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4.2 · Polycystic Kidney Disease
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Signs on CT
5 Both kidneys are massively enlarged while
maintaining a reniform shape (. Fig. 4.2.3 ) .
a
187
4
b
. Fig. 4.2.3 Axial ( a ) and coronal ( b ) CT urography images in a child with ARPKD show massively enlarged kidneys with numerous small
cysts bilaterally
Acquired Polycystic Kidney Disease
Acquired polycystic kidney disease (APKD) is typically seen
in chronic renal failure and dialysis. Chronic potassium
depletion in humans has been associated with the development of renal cysts (e.g., primary hyperaldosteronism). Some
investigators use the term “multiple cystic kidney disease” for
this condition to di erentiate it from the true congenital
polycystic kidney disease.
In contrast to ADPKD and ARPKD, the kidney size is usually normal or smaller than normal. Also, the acquired polycystic kidney has a tendency for malignant transformation.
Signs on CT
5 Bilateral normal size or shrunken kidneys with
multiple cysts (. Fig. 4.2.4 ).
5 Signs of other complication of end-stage disease
or adrenal hyperplasia (hyperaldosteronism) may
be seen.
. Fig. 4.2.4 Axial CT urography in a patient with acquired
polycystic kidney disease shows bilateral normal-sized kidneys
with small cysts
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Chapter 4 · Nephrology
D i erential Diagnoses andRelated Diseases
e human body contains around one million nephrons
in each kidney. e “nephron” is the functional unit of the
Nephronophthisis is an uncommon autosomal dominant disorder characterized by a triad of anemia, salt-wasting, and abnormal levels of nitrogen-containing compounds like urea and
creatinine (azotemia) due to tubulointerstitial nephritis.
Patients are usually young adults or children presenting with
end-stage renal failure. Due to its nonspeci c symptoms, de -
4
nite diagnosis is usually established by kidney biopsy, which
classically shows tubular basement membrane disintegration,
tubular cyst formation, and tubulointerstitial brosis. e disease has three forms: infantile, juvenile, and adolescent.
Nephronophthisis can be associated with retinitis pigmentosa
(Senior–Løken syndrome), cerebellar ataxia and cerebellar vermis hypoplasia (Joubert syndrome), oculomotor apraxia
(Cogan’s syndrome), hepatic brosis and biliary duct proliferation (Boichis syndrome), phalangeal cone- shaped epiphysis
(Saldino-Mainzer disease/conorenal syndrome), hypopituitarism (RHYNS syndrome), ectodermal dysplasia (Sensenbrenner
syndrome), and Leber’s amaurosis (Arima-Dekaban syndrome). Brain MRI shows the characteristic “molar tooth sign”
due to superior cerebellar vermis hypoplasia of Joubert syndrome. On ultrasound, kidneys show multiple cysts up to 2cm
in size, characteristically located at the renal medulla, with
hyperechoic cortex and loss of the corticomedullary di erentiation. Many researches consider the clinical presentation of
nephronophthisis with ultrasound picture of medullary renal
cysts as being characteristic and su cient to establish the diagnosis without the need for renal biopsy. However, renal medullary cysts may be absent in 30 % of cases, so the absence of
medullary renal cysts does not rule out the diagnosis.
kidney, and it is composed of glomerulus and a tubule. e
normal renal parenchyma is divided into:
1 . Glomeruli ( cortex ): it is the functional unit of the kidney,
and it is responsible for plasma ultra ltration. Another
part of the cortex is the juxtaglomerular apparatus and the
cortical proximal and distal tubules , which are responsible
for processing the primary urine, thereby maintaining
body homeostasis.
e glomerulus is a tu of capillaries lined by epithelial cells. e endothelial cell and epithelial cell sandwich the basement membrane, and these structures
together constitute a sieve which results in a glomerular
ultra ltrate passing into Bowman’s space at the start of
the tubule.
e average adult glomerular ltration rate (GFR) is
2
125ml/min/1.73m
. erefore, the glomeruli of a healthy
adult lter 180L of plasma each day (around 120 times the
normal daily adult urine production).
2 . Renal tubules ( cortex and medulla ): the renal tubules
include the proximal tubule ( lies in the cortex ), the loop
of Henle ( lies in the medulla ), the distal tubule ( lies in the
cortex ), and the collecting duct ( lies in the medulla ).
