RUPTURED ANEURYSMS OF THE AORTA

VAISHNAVI SURESH NAIR

The aorta is the main trunk of a series of vessels which convey the oxygenated blood to the tissues of the body for their nutrition.

It commences at the upper part of the left ventricle, where it is about 3 cm in diameter, and after ascending for a short distance, arches backward and to the left side, over the root of the left lung.

It then descends within the thorax on the left side of the vertebral column, passes into the abdominal cavity through the aortic hiatus in the diaphragm, and ends, considerably diminished in size (about 1.75 cm. in diameter), opposite the lower border of the fourth lumbar vertebra, by dividing into the right and left common iliac arteries.

Branches: The ascending aorta, the arch of the

aorta, and the descending aorta, which is again divided into the thoracic and abdominal aorta.

THE AORTA

THE AORTIC VALVE

The aortic valve, or aortic semilunar valve, has three leaflets or cusps. It is located at the base of the aorta. It opens to allow blood to leave the left ventricle as it contracts. When the ventricular muscles relax, the valve closes to prevent blood from backing up into the ventricular chamber.

ASCENDING AORTA (Aorta Ascendens)

The ascending aorta is about 5 cm. in length. It commences at the upper part of the base of the left ventricle, on a level with the lower border

of the third costal cartilage behind the left half of the sternum; it passes obliquely upward, forward, and to the right, in the direction of the heart’s axis, as high as the upper border of the second right costal cartilage, describing a slight curve in its course, and being situated, about 6 cm. behind the posterior surface of the sternum.

At its origin it presents, opposite the segments of the aortic valve, three small dilatations called the aortic sinuses.

At the union of the ascending aorta with the aortic arch the caliber of the vessel is increased, owing to a bulging of its right wall. This dilatation is termed the bulb of the aorta, and on transverse section presents a somewhat oval figure.

The ascending aorta is contained within the pericardium, and is enclosed in a tube of the serous pericardium, common to it and the pulmonary artery

Branches: The only branches of the ascending aorta are the two coronary arteries (Right &

Left) which supply the heart; they arise near the commencement of the aorta immediately above the attached margins of the semilunar valves.

ARCH OF AORTA (Arcus aorta/transverse aorta)

The arch of the aorta is the second major anatomical region of the aorta; it curves above the heart between the ascending and descending aorta. All of the blood delivered from the heart to the systemic tissues of the body passes through the aorta, making it the largest artery in the human body. As the aorta extends from the heart, it begins as the ascending aorta before turning 180 degrees towards the body’s left side in the aortic arch. From the arch the aorta passes posterior to the heart and descends through the thorax and abdomen as the descending aorta.

Branches: Three major arteries branch off from the superior

arterial wall of the aortic arch to supply blood to the tissues of the superior regions of the body: the brachiocephalic trunk, left common carotid artery, and left subclavian artery.

The brachiocephalic trunk is the first artery to arise from the aortic arch, carrying blood to the right arm and the right side of the head and neck. Next to branch from the aorta is the left common carotid artery that supplies blood to the left side of the head and neck. Finally, the left subclavian artery arises from the aortic arch and supplies blood to the left arm.

DESCENDING AORTA

Although the descending aorta is positioned to the left of the body's midline, it gradually descends to directly in front of the vertebral column at the left of the 12th thoracic vertebra.

The portion of the descending aorta above the diaphragm is called the thoracic aorta, and gives off branches into the thoracic wall.

Branches of thoracic aorta: The Bronchial

arteries, Mediastinal arteries, Esophageal arteries, Pericardial arteries, Superior phrenic arteries & supply blood to the organs for which they were named.

Below the diaphragm, the descending aorta become the abdominal aorta and stems off into branches that reach the abdominal wall and various tissues and organs of the abdomen.

Branches of abdominal aorta:

Epidemiology

Ruptured abdominal aortic aneurysms (AAAs) cause 12,000 deaths per year, 8,000 of these are infra-renal.

Women are much less frequently affected.

