aortic disasters ahmed

AORTIC DISASTERSAhmed Alhubaishi

R3

OBJECTIVES:

1. Discuss risk factors for aortic aneurysm and aortic dissection

2. Discuss the clinical presentation of aortic aneurysm and aortic dissection

3. Discuss appropriate diagnostic imaging and treatment

4. Discuss can’t miss atypical presentations of dissection and aneurysm

WHY IS AORTIC DISSECTION AN IMPORTANT TOPIC FOR EMERGENCY PHYSICIANS TO KNOWABOUT?

Thoracic aortic dissection can be extremely difficult to diagnose.

Mortality rates are estimated at 50% by 48 hours if undiagnosed.

Mortality rates increase by 1-2%/hour if undiagnosed.

Prompt detection and therapy impact on survival rates.

Knowledge of common/atypical presentations and current acute aortic disease

literature will decrease the chance of a missed or delayed diagnosis

OUTLINES AORTIC DISSECTION Perspective Principles of disease Clinical features Diagnostic strategies Differential diagnosis Management Disposition pitfalls

DEFINITIONS AND ANATOMY AND CLASSIFICATION SYSTEMS aorta is composed of three layers Aortic dissection occurs when ........ Classification

Stanford DeBakey acute Vs chronic [ chronic if> 2 wks]

Stanford- classification based on involvement of ascending aorta Type A- ascending aorta (prox. to L subclavian) Type B- descending aorta (distal to L subclavian)

  Debakey

Type I- involves ascending aorta and the arch Type II- confined to ascending aorta Type III- confined to descending aorta distal to left

subclavian IIIA- above diaphragm IIIB- below diaphragm

 Type A = Type I and II These require surgical repairType B = Type III These may be treated medically

Stanford type B or DeBakey type III

dissection distal to the subclavian artery

2/3 Younger than type B Treated surgically mortality is 70% by

1 week, 80% at 2 weeks

1/3 Older patients generalized

atherosclerosis hypertensive smokers Chronic lung disease Managed medically 50% two week

mortality

Type A Type B

WHERE DO DISSECTION COMMONLY OCCUR?

The most common site is the first few centimeters of the ascending aorta, with 90% found within 10 centimeters of the aortic valve. The second most common site is just distal to

the left subclavian artery

AORTIC DISSECTION RISK FACTORS

Hypertension Male sex Age Pregnancy Family history Connective tissue

diseaes

Cocaine Turner’s syndrome Bicuspid aortic valve Iatrogenic Coarctaion Trauma Ecstasy Weight lifting

Traditional Less common

KLOMPAS M. DOES THIS PATIENT HAVE AN ACUTE THORACIC AORTIC DISSECTION?J AM MED ASSOC 2002

CLINICAL FEATURES

The key to making the diagnosis of this lethal aortic disease may depend on how familiar you are with well-described atypical and subtle presentations? Although

textbook presentations may occasionally occur, they tend to be the exception rather than the rule.

Atypical really is typical.

Wide range of presentaions depending on area affected and aortic branch involved

Usaual presentaion is with sudden severe central tearing chest pain

May present as : acute MI, acute AR, cardiac tamponade, CV collapse, limb ischemia,syncope, stroke or spinal cord syndrome

Cardinal signs” pulse deficits, asymmetric BP , evolving AR murmur

Characteristics of Aortic Dissection from the International Registry of Acute Aortic Dissection[4]

CHEST PAIN )%(

SYNCOPE)%(

AORTIC INSUFFICiENCY

MURMUR)%(

PULSE DEFICIT )%(

NORMAL CXR)%(

WIDENED MEDIASTINUM ON

CXR)%( NORMAL

ECG)%(

ISCHEMIA )%(

LEFT VENTRICULAR HYPERTROPHY)%(

All (n= 464)73932151262311526

Type A (n= 289)

791344191163311725

Type B (n= 175)

6341291656321332

INTERNATIONAL REGISTRY OF AORTIC DISSECTION (IRAD)-STUDY BY HAGAN, ET AL .

involved 464 patients with confirmed TAD. Mean age: 63 years, 65.3 % males, 62% type A dissections

The findings: pulse deficit 15 % aortic murmur 31.6 % normal chest x-ray 12 % absence of mediastinal widening 34 % syncope 12 % painless 2.2%

CONCLUSIONS FROM THIS STUDY:

(1) Classic findings of aortic dissection are often absent

(2) Don’t rely on textbook presentations

KLOMPAS M. DOES THIS PATIENT HAVE AN ACUTE THORACIC AORTIC DISSECTION?J AM MED ASSOC 2002

PRESENTATIONS REPRESENT COMMON, RECURRING THEMES AMONG MISSEDAORTIC DISSECTION CASES

(1) TAD and Stroke consider TAD in the following scenarios:

Chest pain and any neurologic symptoms (CVA, dysphagia, etc.)

