Abodominal Aortic Aneurysm (AAA)
• Pertinent anatomic dimensions include the
diameter of the Proximal nondilated
– Infrarenal aortic neck, which can range from
18 to 30 mm;
– Common iliac artery, which can range from 8 to 16
mm.
– External iliac arteries, which can range from
6 to 10 mm
ABDOMINAL AORTIC ANEURYSM
• AAA is defined as a pathologic focal
dilation of the aorta that is greater than 30
mm or 1.5 times the adjacent diameter of
the normal aorta.
• Male aortas tend to be larger than female
aortas, and
• There is generalized growth of the aortic
diameter with each decade of life.
• Incidence of abdominal aortic aneurysm
(AAA), based on large screening studies, is
estimated to range from 3% to 10%.
• Incidence appears to be increasing,
– Due in part to improvements in diagnostic
imaging and,
– More importantly, a growing elderly population
• overall mortality of AAA rupture is 71% to
77%, which includes all out-of-hospital
• surgical mortality is 45% to 50% and has not
substantially changed in the last 30 years.
PATHOGENESIS
• Factors that contribute to
– The degradation of collagen and elastin are also
associated with aneurysmal disease, and
– Research in this area has focused on the role of matrix
metalloproteinases and other
– Mediators of tissue enzyme function immune response
and
– Hormone milieu.
• Aneurysms do also occur as a degenerative
complication after aortic dissection.
ETIOLOGY
• Degenerative process in the aortic wall is the
– Most common cause of AAA development.
– Matrix metalloproteinases (MMP), proteolytic enzymes,
are found abundantly in the wall of AAA
• Inflammatory AAA accounts for 5% to 10% of all
AAA
• Infectious or mycotic AAA is rare but is associated
with high mortality
• Connective tissue disorders
– Such as Marfan’s syndrome and Ehlers-Danlos syndrome
– Tend to have more extensive and larger aneurysms at a
younger age
Risk of Rupture
• A rate of growth of more than 5 mm in 6
months or more than 1 cm per year has been
widely adopted as an indication for repair,
independent of aneurysm size.
• Size is an imperfect predictor of rupture risk;
– Autopsy studies have discovered evidence of rupture
in up to 12% of aneurysms less than 5 cm in diameter
• Maximum transverse diameter remains the
standard method of risk assessment for aneurysm
rupture.
• The most widely adopted surrogate for rupture
risk is maximal cross-sectional aneurysm
diameter although the implications for rupture
risk of a particular aortic diameter remain
debated.
Natural History of Aortic Aneurysm
• AAA exhibits a “staccato” pattern of
growth”
– Where periods of relative quiescence may alternate
with expansion.
– Therefore, although an individual pattern of
growth cannot be predicted,
– Average aggregate growth is approximately 3 to 4
mm/year.
Clinical Manifestations
• Most AAAs are asymptomatic and are usually found
incidentally during workup for chronic back pain or
kidney stones.
• physical examination as a
– palpable pulsatile mass, most commonly supraumbilical
and in the midline.
• Patients with these symptoms must be treated as a rupture
until proven otherwise
– It is neither sensitive nor specific except in thin patients.
– Large aneurysms may be missed in the obese, while normal
aortic pulsations may be mistaken for an aneurysm in thin
individuals
Diagnostic Evaluation
Preoperative evaluation should include routine history and
physical exam with particular attention to
a. Any symptoms referable to the aneurysm, which may
impact the timing of repair;
b. History of pelvic surgery or radiation, in the event
retroperitoneal exposure is required or interruption of
hypogastric circulation is planned;
c. Claudication suggestive of significant iliac occlusive
disease;
d. Lower extremity bypass or other femoral reconstructive
procedures; and
e. Chronic renal insufficiency or contrast allergy.
• Ultrasonography:
– Safe, widely available, relatively accurate, and
inexpensive.
– Afford excellent sensitivity and specificity thus the
screening modality of choice.
• Ultrasound may be limited
– By the patient’s habitus or bowel gas,
– Not an ideal method for detecting rupture;
• it is unable to image all portions of the aortic wall, and
• the nonfasting status of emergently examined patients
may further preclude ideal image acquisition.
• It has been estimated that ultrasound may fail to
detect up to 50% of aneurysm ruptures.
