Prehospital Management Of Ruptured Aortic Aneurysm

A ruptured Aortic Aneurysm (rAA) is a catastrophic vascular emergency with an extremely high mortality rate. Up to 85% of patients die before reaching the hospital, highlighting the importance of immediate and effective prehospital intervention.

Pathophysiology of Aortic Aneurysm

An aortic aneurysm (AA) is a localised dilation of the aorta, typically defined as an enlargement greater than 3 cm in diameter. The pathophysiology of aortic aneurysm involves a complex interplay of genetic, biochemical, and biomechanical factors leading to progressive weakening of the aortic wall, culminating in aneurysm formation and eventual rupture if left untreated.

The normal aortic wall consists of three layers:

• Tunica intima: The innermost layer, a single layer of endothelial cells.
• Tunica media: The middle layer, composed of smooth muscle cells, elastin, and collagen fibres that provide structural integrity and elasticity.
• Tunica adventitia: The outer layer, composed of collagen and connective tissue, providing tensile strength to the aorta.

In aortic aneurysm, these layers undergo degeneration and structural changes, weakening the arterial wall and allowing the aorta to progressively dilate.

In aortic aneurysm, these layers undergo degeneration and structural changes, weakening the arterial wall and allowing the aorta to progressively dilate.

The formation of an aoritc aneurysm is often attributed to several key processes, including:

Atherosclerosis

Atherosclerotic plaques accumulate within the arterial wall, leading to inflammation, lipid deposition, and oxidative stress. This weakens the aorta’s structural components and initiates aneurysm formation. As plaques build up in the tunica intima, they restrict blood flow and compromise the vascular integrity of the aortic wall.

Inflammation

Chronic inflammation plays a central role in aortic aneurysm development. Inflammatory cells, such as macrophages and T-lymphocytes, infiltrate the aortic wall, releasing cytokines and proteolytic enzymes like matrix metalloproteinases (MMPs). MMPs degrade elastin and collagen in the tunica media, weakening the arterial wall and causing it to lose its elastic recoil, making it more prone to dilation.

Elastin and Collagen Degradation

Elastin provides the aortic wall with its ability to stretch and recoil. In aortic aneurysm, the balance between elastin synthesis and degradation is disrupted, with increased elastin breakdown leading to a weakened arterial wall. Collagen, which provides tensile strength, also becomes degraded, further contributing to structural weakening.

Vascular Smooth Muscle Cell (VSMC) Dysfunction

VSMCs are responsible for maintaining the structural integrity of the aortic wall. In aortic aneurysm, VSMCs undergo apoptosis (programmed cell death) or senescence (loss of function due to aging), which results in reduced repair and maintenance of the vessel wall, further weakening it.

Oxidative Stress

Reactive oxygen species (ROS) generated by inflammatory processes contribute to the degradation of extracellular matrix proteins (elastin and collagen) and induce VSMC apoptosis. This oxidative damage weakens the aorta’s structural integrity.

Aortic aneurysms can occur in different regions along the aorta, and they are classified based on their location. Here are the key locations where aneurysms can develop:

Ascending Aorta Aneurysm

The part of the aorta that arises from the left ventricle of the heart and extends to the aortic arch.

Aneurysms in this region can lead to complications such as hemopericardium (blood in the pericardial sac) and right sided haemothorax (blood in the pleural cavity).

 Aortic Arch Aneurysm

The portion of the aorta that curves over the heart, between the ascending and descending aorta.

Aneurysms here can result in a mediastinal haematoma (bleeding into the central chest cavity), compression of the pulmonary arteries, or obstruction of blood flow to the brain or upper limbs.

 Descending Aorta Aneurysm

The part of the aorta that runs down the chest from the aortic arch to the diaphragm.

Aneurysms in this region can compress the pulmonary arteries, lead to a left-sided haemothorax, or very rarely, erode into the oesophagus, causing severe bleeding.

 Abdominal Aorta Aneurysm

The most common site for aneurysms, located below the diaphragm and extending to the point where the aorta bifurcates into the iliac arteries.

Abdominal aortic aneurysms (AAA) typically result in retroperitoneal or intraperitoneal haemorrhage when they rupture, leading to back or abdominal pain, and often, shock.

As the aneurysm expands, the aortic wall continues to weaken, and the aorta dilates further. This progressive dilation increases wall tension. As the diameter of the aneurysm increases, the tension on the aortic wall grows, further increasing the risk of rupture.

Several factors can influence the rate of aneurysm growth:

Size of the aneurysm: Larger aneurysms tend to grow more rapidly than smaller ones, and those over 5.5 cm in diameter have a significantly higher risk of rupture.

Blood pressure: Hypertension exerts greater pressure on the weakened aortic wall, accelerating the expansion of the aneurysm.

Smoking: Smoking increases the risk of AAA development and rupture by promoting inflammation and oxidative stress within the aortic wall.