Chest pain and limb paresthesia (2) Painless TAD and Syncope

Add TAD to your differential diagnosis of unexplained syncope

CONT.

3) TAD and Paralysis Consider TAD in the following scenarios:

Chest pain and limb (particularly lower extremity) weakness or paresthesia

Chest pain and spinal cord syndromes Unexplained lower extremity weakness

(4) TAD and Myocardial Infarction

(5) Isolated Abdominal Pain Consider TAD in the following scenarios:

Unexplained abdominal pain in the presence of hypertension

Combination of chest and abdominal pain Abdominal pain and cocaine use Unexplained abdominal pain and an “ill-appearing”

patient (6) TAD and “the other complaint’’ Consider TAD under the following

circumstance: Chest pain combined with “the other complaint”

(especially neurologic symptoms)

(7) Cough, Hoarseness, and SVC Syndrome

(8)Young patients with TAD (9) pt with Congestive Heart Failure

Consider TAD in patients with new onset CHF

Januzzi, JL et al. Acute Aortic Dissection Presenting With Congestive Heart Failure: Results From the International Registry of Acute Aortic Dissection. J Am Coll Cardiol, 2005

Patients who present with CHF symptoms secondary to acute aortic dissection are

much more likely to have none or mild pain compared to patients with aortic dissection

without CHF symptoms

THINGS TO BE DOCUMENTED:

Consider documenting the following in all chest pain patients: Risk factor profile for TAD (HTN, cocaine, family

history, etc) Blood pressure in both arms (equal) Pulses (symmetric) Absence of aortic murmur Absence of marfanoid body habitus

LIMITATIONS OF THE PHYSICAL EXAMINATION Bilateral BP measurement

19% of the population may have arm differences greater than 20 mm Hg

Von Kodolitsch et al. did show that a BP differential > 20 mm Hg was an independent predictor of TAD

50% of patients who present with TAD are hypertensive

Aortic murmur: 1/3 of patients with TAD Pulse deficit: 15% of cases of TAD

Pitfall: Over-reliance on a “classic”presentation for diagnosis of AD

DIAGNOSTIC STRATEGIES

Gold standards

  -- Sensitivities and Specificities of Imaging Modalities for Diagnosing Aortic Dissection

TESTTEEHELICAL CTMRI

Sensitivity(%) 9810098

Specificity(%) 959898

(From Shiga T, Wajima Z, Apfel CC, et al: Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging for suspected thoracic aortic dissection :

Systematic review and meta-analysis. Arch Intern Med 166:1350–1356, 2006).

SensSpecAdvantagesDisadvantages

TTE80%95% Too many false negatives

TEE98%90-100% Rapid (10-30 minutes)Bedside testInexpensiveID’s site of tear in 75%No contraindiciationsNo radiation/contrastGives info about aortic regurgitation

Tough to see ascending aorta

CT scan95%90-100% Rapid (20-40 minutes)Low FP and FN ratesDynamic scanning detects different filling

rates

ExpensiveUses contrastOutside ED (no monitor)No info re: regurg

MRI98%98% Non-invasiveNo radiation/contrastGives excellent detail of dissection,

including branches

Slow (up to 75 minutes)No monitoringContraindicationsExpensive

Aorto-graphy88%95% Intimal tear seen in 56%Identifies AI, coronary and carotid extension

Not as sensitive as MRI or TEENeeds contrastInvasiveSlow (1-2 hours)Thrombosed lumen may be obscured

WHEN TO USE THE ABOVE MODALITIES?

  Hemodynamically unstable- TEE Surgeon requires definitive anatomical

delineation- CT, MRI, Aortography R/O dissection for MI- TEE would be

adequate Hemodynamically stable- CT, MRI,

Computed tomography scan demonstrating the true lumen and false lumen

ECG PITFALLS 

ECG commonly shows LVH, reflecting long-standing hypertension

ST-T changes or heart blocks can occur Note that 10-40% with dissection may

have ECG changes suggestive of MI Unclear if due to dissection or possible

coronary dissection ST changes imply a much worse prognosis

12 lead ECG of a young patient with confirmed proximal TAD.

The ECG shows inverted T-waves and ST-depression in the inferior leads. During operative repair, the right coronary ostia was found to be occluded.

