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Case report

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Title: Case report


1
Case report
  • 90-12-11 616 pm
  • ??? ?? 64
  • ?????,?????
  • ?? LMD??, bradycardia
  • vital signs BT 36.4, PR 50, RR 20, BP 120/60
  • Triage class 1

2
  • LMD Transfer note
  • A middle aged male patient suffered from chest
    distress with SOB, and he was sent to our H. At
    ER complete ECG revealed mild ST-T elevation in
    II and aVF, and bradycardia was also noted and he
    received NTG 1 sl st and nasal O2 therapy, but
    s/s persisted
  • R/O inf. MI Thanks for your attention

3
  • Chief Complaint OPD ?, R/O AMI
  • Present Illness
  • Chest pain onset at 500 pm
  • No radiate to back
  • Radiate to neck
  • Past personal and medical history
  • ??????
  • Smoking drinking
  • HTN(-)

4
PE
  • vital signs BT 36.4, PR 50, RR 20, BP 120/60
  • Consciousness clear
  • HEENT and neck No JVD
  • Chest regular heart beat, bradycardia
  • Abdomen Soft
  • Pelvix Stable
  • Ext symmetric 4 limbs pulse
  • NE normal
  • Impression???

5
Impression
  • R/O AMI

6
Order sheet
  • CBC/DC/PLT
  • PT,aPTT
  • ??
  • N/S KVO
  • NTG spray sl 2
  • Morphine 3 mg iv st
  • millisrol 3 cc/hr
  • on monitor

7
Order sheet
  • Troponin T
  • portable CXR
  • Rt side ECG
  • ECG

8
ECG bradycardia
9
710 pm order
  • Impression bradycardia, r/o hyperkalemia
  • Calcium gluconate 1 amp iv st

10
750 pm Lab Data
  • Glu110, BUN15, Cr1.1, Na146, K4.1
  • CPK 107, CKMB 13
  • Troponin Ilt 0.5

11
750 pm progress note
  • S still chest pain
  • O nausea(), Vomiting() 2 times
  • pain will increase by inspiration or swallowing
  • radiate to neck
  • Not chest tightness
  • Lab data K4.1 Tro.Ilt0.5 CKMB13 CK107
  • A chest pain and bradycardia, cause ?
  • P
  • f/u cardiac enzyme
  • check 4 limbs BP

12
Order sheet 810 pm
  • F/U Troponin I, CPK, CKMB at 830 pm
  • check 4 limbs BP st
  • F/U ECG at 830 pm

13
845 ECG
14
840 pm
  • 4 limbs BP
  • RU 89/72 mmHg, LU 117/68 mmHg
  • RL 151/81 mmHg, LL 141/78 mmHg

15
900 pm Progress note
  • Rt upper limb cold, weak pulse
  • Still chest pain
  • CXR boulderline widening mediastinum
  • R/O aortic disection
  • arrange chest CT

16
919 pm Lab Data
  • CPK 100
  • CKMB 10
  • Troponin I lt 0.5

17
920 pm progress note
  • S chest severe pain
  • O consciousness slear
  • BP 100/60, PR 50 RR 16/min
  • Neck supple
  • Heart RHB with murmur
  • lung clear
  • Abdomen soft.normal active bowel sounds

18
920 pm progress note
  • Ext
  • muscle power 4 symmetric,
  • Pulse RU limb , LU limb , RL and LL limb
  • Aortic CT definite dissection in ascending aorta
  • P
  • control BP and PR
  • consult CVS

19
1030 pm CVS note
  • Aortic dissection, type A
  • surgical repair is indicated
  • admit to SICU for BP control and preop preparation

20
Aortic Dissection
  • Manifestation
  • Pain gt 90
  • vasovagal symptoms
  • Syncope 5
  • neurologic deficit 20

21
Pain
  • the most common complaint (gt 90 of cases)
  • In almost all cases in which pain is not present,
    the patient either is unconscious or has a
    neurologic deficit that impairs pain perception.
  • tearing, ripping, and knifelike, but
    may be characterized by different patients in
    many different ways.
  • Typically the pain occurs abruptly and is most
    severe at onset.

22
  • The location of the pain
  • Anterior chest pain -- dissection of the
    ascending aorta
  • neck and jaw -- dissection of the aortic arch,
  • in the interscapular area --descending thoracic
    aorta
  • in the lumbar area or abdomen-- involvement below
    the diaphragm
  • migration -- propagation of the dissection
  • has very high diagnostic accuracy for aortic
    dissection.
  • In one study, 71 of patients with aortic
    dissection had migration of pain.