Ruptured abdominal aortic aneurysm (AAA) is one of the most fatal surgical emergencies, with an overall

mortality rate of 90%.

Rupture of a thoracic aneurysm has a greater than 97% fatality rate.

Risk factors

The presence of an aneurysm is a risk for rupture.

The larger the lesion, the more likely it is to bleed; aneurysms over 6 cm have a 25% annual risk of rupture.

Smoking and hypertension are additional risks.

A ruptured aneurysm should be considered whenever a man aged over 55 or a

woman aged over 70 presents with circulatory collapse.

PATHOPHYSIOLOGY

Aorta consists of 3 layers- Intima, Media & Adventitia.

Certain diseases causes weakening of the aortic walls , reduces its elasticity.

When blood is pumped through these weakened areas, it bulges out, which are

called aneurysms.

As the flow and thus the pressure through this area increases, it causes the

rupture of the aneurysm of the aortic wall.

Clinical Presentation

A ruptured aneurysm usually presents with pain.

Ruptured Thoracic aortic aneurysm (RTAA)

It will cause chest pain , Ripping sensation in chest, Severe back pain, between shoulder

blades

Haemoptysis (erodes to trachea), Hematemesis (erodes into esophagus) can occur.

Dizziness, Hypotension, Syncope

Difficulty in walking or speaking

If bleeding occurs into the mediastinum, it can cause cardiac tamponade and rapidly be fatal.

The patient will probably never reach hospital alive and the diagnosis is made post-mortem.

Ruptured Abdominal aortic aneurysm (RAAA)

Ruptured AAA presents with a classical triad of pain in the flank or back, hypotension and a

pulsatile abdominal mass; however, only about half have the full triad. Tachycardia

develops. Shock may occur.

The patient will complain of the pain and may feel cold, sweaty and faint on standing.

The following symptoms are listed with approximate frequency of presentation

• Abdominal pain (60%)

• Back pain (70%)

• Syncope (30%)

• Vomiting (20%)

RUPTURED ABDOMINAL AORTIC ANEURYSM

RUPTURED ABDOMINAL AORTIC ANEURYSM

Abdominal aortic aneurysm (AAA) - sites of rupture and their

incidence

•Intraperitoneal rupture (20%)

•Retroperitoneal rupture (80%)

•Aortocaval fistula (3–4%)

•Primary aortoduodenal fistula (<1%)

•Rarely, Into the abdominal veins or

the bowel.

Pressure builds within aneurysm

Rupture of aortic aneurysm

Normal abdominal aorta Aneurysm

Anterior intraperitoneal rupture

A tear in the anterior wall of the aneurysm results in sudden severe abdominal or back pain and collapse.

The resultant bleeding into the peritoneal cavity is so rapid that exsanguination and death usually occur before

the patient reaches the hospital.

Posterior retroperitoneal rupture

Classical clinical picture

Rupture into the retroperitoneal cavity is the most common site of ruptured AAA .

A tear in the posterolateral aneurysm wall leads to retroperitoneal bleeding which manifests clinically as back pain

with or without abdominal pain and hypotension.

This tear is often sealed for a few hours, which allows time for the transfer of the patient to the hospital,

diagnosis, and treatment.

On examination, a pulsatile epigastric mass is often palpable, particularly in a thin patient. But this mass may not

be palpable in obese or distended patients or in those with severe hypovolaemia.

Unusual presentations of ruptured abdominal aortic aneurysm

The temporary sealing of the tear in the aneurysm wall may rarely extend beyond a few hours. This results in a variety

of misleading symptoms and signs because of the extension of the retroperitoneal haematoma and its compressive

effects.

In ruptured AAA the duration of symptoms may be unusually long, and that an abdominal pulsatile mass may be

absent.