Each renal tubule is responsible for reabsorption or
secretion of di erent metabolites. e reabsorption may
be across the tubular cells (transcellular) or passively
across the tight junctions in between tubular cells (paracellular).
3 . Interstitium : it refers to the “connective tissue” of both
compartments (cortex and medulla) including the
lymphatic tissue.
Further Reading
Blowey DL, et al. Ultrasound ndings in juvenile nephro-
4 . Renal vessels : these include the intrarenal and the arcuate
arteries.
nophthisis. Pediatr Nephrol. 1996;10:22–4.
Capisonda R, et al. Autosomal recessive polycystic kidney
disease: outcomes from a single-center experience. Pediatr Nephrol. 2003;18:119–26.
Examples ofRenal Parenchymal Disorders
According toTheir Anatomical Involvement
Grossman H, et al. Sonographic diagnosis of renal cystic dis-
eases. AJR. 1963;140:81–5.
Martinez JR, et al. Polycystic kidney disease: etiology, patho-
genesis and treatment. Dis Mon. 1995;41(11):693–765.
Roche CJ, et al. Selections from the bu et of food signs in
radiology. Radiographics. 2002;22:1369–84.
Salomon R, et al. Nephronophthisis. Pediatr Nephrol.
2009;24:2333–44.
Vauthey JN, et al. Adult polycystic disease of the liver. Br J Surg.
1991;78:524–7.
A . Glomerulonephritis (acute nephritis syndrome) : presents
mainly with hematuria and hypertension. Other signs
include proteinuria and impaired renal function (e.g.,
oliguria ). Oliguria de ned as a urine
2
volume < 400ml/24h/1.73m
body surface area (BSA).
Serum complements is an important test to be done in a
patient suspected with glomerulonephritis.
B . Renal tubular disorder : presents mainly with polyuria/
polydipsia and electrolytes imbalance (e.g., metabolic
acidosis, metabolic alkalosis, hyponatremia, hypokalemia,
etc . ). Chronic renal tubular disease results in failure to
4.3 Renal Failure
thrive, nephrolithiasis, nephrocalcinosis (mainly
medullary type), refractory rickets and osteomalacia,
A renal parenchymal disorder (RPD) is a term used to
describe a disease that involves one or more compartments o
the renal parenchyma. When this parenchymal injury causes
impairment of renal functions, the term “renal failure” is
applied to the disease as a progression of parenchymal injury.
and hypertension.
C . Renal interstitial disorder : typically present with chronic
renal failure due to renal parenchymal brosis and
atrophy. Examples of renal interstitial disorders include
analgesic nephropathy (e.g . , NSAIDs, Chinese herbs ),
4.3 · Renal Failure
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toxic materials (e.g., lithium, lead, cadmium ), interstitial
nephritis (e.g., Lupus nephritis, Sjögren’s syndrome ),
infections (CMV, nephropathia epidemica ), and
granulomas (e.g., sarcoidosis, TB ).
D . Renal vascular disorders : typically present with
hypertension (e.g . , vasculitis, nutcracker syndrome,
hemolytic uremic syndrome , etc. )
Acute renal failure (ARF) is a disease characterized by
decrease/impaired renal functions. ARF can be subdivided
into three main subtypes based on the etiology:
1 . Prerenal ARF : the main cause is hypoperfusion of the kid-
ney that can be due to hemorrhage, shock, hepatorenal
syndrome, renal artery stenosis (RAS), and congestive
heart failure. Prerenal ARF can occur in patients with
RAS who are treated with ACE inhibitors or angiotensin
II blockers ( which are normally highly secreted by the kid-
ney to overcome RAS ). A patient who develops ARF with
ACE inhibitors or angiotensin II blockers should be investigated for RAS.In children, the most common causes of
prerenal ARF include sepsis, hyperviscosity, dehydration,
and heart disease ( patent ductus arteriosus and coarctation
of the aorta ).
2 . Renal ARF : it is caused by a disease that a ects the renal
parenchyma itself ( glomerular, tubular, interstitial, or
vascular ).
3 . Postrenal AR F: it is caused by obstruction of the urine
out ow at di erent levels:
(a) Ureter : stones, strictures, and retrocaval course
(b) Bladder : neurogenic bladder, bladder carcinoma, and
stones (rare)
(c) Prostate : benign prostatic hyperplasia and prostate
cancers
Signs of ARF include oliguria, increased serum bloodurea nitrogen (BUN) and creatinine levels, increased uric
acid levels, metabolic acidosis, hyponatremia, hyperkalemia
( if not corrected pharmacologically consider dialysis ), hyper-
phosphatemia, hypocalcemia, anemia ( due to decreased
erythropoiesis ), leukopenia, and platelet dysfunctions. Urinalysis shows low urea and creatinine levels, proteinuria, and
low concentrations of chloride, sodium, and potassium.