23
  • Aortic dissection accompanied by vasovagal
    symptoms
  • diaphoresis, nausea, vomiting, light-headedness,
    and severe apprehension.
  • Syncope
  • early course of aortic dissection, about 5 of
    cases.
  • most associated with ascending aorta dissection
  • dissection into the pericardium?pericardial
    tamponade
  • Other causes of syncope secondary to aortic
    dissection are hypovolemia, excessive vagal tone,
    and cardiac conduction abnormalities.

24
  • In approximately 20 of patients, neurologic
    deficit is the presenting manifestation of aortic
    dissection.
  • The neurologic presentations are CVA, spinal cord
    ischemia, and peripheral nerve ischemia

25
Physical Examination.
  • Appearance very apprehensive
  • Tachycardia and signs of inadequate end-organ
    perfusion may be present even in the face of an
    elevated blood pressure.
  • e.g., clammy skin, altered mental status, delayed
    capillary refill
  • chronic hypertension gt 75 of patients
  • may be exacerbated by a catecholamine release
    related to the acute event

26
  • Severe hypertension refractory to medical therapy
  • may occur if the dissection involvesthe renal
    arteries with subsequent renin release
  • hypotension
  • dissection has progressed back into the
    pericardium with resulting pericardial tamponade
  • hypovolemia occurred from rupture along the aorta
  • pseudohypotension
  • the blood pressure in the arms is low or
    unobtainable and the central arterial pressure is
    normal orhigh.
  • results from the interruption of blood flow to
    the subclavian arteries

27
Pulse deficits and discrepancies in blood
pressure between limbs
  • Pulse deficits(a unilaterally weakened or absent
    pulse) in almost 50 of patients with proximal
    dissections
  • Usually in the upper extremities
  • mechanisms
  • An intimal flap cover the true lumen of a branch
    vessel
  • dissecting hematoma compress an adjacent true
    lumen.
  • Careful documentation of pulses and frequent
    reexamination are important because pulse
    deficits are commonly transient

28
Acute aortic regurgitation
  • This is identified clinically by
  • Hypotension
  • fulminant pulmonary edema
  • aortic diastolic murmur (musical, vibrating
    quality with variable intensity)
  • widened mediastinum on CXR
  • Aortic regurgitation in 50 of type A
    dissections
  • Rapid surgical correction affords the only chance
    for survival

29
  • Hemorrhage into the pericardium or tamponade
    ???????
  • Pericardial friction rub
  • Jugular venous distension
  • Pulsus paradoxus
  • Muffled heart sounds
  • Tachycardia
  • Hypotension

30
Neurologic findings
  • most common altered sensorium
  • The most common focal neurologic abnormalities
  • Hemiplegia
  • Hemianesthesia
  • Gaze preference to the affected side
  • Ischemic paraparesis
  • occurs in approximately 4 of dissections
  • result of interruption of blood flow in the
    intercostal, lumbar, and anterior spinal
    arteries.
  • Ischemic peripheral neuropathy
  • may follow obstruction of the vessels that supply
    the upper and lower extremities

31
Uncommon clinical manifestations
  • Hemoptysis
  • a rare finding in aortic dissection and usually
    is caused by rupture of the aorta into lung
    tissue or by dissection of bronchial arteries
  • Hoarseness
  • from vocal cord paralysis may be caused by
    compression of the recurrent laryngeal nerve by
    the expanding dissecting hematoma
  • Horners syndrome
  • may result from compression of the superior
    cervical sympathetic ganglion by the dissected
    aorta.
  • Superior vena cava syndrome

32
  • Hematemesis
  • Rupture of the aorta into the esophagus
  • Bronchospasm
  • Bronchial or tracheal compression
  • Mesenteric infarction and myocardial infarction
    (MI) unusual
  • Rarely, aortic dissection may present as a fever
    of unknown origin

33
Ancillary Evaluation
  • Routine Laboratory Tests.
  • of little value.
  • Serial analysis of cardiac enzymes is usually
    negative.
  • Microscopic hematuria may occur where the renal
    artery is involved

34
ECG
  • EKG
  • Commonly shows LVH reflecting long-standing
    hypertension
  • Useful in excluding MI however, 10 to 40 of
    patients with aortic dissection may have EKG
    abnormalities suggesting ischemia or infarction
  • Acute MI
  • Proximal dissection that involves a coronary
    artery
  • Heart block
  • retrograde dissection into the interatrial septum
    with compression of the AV node

35
Chest X-Ray
  • Routine chest x-ray studies will be abnormal in
    80 to 90 of cases.
  • mediastinal widening gt75 of cases.
  • The calcium sign uncommon but highly specific
  • the calcium deposit separated from the outermost
    portion of the aorta gt 5 mm
  • Double-density appearance of the aorta
  • suggesting true and false channels

