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Examination of the ribs and chest wall begins with an assessment of localized

swelling, such as the sternoclavicular joints and costochondral junctions. The


articulations at either end of the clavicle shouldbe palpated. Along the course of the
sternum in the midline, tenderness may befound beside the sternalis muscles, the
manubriosternal and xiphisternal joints, or the xiphoid process. In addition,
tenderness shoul be sought at the costochondral junctions along the sides of the
sternum and over the lower rib tips laterally. In the posterior thorax, costovertebral
joint dysfunction may be assessed by palpation over the areas just lateral to the
vertebral bodies or over the affected rib.
In addition to direct palpation, various maneuvers have been utilized to reproduce
chest wall pain. These include the Crowing rooster maneuver, horizontal arm
flexion and the hooking maneuver.
The Crowing rooster maneuver (Fig. 8.3) is done with clinician standing behind the
patient and extending traction on the upper arms by pulling them backward and
slightly superiorly. Pain originating from cervical spine or anterior chest wall (or
both) will be reproduced.
In horizontalarm flexion, the arms is flexed across the anterior chest and steadied,
prolonged tractionis applied in a horizontal direction. Both horizontal arm flexion
and the Crowing rooster maneuver may be done at the same time with neck
extension or rotation.
The hooking maneuver (Fig. 8.4) is done by hooking the fingers under anterior
costal margins and by pulling the rib cage anteriorly. This will reproduce pain in
cases of costochondritis, traumatic or slipping rib syndrome.
As witth palpation, the findings with all three of these maneuvers should be
considered diagnostic only if the patients presenting pain is reproduced.

DIAGNOSTIC TESTING AND EVALUATION


After history and physical examination, the differential diagnosie is narrowed down,
various investigations related to thesuspected diagnosis helps to determine whether
the patient has a serious condition. It also helps to reach a final diagnosis in most of
the adults presenting with chest pain.
Acute Coronary Syndrome and CAD
Important diagnostic test when evaluating for acute coronary syndrome include the
12 lead ECD, serum markers of myocardial damage, and cardia testing with stress
testing or nuclear imaging. ECG findings that most strongly suggest MI are ST
segment elevation, Q waves, and a conduction defect, especially if such findings are
new compared wih a previous ECG. New T wave inversion also increases the

likelihood of MI. however, none of theses findings is sensitive enough that its
absence can exclude MI. other routine measure include using supplemental oxygen,
establishing continous access, and giving aspirin as well as sublingual nitroglycerin
for pain.
Echocardiography can detect regional left ventricular wall motion abnormalities
within seconds of coronary artery occlusion. The sensitivity of this procedure is high
but specificity is limited due to the large number of alternative causes of regional
wall motion abnormalities. Thus, echocardiography may be used to exclude MI
during or immediately after an episode of chest pain but not to diagnose it.
Individuals with chest pain, who have a history that indicates low risk of cardio
vascular disease, a normal or near normal ECG, and normal troponin levels can
safety be evaluated as outpatients.
Patients at low risk usually do not need further testing unless there are other risk
factors in their family or medical history that markedly increase their likelihood of
CAD. Patients at intermediate risk for CAD who can exercise and have no left bundle
branch block, pre excitation, or significant resting ST depression on their ECG can
be evaluated with an exercise stress ECG. Patients with baseline ECG abnormalities
should have perfussion imaging performed along with a stress ECG and patients
who cannot exercise may be evaluated with a pharmacologic stress or vasodilator
test (e.g. dobutamine, adenosine). Patients at high risk for CAD generally should
proceed directly to angiography, which allows definitive assessment of coronary
artery anatomy and also for patients in whom other tests are nondiagnostic and for
those who could benefit from revascularization. A cardiologist is the best person to
deal with cardiac type of pain.

Pulmonary Embolism
A low clinical suspicion for PE [e.g. Wells score (Table 8.3) less than 2] plus a normal
quantitative D-dimer assay safely rules out PE, with a negative predicitive value
greater than 99,5 percent. If further testing is needed, helical computed
tomography (CT), combined with clinical suspicion and other testings such as lower
extremity venous ultrasound, can be used to rule in or rule out PE.
A number of different sequential testing protocols have been prposed, all of which
involve the same basic elements: (i) for patients with low clinical suspicion and a
normal D-dimer, no further evaluation or treatment is needed unless symptoms
change or progress; (ii) for patients with low clinical suspicion and an abnormal Ddimer, or moderate to high clinical suspicion, helical CT and lower extremity venous
ultrasound examination should be ordered; (iii) for patients with moderate or high
clinical suspicion and an abnormal CT scan or venous ultrasound, treatment should
be given for PE or DVT regardless of D-dimer; and (iv) for patients with an abnormal

D-dimer plus a normalCT scan and a normal venous ultrasound, serial ultrasound
shoul be considered if clinical suspicion is low to moderate and pulmonari
angiography should be considered if clinical suspicion is high.