CXR PITFALLS   abnormal in 80-90% of cases Mediastinal widening- in 75% “Calcium sign Aortic double density Disparity in caliber between ascending and

descending aorta Localized bulge on the aorta Obliteration of the aortic knob NG tube, trachea or ETT displaced to the right Pleural effusions- common and usually on the left

HAGAN P, NIENABER CA, ISSELBACHER EM, ET AL. THE INTERNATIONALREGISTRY OF ACUTE AORTIC DISSECTION (IRAD): NEW INSIGHTS INTOAN OLD DISEASE. J AM MED ASSOC 2000

Pitfall : Use of the chest X-ray to excludethe diagnosis of AD

Myocin heavy-chain concentrations D-dimer levels soluble elastin fragments

newer tools that may be helpful to the diagnosis of aortic dissection and await prospective clinical trails to evaluate their usefulness

D dimer Not ready for prime time as a rule-out strategy

Sodeck, et al. D-dimer in ruling out acute aortic dissection: a systematic review and prospective cohort study. European Heart Journal 2007

DDX

acute MI pulmonary embolus Pericarditis CCF ….. etc

MANAGEMENT

ABC’s above all else Ultimately, a transfer to a hospital with a CVT

surgical service should be done once patient is stable enough.

Resuscitate with fluids or blood as needed if hypotensive

BLOOD PRESSURE CONTROL IS THE KEY TO MANAGEMENT

Maintain systolic blood pressure between 100- 120 mmHg and reduce force of cardiac contraction

Nitroprusside 50-100mg in 500cc D5W at rate 0.5-3 ug/kg/min (titrate to BP) **** Increases heart rate, so if given alone it may worsen the dissection

B-Blockers Propanolol- used inconjunction with Nipride

1 mg IV every 5 minutes (max 0.15 mg/kg) Later given as 2-6mg every 4-6 hours

  Esmolol- also given with Nipride

500 mg/kg over 1 min, then infusion of 50 to 150 mg/kg per minute.

Labetalol- used as a single agent (α-effects attenuates heart rate) Bolus of 5-20 mg, then infusion of 1-2 mg/min

DISPOSITION

Surgery for type A not type B hospital mortality in type B dissections

treated without surgery is 15-20%, which is comparable to or better than the operative mortality rate.

OR mortality rate is decreasing for type B though

OR mortality rate for type A is about 7% (and decreasing)

HOW CAN WE DECREASE CHANCES OF MISSING THE DIAGNOSIS OF TAD?

In reality: no way that every case of A.D can be diagnosed in ED

Know the subtle and atypical presentations well. Think beyond classic textbook descriptions and

think of TAD more often Perform a detailed risk factor profile for TAD

on every chest pain patient

CONT.

Decrease your own threshold to obtain CT scans in chest pain patients

Approach every chest pain patient as if they could have a TAD and convince yourself the patient doesn’t have it.

• Realize that young patients without connective tissue disease can have TAD

ABDOMINAL AORTIC ANEURYSM

■ A true aneurysm involves all three layers of vessel wall.

■ A false aneurysm or pseudoaneurysm communicates with the vessel lumen, but is contained only by adventitia or surrounding soft tissues.

Types of aortic aneurysms

(AAAs) is true aneurysms involve the infrarenal aorta. aortic diameter >3 cm = AAA.

An AAA of any size can rupture, but those >5 cm are more likely to rupture.

size is the most important factor in determining rupture risk

The most common location of rupture retroperitoneum

Rupture is associated with an 80–90% overall mortality

PRIMARY RISK FACTORS FOR AAA

Increasing age > 65 Family history ,? Genetic ( 1st degree

relatives have 10-20 times the risk) Atherosclerotic risk factors ie htn ,dm,

smoking,cad,male

Other predisposing factors include infection, trauma, connective tissue disease, and arteritis.

Table 84-1   -- Prevalence of Abdominal Aortic Aneurysms (AAAs) in Selected Risk Groups

GROUPINCIDENCE)%(

Autopsy subjects aged 50 years or old5,6]2–4

Men aged 65 years or older[4,7]5–10

Patients with coronary artery disease[8] or occlusive peripheral vascular disease[9,10]10–15

Brothers of patients with AAAs[11,12]20–30

SYMPTOMS

■ Most aneurysms are asymptomatic when discovered (60-80%)and become symptomatic when expanding or ruptured.

■ Acute pain in abdomen, back, or flank [ 75% ]■ Nausea and vomiting■ Syncope or near syncope urologic symptoms 10%

EXAM■ Vital signs may be surprisingly normal.

■ Hypotension and shock if rupture with significant blood loss

■ Abdominal tenderness, distension, or pulsatile abdominal mass [75% above umbilicus]

■ Evidence for retroperitoneal hematoma ■ Periumbilical ecchymosis (Cullen’s sign) ■ Flank ecchymosis (Grey-Turner’s sign)

■ Massive GI bleed if rupture into GI tract (aortoenteric fistula)

■ High-output heart failure if rupture into vena cava (aortocaval fistula)

Triad of abdominal pain,hypotension, pulsatile

abdominal mass = AAA untilproven otherwise, although

triad is rare.

