedure may be considered in very early, less severe cases without significant duodenal dilatation.

Key References

• Guidelines: Given the rarity, there are no specific standalone clinical practice guidelines from major societies for SMA syndrome. Management principles are derived from consensus expert opinion and synthesis of case series/reviews.

  • General guidelines on Nutritional Support from societies like ASPEN (American Society for Parenteral and Enteral Nutrition) and ESPEN (European Society for Clinical Nutrition and Metabolism) are highly relevant for management.
  • Guidelines for Eating Disorder Management from psychiatric and psychological associations are crucial when SMA syndrome coexists with these conditions.

• Studies:

  • Numerous case reports and series published in surgical and gastroenterological journals describe diagnostic features, management strategies, and outcomes. Search terms like "Superior Mesenteric Artery Syndrome," "Wilkie's Syndrome," "duodenal compression" in PubMed or similar databases will yield relevant clinical studies.
  • Meta-analyses and systematic reviews synthesizing outcomes of surgical vs. conservative management for SMA syndrome.

• Reviews:

  • Comprehensive review articles in major gastroenterology and surgical journals (e.g., World Journal of Surgery, Journal of Gastrointestinal Surgery, Clinical Gastroenterology and Hepatology) offer detailed summaries of the pathophysiology, diagnosis, and management of SMA syndrome.