Transient lower limb paralysis

Right hypochondrial pain

Nephro ureterolithiasis

Groin pain

Testicular pain

Testicular ecchymosis (blue scrotum sign of Bryant)

Iliofemoral venous thrombosis

Inguinoscrotal mass mimicking a hernia

The three most frequent emergency presentations of ruptured AAA and their immediate management are:

•A patient known to have an AAA presents with a sudden onset of abdominal or back pain and

hypotension

•A patient presents with the classical triad of pain, hypotension, and a pulsatile mass.

In the two previous scenarios, a haemodynamically unstable patient should be immediately transferred to the

operating theatre for emergency open repair. Recently, endovascular aneurysm repair (EVAR) has been successfully

used to treat ruptured AAA.

In hospitals with capabilities for EVAR, a haemodynamically stable patient can undergo a preoperative computed

tomography (CT) scan, and if the anatomy of the aneurysm is suitable, the patient can undergo endovascular repair

for his/her ruptured aneurysm.

•A patient is suspected of having a ruptured AAA, regardless of the symptoms and signs, and is

haemodynamically stable.

This patient should undergo a CT scan to confirm the diagnosis and assess his/her suitability for EVAR.

Emergency presentations of ruptured AAA

Chronic contained rupture of AAA

Although most patients with ruptured AAA have an acute presentation, some patients may escape detection for

weeks or months after the aneurysm ruptures. This usually occurs when a retroperitoneal rupture leads to slow

progressive bleeding which forms a large haematoma that is contained by the resistance of the periaortic tissues.

Approximately 4% of ruptured AAA are contained ruptures . They are also known as "sealed" or "spontaneously

healed" aneurysms.

Most patients with a contained rupture are haemodynamically stable with no manifestations of acute blood

loss. But a contained rupture is a ruptured aneurysm in a stable patient that may progress to free rupture at any

time. Thus, urgent surgical treatment within 24 h, preferably after admission to an intensive care unit, is

necessary.

Most patients with a contained rupture present with chronic back pain that may radiate to the groin. Other

reported presentations includes lumbar vertebral erosion, lumbar spondylitis-like symptoms, left lower limb

weakness or neuropathy, crural neuropathy, left psoas muscle haematoma, and obstructive jaundice.

Rupture into the abdominal veins

Rarely, AAA ruptures into the inferior vena cava or the left renal vein. This results in an aortocaval fistula or an

aorta–left renal vein fistula, respectively.

Aortocaval fistula

A spontaneous aortocaval fistula most commonly occurs when an AAA erodes (ruptures) into the inferior

vena cava

Approximately 3–4% of patients with ruptured AAA have an aortocaval fistula.

In these patients, the manifestations of rupture usually dominate the clinical picture and significantly

diminish the chance of preoperative diagnosis.

Aortocaval fistulae are probably missed in 50% of patients and are discovered accidentally during elective

repair of AAA.

Trauma and surgery of the lumbar spine are other known causes of aortocaval fistulae.

The manifestations of an aortocaval fistula are variable because they depend on the size of the communication

between the aorta and the inferior vena cava.

Thus, temporary or permanent closure of this communication by an aortic mural thrombus or by a

compressing aneurysm will change the clinical picture.

The discovery of an aortocaval fistula during surgery is associated with major blood loss and the possibility of

pulmonary embolization with thrombus material from the aneurysm sac. Thus, unless the patient presents in

extremis due to the rupture, every effort should be made to detect the fistula preoperatively.

Abdominal CT scan is the definitive imaging test for the evaluation of AAA, and all patients suspected of

having an aortocaval fistula should undergo a contrast CT whenever possible.

Characteristic CT findings are loss of the fat plane between the aorta and inferior vena cava, vena caval

effacement, and direct inflow of contrast from the aorta to the inferior vena cava.

Clinically, a patient with an aortocaval fistula presents with a classical triad of abdominal or back pain, a

pulsatile abdominal mass, and a continuous bruit on abdominal auscultation.

This triad is reported in 50–90% of patients.

Patients with an aortocaval fistula may also present with manifestations of high output heart failure such as

dyspnoea, tachycardia, wide pulse pressure, cyanosis, and lower limb oedema.