Other signs of ARF include nausea and vomiting, brown
tongue, gastrointestinal bleeding, le heart failure, and
maybe pericarditis. Neurological manifestations include fatigability, muscle twitching, and maybe excessive sleeping
(hypersomnolence).
In a busy radiology department, many of the ultrasound referrals are from the nephrology and/or the urology department. Renal ultrasound is an essential integral
part of the investigation of many renal disorders because of
its easy accessibility, its high accuracy, lack of radiation
exposure, and lack or radiological contrast exposure. It is
the intention of this theme to concentrate on the sonographic signs of di erent renal disorders that will help the
radiologist to characterize the renal status for the referring
clinician.
189
Signs on Ultrasound
1 . Normal kidney is ovoid shape with a diameter of
9–12cm, width 4–6cm, and normal thickness of the
parenchyma 15–25mm; the pyramids are more
echo-poor than the cortex ( good contrast in children,
less in elderly persons ); and the cortex is hypoechoic
compared to the liver.
2. For renal size, the mean right renal length is
10.74 ± 1.35cm and mean left renal length is
11.10 ± 1.15cm, measured as the longest diameter
obtained on a posterior oblique image. Asymmetry
in renal size can be suggestive of ischemic renal
disease (2cm di erence between the two kidneys is
a signi cant measurement of ischemic lesion).
3 . Renal volume is measured via the following equation:
volume (V) = craniocaudal diameter ×
anteroposterior diameter × transverse diameter ×
0.5233. To adjust it to the patient’s body size, the
volume is then divided by the patient’s body mass
index (V/BMI × 25). The normal renal volume after
adjustment to the body mass index is 231–281.
Increased renal volume > 281 means nephromegaly.
4 . Parenchymal echogenicity is a nonspeci c sign that
re ects nephropathy, which is classi ed as the
following: grade 0 , echogenicity poorer than that of
the liver parenchyma (normal nding); grade I ,
echogenicity identical to that of the liver
parenchyma (normal nding); grade II , echogenicity
more intense than that of the liver parenchyma
(pathological nding); and grade III , echogenicity
identical to that of the renal sinus (pathological
nding). Parenchymal echogenicity varies also with
the patient’s age ( it is increased in newborn babies up
to 6 months of age due to elevated cellularity and in
elderly patients due to brosis ).
5 . On normal Doppler sonography , the renal artery
shows diameter of 5–8mm, maximum velocity (V
of 60–180cm / s, intrarenal RI = 0.6–0.7, and < 10 %
di erence between right and left kidney. The
intrarenal RI is measured from the arcuate arteries (at
the corticomedullary junction) or interlobar arteries
(adjacent to medullary pyramids). Three to ve
reproducible waveforms from each kidney are
obtained, and RIs from these waveforms are
averaged to arrive at mean RI values for each kidney
(. Fig. 4.3.1 ).
In children, it is common for the mean RI to
exceed 0.70 through the rst year of life, and a mean
RI greater than 0.70 can be seen through at least the
rst 4 years of life. In elderly patients without renal
insu ciency, the normal RI can also exceed 0.70. An
RI di erence greater than 0.10 between the kidneys
is seen only with true obstructive renal disease.
6 . I n acute renal failure , morphological abnormalities in
B-mode are only seen in 11 % of patients. However,
max
4
)
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Chapter 4 · Nephrology
almost 70 % of patients show intrarenal elevated RI
(>0.7) and normal or low RI in prerenal causes (<0.7)
on Doppler sonography.
7 . I n chronic renal failure , renal size < 8cm is a sign of
chronic renal failure. Reduced renal volume is a
negative prognostic sign and correlates
histopathologically with the degree of atrophy,
4
necrosis, and brosis. It can be seen in chronic
glomerulonephritis, papillary necrosis, hereditary
nephropathy, widespread nephrosclerosis, and
end-stage chronic renal failure. In patients with
chronic renal failure, RI > 0.80 on Doppler sonography
predicts progression of nephropathy more accurately
than creatinine clearance and proteinuria, showing
sensitivity (64 %) and speci city (98 %).