• CT scan remains
– The gold standard for determination of anatomic
eligibility for endovascular repair.
– Size of AAA may differ up to 1 cm between CT and
ultrasound, and during longitudinal follow-up,
comparisons should be made between identical
modalities
• CT angiography (CTA), provides
– It detects vessel calcification,
– thrombus,
– concurrent arterial occlusive disease
– permits multiplanar and three-dimensional
reconstruction and analysis for operative planning
• The only major drawback to CT is the risk of
contrast nephropathy in diabetics and in
patients with renal insufficiency.
• Angiography is
– Invasive
– With an increased risk of complications.
– Indications for angiography are
• Isolated to concomitant iliac occlusive disease and
• Unusual renovascular anatomy.
MRA
• The ability to acquire dynamic images
throughout the cardiac cycle may ultimately
prove clinically useful.
Limitation of MRA
• Use of gadolinium, which has been associated
with the development of nephrogenic
systemic fibrosis in patients with low
glomerular filtration rate.
• Limited by the presence of incompatible
metallic implants or foreign bodies.
Screening and Surveillance
Recommendations.
• Screening recommendations for AAA are
informed by the sensitivity and specificity of
ultrasound screening.
• A major recent compilation of evidence-
based recommendations for screening and
surveillance of AAA is provided by the 2009
Practice Guidelines developed by the Clinical
Practice Council of the Society for Vascular
Surgery.
Screening made a strong recommendation for One-
time
– Screening of all men aged 65 years and older or men
55 years and older with a family history of AAA.
– Screening of women is also strongly recommended
for those aged 65 years and older with a family history
of AAA or a personal smoking history.
• Once an aneurysm has been detected, the
Society for Vascular Surgery Clinical Practice
Council recommends further screening intervals
as follows, based on aneurysm size (maximum
external aortic diameter) and associated risk of
rupture:
– <2.6 cm: No further screening recommended
– 2.6-2.9 cm: Reexamination at 5 years
– 3-3.4 cm: Reexamination at 3 years
– 3.5-4.4 cm: Reexamination at 12 months
– 4.5-5.4 cm: Reexamination at 6 months
Treatment
• Medical management: Dual purpose
– To potentially minimize the rate of aneurysm
expansion or rupture and
– To medically prepare for potential repair.
– BLOOD PRESSURE MANAGEMENT WITH
ANTIHYPERTENISIVE DUGS
– CESSATION OF SMOKING
–The bottom line is that no drug can
currently be recommended for the
indication of reducing AAA
enlargement.
Surgical treatment
Surgical treatment is generally recommended for
aneurysms
– More than 5.5 cm in maximal diameter,
– Those demonstrating more than 5 mm of growth
in 6 months or more than 1 cm in a year, and
– Aneurysms with a saccular rather than the
typical fusiform anatomy
– Consideration of aneurysm repair at a smaller
size in women.
• Presence of significant aneurysm-related
anxiety associated with awareness of the
presence of an unrepaired aneurysm has also
been cited as affecting quality of life and
presenting a potential consideration in
managing aneurysms below 5.5 cm in
diameter.
• Open repair
• Endovascular repair
Open Surgical Repair
• Open surgical repairof AAA may be
accomplished by either a
– Transperitoneal or
– Retroperitoneal approach
• Transperitoneal repair
– Through a midline laparotomy incision
– The most widely used approach to the usual
infrarenal aneurysm and
– Offers a rapid exposure,
– Excellent access to renal and iliac vessels, and
– The ability to fully examine the abdominal
contents
Retroperitoneal approach
• Afford greater access to the visceral segment of the
abdominal aorta and may be aided,
• where required, by thoracic extension of the incision
and exposure with or without division of the
diaphragm.
• Advantage
– To reduce physiologic stress on the patient
– To result in fewer postoperative pulmonary
complications.
– Reduction of postoperative ileus
• Disadvantage
– Persistent postoperative pain,
– Flank wall laxity, and
– Hernia have been described complicating
retroperitoneal repair
Advantages Open Abdominal Aortic
Aneurysm Repair
• AAA is permanently eliminated because it is entirely
replaced by a prosthetic aortic graft.
– longterm imaging surveillance is not needed with these
patients
• Direct assessment of the circulatory integrity of the
colon.
– If signs of colonic ischemia become evident after aortic
bypass grafting, a concomitant mesenteric artery bypass
can be performed to revascularize the colonic circulation.
