Acute aortic emergencies

Introduction

• Acute aortic syndromes
  • Aortic dissection, penetrating atherosclerotic ulcer, intramural haematoma and aortic aneurysm leakage/rupture
  • 3-6 cases per 100 000 per year
  • Most common cardiovascular complication of Marfan’s syndrome is aortic root disease and type A dissection
  • Identification of gene mutations associated with Marfan’s (TGFBR2 and FBN1), combined with regular follow-up can reduce fatal outcomes

Pathophysiology

• Degeneration of the media of the aortic wall with intimal stress leading to:
  • Aortic dilation
  • Aneurysm formation
  • Development of penetrating ulcer
  • Intramural haemorrhage
  • Aortic dissection
  • Aortic rupture
• Aortic dissection
  • Violation of intima allowing blood to enter media and dissect between the intima and adventitia
  • Dissecting column of blood forms a false lumen and can re-enter lumen (spontaneous clinical recovery) or dissect through adventitia with exsanguination
  • First peak in younger patients with connective tissue disorders and second peak in those >50yo with chronic hypertension
  • Other atherosclerotic risk factors are relatively weak compared to chronic HTN
  • Atherosclerosis is NOT a major risk factor for aortic dissection and is rarely present at site of dissection
• Aortic intramural haematoma
  • Results from infarction of the aortic media due to injury to vasa vasorum
  • May resolve spontaneously or dissect
  • 5-20% of cases of acute aortic syndrome
  • Treated as for dissection
  • High-risk features
    • Thickness >10mm in ascending or >13mm in descending aorta
    • Underlying aneurysm
    • Intramural blood pools
      • Occur at aortic branch arteries with small contrast-filled focal collections
      • “Chinese ring sword sign”
• Penetrating atherosclerotic ulcer
  • Mushroom-shaped, smooth, crater
  • Mostly descending aorta

Risk factors

• Risk factors
  • Male (65% of cases)
  • Chronic hypertension (70-90% of cases)
  • Arteritis/syphilis
  • Bicuspid aortic valve
  • Marfan’s syndrome
  • Ehlers-Danlos syndrome
  • Family history of aortic dissection
  • Chronic cocaine/amphetamine use
  • Prior cardiac surgery

Aortic dissection

• 5-10 patients per million per year
• 2-3x more common than ruptured AAA
• 90% fatal in 3 months; 28% fatal in 24 hours
• In-hospital mortality 25%
• Distribution
  • 50% begin in ascending aorta
  • 30% begin in the arch
  • 20% begin distally
  • Usually re-enter aorta just above bifurcation

Complications

• Dissection of other vessels
  • Coronaries, brachiocephalic trunk, carotids, left subclavian, spinal, mesenteric, renal, iliacs
  • Free rupture – Haemothorax/sudden death/retroperitoneal/peritoneal
  • Acute aortic regurgitation
  • Haemopericardium/tamponade
  • Aneurysm formation

Clinical features

• History
  • Always think if chest pain PLUS
    • Back pain
    • Abdominal pain
    • Neurological deficits
    • Limb ischaemia
  • Classically tearing chest pain radiating to interscapular region with impending doom
  • 60% of patients had anterior chest pain (most common in Stanford A); 50% have back pain
  • Abdominal pain (30%) and back pain are more common in Stanford B
  • 25% have no chest pain
  • 5% have no pain at all
  • Most patients describe pain as worst pain they’ve ever had and abrupt onset (85%) – if not rapid onset LR -0.3 to -0.07
  • 64% describe sharp pain and 50% as tearing
  • Syncope seen in 10% (mostly Stanford A)
  • 22% occur in patients with prior cardiac surgery
  • May present with stroke symptoms with carotid involvement
    • 20% of type A dissections display neurological findings (poor prognosis)
    • Focal neuro deficit + chest pain = LR + 6.6 to 33
  • Paraplegia if blood supply to spinal cord interrupted
  • Further distal dissection may lead to flank/back or abdominal pain
  • Cardiac tamponade if more proximal dissection ensues +- ECG showing ACS-type findings if coronary arteries involved
• Examination
  • 1/3 have aortic insufficiency murmur – LR + 9.0
  • 15% have pulse deficit in radial or femoral arteries
    • 20% sensitive but 95% specific – LR + 29-33
  • BP discrepancy of >20mmHg between arms – significant
    • 30% sensitive and 85% specific for dissection
  • 50% have hypertension (>150mmHg)
    • Seen in 35% of Type A and 70% of type B
  • Hypotension in 18-25% (worse prognosis)
  • Pericardial tamponade occurs in 25% of type A dissections
  • Aneurysmal aortic dilatation can compress surrounding structures
    • Oesophagus (dysphagia)
    • Recurrent laryngeal nerve (hoarsenss)
    • Superior cervical sympathetic ganglion (Horner’s)
• DDx
  • MI/ACS
  • Pericardial disease
  • Stroke
  • Spinal cord injury/disorders
  • Intra-abdominal disorders
  • PE, pneumonia, pleurisy, pneumothorax

