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Aortic Dissection

25

 

Shyam Sunder Tipparaju, Gopinath Ramachandran,

Ravinuthala Venkat Kumar, and Muppiri Vijay Kumar

A 57-year-old male patient with long-term, poorly controlled hypertension developed severe precordial chest pain, radiating to the back while gardening. The physical examination showed temperature 99°F, pulse 110/min, respiration 20/min, BP 200/100 mmHg (right arm) and 180/90 mmHg (left arm), decreased left brachial and radial pulses, and diastolic murmur along the left sternal border.

Aortic dissection is a relatively uncommon disorder as compared to other cardiac emergencies such as acute myocardial infarction (AMI) or congestive heart failure (CHF). It carries a high mortality of 1% every hour for initial 48 h, if not properly recognized and managed.

Step 1: Resuscitate urgently

Emergent control of hypertension and maintaining organ perfusion is the priority in initial resuscitation (see Chap. 24).

Step 2: Assess urgently

Time is of essence in managing aortic dissection, and a focused history and focused physical examination should be quickly performed to differentiate causes of acute chest pain (Tables 25.1 and 25.2).

S.S. Tipparaju, M.D., P.D.C.C. (*)

Critical Care, Continental Hospitals, Hyderabad, India e-mail: shyamsundert@rediffmail.com

G. Ramachandran, M.D., F.F.A.R.C.S.

Department of Anaesthesiology & Critical Care, Nizam Institute of Medical Sciences, Hyderabad, India

R.V. Kumar, M.S., M.Ch. • M.V. Kumar, M.S., M.Ch.

Department of Cardiothoracic Surgery, Nizam’s Institute of Medical Sciences, Hyderabad, India

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,

203

DOI 10.1007/978-81-322-0535-7_25, © Springer India 2012

 

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S.S. Tipparaju et al.

 

 

Table 25.1 Causes of acute

Acute coronary syndrome with and without ST elevation

chest pain

Acute aortic regurgitation without dissection

 

 

Aortic aneurysms without dissection

 

Musculoskeletal pain

 

Pericarditis

 

Mediastinal tumors

 

Pleuritis

 

Pulmonary embolism

 

Cholecystitis

Table 25.2 Clinical features of aortic dissection

Sudden severe chest pain radiating to back

96%

Syncope (cardiac tamponade or new stroke)

13%

Congestive cardiac failure (severe AR or

7%

tamponade)

 

Cerebrovascular accident

6%

Ischemic peripheral neuropathy/paraplegia/

 

cardiac arrest/sudden death

 

Hypertension

70% of cases with type B dissections and

 

36% with type A dissection

Hypotension

25% of cases with proximal dissections and

 

4% with distal dissection

Acute severe aortic regurgitation

33%

Pulse deficit

30% of proximal dissection and 15% of

 

distal dissection

Neurological manifestations

6–19%

Acute MI

1–2%

Renal ischemia

5–8%

Mesenteric ischemia

3–5%

Diminished femoral pulses

12%

An urgent 12-lead ECG should be performed to look for features of AMI.

If aortic dissection is a possibility, antiplatelet, anticoagulant, and thrombolysis should be avoided.

Chest X-ray—a routine chest radiograph is abnormal in 60% of cases with suspected aortic dissection; the commonest finding are widening of mediastinum and left-sided pleural effusion.

D-dimer may be falsely elevated in some cases.

Step 3: Initiate treatment for suspected aortic dissection (Table 25.3)

All patients suspected of having acute aortic syndrome should be admitted to the ICU for invasive monitoring and hemodynamic stabilization.

Pain control with morphine should be started.

25 Aortic Dissection

205

 

 

Table 25.3 Antihypertensive and heart rate control therapy

 

Drug

Dosing

Remarks

Labetalol

20 mg IV over 2 min, then 40–80 mg every 15 min

Alphaand beta-blocker

 

until adequate response or excessive bradycardia,

 

 

then continuous. IV infusion at 2–10 mg/min,

 

 

(maximum daily IV dose is 300 mg) titrated

 

 

to effect (maximum daily IV dose is 300 mg),

 

 

may be switched to oral once stabilized

 

Esmolol

500 mcg/Kg IV bolus, then continuous infusion at

Short half-life

 

50–200 mcg/Kg/min

 

 

Titrated to effect

 

Sodium

No bolus, continuous infusion titrated to effect,

Use only in presence of

nitroprusside

0.3–0.5 mcg/Kg/min titrated to a maximum of

rate-controlling agent

 

10 mcg/Kg/min

 

Enalapril

0.625–1.25 mg IV, then increase every 6 h to a

Ideal for renal artery

 

maximum of 5 mg every 6 h

dissection

Diltiazem

0.25 mg/Kg IV over 2 min, then continuous IV

Use when beta-blocker is

 

infusion at 5–15 mg/h

contraindicated

An arterial line in the well-perfused hand should be inserted.

Reduction of systolic blood pressure, decreasing heart rate, and diminution of the rate of rise of the left ventricular ejection time (dP/dT) are the goals of the primary medical treatment.

Beta-blockers (labetalol and esmolol) as a group of drugs that have the most desirable effect in reducing the force of the left ventricular ejection (dP/dT). However, if beta-blockers alone do not control hypertension, vasodilators are ideal additional agents to control blood pressure. Because vasodilators alone can increase the left ventricular ejection, they should always be combined with beta-blockers.

The goal of therapy is to manage the heart rate less than 70 beats/min and to keep blood pressure as low as possible without compromising organ perfusion.

In patients with hypotension at presentation, possible volume depletion, which may be the result of blood sequestration in the false lumen, pleura, or pericardial space, has to be ruled out.