• Permits the surgeons to explore for other abdominal
pathologies, such as gastrointestinal tumors, liver
mass, or cholelithiasis.
Risks associated with Open Repair
• Cardiac complications in the form of either myocardial
infarction or arrhythmias.
• Renal failure or transient renal insufficiency as a result of
– perioperative hypotension,
– atheromatous embolization,
– Inadvertent injury to the ureter,
– preoperative contrast-induced nephropathy, or
– suprarenal aortic clamping
• Ischemic colitis is a devastating potential complication after
open repair
• Prosthetic graft infection ranges between 1% and 4% after
open repair
• If the prosthetic graft is not fully covered by the aneurysm sac
or retroperitoneum, intestinal adhesion with subsequent bowel
erosion may occur, resulting in an aortoenteric fistula.
Endovascular repair
Management of the Ruptured
Aneurysm
• Patients who survive to present to the hospital with a ruptured AAA
may range from relatively stable to circulatory collapse.
• key principles of management must be considered.
– First, the appropriate hemodynamic parameters are those of
permissive hypotension, with systolic blood pressures as low as
50 to 70 mm Hg considered adequate in a conscious patient,
– Avoidance of aggressive volume resuscitation.
• Management of a hemodynamically unstable patient or one in
whom aortic control is expected to be delayed, prolonged, or
complex, whether open or endovascular, may use percutaneous
balloon control of the proximal aorta
• When possible contrast-enhanced CTA should
be performed preoperatively, although
techniques that rely exclusively on
angiography have been described
• This may establish whether endovascular
repair is possible or preferred.
In the operating room,
 Consideration should be given to the method and
timing of anesthesia.
 If Endovascular repair may be performed initially
or in its entirety under local anesthesia.
 When open repair and general anesthesia are
required,
• It is prudent to complete positioning,
• Sterile preparation, and
• Draping of the field before induction of anesthesia. In
treating a ruptured aneurysm,
• Supraceliac control clamp should greatly facilitate
resuscitation and provide a measure of hemodynamic
stability
Endovascular aneurysm repair
• First reported by Parodi and colleagues in 1991
• Widely adopted since the first Food and Drug
Administration (FDA)–approved devices for
EVAR, the AneuRx (Medtronic, Minneapolis,
Minn) and the Ancure (Guidant Corporation,
Menlo Park, Calif), became available in 1999
• EVAR more frequently performed in recent years
than open surgical repair for aneurysms with
suitable anatomy
• EVAR has advantage.
– Shorter length of stay,
– Lower 30-day morbidity and mortality Does not improve quality of life beyond 3
months or survival beyond 2 years
• Early, periprocedural complications include
– Endoleak; access-related complications, which occur in up to 3% of cases.
– Hematoma,
– Pseudoaneurysm,
– Arterial occlusion or dissection, and Iliac artery rupture or transection;
– Peripheral embolization;
– Renal insufficiency;
– Local wound complications;
– Inadvertentrenal or hypogastric artery occlusion; and
– Rare occurrences, such as colon or spine ischemia
Late complication
– Rupture, which occurs rarely but at a higher rate than after open repair;
– Graft limb occlusion;
– Endoleak or sac enlargement
– Graft infections
Endoleak
• An endoleak occurs when there is a persistent
flow of blood (visible on radiologic imaging)
into the aneurysm sac, and it may occur during
the initial procedure or develop over time.
• A relatively common complication.
• They are not benign, because they lead to
continual pressurization of the sac, which can
cause expansion or even rupture.
Enodleak
Postoperative Management
 Patients are typically admitted to an intensive care unit,
with
 Continuous cardiopulmonary monitoring.
 Adequate pain control,
 Appropriate resuscitation, adequate oxygenation, and
heart rate control all serve to minimize the risk of
postoperative myocardial infarction.
 Epidural anesthesia and patient-controlled analgesia are
both excellent options for postoperative pain
management.
 Prophylaxis for deep venous thrombosis is important .
 Attention to early mobilization and nutrition of the
patient are also essential to recovery.
Post operative imaging
• Image patients with CT initially, then at 5-year
intervals after repair.
• CT for detecting anastomotic or para-
anastomotic changes
• Ultrasound may also be used for surveillance
but is operator dependent and lacks the
sensitivity as of CT
• Thanks

Abominal aneurysm

  • 1.