Additional symptoms and signs include angina, palpitations hypotension, fever, oliguria,

haematuria, pulsatile peripheral veins, and diminished lower limb pulses.

Aorta–left renal vein fistula

It most commonly occurs when the wall of an infrarenal AAA erodes into the left renal vein.

The left renal vein normally crosses in front of the abdominal aorta on its way to the inferior vena cava. In 1–

2.4% of people, however, the vein crosses behind the aorta.

A retro aortic left renal vein is involved in more than 90% of cases of aorta–left renal vein fistula.

The "abdominal pain, haematuria, silent left kidney" syndrome described by Mansour et al summarises

the clinical features of aorta–left renal vein fistula.

Haematuria is the most important clinical feature in this condition, followed by pain which is usually felt in the

left flank and radiates to the groin, mimicking ureteric colic.

A pulsatile abdominal mass and a left sided continuous bruit are detected in approximately 60% and

70% of patients, respectively.

Renal dysfunction is usually seen in 85% of patients.

High output heart failure, similar to that seen in an aortocaval fistula, can also be seen in patients with an

aorta–left renal vein fistula. The degree of heart failure depends mostly on the size of the fistula.

Although extremely rare, an aorta–left renal vein fistula should be ruled out if a patient with an AAA develops

haematuria, left loin pain, or manifestations of renal dysfunction.

A contrast CT scan of the aorta can visualise the fistula, which should be looked for if a retro aortic left renal vein

is seen.

Preoperative diagnosis can avoid unnecessary blood loss when the aneurysm is opened during surgery. Intra

operatively, a palpable thrill over the aneurysm, or an absent left renal vein anterior to the aorta, should raise

suspicion of an aorta–left renal vein fistula.

An extremely rare cause of haematuria is an aortoureteric fistula. Here, the communication is usually between the

ureter and a previously inserted aortic graft, but it can also occur with an aortoiliac aneurysm.

The triad of unilateral hydronephrosis, intermittent haematuria, and previous aortic surgery should alert the

clinician to this life threatening but potentially curable disease.

Rupture into the bowel (aorto enteric fistula)

An aorto enteric fistula is an abnormal communication between the abdominal aorta and the bowel; it may be

primary or secondary.

A primary aorto enteric fistula connects an infra renal AAA to the bowel, most commonly the duodenum

(aortoduodenal fistula). This condition is often fatal but fortunately rare, with an estimated incidence at autopsy of

0.04–0.07%.

A secondary aorto enteric fistula is a late postoperative complication due to erosion of a prosthetic aortic

graft into the duodenum. This condition is more common, occurring in 0.5–2.3% of patients after aortic surgery.

The third and fourth parts of the duodenum are most commonly involved in an aorto enteric fistula because this

duodenal segment is closely applied to the anterior wall of the aorta, being fixed posteriorly by the ligament of

Treitz. However, communications with other parts of the gastrointestinal tract have also been reported.

Patients with a primary aortoduodenal fistula commonly present with upper gastrointestinal haemorrhage

(hematemesis, melena, haematochezia). Abdominal pain and a pulsatile abdominal mass may also be

present; however, patients rarely have all three findings.

Gastrointestinal haemorrhage was the most common presentation in patients with primary aortoduodenal fistula,

occurring in 96% of patients. Massive haemorrhage is uncommon initially; patients usually experience an episode

of small brisk bleeding which stops spontaneously. This "herald bleed" is characteristic of an aortoduodenal

fistula

Oesophagogastroduodenoscopy (OGD) is likely to be the first diagnostic test done in patients with upper

gastrointestinal haemorrhage, even if the cause of the bleeding is an aortoduodenal fistula.

OGD is useful to rule out the much more common causes of bleeding such as gastroduodenal ulcers and

oesophageal varices. If bleeding is due to an aortoduodenal fistula, OGD may not be precise in visualising the

fistula because of failure to pass the endoscope into the third or fourth parts of the duodenum.