8 . Nephromegaly is detected when the renal length size
is > 13cm in length or renal volume > 281. In newly
diagnosed diabetics, the kidney size is normal or
enlarged (>13cm in diameter) due to glomerular
hyper ltration.
Nephromegaly with high renal volume can be seen
in renal hyper ltration due to insulin therapy, acute
tubular necrosis (ATN), acute interstitial nephritis,
accumulating diseases ( amyloid, glycogen, lipids ), and
liver cirrhosis. Particularly ATN leads to a substantial
increase in the anteroposterior diameter of both
kidneys, while the length is generally normal.
9 . I n nephrocalcinosis , the hypoechoic medulla appears
echogenic with or without shadow re ection in
medullary nephrocalcinosis , and the cortex appears
echogenic with or without shadow re ection in
cortical nephrocalcinosis . Cortical nephrocalcinosis
usually arises due to ischemic injury.
10. Hyperechoic medullae can be seen in medullary
brosis or nephrocalcinosis due to gout, medullary
sponge kidney, primary hyperaldosteronism,
hyperparathyroidism, glycogenosis, and Wilson’s
disease.
11. For hyperechoic corticomedullary junction , this sign is
not speci c to a disease but can be seen in diabetes,
pseudoxanthoma elasticum, and arterial
hypertension.
12. Di usely hypoechoic kidney is an uncommon sign that
can be seen in acute pyelonephritis, lymphoma, and
nephroblastomatosis.
13. Glomerular diseases show normal kidneys in US
examination until later stages of the disease. In later
stages of the disease, the kidney shrinks (size < 8cm),
and the cortex starts to show increased echogenicity
due to in ammation with or without brosis
(
. Fig. 4.3.2 ). In contrast to tubulointerstitial
diseases, the RI on Doppler sonography is usually
normal in glomerular diseases (mean = 0.58).
14. In tubulointerstitial nephritis , the hallmark of
tubulointerstitial nephritis is increased medullary
echogenicity, which correlates with the degree of
glomerular sclerosis and interstitial brosis. The RI on
Doppler sonography is almost always high (>0.75) in
interstitial parenchymal pathologies.
a
. Fig. 4.3.1 Ultrasound image B-mode ( a ) and Doppler mode ( b ) of a normal kidney
b
4.3 · Renal Failure
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a
. Fig. 4.3.2 Ultrasound image B-mode ( a ) and power Doppler mode ( b ) of a left kidney with glomerulonephritis due to Streptococcal
infection. A localized area of hyperechoic cortex is detected ( arrowhead ) with subsequent hyperemia on power Doppler mode ( b )
b
191
4
References
Abernethy LJ, et al. Fibromuscular dysplasia of the renal
artery in a child: detection by Doppler ultrasound and
correction by percutaneous transluminal angioplasty.
Pediatr Radiol. 1989;19:539–40.
Arnerlöv C, et al. Dynamic sonography with provocation of
pain for diagnosis of symptomatic mobile kidneys. Eur J
Surg. 2001;167:218–21.
Bagga A, et al. Approach to renal tubular disorders. Indian J
Pediatr. 2005;72(9):771–6.
Beland MD, et al. Renal cortical thickness measured at ultra-
sound: is it better than renal length as an indicator of renal
function in chronic kidney disease? AJR. 2010;195:W146–9.
Buturovic-Ponikvar J, et al. Ultrasonography in chronic renal
failure. Eur J Radiol. 2003;46:115–22.
Christian MT. Renal tubular disorders. Paediatr Child
Health. 2010;20(6):266–73.
Fiorini F, et al. e role of ultrasonography in the study of
medical nephropathy. J Ultrasound. 2007;10:161–7.
Fredericks BJ, et al. Glomerulocystic renal disease: ultra-
sound appearances. Pediatr Radiol. 1989;19:184–6.
Meola M, et al. Color Doppler sonography in the study of
chronic ischemic nephropathy. J Ultrasound. 2008;11:55–73.
Mercado-Deane MG, et al. US of renal insu ciency in neo-
nates. Radiographics. 2002;22:1429–38.
Riccabona M. Renal failure in neonates, infants, and children:
the role of ultrasound. Ultrasound Clin. 2006;1:457–69.
Ries M, et al. Parapelvic kidney cysts: a distinguishing feature
with high prevalence in Fabry disease. Kidney Int.