  • 3.
    • Pertinent anatomicdimensions include the diameter of the Proximal nondilated – Infrarenal aortic neck, which can range from 18 to 30 mm; – Common iliac artery, which can range from 8 to 16 mm. – External iliac arteries, which can range from 6 to 10 mm
  • 4.
  • 5.
    • AAA isdefined as a pathologic focal dilation of the aorta that is greater than 30 mm or 1.5 times the adjacent diameter of the normal aorta. • Male aortas tend to be larger than female aortas, and • There is generalized growth of the aortic diameter with each decade of life.
  • 6.
    • Incidence ofabdominal aortic aneurysm (AAA), based on large screening studies, is estimated to range from 3% to 10%. • Incidence appears to be increasing, – Due in part to improvements in diagnostic imaging and, – More importantly, a growing elderly population
  • 7.
    • overall mortalityof AAA rupture is 71% to 77%, which includes all out-of-hospital • surgical mortality is 45% to 50% and has not substantially changed in the last 30 years.
  • 8.
    PATHOGENESIS • Factors thatcontribute to – The degradation of collagen and elastin are also associated with aneurysmal disease, and – Research in this area has focused on the role of matrix metalloproteinases and other – Mediators of tissue enzyme function immune response and – Hormone milieu. • Aneurysms do also occur as a degenerative complication after aortic dissection.
  • 9.
    ETIOLOGY • Degenerative processin the aortic wall is the – Most common cause of AAA development. – Matrix metalloproteinases (MMP), proteolytic enzymes, are found abundantly in the wall of AAA • Inflammatory AAA accounts for 5% to 10% of all AAA • Infectious or mycotic AAA is rare but is associated with high mortality • Connective tissue disorders – Such as Marfan’s syndrome and Ehlers-Danlos syndrome – Tend to have more extensive and larger aneurysms at a younger age
  • 11.
    Risk of Rupture •A rate of growth of more than 5 mm in 6 months or more than 1 cm per year has been widely adopted as an indication for repair, independent of aneurysm size. • Size is an imperfect predictor of rupture risk; – Autopsy studies have discovered evidence of rupture in up to 12% of aneurysms less than 5 cm in diameter • Maximum transverse diameter remains the standard method of risk assessment for aneurysm rupture.
  • 12.
    • The mostwidely adopted surrogate for rupture risk is maximal cross-sectional aneurysm diameter although the implications for rupture risk of a particular aortic diameter remain debated.
  • 13.
    Natural History ofAortic Aneurysm • AAA exhibits a “staccato” pattern of growth” – Where periods of relative quiescence may alternate with expansion. – Therefore, although an individual pattern of growth cannot be predicted, – Average aggregate growth is approximately 3 to 4 mm/year.
  • 14.
    Clinical Manifestations • MostAAAs are asymptomatic and are usually found incidentally during workup for chronic back pain or kidney stones. • physical examination as a – palpable pulsatile mass, most commonly supraumbilical and in the midline. • Patients with these symptoms must be treated as a rupture until proven otherwise – It is neither sensitive nor specific except in thin patients. – Large aneurysms may be missed in the obese, while normal aortic pulsations may be mistaken for an aneurysm in thin individuals
  • 15.
    Diagnostic Evaluation Preoperative evaluationshould include routine history and physical exam with particular attention to a. Any symptoms referable to the aneurysm, which may impact the timing of repair; b. History of pelvic surgery or radiation, in the event retroperitoneal exposure is required or interruption of hypogastric circulation is planned; c. Claudication suggestive of significant iliac occlusive disease; d. Lower extremity bypass or other femoral reconstructive procedures; and e. Chronic renal insufficiency or contrast allergy.
  • 16.
    • Ultrasonography: – Safe,widely available, relatively accurate, and inexpensive. – Afford excellent sensitivity and specificity thus the screening modality of choice. • Ultrasound may be limited – By the patient’s habitus or bowel gas, – Not an ideal method for detecting rupture; • it is unable to image all portions of the aortic wall, and • the nonfasting status of emergently examined patients may further preclude ideal image acquisition. • It has been estimated that ultrasound may fail to detect up to 50% of aneurysm ruptures.
  • 18.