Diagnosis

• ECG – Normal in 19-31%. Majority have non-specific ST/T wave changes or ST depression
  • 25% have features suggestive of ACS (usually type I dissection)
• D-dimer
  • False negative rate as high as 18%. Especially useless in younger patients with short dissection length and thrombosed false lumen
  • Not to be used as sole rule-out criterion and not routinely used in workup at all
• Imaging
  • 12-37% of patients have normal CXR; conversely 90% of cases have some abnormality
    • 60% widened mediastinum; 50% abnormal aortic contour
  • Normal CXR more common if younger (connective tissue) or pregnancy-related
  • CT (MDCT) is the modality of choice
    • Highly sensitive/specific and can diagnose atherosclerotic ulcers and intramural haematomas
    • Provides information on extent of dissection, other organs involved and signs of aortic rupture
    • More accurate for proximal than distal aortic dissections; Sensitivity 95%, specificity 95-100%
    • False lumen vs. true lumen
      • False lumen has beaks at each edge
      • Usually larger
      • Shows cobwebs within lumen
      • May surround the true lumen
      • Left renal artery usually comes off false lumen
    • TTE
      • Limited sensitivity but highly specific if intimal flap seen. Sensitive for ascending dissections within 2-3cm of aortic valve
    • TOE may be as sensitive and specific as CT
      • Requires moderate sedation and highly operator dependent
      • Sensitivity 80-100%; specificity 70-95%
      • Less accurate for aortic ulcers and intramural haematomas
    • Coronary CT angiography (triple rule-out)
      • Can diagnosed and differentiate coronary artery disease, PE and acute aortic dissection
      • Requires special infusion protocol and has not been shown to improve diagnostic yield, reduce clinical events or diminish downstream resource use

CXR findings

• Double density of aorta
• Tracheal deviation to the right and anteriorly
• Depression of left main bronchus
• NGT deviation to the right
• Cardiomegaly
• Left sided pleural effusion
• Apical capping

• Left mediastinal width at level of aortic knob >5cm – 90% sensitive and specific
• Blurred aortic knob – 70% sensitive
• Loss of aortopulmonary window
• Mediastinum > 7.5cm at level of aortic knob – 90% sensitive and specific
• Mediastinum >25% chest width
• Subjective widening – Sensitivity of 65%; LR + 2.0
• Disparity between ascending and descending aorta diameter

Treatment

• Vasodilators
  • Nitroprusside can be added once HR <60
  • GTN preferred if coronary ischaemia evident
  • Hydralazine 5-10mg IV over 5-10 min repeated q15-20min
• Definitive repair
  • Type A require prompt surgical repair
  • Endovascular stent repairs with fenetrations can be used for some type A and complicated type B dissections (malperfusion, resistent hypertension, persistent severe pain, persistent false lumens or expanding aortic diameter), penetrating ulcers and intramural haematomas
• All other Type B get medical management and ongoing management from Cardiology/Vascular Surgery

Aneurysmal disease

• Aneurysm = Dilatation >1.5x normal diameter
  • True aneurysm – involves all three layers of wall
    • Risk factors:
      • Connective tissue disorders
      • Family Hx of aneurysm
      • Atherosclerosis risk factors
    • Thinning of media and reduced tensile strength
    • Increased wall force and dilatation are intertwined as per LaPlace law: wall tension = pressure x radius
    • Larger aneurysms expand more quickly due to this (0.25-0.5cm per year)
    • Abrupt expansion and rupture can occur and is not predictable