36
  • localized bulge along a normally smooth aortic
    contour
  • disparity in the caliber between the descending
    and ascending aorta
  • Displacement of the trachea or nasogastric tube
    to the right by the dissection
  • Previous CXR very useful for comparison
  • Pleural effusions are common and usually occur on
    the left side
  • small effusion periaortic inflammation
  • a large effusion leaking or rupture of the
    dissection into the pleural space? Thoracentesis

37
Echocardiography
  • Until recently, echocardiography has not been a
    useful tool in the detection and delineation of
    aortic dissection
  • M-mode and 2-D ultrasound through a transthoracic
    approach have a sensitivity and specificity that
    is unacceptably low, ranging from 77 to 80 and
    93 to 96, respectively, giving a predictive
    value that results in too many false-negative
    tests
  • The transthoracic approach is hindered by
    overlying sternum, ribs, and lungs

38
Transesophageal Echocardiography
  • Dramatically improved the quality of
    echocardiography in the diagnosis of aortic
    dissection
  • This modality has been shown to be 97 to 100
    sensitive and 90 to 100 specific
  • There can be some difficulty in evaluating the
    ascending aorta and proximal arch because of the
    interposition of the air-filled trachea and left
    main bronchus, but this problem has been largely
    overcome by the use of the newer biplane probes.

39
TEE
  • Multiplane (or omniplane) probes may be of still
    greater usefulness because they allow additional
    views of cardiovascular structures in oblique
    planes
  • Transesophageal echocardiography (TEE) is quick
    and can be easily performed at the bedside in the
    ED.
  • Few serious side effects or contraindications
  • Requires no radiation or contrast injection.

40
TEE
  • TEE is excellent at detecting pericardial
    effusion and compares favorably with other
    modalities in evaluating aortic regurgitation,
    flow in the proximal coronary arteries, the
    intimal flap, and site of entry.
  • For these reasons, TEE has become the primary
    diagnostic method for detecting aortic dissection
    in many institutions

41
CT
  • The rates of both false-positive and
    false-negative diagnoses of aortic dissection
    appear to be less than 5.
  • Signs on the CT scan that are particularly
    suggestive of aortic dissection include
    dilatation of the aorta, identification of an
    intimal flap, differential rates of flow in true
    and false channels, and the clear demonstration
    of both the false and true lumina.

42
Limitations of the CT scan
  • It does not provide information about the
    presence of aortic regurgitation, which is
    important in determining appropriate therapy
  • Fails to provide reliable information about the
    relationship of the dissection to the major
    arterial branches of the aorta
  • Some patients have serious adverse reactions to
    the administration of IV contrast material
  • A CT scan is time consuming and requires the
    patient to be outside of the ED or intensive care
    unit

43
Aortography
  • In most institutions, aortography remains the
    standard imaging modality for detection of aortic
    dissection against which all other modalities are
    measured
  • In skilled hands, this procedure can be performed
    with low morbidity and mortality and with high
    diagnostic accuracy

44
Aortography
  • Filling of a false channel
  • Channels with or without an intervening intimal
    flap
  • Distortion of the true lumen by either a patent
    or thrombosed false lumen
  • Thickening of the aortic wall by more than 5 to 6
    mm caused by a thrombosed false lumen
  • Displaced intimal calcification

45
Aortography
  • Misdiagnoses occur in one of several situations
  • Thrombosis of the false channel may prevent
    visualization of either the intimal flap or a
    double lumen.
  • The true and false lumina may opacify
    simultaneously and, therefore, may not be clearly
    delineated from one another.
  • The intimal flap may not be visualized when it is
    located in a plane tangential to the x-ray beam

46
The disadvantages of aortography
  • invasive techniques, requires that a catheter be
    inserted into a potentially abnormal aorta.
  • It is also the most expensive of the modalities
    available.
  • Specialized personnel are required, and the
    patient must be removed from the ED.
  • Other disadvantages are the risks of IV contrast
    material and inadequate detection of pleural leak

47
Aortography
  • Despite these limitations, aortography remains an
    informative procedure to diagnose aortic
    dissection.
  • It is a sensitive test for detecting aortic
    dissection and very accurate for determining the
    site of the intimal tear and the extent of the
    dissection
  • Aortic regurgitation is easily demonstrated with
    aortography, and it is the only procedure that
    demonstrates the extent and location of
    dissection into aortic side branches

48
CT versus Aortography
  • The CT scan has greater contrast resolution and
    detects small or delayed differences in the
    opacification of true and false channels.
  • A CT scan may be able to detect a thrombosed
    false lumen despite nonopacification, whereas
    aortography cannot.
  • The axial scanning plane in a CT scan is
    perpendicular to the intimal flap so that the
    detection of the intimal flap is easier.
  • Does not require arterial catheterization, and
    may reveal other abnormalities that explain the
    patients clinical presentation

49
MRI
  • For the evaluation of the stable patient with
    suspected aortic dissection
  • Useful in
  • the evaluation of chronic aortic dissection,
  • in the follow-up of postoperative patients
  • for monitoring nonoperative patients for
    progression of the dissection

50
TREATMENT
51
Treatment at Emergency Department
  • All patients suspected of having an acute aortic
    dissection should receive careful monitoring of
    cardiac rhythm, blood pressure, and urine output
  • The objectives of early management are to
    eliminate the forces favoring progression of the
    dissection by maintaining systolic blood pressure
    between 100 and 120 mm Hg (or the lowest level
    commensurate with vital organ perfusion) and by
    reducing the force of cardiac contraction and the
    rate of rise of the arterial pulse (dP/dT).