Kiell CS and C.B. Ernst, Advances in management of abdominal aortic aneurysm,Adv Surg 26 (1993),

Exam – limited sensitivity Improves as AAA enlarges Worsens with obesity Unknown value in rupture Do not use to exclude AAA

Lederle FA, Simel DL. The rational clinical examination. Does this patient haveabdominal aortic aneurysm? JAMA. 1999 Jan 6

DIAGNOSIS

The diagnosis should be suspected in any patient >50 years old presenting with abdominal pain, flank pain, or

hypotension. Delay in diagnosis of these conditions is

commonAAA rupture (30% misdiagnosed initially)

ABDOMINAL X RAY Abnormalities seen in 2/3 to ¾ of cases But AXR rarely ordered for AAA Retrospectively apparent in 90%

Most common signs are wall calcifications and a paravertebral soft tissue mass, both seen in 65%

Other signs include loss of psoas or renal outlines, renal displacement, and occasionally a properitoneal flank stripe

AXR cannot be used to rule out an AAA

Anteroposterior (A) and lateral (B) views of large abdominal aortic aneurysms with calcification of the aortic wall

Ultrasound 100% sensitive when aorta is visualized Modality of choice in the unstable patient May not be able to identify rupture, site of leak,

or retroperitoneal hematoma

Cross-sectional ultrasound of a 6-cm abdominal aortic aneurysm. Note mural thrombus and eccentrically shaped patent lumen.

Widely cited as sensitive for AAA (98%) But not for rupture

Combination: US confirmation of aneurysm abdominal pain unstable hemodynamics

95% sensitive in determining need for emergency surgery for AAA

Costantino TG, Bruno EC, Handly N, Dean AJ. Accuracy of emergency medicine ultrasound in the evaluation of abdominal aortic aneurysm. J Emerg Med. 2005

CT - Highly sensitive

- Requires stable patient for transport -Better than ultrasound at detecting rupture

and retroperitoneal blood MRI or aortography are rarely indicated

in the ED.

Sharma U, Ghai S, Paul SB, Gulati MS, Bahl VK, Rajani M, Mukhopadhyay S.Helical CT evaluation of aortic aneurysms and dissection: a pictorial essay. ClinImaging. 2003

Computed tomography scan of ruptured abdominal aortic aneurysm, with calcification of the aortic wall and intraluminal thrombus. The patent lumen enhances with the administration of contrast material, but the periaortic hematoma )arrow( does not.

“Acute abdomen ”

COMMON MISDIAGNOSES IN PATIENTS WITH RUPTURED ABDOMINAL AORTIC ANEURYSMS

  Renal colic  “Acute abdomen”   Pancreatitis

  Intestinal ischemia  Diverticulitis  Cholecystitis  Appendicitis  Perforated viscus  Bowel obstruction

  Musculoskeletal back pain  Acute myocardial infarction

‘Mimic’Reasons why

PancreatitisPain pattern is similar

Bowel obstructionIf duodenum is stretched over AAA

DiverticulitisVague LLQ pain occasionally seen in AAA

Obstructive jaundiceRare- if CBD is compressed

Renal colicAAA compresses ureterHematuria occurs infrequently (more when AV fistula present)

Testicular painHemorrhage to scrotumExtension to Iliac vessels with compression of inguinal canal

Inguinal herniaExtension to iliac vessels

Hip painExtension to iliac vessels

Sciatica/Femoral nerve painCompression of femoral nerve in retroperitoneum

Ischemic bowelVague abdominal pain, dull

PyelonephritisBack/flank pain

Chronic abd. Pain NYD10% live >6 weeks after onset of symptoms

•*** Anemia in conjunction with chronic back pain- think AAA

TREATMENT

Ruptured aneurysms require immediate surgical intervention with operative or endovascular repair. 50% operative mortality

Fluid and blood resuscitation: To SBP 90–100 mmHg.

Thoracotomy with cross clamping of aorta: If severe hemodynamic compromise or cardiac arrest

CONT.

Asymptomatic aneurysms can be scheduled for repair based on aneurysm size and patient comorbidities.

Endovascular repair with stent graft is increasingly used.

surgically repaired ruptured AAA, mortality 46%

Once in ED, early diagnosis decreases mortality from 75 to 35%

Wainess RM, Dimick JB, Cowan JA Jr, Henke PK, Stanley JC, Upchurch GR Jr. Epidemiology of surgically treated abdominal aortic aneurysms in the United States,1988 to 2000. Vascular. 2004 Jul-Aug

COMPLICATIONS

Rupture Atheroembolism: Microemboli from

atherosclerotic aneurysms Lodge in distal small vessels “Blue toe syndrome” is classic presentation. Can also occur from nonaneurysmal atherosclerotic

plaques Graft complications

■ Graft infection ■ Secondary aortoenteric fistula ■ Endoleak: Leak outside of graft lumen, but

within existing aneurysm sac (continued risk for AAA rupture!)

Thank you