    • CT scanremains – The gold standard for determination of anatomic eligibility for endovascular repair. – Size of AAA may differ up to 1 cm between CT and ultrasound, and during longitudinal follow-up, comparisons should be made between identical modalities • CT angiography (CTA), provides – It detects vessel calcification, – thrombus, – concurrent arterial occlusive disease – permits multiplanar and three-dimensional reconstruction and analysis for operative planning
  • 20.
    • The onlymajor drawback to CT is the risk of contrast nephropathy in diabetics and in patients with renal insufficiency.
  • 21.
    • Angiography is –Invasive – With an increased risk of complications. – Indications for angiography are • Isolated to concomitant iliac occlusive disease and • Unusual renovascular anatomy.
  • 22.
    MRA • The abilityto acquire dynamic images throughout the cardiac cycle may ultimately prove clinically useful.
  • 23.
    Limitation of MRA •Use of gadolinium, which has been associated with the development of nephrogenic systemic fibrosis in patients with low glomerular filtration rate. • Limited by the presence of incompatible metallic implants or foreign bodies.
  • 24.
    Screening and Surveillance Recommendations. •Screening recommendations for AAA are informed by the sensitivity and specificity of ultrasound screening. • A major recent compilation of evidence- based recommendations for screening and surveillance of AAA is provided by the 2009 Practice Guidelines developed by the Clinical Practice Council of the Society for Vascular Surgery.
  • 25.
    Screening made astrong recommendation for One- time – Screening of all men aged 65 years and older or men 55 years and older with a family history of AAA. – Screening of women is also strongly recommended for those aged 65 years and older with a family history of AAA or a personal smoking history.
  • 26.
    • Once ananeurysm has been detected, the Society for Vascular Surgery Clinical Practice Council recommends further screening intervals as follows, based on aneurysm size (maximum external aortic diameter) and associated risk of rupture: – <2.6 cm: No further screening recommended – 2.6-2.9 cm: Reexamination at 5 years – 3-3.4 cm: Reexamination at 3 years – 3.5-4.4 cm: Reexamination at 12 months – 4.5-5.4 cm: Reexamination at 6 months
  • 27.
  • 28.
    • Medical management:Dual purpose – To potentially minimize the rate of aneurysm expansion or rupture and – To medically prepare for potential repair. – BLOOD PRESSURE MANAGEMENT WITH ANTIHYPERTENISIVE DUGS – CESSATION OF SMOKING –The bottom line is that no drug can currently be recommended for the indication of reducing AAA enlargement.
  • 29.
    Surgical treatment Surgical treatmentis generally recommended for aneurysms – More than 5.5 cm in maximal diameter, – Those demonstrating more than 5 mm of growth in 6 months or more than 1 cm in a year, and – Aneurysms with a saccular rather than the typical fusiform anatomy – Consideration of aneurysm repair at a smaller size in women.
  • 30.
    • Presence ofsignificant aneurysm-related anxiety associated with awareness of the presence of an unrepaired aneurysm has also been cited as affecting quality of life and presenting a potential consideration in managing aneurysms below 5.5 cm in diameter.
  • 31.
    • Open repair •Endovascular repair
  • 32.
    Open Surgical Repair •Open surgical repairof AAA may be accomplished by either a – Transperitoneal or – Retroperitoneal approach
  • 33.
    • Transperitoneal repair –Through a midline laparotomy incision – The most widely used approach to the usual infrarenal aneurysm and – Offers a rapid exposure, – Excellent access to renal and iliac vessels, and – The ability to fully examine the abdominal contents
  • 36.
    Retroperitoneal approach • Affordgreater access to the visceral segment of the abdominal aorta and may be aided, • where required, by thoracic extension of the incision and exposure with or without division of the diaphragm.
  • 37.
    • Advantage – Toreduce physiologic stress on the patient – To result in fewer postoperative pulmonary complications. – Reduction of postoperative ileus • Disadvantage – Persistent postoperative pain, – Flank wall laxity, and – Hernia have been described complicating retroperitoneal repair
  • 38.
    Advantages Open AbdominalAortic Aneurysm Repair • AAA is permanently eliminated because it is entirely replaced by a prosthetic aortic graft. – longterm imaging surveillance is not needed with these patients • Direct assessment of the circulatory integrity of the colon. – If signs of colonic ischemia become evident after aortic bypass grafting, a concomitant mesenteric artery bypass can be performed to revascularize the colonic circulation. • Permits the surgeons to explore for other abdominal pathologies, such as gastrointestinal tumors, liver mass, or cholelithiasis.