Aneurysmal disease

• Pseudoaneurysm – Partly vessel wall and partly fibrous tissues
  • Usually at site of previous cannulation, anastamoses of prior reconstructions, trauma or infection
  • Small ones may thrombose spontaneously
• Mycotic aneurysm – Infection in blood vessel wall, often in immunocompromised
  • Can be direct extension or embolisation from IE
• Peripheral and visceral aneurysms
  • Popliteal artery most common (often co-exist with AAA)
  • Renal, splenic and hepatic arteries most common visceral aneurysms
    • Usually silent until rupture or thrombosis/embolic phenomena

Abdominal Aortic Aneurysm

• Defined as aorta >=3cm in diameter
• Repair considered for aneurysm >5cm
• 20% have first-degree relative with AAA
• Most patients >60 and more commonly male
• Clinical features
  • Syncope, back, flank, abdominal pain, GI bleeding, extremity ischaemia from embolisation from intramural thrombus, shock or sudden death
  • Sudden death usually occurs from intraperitoneal rupture
  • Syncope without warning symptoms and subsequent severe pain suggests rupture with some temporary containment
    • Patients may regain consciousness but irreversible haemorrhagic shock ensues if not promptly diagnosed
  • Typically back or abdominal pain, 50% describe as ripping/tearing and 10% have syncope
  • Non-classic sites of pain are still common (flank, groin, isolated quadrants, hip)
  • Uncommon presentations are Grey-Turner, Cullen, scrotal haematoma, inguinal mass and femoral neuropathy from compression

AAA

• Prevalence
  • 1% at age 50
  • 4% at age 60
  • 5-10% at age 70
  • 10% at age 80
• Rupture <1% per year if <5cm and 17% per year if >6cm
• Risk of rupture higher in women (growth rate is faster) and in current smokers/hypertension
• 0.3cm/year expansion if <5cm and 0.5cm/year if >5cm

AAA

• Diagnosis
  • Abdominal palpation
    • Sensitivity 29% for 3-4cm; 50% for 4-5cm; 76% for >5cm
    • Lack of tenderness does not indicate intact aorta
    • Periumbilical ecchymosis (Cullen sign) and flank ecchymosis (Grey-Turner sign) are rare
    • Scrotal or vulvar haematomas or inguinal masses can be seen if retroperitoneal blood dissects down
  • Aortoenteric fistulas may present with small sentinel bleed followed by catastrophic haemorrhage
  • Aortovenous fistulas can cause high-output cardiac failure

AAA

• Imaging
  • Plain film – May show calcified aneurysm but cannot determine rupture
  • Bedside USS – >90% sensitivity for demonstrating aneurysm and measuring diameter if technically adequate
    • Obesity, bowel gas and abdominal tenderness make study difficult
    • Need to measure transverse and longitudinally
    • Identifying SMA distinguishes aorta from IVC
    • If <3cm, this excludes aneurysmal disease
  • CT with contrast
    • Unenhanced CT still identifies aneurysm size and retroperitoneal haemorrhage
  • CT Aortogram
    • Impending rupture appears as a dense rim of new thrombus within the lumen and/or contrast fissuring into the luminal thrombus

AAA

• Treatment
  • Consultation
  • Permissive hypotension to 90mmHg or LOC with blood products
  • Pain control
  • Use imaging only in those fully compensated or unlikely to have ruptured their aneurysm
  • If asymptomatic
    • >5cm needs follow-up within days
    • >3cm needs follow-up at some point
    • Repairing AAA <5.5cm does not improve survival in men but may do so in women
  • Perioperative mortality for elective repair is 5% for open and 1.5% for endovascular repair (although 2 year survival rates are the same for either method = 90%)
  • Endovascular repair does NOT improve survival if deemed medically unfit for open repair
  • Operative mortality is 15% if urgently repaired (non-ruptured) and 50% if ruptured

Thoracic aortic aneurysm

• Presenting symptoms often from compression of oesophagus, trachea, bronchi, sympathetic ganglia or recurrent laryngeal
• If erodes into another structure, almost invariably fatal
• Refer any patient with asymptomatic TAA to surgeon and primary care provider for operative repair and blood pressure control respectively