When an aneurysm ruptures, it often leads to massive internal bleeding. The rupture usually occurs at the site of the greatest wall tension, typically at the posterior wall of the aneurysm. Rupture can result in:

Retroperitoneal haemorrhage: Blood leaks into the retroperitoneal space, often causing severe back pain and initial containment by surrounding structures. This sometimes delays collapse.

Intraperitoneal haemorrhage: This occurs when blood leaks into the abdominal cavity, causing rapid circulatory collapse and high mortality rates.

Rupture is the most feared complication of aortic aneurysm and is associated with a high mortality rate. As the aneurysm enlarges, the risk of rupture increases exponentially. For example:

• Aneurysms less than 4 cm in diameter have a rupture risk of less than 1% per year.
• Aneurysms between 4.0-5.4 cm carry a rupture risk of approximately 1-11% per year.
• Aneurysms greater than 5.5 cm have a rupture risk exceeding 10% per year.

Once rupture occurs, the patient rapidly deteriorates, presenting with severe pain, haemodynamic instability, and signs of hypovolaemic shock.

Risk Factors

Although the exact aetiology of AAA remains unclear, several risk factors contribute to its development, including:

General Clinical Features Of rAA

The clinical presentation may vary depending on the location of the aneurysm (ascending aorta, aortic arch, descending thoracic aorta, or abdominal aorta), but there are some common features across all types.

Severe, Sudden-Onset Pain

The most characteristic symptom of a ruptured aortic aneurysm is the abrupt onset of severe pain.

• Ascending Aorta: Pain is typically located in the chest and may radiate to the back, neck, or jaw. This pain may be mistaken for myocardial infarction.
• Aortic Arch: Pain in the chest, back, or neck is common, along with symptoms of upper body or cerebral ischemia due to compression of vessels branching off the arch.
• Descending Thoracic Aorta: Severe, tearing pain in the chest, back, or interscapular area is common. It may radiate to the abdomen or lower back.
• Abdominal Aorta: Severe, sharp, or tearing abdominal, flank, or back pain. It can radiate to the groin, hips, or legs.

Syncope or Collapse:

• Patients may experience syncope (fainting) due to sudden blood loss and cardiovascular collapse. This is a sign of haemodynamic instability and a poor prognostic indicator.
• In some cases, collapse may precede the onset of pain, especially if the rupture causes immediate and massive internal bleeding.

Hypotension

• Profound hypotension or shock is a hallmark of rupture due to massive blood loss. Hypotension is more common in intraperitoneal or intrathoracic ruptures, where the bleeding is less contained.
• Retroperitoneal bleeding, which may occur in abdominal aortic aneurysm (AAA) rupture, can be contained temporarily, delaying the onset of hypotension.

Pallor, Sweating, and Clamminess

• Patients with ruptured aortic aneurysm often appear pale and diaphoretic (sweating), which are classic signs of hypovolaemic shock.

Nausea and Vomiting

• Nausea and vomiting can occur, especially in abdominal aortic aneurysm ruptures, due to severe abdominal pain and visceral irritation.

Signs of Hypovolaemic Shock

• Cold, clammy skin, weak peripheral pulses, and delayed capillary refill indicate poor perfusion and impending cardiovascular collapse.

Location Specific Clinical Features Of rAA

Ascending Aortic Aneurysm Rupture

• Can lead to hemopericardium (blood accumulating in the pericardial sac), resulting in cardiac tamponade, which can cause rapid cardiovascular collapse, syncope, and death.
• May cause right haemothorax, leading to respiratory distress, hypotension, and immediate life-threatening complications.

Aortic Arch Aneurysm Rupture

• Compression of the pulmonary arteries or pulmonary trunk may lead to respiratory distress and cardiac complications.
• Mediastinal haematoma can cause severe chest pain and pressure on surrounding structures, potentially resulting in airway compromise or vascular obstruction.

Descending Thoracic Aortic Aneurysm Rupture

• May cause left-sided haemothorax, leading to respiratory distress and shock.
• Rarely, it may erode into the oesophagus, resulting in catastrophic upper gastrointestinal bleeding (haematemesis).

Abdominal Aortic Aneurysm (AAA) Rupture

• Typically leads to retroperitoneal haemorrhage, causing severe back or loin pain. This can be temporarily contained, providing a brief window for intervention.
• Intraperitoneal haemorrhage is more catastrophic, with diffuse abdominal pain, rapid cardiovascular collapse, and high mortality rates.
• Sometimes, there may be erosion into the gastrointestinal tract, causing a “herald” bleed, which can present as gastrointestinal bleeding before full rupture.

Examination Findings of rAA 

Pulsatile Mass (AAA)

A pulsatile mass may be palpable in the abdomen in cases of ruptured abdominal aortic aneurysm. However, in up to 50% of cases, a pulsatile mass may not be detected.

Abdominal or Chest Tenderness

Tenderness in the abdomen or chest may be present, depending on the location of the aneurysm. The tenderness is usually localised to the site of the aneurysm.

Signs of Poor Peripheral Perfusion

Cool extremities, mottling, weak or absent peripheral pulses, and delayed capillary refill indicate poor blood flow secondary to haemodynamic compromise.