  • 39.
    Risks associated withOpen Repair • Cardiac complications in the form of either myocardial infarction or arrhythmias. • Renal failure or transient renal insufficiency as a result of – perioperative hypotension, – atheromatous embolization, – Inadvertent injury to the ureter, – preoperative contrast-induced nephropathy, or – suprarenal aortic clamping • Ischemic colitis is a devastating potential complication after open repair • Prosthetic graft infection ranges between 1% and 4% after open repair • If the prosthetic graft is not fully covered by the aneurysm sac or retroperitoneum, intestinal adhesion with subsequent bowel erosion may occur, resulting in an aortoenteric fistula.
  • 40.
  • 41.
    Management of theRuptured Aneurysm • Patients who survive to present to the hospital with a ruptured AAA may range from relatively stable to circulatory collapse. • key principles of management must be considered. – First, the appropriate hemodynamic parameters are those of permissive hypotension, with systolic blood pressures as low as 50 to 70 mm Hg considered adequate in a conscious patient, – Avoidance of aggressive volume resuscitation. • Management of a hemodynamically unstable patient or one in whom aortic control is expected to be delayed, prolonged, or complex, whether open or endovascular, may use percutaneous balloon control of the proximal aorta
  • 42.
    • When possiblecontrast-enhanced CTA should be performed preoperatively, although techniques that rely exclusively on angiography have been described • This may establish whether endovascular repair is possible or preferred.
  • 43.
    In the operatingroom,  Consideration should be given to the method and timing of anesthesia.  If Endovascular repair may be performed initially or in its entirety under local anesthesia.  When open repair and general anesthesia are required, • It is prudent to complete positioning, • Sterile preparation, and • Draping of the field before induction of anesthesia. In treating a ruptured aneurysm, • Supraceliac control clamp should greatly facilitate resuscitation and provide a measure of hemodynamic stability
  • 44.
    Endovascular aneurysm repair •First reported by Parodi and colleagues in 1991 • Widely adopted since the first Food and Drug Administration (FDA)–approved devices for EVAR, the AneuRx (Medtronic, Minneapolis, Minn) and the Ancure (Guidant Corporation, Menlo Park, Calif), became available in 1999 • EVAR more frequently performed in recent years than open surgical repair for aneurysms with suitable anatomy
  • 48.
    • EVAR hasadvantage. – Shorter length of stay, – Lower 30-day morbidity and mortality Does not improve quality of life beyond 3 months or survival beyond 2 years • Early, periprocedural complications include – Endoleak; access-related complications, which occur in up to 3% of cases. – Hematoma, – Pseudoaneurysm, – Arterial occlusion or dissection, and Iliac artery rupture or transection; – Peripheral embolization; – Renal insufficiency; – Local wound complications; – Inadvertentrenal or hypogastric artery occlusion; and – Rare occurrences, such as colon or spine ischemia Late complication – Rupture, which occurs rarely but at a higher rate than after open repair; – Graft limb occlusion; – Endoleak or sac enlargement – Graft infections
  • 49.
    Endoleak • An endoleakoccurs when there is a persistent flow of blood (visible on radiologic imaging) into the aneurysm sac, and it may occur during the initial procedure or develop over time. • A relatively common complication. • They are not benign, because they lead to continual pressurization of the sac, which can cause expansion or even rupture.
  • 50.
  • 52.
    Postoperative Management  Patientsare typically admitted to an intensive care unit, with  Continuous cardiopulmonary monitoring.  Adequate pain control,  Appropriate resuscitation, adequate oxygenation, and heart rate control all serve to minimize the risk of postoperative myocardial infarction.  Epidural anesthesia and patient-controlled analgesia are both excellent options for postoperative pain management.  Prophylaxis for deep venous thrombosis is important .  Attention to early mobilization and nutrition of the patient are also essential to recovery.
  • 53.
    Post operative imaging •Image patients with CT initially, then at 5-year intervals after repair. • CT for detecting anastomotic or para- anastomotic changes • Ultrasound may also be used for surveillance but is operator dependent and lacks the sensitivity as of CT
  • 54.