Definition

• Traditionally >1.5 x normal (1.5 x 35mm = near 50mm)
• The problem with this definition is that an aneurysm of the thoracic aorta would have to be near 50mm in size and 60% of dissections have a thoracic aorta diameter <55mm
• Normal aortic calibre for an adult male is around 35mm
• Compared to this:
  • 40-44mm = 89 x risk of dissection
  • >45mm = 6000x risk of dissection
• Probably the best way to measure is indexed to body size (height and/or surface area)

Thoracic aortic aneurysm

• Indications for repair
  • Symptomatic
  • Ruptured
  • Dissection
  • Asymptomatic
    • Ascending
      • End-diastolic aortic diameter >5.5cm
    • Descending
      • >5.5cm
      • >7cm if high surgical risk
    • Rapid expansion >0.5-1cm per year for aneurysms <5cm in diameter

Spontaneous retroperitoneal haemorrhage

• Usually associated with vascular or malignant disease of the kidney or adrenal gland, spontaneous rupture of retroperitoneal veins or with anticoagulant therapy
• Presents as acute abdominal pain, shock and palpable abdominal or groin mass
• Confirmed by CT
• IR is often the treatment of choice

Visceral arterial aneurysms

• Defined as those affecting celiac, SMA, IMA and their branches
• Splenic artery (70%) and hepatic artery (20%) most commonly
• Often present with life-threatening haemorrhage due to delayed diagnosis and high incidence of rupture
• Usual treatment is therefore early elective intervention rather than watchful waiting
• Aneurysmal = 1.5x normal diameter

VAA

• Risk factors
  • Atherosclerosis
  • Pregnancy
  • Portal HTN (splenic)
  • Liver transplant (splenic)
  • Marfan/Ehlers-Danlos
  • Kawasaki
• Presenting complaints
  • Usually vague abdominal pain, nausea/vomiting until rupture

VAA – Splenic

• Third most common true aneurysm after aortic and iliac artery
• 80% in those over 50

VAA – Hepatic

• 80% extrahepatic
• Atherosclerosis is the most common underlying cause
• Symptomatic – Nausea and RUQ pain but most diagnosed incidentally
• Erosion into biliary tree leads to haemobilia
  • Quincke’s triad = Jaundice, biliary colic and GI bleeding
  • Occurs in 1/3

Aortic Dissection Summary

Hot Note – Aortic Dissection

• Type A —> Cardiothoracics for surgical repair
• Type B —> Vascular surgeons for either endovascular repair to medical management
• Key Targets in ED
  • HR < 60
  • BP 100 – 120 
  • Pain free  
• Most physical exam findings are not very useful
• Best diagnostic test is any of:
  • TOE
  • CT – gated CTA
  • MRI 

Introduction

• An aortic dissection involves the longitudinal cleavage of the aortic media by a dissecting column of blood. 
• Despite advances in medical diagnostics and treatment, mortality rate of aortic dissection remains high —> 27% 

Epidemiology

• Mortality = 27%
• Men : Women    3 : 1
• Women more likely to present later and have poorer prognosis
• Hypertension is most common risk factor (and is seen in MOST, but not all patients)
• Other associations:
  • History of cardiac surgery (18%)
  • Bicuspid aortic valve (14%) 
  • Congenital Heart Disease
  • Connective Tissue Disorder
    • Marfan’s Syndrome
    • SLE
    • Scleroderma
  • Inflammatory Vasculitic disorders
    • Takayasu arteritis
    • Giant Cell Arteritis
    • Behcet’s Disease
    • Syphillis 
  • Stimulant use, exertion, cardiac surgery and IA balloon insertion 
• NOTE – Atherosclerosis rarely found at the site of dissection 

Pathophysiology

• Each heart beat results in flexion of the ascending and descending aorta due to the ‘swinging’ of the heart beat to beat
• The descending aorta flexes at the left subclavian artery, due to the tethering of the the aorta at this point by the ligamentum arteriosum 
• The middle layer of the aortic wall (the media) degenerates and is the precursor to aortic dissection.
  • Hydrodynamic stress tears the aortic intima, and a column of blood under pressure enters the media
  • Migration of this invading haematoma can occur either anterograde or retrograde 
  • Results in a false lumen
  • The extent of the haematoma extension relies upon two factors
    • Slope of the pulse wave upstroke (shear stress) related to heart rate
    • Systolic blood pressure

Classification of Aortic Dissections:

1. Stanford Classification
   • Type A (62%)
     • Ascending aorta +/- descending aorta
     • More lethal
     • Require surgical repair
   • Type B (38%)
     • Descending aorta only 
     • Less lethal
     • Often repaired endovascularly 
     • Can have conservative management 

Image Reference – https://www.saem.org/cdem/education/online-education/m4-curriculum/group-m4-cardiovascular/thoracic-aortic-dissection

Clinical Features/Discriminating Features 

• Pain is the most common presenting complaint in aortic dissection
  • 90% of patients present with pain
• Pain is rapid onset, severe and usually described as sharp or tearing or ripping
• Migration of pain from chest to abdomen is useful and more specific but only occurs in 17% of dissections
• Pain that radiates into the back or up into the neck is non-specific 
• Syncope occurs in 9% of patients with aortic dissection
• THINK ABOUT CHEST PAIN + 1
  • Chest pain + abdo pain
  • Chest pain + neurological finding 
  • Chest pain + headache 
  • Chest pain + cardiac tamponade
  • Chest pain + syncope 
• Also think about ‘renal colic of the chest’ 
• Aortic regurgitation occurs in 32% of patients with dissection, so listen carefully to heart sounds for the diastolic murmur
• Pulse deficits and discrepancies in BP between arms has a Sn = 30% —> basically useless 
• Complications of the dissection can be present on history and clinical examination:
  • STEMI picture with dissection down coronary artery (most commonly RCA)
  • Anterior spinal artery ischaemia with secondary anterior cord syndrome features
  • Mesenteric ischaemia
  • Renal ischaemia (refractory hypertension and renal failure) 
  • Lower extremity ischaemia 
• Diagnostic Testing in Aortic Dissection
  • Routine lab tests are basically useless for aortic dissection
  • D-Dimer
    • Negative D-dimer makes dissection less likely
    • However not studied rigorously enough to be used as rule out test
  • ECG
    • May show inferior ischaemia due to dissection down RCA
    • LVH is common finding in dissection due to the long-standing hypertension being risk factor for the dissection 
    • Small voltage ECG and electrical alternans can occur with the complication of pericardial effusion 
  • CXR
    • 80 – 90% of CXRs are abnormal in aortic dissection. HOWEVER, the abnormalities are non-specific and not diagnostic
    • Mediastinal widening present in ~ 60%
      • >8cm at aortic knob (T2)
    • Other useful signs on CXR
      • Double egg-shell sign
      • Obliteration of the aortic knob
      • Displacement of the trachea or NG tube to the right
      • Left sided pleural effusion 
  • Echocardiogram
    • Transthoracic echocardiogram is insensitive for detecting aortic dissection
      • However might be useful in diagnosis of associated pericardial effusion or aortic insufficiency 
    • Transoesophageal echocardiogram is HIGHLY SENSITIVE for diagnosis of aortic dissection
      • TOE – Sn = 98%
      • TOE – Sp = 95% 
  • CT
    • Sn = 100%
    • Sp = 98%
    • Diagnostic test of choice for aortic dissection
    • Findings on CT suggestive of aortic dissection:
      • Dilation of the aorta
      • Intimal Flap
      • Demonstrates false and true lumen
    • CT also useful for planning operations and endovascular surgery. Also useful for defining adventitia rupture 

Complications of Aortic Dissection:

• Aortic rupture with haemorrhage
  • Pericardial effusion and tamponade if retrograde tear to Type A 
  • Pleural effusion if tears in descending aorta 
• Stroke syndrome secondary to occlusion/embolis from carotid extension 
• Inferior MI from dissection down the RCA 
• Anterior Spinal Cord Syndrome 
• Mesenteric Ischaemia 
• Lower Limb Ischaemia 
• Renal Infarction 

Key Differential Diagnosis – Cognitive Reasoning

• MI (always check ECG, much more likely to be MI and dissection)
• Boehaave’s Syndrome (alcoholics, history of vomiting)
• Pneumothorax (associated respiratory distress, risk factors)
• Musculoskeletal tear (usually preceded by activity or repetitive strain)