Diminished Breath Sounds (Thoracic Aneurysm Rupture)

In cases of haemothorax, breath sounds may be diminished on the affected side, particularly in thoracic aortic aneurysm rupture.

Prehospital Management of Ruptured Aortic Aneurysm

An immediate structured approach based on the <C>ABCDE framework ensures systematic assessment and management of the patient. This should be supplemented by a high index of suspicion in at-risk populations, particularly older men with cardiovascular comorbidities and known aortic aneurysm. A time-critical transfer is needed for all suspected ruptured aortic aneurysm.

External haemorrhage is not typically a feature of ruptured aortic aneurysm, but internal catastrophic bleeding must be recognised early.

Prehospital haemorrhage control focuses on managing the consequences of internal blood loss through rapid diagnosis and stabilisation.

Ensure the airway is patent. An altered level of consciousness may compromise airway patency.

Consider advanced airway management if there is a risk of airway compromise.

Administer high-flow oxygen, aiming for SpO2 between 94% and 98%.

Monitor respiratory rate and effort. Patients in hypovolaemic shock may present with tachypnoea.

Be cautious of hypoxia, as it exacerbates end-organ hypoperfusion.

Obtain vital signs, including blood pressure, heart rate, and capillary refill time.

Permissive hypotension: Avoid aggressive intravenous fluid resuscitation unless there are signs of impaired cerebral perfusion. Excessive fluids can dislodge clot formation and exacerbate haemorrhage. A systolic blood pressure target of 70-90 mmHg is generally recommended until surgical intervention is available.

If fluid resuscitation is necessary, use small boluses (250ml) of 0.9% sodium chloride to maintain cerebral perfusion, being cautious not to increase blood pressure excessively.

Assess neurological status, including Glasgow Coma Scale (GCS) score and pupillary response.

Check blood glucose levels to rule out hypoglycaemia as a cause of altered mental status.

Fully expose the patient to assess for signs of shock, including pallor, cold and clammy skin, and diminished peripheral pulses.

Palpate the abdomen for a pulsatile mass, though it may not be present in all cases.

Ensure the patient remains warm to prevent hypothermia, which can worsen coagulopathy.

Pain relief is a crucial component of prehospital care, but caution is required when administering strong analgesics. Opioids such as morphine can reduce abdominal muscle tone, which may inadvertently increase blood flow to the rupture site, leading to worsened haemorrhage so should be avoided.

Continually reassess the patient’s pain score and response to treatment.

Patients with suspected ruptured aortic aneurysm require immediate transportation to an arterial centre with vascular surgery capability. Every minute counts, as delays in surgical repair can lead to rapid deterioration. While enroute, continue to monitor and reassess the patient’s condition, focusing on maintaining airway patency, oxygenation, and permissive hypotension.

During the transfer, communicate with the receiving hospital using an ATMIST handover

The ultimate goal is to minimise the prehospital time and ensure the patient receives timely vascular surgical intervention, whether through open repair or endovascular aneurysm repair (EVAR).

In the following instances, the patient should be taken to the nearest ED or managed at home according to their individual care plan:

• The patient has experienced cardiac arrest or is at imminent risk of arrest.
• The airway cannot be safely managed.
• The patient was previously identified as being in the final stages of life and is on an end-of-life care pathway.
• The patient has an advanced directive declining surgery, even if their life is in danger.
• It has been previously agreed that the patient is not a candidate for surgical intervention and is unlikely to survive either elective or emergency surgery.

Differential Diagnosis

While managing a patient with suspected ruptured aortic aneurysm, consider other causes of abdominal pain and haemodynamic instability.

Renal colic is a common differential, particularly in patients presenting with acute loin-to-groin pain, but the absence of hypotension usually differentiates it from ruptured aortic aneurysm. Other potential diagnoses include gastrointestinal perforation, pancreatitis, and myocardial infarction.

JRCALC Flowchart

Conclusion

The prehospital management of a ruptured aortic aneurysm is a complex and high-risk task that demands rapid decision-making and well-coordinated care. It is crucial for responders to quickly identify the signs and symptoms of ruptured aortic aneurysm, initiate proper treatment, and ensure timely transport to a specialised vascular centre. Adhering to structured protocols like <C>ABCDE, using permissive hypotension, and delivering effective pain relief are essential steps that can significantly improve patient outcomes in this life-threatening emergency.

Key Points

Bibliography

Joint Royal Colleges Ambulance Liaison Committee, & Association of Ambulance Chief Executives. (2022). JRCALC Clinical Guidelines 2022. Class Professional Publishing.

NHS (2019). Overview – Abdominal aortic aneurysm. NHS. https://www.nhs.uk/conditions/abdominal-aortic-aneurysm

NICE (2020). Overview | Abdominal aortic aneurysm: diagnosis and management | Guidance | NICE. https://www.nice.org.uk/guidance/ng156

Shaw, P.M., Loree, J. and Gibbons, R.C. (2023). Abdominal Aortic Aneurysm (AAA). PubMed. Available at: https://www.ncbi.nlm.nih.gov/books/NBK470237