Consequently, in patients with known or previously treated AAApresenting with unexplained upper

gastrointestinal haemorrhage, CT has emerged as the most important initial diagnostic test to rule out an

aortoduodenal fistula. Highly suggestive findings on CT include loss of the fat plane between the aorta and

duodenum and the presence of air in the retroperitoneal cavity.

Unless a primary gastrointestinal source of bleeding has been unequivocally identified in a bleeding patient

with AAA, an aortoduodenal fistula should always be ruled out.

Currently, the preoperative diagnosis of aortoduodenal fistulae is reached in only 50% of patients.

RUPTURED AAA IN CHILDREN

• Aortic aneurysms are extremely rare in children, and their aetiology is different from those in adults.

• In children, aortic wall infection, vasculitis, and connective tissue disorders are important causative

factors for AAA.

• Umbilical vein catheterisation is also a well recognised cause of childhood AAA, possibly

through infection.

• Most AAAs in children present as painless pulsatile masses; But a few alarming cases of rupture

have been reported.

• Ruptured AAA is not often suspected in children; But its fatal & should immediately rule out ruptured

AAA in children if it is suspected.

Physical Examination

A patient with a ruptured aneurysm at any level is likely to look pale and unwell and to be cold and sweaty.

The pulse will be rapid, weak and thready. Hypotension is common.

With a ruptured AAA there may well be a pulsatile mass in the vicinity of the bifurcation of the aorta. This is a few

centimetres above the umbilicus and a little to the left.

It may be tender and a bruit may be audible. Bleeding causes peritoneal irritation and it may appear as an acute

abdomen.

The following findings are listed with approximate frequency:

Palpable mass (90%).

Tenderness (80%).

Systolic blood pressure (BP) below 80 mm Hg (40%).

NB: presentation can be atypical, eg: intestinal obstruction from haematoma or an apparent irreducible inguinal

hernia.

Rare presentations are:

Severe hematemesis from an aorto -duodenal fistula.

A fistula into the inferior vena cava, producing lower limb oedema and high-output cardiac failure.

Differential diagnosis

The differential diagnosis for a ruptured TAA is that of chest pain, especially MI with cardiogenic shock but

also massive pulmonary embolism.

The differential diagnosis for ruptured AAA involves other causes of abdominal pain, including acute abdomen.

Investigations

If an aneurysm is ruptured, investigations need to be swift and pertinent.

Laboratory studies

CBC: NB: if there has not been time for haemodilution then haemoglobin will be normal. Anaemia is present in

less than half of patients. Around 80% have a white cell count of 10 x 109/L or more.

CMP

Group and rapid cross-match: whilst arranging surgery.

Baseline biochemistry of U&Es: should be performed.

Radiology

CXR: for a TAA the CXR may well show an enlarged base of aorta.

Plain abdominal X-ray: for an AAA this will show the lesion in about 75%, as it is often calcified.

Portable ultrasound: this examination may be helpful but there is not time for detailed assessment. If there is

strong suspicion of a ruptured aneurysm then immediate surgery may be the investigation of choice.

Other investigations: CT angiography will confirm the diagnosis. MRI and angiography are an alternative

but, practically, more time-consuming so probably only suitable for the stable patient.

ECG ECG: is important In patients presenting with chest pain.

TREATMENT

Abdominal aortic aneurysms (AAAs) are typically repaired by an operative intervention.

The possible approaches are the traditional open laparotomy, newer minimally invasive methodologies, or by

the placement of endovascular stents.

INDICATIONS:

Open repair:

Diameter of the aneurysm greater than 2 inchesAbdominal PainAbdominal Pulsation

Endovascular repair:

Severe Heart diseasesAge risksOther underlying medical conditions

PRE-OPERATIVE MEASURES

•Type and cross match blood

•IV line (fluids, antibiotics, anesthesia)

•Administer prophylactic antibiotics (cefazolin, 1 g intravenous piggyback)

•Insert a Foley catheter

•Monitor central venous pressure or establish Swan-Ganz catheterization (if

indicated)

•Prepare the skin from the nipples to the mid thigh

•Administer general anesthesia (open), general/regional anesthesia (endovascular)

•Insert a nasogastric tube

Open repair of an abdominal aortic aneurysm involves

an incision of the abdomen to directly visualize the aortic

aneurysm. The procedure is performed in an operating

room under general anaesthesia.