Management

• Resus Management
  • STOP THE SPREADING TEAR
    • Reduce Heart Rate (Target HR < 60) 
      • Beta blocker therapy
        • Esmolol 250mcg/kg bolus, followed by 50 – 200mcg/kg/min infusion OR; 
        • Metoprolol IV 5mg Q20mins up to 15mg 
    • Reduce Blood Pressure (Sys 100 – 120) 
      • ONLY AFTER BETA BLOCKADE
      • Hydralazine 5mg IV Q20mins to maximum 20mg 
      • Glyceryl Trinitrate 5 – 100mcg/min 
      • Sodium nitroprusside 0.5 – 3mcg/kg/min infusion 
  • May require management of haemorrhagic shock
    • These cases need urgent surgical repair and transfer to theatre

• Definitive Management
  • Type A Dissection
    • Urgent Referral to Cardiothoracic Surgeon
    • Surgery significantly reduces mortality (27% operative group, 56% conservative group) 
  • Type B Dissection
    • Urgent Referral to Vascular Surgeon 
    • Definitive management not as clear cut as Type A
    • Any complicated dissection (end-organ ischaemia, leaking/rupture, aortic dilation or intractable pain) usually managed surgically with Thoracic Endovascular Aneurysm Repair (TEVAR) 
    • Uncomplicated dissections can be treated medically with beta-blocker therapy and antihypertensives 

• Supportive Management
  • Analgesia
    • Fentanyl 25 – 50mcg Q20mins for pain 
  • Remain NBM
    • Maintenance Fluids 

• Colleagues Expectation
  • CT when possible
    • Allows identification of site of dissection and also any complications associated with it
  • Remember the targets
    • HR < 60
    • BP 100 – 120 

• Disposition
  • Admitted often via theatre/interventional suite, sometimes to ICU depending on the post-operative course

Key Decision Points/Consultant Level Thinking

• Think about dissection in any of the following:
  • Chest pain + 1 scenarios
  • Renal colic of the chest
  • Chest pain + syncope 
• If you think about it, test for it 
• Refer early
• Be aggressive with your beta-blocker therapy and target HR 60, BP 100 – 120 

Critical Interventions for this Topic (what will actually make a difference to outcomes)

• ED management limited to four things:
  • Control the HR < 60
  • Control the BP 100 – 120 
  • Manage the patients pain 
  • Facilitate transfer to theatre for:
    • Type A dissections (cardiothoracics)
    • Complicated Type B dissections (vascular)

Case Specifically for This Topic

• Too follow

Aortic Aneurysm Summary

Hot Note – Aortic Aneurysms

• Abdominal aorta > 3cm = abdominal aortic aneurysm   
• Ruptured AAA are uniformly fatal unless treated
• Preoperative hypotension is the most significant predictor of mortality in patients undergoing surgery for AAA repair 
• Most important clinical risk factor for rupture is size of the aneurysm
  • Most ruptured AAA > 5cm 

Introduction

• An aneurysm is dilation of an arterial wall > 1.5 times normal diameter
• A true aneurysm has dilation of all layers of the vessel wall
• Aneurysms of the aorta can develop in any segment, but most are infrarenal. 
• A diameter of >3cm defines an abdominal aortic aneurysm 

Epidemiology

• Average age at diagnosis is 65-70 years
• Male>> Females
• Risk factors for AAA:
  • Atherosclerotic disease
  • Family history of AAA
  • Collagen disease 
  • Increasing age
  • Male sex
• Ruptured AAA are uniformly fatal unless treated
• Preoperative hypotension is the most significant predictor of mortality in patients undergoing surgery for AAA repair 

Pathophysiology

• AAA’s develop when biochemical abnormalities lead to loss of elastin and collagen in the walls of the aorta
• AAA’s will progressively enlarge without intervention
• The natural history of the disease will mean that ultimately the aneurysm will rupture if no intervention is undertaken
• Most important clinical risk factor for rupture is size of the aneurysm
  • Most ruptured AAA > 5cm 
• Rupture of the aneurysm usually occurs posteriorly into the retroperitoneal space
• Posterior rupture can be contained by the smaller retroperitoneal space leading to tamponade and clotting. 
• 10% – 30% of ruptures occur anteriorly into the intraperitoneal space. This space is larger and these ruptures are commonly fatal. 