2004;66:978–82.
Tublin ME, et al. e resistive index in renal Doppler sonog-
raphy: where do we stand? AJR. 2003;180:885–92.
Vester U, et al. e diagnostic value of ultrasound in cystic
kidney diseases. Pediatr Nephrol. 2010;25:231–40.
Cardiology
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5.1 Acute Chest Pain – 194
Acute Coronary Syndrome – 194
Acute Pulmonary Embolism – 197
Aortic Dissection – 199
Aortic Intramural Hematoma – 201
Penetrating Atherosclerotic Ulcer – 202
5.2 Diseases oftheGreat Vessels – 202
Thoracic Aortic Aneurysm – 202
Pulmonary Hypertension – 203
Coral Reef Aorta – 205
Superior Vena Cava Syndrome – 205
193
5
5.3 Myocardial Diseases (Cardiomyopathies) – 206
Hypertrophic Cardiomyopathy – 206
Dilated Cardiomyopathy – 208
Restrictive Cardiomyopathy – 208
Arrhythmogenic Right Ventricular Dysplasia – 208
Noncompaction Cardiomyopathy (Spongy Myocardium) – 209
Peripartum Cardiomyopathy (Cardiomyopathy of Pregnancy) – 210
5.4 Endocarditis – 210
Infective Endocarditis – 211
Lö er’s Endocarditis (Eosinophilic Endomyocardial Disease) – 213
Marantic Endocarditis (Nonbacterial Thrombotic Endocarditis) – 214
5.5 Pericardial Diseases – 215
Di erential Diagnoses andRelated Diseases – 215
© Springer International Publishing Switzerland 2017
J.A. Al-Tubaikh, Internal Medicine, DOI10.1007/978-3-319-39747-4_5
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Chapter 5 · Cardiology
5.1 Acute Chest Pain
Acute chest pain is one of the most common complaints
encountered in medical emergency departments. Chest pain
is divided into cardiac and noncardiac chest pain. Causes of
cardiac chest pain include angina pectoris (stable and unstable), myocardial infarction (MI) (ST-segment elevation and
non-ST-segment elevation), myocarditis, etc. Noncardiac
chest pain includes diseases of the great vessels, esophagitis,
pneumonia, etc.
5
is topic discusses the use of radiology in detecting
acute chest pain and how the radiologist can contribute in
assessing causes of acute chest pain in emergency departments.
Acute Coronary Syndrome
Acute coronary syndrome (CAS) is a term used to describe
symptoms and manifestations of myocardial ischemia
induced by coronary artery disease.
e most important components of CAS are angina pectoris and its severe complication MI. Angina pectoris is a term
used to describe transient myocardial ischemia in the absence
of myocardial cell death. In contrast, MI is a term used to
describe myocardial cell death and necrosis due to ischemia.
Patients with angina pectoris classically present with retrosternal chest pain, which radiates to the neck and the le
shoulder, accompanied by a sensation of numbness in the
ngers. Associated symptoms include tachycardia, dyspnea,
and possibly arrhythmia. e chest pain in angina pectoris
typically lasts <10min in duration. Patients with MI classically present with the symptoms of angina pectoris in a severe
fashion. e retrosternal chest pain is severe and associated
with autonomic nervous system hyperactivity, causing profound sweating and at times loss of consciousness. e chest
pain typically may last up to 30min in duration.
MI can be transmural involving the whole thickness of the
myocardial wall due to complete occlusion of the coronary
artery. MI can also be subendocardial, which is classically
seen in coronary arterial spasm and hypertension due to
hypoperfusion. e vascular supply of the endocardium is the
part of the heart wall that is most sensitive to hypoperfusion.
Cardiac CT is used in patients with acute chest pain to
rule out three main conditions (triple rule out): acute MI,
pulmonary embolism (PE), and aortic dissection. Cardiac
CT can also be used to detect calcium plaques within the
coronary arteries in a technique known as “calcium scoring.”
Calcium scoring is a method that quanti es the atherosclerotic plaques within the coronary vessels. e calcium
score is used to assess the risk of heart events, not to detect
coronary stenosis. e basic idea of calcium scoring is to
perform a noncontrast CT of the heart to detect calci ed
plaques (. Fig. 5.1.1 ). Once a calci ed plaque is identi ed in
the coronary arteries, the examiner encircles the plaque by a
cursor, and a special program will measure the plaque attenuation and express it as a number in Houns eld units as a
. Fig. 5.1.1 Axial nonenhanced cardiac CT examination for calcium
scoring shows calci ed plaque in the right coronary artery
score (Agatston score). Each coronary branch is measured
separately and then the numbers added to give a total calcium burden score. e score predicts the probability of
heart attacks in the next 5–10 years on the current status of
the patient without treatment modi cations.
