aortic disasters ahmed
TRANSCRIPT
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