Pneumonia and Heart Failure


Chest radiograph generally is considered the reference standard for patients
suspected of having pneumonia and it is the standard againts which clinical
evaluations for pneumonia are compared.
An abnormal ECG and cardiomegaly on chest radiograph increases the likelihood of
heart failure among patients with chest pain. Brain natriuretic peptide level has
been found to be reliable for detecting heart failure in patient presenting with acute
dyspnea. An echocardiography is helpful for diagnosis of heart failure.

Chest Wall Pain


Chest wall pain usually can be diagnosed by history and physical examination after
excluding cardiac, pulmonary and abdominal sources of pain. Laboratory and
radiographic studies of the following purposes in the evaluation of a patient with
suspected musculoskeletal chest pain.

To determine whether a suspected chest wall syndrome might be asssociated


with a spesific rheumatoid disease.
To directly assess an anatomic area of the chest wall or surrounding structures.
The evaluatin of such patient should consist of a bood count, routine blood
chemistries (including serum creatinine), urine analysis, chest X-ray and ECG. In
most rheumatoid disease in which the chest wall is involved, the diagnosis is
based upon the pattern of joint involvement outside the chest, extra-articular
features and laboratory abnormalities. As an example , the ESR Is a relatively
nonspecific test for inflammatory disease which is elevated in majority of
patients with septic arthritis, active rheumatoid arthtitis, ankylosing spondylitis
and other spondyloarthropathies. An elevated ESR is not as predictable in
psoriatic arthtritis or sternoclavicular hyperostosis.
In patients with unexplained arthritis of the sternoclavicular joint, an evaluation
for rheumatoid factor is indicated, since some patients with rheumatoid
arthtritis present with monoarticular pattern of arthtritis.
In patients with pain or stiffness in the lower or upper back, with evidence of
sacroiliac tenderness, with limited lumbar flexion or chest expansion on
examination, radiographs of the SI joints is the initial step in evaluating
ankylosing spondylitis. When SI film are equivocal, checking for the HLA B-27
antigen may be useful.

Sometimes a diagnostic trigger point or costochondral site injection, may be helpful.


Gastrointestinal Causes of Chest Pain
Gastrointestinal work up is aimed at demonstrating pathological gastroesophageal
reflux, hypersensitivity of the esophagus, or esophageal motor abnormalities.
Gastroesophageal Reflux Tests
i. Proton pump inhibitors: Empirical PPI therapy (the PPI test) is recommended prior
to any invasive testing to diagnose disease related non cardiac chest pain
(NCCP). The omeprazole dose used in the PPI test range from 40 to 80 mg daily
over a duration of 7 to 28 days. If the symptom score improves by more than
50-70% relative to baseline, the test is considered positive. The PPI test is a
cost-saving approach that significantly reduce the number of invasive diagnostic
tests.
ii. Reflux Monitoring: Esophageal pH monitoring demonstrates pathological GERD in up
to 62% of the patients with NCCP. A group of patients may have normal acid
exposure, but still have a significant temporal relationship between reflux
episodes and chest pain events. These patients considered to have an acidhypersensitiveesophagus.
iii. Endoscopy: it shoul be reserved for patients with NCCP and alarm symptoms
including dysphagia, odynophagia, weight loss, or anemia.
Esophageal Sensitivity Tests
i.

ii.

Acid perfusion tests: Hydrochloric acid, infused into the middle third of the
esophagus, is able to inducechest pain. The acid infusion test is positive in
10-38% of patients with NCCP.
Ballon distension tests: A small ballon is placed in the lower esophagus
and inflated until the patient reports of pain. Richter et al and other
investigators have observed that ballon distension at lower volumes
reproduces chest pain in patients with NCCP than oin controls.

Esophageal Motility Tests


i.

High resolution manometry (HRM): This is the gold standard for


recognition and classification of esophageal motility disorders. A
significant precentage (48-64%) of patients with achalasia experience
chest pain. A recent study using HRM showed that acid sensitive NCCP
patients have distinct hypermotility pattern in the smooth muscle portion
of the esophagus.
Resolusi tinggi manometri (HRM): Adalah standar emas untuk pengakuan
dan klasifikasi gangguan motilitas esofagus. Sebuah persentase yang
signifikan (48-64%) dari pasien dengan nyeri dada mengalami akalasia.
Sebuah penelitian menggunakan HRM terbaru menunjukkan bahwa pasien
NCCP sensitif-asam memiliki pola hipermotilitas berbeda di bagian otot
polos esophagus.

ii.

Pharmacological provocative tests: Provocative tests with edrophonium,


ergonovine, bethanechol, and pentagastrin have been developed to
identify patients with NCCP of esophageal origin. Overall, pharmacological
provocative tests are invasive, associated with adverse events, not
standardize, have l;ow diagnostic sensitivity for NCCP, and fail to predict
therapeutic outcome.
Farmakologi tes provokatif: tes provokatif dengan edrophonium,
ergonovin, bethanechol, dan pentagastrin telah dikembangkan untuk
mengidentifikasi pasien dengan NCCP esofagus. Secara keseluruhan,
farmakologi tes provokatif yang invasif, terkait dengan efek samping,
tidak standarisasi, memiliki sensitivitas diagnostik rendah untuk KOMNAS,
dan gagal untuk memprediksi hasil terapi.

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