The surgeon will make an incision in the abdomen either

lengthwise from below the breastbone to just below the

navel or across the abdomen and down the centre.

Once the abdomen is opened, the aneurysm will be

repaired by the use of a long cylinder-like tube called a

graft. Grafts are made of various materials, such as

Dacron (textile polyester synthetic graft) or

polytetrafluoroethylene (PTFE, a non textile synthetic

graft). The graft is sutured to the aorta connecting one

end of the aorta at the site of the aneurysm to the other

end of the aorta.

4-6hrs duration

5-10 days hospital stay

Open repair

Endo Vascular Aneurysm Repair (EVAR) EVAR is a minimally-invasive (without a large abdominal incision)

procedure performed to repair an abdominal aortic aneurysm. EVAR

may be performed in an operating room, radiology department, or a

catheterization laboratory. Surgeon may use general anesthesia or

regional anesthesia (epidural or spinal anesthesia). The surgeon will

make a small incision in each groin to visualize the femoral arteries in

each leg. With the use of special endovascular instruments, along with

X-ray images for guidance, a stent-graft will be inserted through the

femoral artery and advanced up into the aorta to the site of the

aneurysm. A stent-graft is a long cylinder-like tube made of a thin

metal framework (stent), while the graft portion is made of various

materials such as Dacron or polytetrafluoroethylene (PTFE) and may

cover the stent. The stent helps to hold the graft in place. The stent-

graft is inserted into the aorta in a collapsed position and placed at the

aneurysm site. Once in place, the stent-graft will be expanded (in a

spring-like fashion), attaching to the wall of the aorta to support the

wall of the aorta. The aneurysm will eventually shrink down onto the

stent-graft.

2-3hrs duration

2-3 days hospital stay

Postoperative Details

Fluid shifts are common following aortic surgery. Fluid requirements may be high in the first 12 hours,

depending on the amount of blood loss and fluid resuscitation in the operating room.

Monitor the patient in the surgical intensive care unit for hemodynamic stability, bleeding, urine output, and

peripheral pulses.

A postoperative electrocardiogram and chest radiograph are needed.

Prophylactic antibiotics (eg, cefazolin at 1 g) are administered for 24 hours.

The patient is seen in 1-2 weeks for suture or skin staple removal, then yearly thereafter.

Complications of the procedure

Open repair

• Myocardial infarction (heart attack)

• Irregular heart rhythms (arrhythmias)

• Bleeding during or after surgery

• Injury to the bowel (intestines)

• Limb ischemia (loss of blood flow to legs/ feet)

• Embolus (clot) to other parts of the body

• Infection of the graft

• Lung problems

• Kidney damage

• Spinal cord injury

EVAR

• Damage to surrounding blood vessels, organs, or

other structures by instruments

• Kidney damage

• Limb ischemia (loss of blood flow to leg/feet) from

clots

• Groin wound infection

• Groin hematoma (large blood-filled bruise)

• Bleeding

• Endo leak (continual leaking of blood out of the

graft and into the aneurysm sac with potential

rupture)

• Spinal cord injury

Prognosis

No more than 1 in 3 patients with a ruptured aortic aneurysm will reach hospital alive, and 20% of those who do, fail

to reach theatre.

Delay in diagnosis is a major risk factor. Elective repair of AAA has a mortality of around 5% compared with 60-80%

for emergency repair.

The following factors are associated with a mortality rate in excess of 80%:

Age over 80.

Presentation in shock with free intraperitoneal rupture.

Failure of BP to rise, despite attempts at resuscitation.

Haematocrit below 25% on admission.

Preoperative cardiac arrest.