52
  • Narcotics should be administered in adequate
    amounts for pain control
  • Therapy should begin immediately to attain these
    goals while other diagnostic tests are performed
  • The early hours are a critical period
  • The mortality in the first 24 to 48 hours of
    aortic dissection is between 1 and 2 per hour.
  • Those patients presenting with hypotension
    secondary to aortic rupture or pericardial
    tamponade should be resuscitated with IV fluids
    and blood transfusions
  • More typically, the patient will be hypertensive

53
Sodium nitroprusside
  • Prompt reduction of the blood pressure can be
    accomplished with sodium nitroprusside
  • 50 to 100 mg are mixed in 500 ml of D5W and
    initially infused at a rate of 0.5 to 3 mg/kg/min
  • The rate is adjusted to achieve the desired blood
    pressure
  • The solution is light sensitive, and the bottle
    and tubing containing the mixture should be
    wrapped in aluminum foil

54
Sodium nitroprusside
  • Because sodium nitroprusside increases the heart
    rate and may also increase the dP/dT,
    administration of this drug alone may worsen the
    dissection
  • A b-adrenergic blocker must be used in
    conjunction with sodium nitroprusside to lower
    the dP/dT
  • Propranolol
  • more selective b-blocking agent such as
    metoprolol.
  • Esmolol short-acting (continuous infusion)

55
  • Trimethaphan camsylate
  • effective in the initial treatment of acute
    aortic dissection
  • It is generally used as a single agent and is the
    preferred drug in a patient who has a
    contraindication to b-blockers
  • IV labetalol
  • This drug has both a- and b-blockade properties
  • May be used as a single agent for the management
    of aortic dissection

56
Definitive Therapy
  • Type A acute aortic dissections require surgical
    treatment.
  • The aortic segment containing the original
    intimal tear is resected when possible, with
    graft replacement of the ascending aorta to
    redirect blood into the true lumen.
  • An operative mortality rate of 7 has recently
    been reported
  • If aortic insufficiency is present, it can be
    corrected through aortic valve resuspension or
    replacement

57
  • The only contraindication to immediate surgical
    repair of a type A dissection is the simultaneous
    occurrence of a progressing stroke.

58
Type B acute aortic dissections
  • Definitive treatment is less clear
  • Generally, these patients tend to be worse
    surgical risks
  • The hospital mortality in patients treated
    without surgery who have acute type B dissections
    is 15 to 20, and that is comparable to or
    better than the mortality rate with surgery in
    most institutions, although the mortality rate in
    surgery for type B dissections appears to be
    decreasing

59
Uncomplicated distal dissections
  • Patients who present with chronic aortic
    dissection have already survived their period of
    greatest mortality risk and are usually treated
    by blood pressure control unless complications
    mandate surgery
  • Treated with blood pressure control
  • Surgery has been reserved for those patients who
    have persistent pain, uncontrolled hypertension,
    occlusion of a major arterial trunk, frank aortic
    leaking or rupture, or development of a localized
    aneurysm

60
  • However, as surgical management for these
    patients improves, medical therapy may be
    replaced by operative treatment as the preferred
    definitive approach
  • All patients who have sustained and survived an
    aortic dissection, regardless of the type of
    definitive therapy used, require careful
    long-term management
  • Major complications that may occur with time are
    redissection, the development of a localized
    aneurysm, and progressive aortic insufficiency

61
  • Control of blood pressure is the cornerstone of
    therapy
  • b-Blocking agents are the most commonly used oral
    antihypertensive drugs in the treatment of these
    patients
  • other agents, such as thiazide diuretics, calcium
    channel blockers, and angiotensin-converting
    enzyme inhibitors, may need to be added.

62
Follow-up visits
  • Blood pressure monitoring
  • Detecting signs of recurrence or progression of
    disease
  • Chest pain
  • Signs of congestive heart failure
  • Presence of aortic insufficiency
  • Mediastinal size can be followed by chest x-ray
    studies.
  • Periodically these patients should undergo either
    a CT scan or MRI scan to determine the status of
    the aorta
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