Pericardiocentesis is usually avoided for cardiac tamponade secondary to dissection, as bleeding is recurrent. A definitive surgery is indicated in these cases.

Step 4: Perform confirmatory investigation for acute aortic dissection (Table 25.4)

The diagnostic goal of imaging is to achieve the following:

Confirm diagnosis.

Classify the dissection/delineate the extent.

Differentiate true and false lumen, localize intimal tears, and distinguish between communicating and noncommunicating dissection.

Assess side branch involvement (including coronary arteries).

Detect and grade aortic regurgitation.

Detect extravasation (periaortic or mediastinal hematoma, pleural or pericardial effusion).

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S.S. Tipparaju et al.

 

 

 

Table 25.4 Diagnostic imaging

 

 

Modality

Sensitivity (%)

Specificity (%)

Comments

CT scan

90–100

90–100

Quick, readily available, familiarity

 

 

 

Shows pleural/pericardial spaces

 

 

 

Shows head and neck vessels

 

 

 

IV contrast may cause renal failure

MRI

98–100

98–100

Gold standard

 

 

 

Detailed dynamic images

 

 

 

Flow in true and false lumen

 

 

 

Branched vessels

 

 

 

Limitation is availability

 

 

 

Time taken in emergency situation

Echo

 

 

 

Transthoracic

60–80

86–90

Readily available and can be used in

 

 

 

emergency situations

Transesophageal

90–99

85–98

Shows coronary ostia, AR, and

 

 

 

pericardium

 

 

 

LV function

 

 

 

Contraindicated in esophageal and

 

 

 

cervical pathology

Aortography

80–90

88–94

Shows true and false lumen perfusion

 

 

 

Flap, coronaries, AR

 

 

 

Invasive, can precipitate rupture

 

 

 

Facilities and expertise not widely

 

 

 

available

Intravascular

94–100

97–100

Used to complement information of

ultrasound

 

 

aortography

 

 

 

Clearly differentiates dissection

 

 

 

Intramural hematoma, and

 

 

 

penetrating ulcer

Assess clinical stability (for transport), availability, and experience with the investigation before deciding on the confirmatory imaging modality.

Because of good sensitivity and specificity, CT angiography and MRI angiography are considered current standards of evaluation.

If the patient is hemodynamically unstable and cannot be shifted for imaging, transesophageal echocardiography can be done to confirm the diagnosis.

Transthoracic echo has a low sensitivity and specificity especially for type B dissection.

Coronary angiography—because the recent generation CT/MRI imaging modalities can demonstrate proximal third of coronary arteries, routine use of conventional coronary angiogram is not recommended.

Step 5: Understand types of aortic dissection and their outcome (Fig. 25.1)

Aortic dissection refers to formation of a tear in aortic intima, directly exposing the blood to the diseased medial layer and splitting the aortic wall, producing true lumen and false lumen with driving force (pulse pressure).

25 Aortic Dissection

207

 

 

Fig. 25.1 Classification of aortic dissection

The dissecting process extends antegradely but sometimes retrogradely from the site of intimal tear.

For prognostic and therapeutic reasons, aortic dissections are classified into three major types, which share the basic principle whether the ascending aorta is involved (Fig. 25.1).

Proximal dissection (involves ascending aorta) includes De Bakey type I and type II or Stanford type A.

Distal dissection (spares ascending aorta) includes De Bakey type III or Stanford type B.

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For prognostic reasons, dissection has also been classified as acute or chronic depending on duration (less or more than 2 weeks).

Recent years have brought recognition of two important variants of aortic dissection.

Intramural hematoma (IMH)

Aortic IMH is considered as a precursor of dissection originating from ruptured vasa vasorum in the aortic medial wall layer and resulting in an aortic wall infarct that may provoke a secondary tear, causing a classic aortic dissection. Although clinical manifestations of IMH are similar to acute aortic dissection, IMH is an imaging diagnosis in an appropriate clinical setting. Treatment is similar to classic aortic dissection.

Penetrating aortic ulcer

Deep ulceration of atherosclerotic plaque can lead to IMH, aortic dissection, or perforation. In association with IMH, these ulcers are seen almost exclusively with type B dissection.

At present, these three lesions—aortic dissection, IMH, and penetrating aortic ulcers—are called acute aortic syndromes.

Acute aortic dissection of ascending aorta (De Bakey type I and type II, Stanford type A) is highly lethal, with a mortality rate of 1–2% every hour after the onset of symptoms. Without surgery, the mortality rate exceeds 50% after 1 month.

Uncomplicated type B (De Bakey type III) aortic dissection has a 30-day mortality of 10% and may be managed medically.

Intramural hematoma of ascending aorta has a prognosis similar to type A dissection.

Step 6: Definitive surgery

Type I and II (A) dissections are managed primarily by surgery.

Type III (B) is managed conservatively, and surgery is only indicated if complications such as organ hypoperfusion, refractory hypotension, refractory pain, or aortic rupture occur.

There is increasingly use of percutaneous endovascular stent grafting in selected cases of distal dissection.

Step 7: Identify underlying risk factors for aortic dissection

These include hypertension, hyperlipidemia, trauma, hereditary connective tissue disorders like Marfan’s syndrome, arteritis, and cocaine use.

Step 8: Long-term follow-up and treatment

The cornerstone of medical therapy is with beta-blockers. Excellent blood pressure control, less than 120/80 mmHg, is paramount to prevent long-term complications. Close follow-up by a specialized team includes the assessment of signs of aortic expansion, aneurysm formation, signs of leakages at anastomoses/ stent sites, and malperfusion.

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