Clinical Features/Discriminating Features 

• Most AAAs are asymptomatic
• The first sign may be the rupture of the AAA
• Unruptured AAAs can present in several ways:
  • Back or abdominal pain
  • Distal limb ischaemia from embolus 
  • Palpable pulsatile abdominal mass (becomes more obvious as the AAA gets larger) Sn ~ 75% of AAA > 5cm 
• Ruptured AAA presentation:
  • Classic teaching is a triad:
    • PAIN + HYPOTENSION + PALPABLE MASS 
  • Often severe pain in the abdomen or back
  • Usually described as sharp or tearing pain
  • 10% associated with syncope, which heralds likely anterior rupture and increased mortality and haemorrhage 
  • Often pain associated with abdominal gaurding
  • Look for Grey-Turner’s sign or Cullen’s sign to indicate retroperitoneal bleeding
• Diagnosis of Ruptured AAA:
  • CT Aorta gold standard
  • Bedside USS looking for AAA > 3cm (>5cm more likely to rupture) can be used to guide likelihood of AAA rupture as diagnosis
• Aortoenteric Fistula
  • An unprepared AAA can erode into the GI tract (usually into the duodenum) leading to an aortoenteric fistula formation
  • This can lead to massive GI haemorrhage with haematemisis and PR bleeding
  • In a patient with recent endovascular graft with GI haemorrhage always consider aorto-enteric fistula 
• Diagnosis of a AAA:
  • Ultrasound
    • In technically adequate study, Sn=100% for diagnosis of AAA
    • NOTE – CANNOT DIAGNOSE RUPTURE OF AAA
    • Useful for AAA as:
      • Available at the bedside
      • Reproducible 
      • Quick
      • No contrast required 
      • If negative scan, NOT AAA 
  • CT Angiography
    • Diagnostic test of choice for suspected AAA and also for ruptured AAA
    • 100% accurate for diagnosis of both AAA and also ruptured AAA
    • Use of IV contrast will improve scan quality and idenfication of rupture site

Key Differential Diagnosis – Cognitive Reasoning

• Renal calculi
• Surgical Abdomen of any cause
  • Intestinal Ischaemia
  • Diverticulitis
  • Appendicitis
  • Perforated viscous
  • Bowel Obstruction 
• Pancreatitis 
• MSK back pain
• Acute MI
• Aortic Dissection 
• Ovarian Torsion 

Emergency Disease Spectrum

Small, stable AAA —> Large AAA —> Ruptured AAA (posterior) —> Ruptured AAA (anterior) with collapse 

Management

• Resus Management
  • Requires urgent transfer to theatre to cross clamp the aorta and repair the tear… Everything else is temporising and unlikely to help
    • RUPTURED AAA IS A TIME DEPENDENT DISEASE STATE, ED SHOULD NOT DELAY TRANSFER TO THEATRE FOR ANY ATTEMPT OF STABILISING THE PATIENT
  • Manage the haemorrhagic shock
    • 10mL/kg PRBC
    • If > 4 units, switch to MTP 1 : 1 : 1 PRBC : FFP : Platelets or guided by ROTEM or TEG 
    • Minimise crystalloid administration 
    • Target MAP 65 or Systolic 90 with normal mental state and palpable radial pulse 
    • Reverse any anticoagulation if possible
    • Early use of TXA
    • Keep the patient warm

• Definitive Management
  • Urgent referral to vascular surgeon
    • Open repair
    • Endovascular repair 

• Supportive Management
  • Analgesia —> Fentanyl 

• Colleagues Expectation
  • Where possible —> CT 

• Patient Expectation
  • Explanation of diagnosis
  • Explanation of mortality risk
  • Consideration of palliative management 

• Disposition
  • Theatre
  • Palliative approach —> medicine 

Key Decision Points/Consultant Level Thinking

• Clinical suspicion of AAA
  • Make the diagnosis (either US or CT) 
  • Contact the vascular surgeon
  • Don’t let anything delay transfer to theatre 
• Consider how to optimise the patient on route to theatre
  • TREAT AS BLEEDING TRAUMA PATIENT 
• Think about aortoenteric fistula in patient with recent graft and GI haemorrhage 
• Any older patient with abdo pain, consider AAA 

Critical Interventions for this Topic (what will actually make a difference to outcomes)

• The only useful intervention in ruptured AAA is surgical repair, don’t ever delay in ED

Case Specifically for This Topic

• To follow

Special Population – To Follow

1) Paediatrics 
2) Pregnant Women
3) The Elderly 
4) High Risk Groups (Immunocompromised, IVDU, vulnerable etc) 

Last Updated on September 5, 2024 by Andrew Crofton