Uncalci ed atherosclerotic plaques take up to 15 years
before they are calci ed and visualized in a calcium scoring
study or noncontrast CT study. e uncalci ed (vulnerable)
plaque appears inhomogeneous or with low density on CT
scan (25 ± 15 HU). Uncalci ed and partially calci ed plaques
are more associated with ACS than are calci ed plaques,
because they are unstable and can be dislodged, initiating a
coronary embolic attack.
Cardiac MRI in CAS patients is mainly used to study
myocardial wall motion ( myocardial function study ), perfu-
sion (same as the thallium perfusion study ), viability, and
ejection fraction measurement like cardiac Doppler study
( phase-contrast ow quanti cation ). e role of cardiac MRI
postinfarction is to identify viable (salvageable) myocardium, which is mainly detected by the ( myocardial viability
study ).
e basic concept of the myocardial viability study is to
detect how much viable (alive and contractile) myocardium
is le a er MI. e technique depends upon the fact that
gadolinium di uses into the myocardial interstitial spaces
a er its injection into the body. As long as the myocardial
membrane (sarcolemma) is intact, the gadolinium is pumped
out of the intracellular compartment and concentrated in the
extracellular compartment until it is washed out 10min a er
its injection. is scenario occurs with normal and viable
myocardium. If the myocardium is diseased or infarcted, the
gadolinium will di use inside the extra- and intracellular
compartments, which makes its clearance take longer time
5.1 · Acute Chest Pain
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than 10min. Myocardial contrast enhancement that exceeds
10min from gadolinium injection is called “late gadolinium
enhancement,” which is considered pathological, and the test
is considered positive for nonviable myocardium.
Loss of cardiac wall motion, which is assessed in the myocardial function study, is another important sign of nonviable
myocardium. However, there are two situations where the
myocardium is viable but is not contracting: myocardial
stunning and hibernating myocardium. Myocardial stunning
is a situation where the cardiac muscles are viable, but they
do not contract as a transient phenomenon a er MI (like
penumbra a er stroke). Hibernating myocardium is a situa-
tion where the cardiac muscles are viable, but are not contracting a er reestablishing coronary perfusion due to a long
period of chronic perfusion abnormalities. is situation is
typically seen in patients with long-standing, compromised
coronary perfusion who have undergone coronary artery
bypass surgery (CABG). Although the perfusion is normally
established a er a long period of hypoperfusion, the muscles
are not contracting due to a long period of cardiac muscle
ischemia and hypofunction.
Signs on Cardiac CT
5 In a patient with acute chest pain, detection of
calcified plaques on the nonenhanced coronary
vessels with absence of signs of aortic dissection
or embolism confirms the diagnosis of
CAS.However, absence of the coronary calcified
plaques does not rule out CAS because uncalcified
plaques can be present. Up to 50 % of patients
with sudden cardiac arrests show calcified lesions
in their coronary arteries (. Fig. 5.1.1 ).
5 MI may be seen as a subendocardial ventricular
hypodense area depending upon the blocked
coronary artery and its vascular territory.
5 Post-myocardial infarction calcification and
ventricular dilatation may occur (. Fig. 5.1.3 ).
a
195
5
Signs on Chest Radiographs
5 Indirect signs of CAS include aortic calcification of
aorta or coronary arteries calcification.
5 If the MI is complicated by heart failure, signs of
pulmonary edema may be detected such as upper
lobe vessel cephalization and enlarged cardiac
silhouette (. Fig. 5.1.2 ).
b
. Fig. 5.1.2 Anteroposterior chest radiograph of a bedridden
patient with myocardial infarction (MI) shows congested hilar
vessels and beginning of pulmonary edema
. Fig. 5.1.3 Posteroanterior chest radiograph ( a ) and thorax
CT ( b ) shows focal apical left ventricular dilatation with calci ed
rim due to old MI of this region ( arrowheads )
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Chapter 5 · Cardiology
Signs of MI on MRI
5 Wall motion abnormalities (akinesia or hypokinesia)
on cine MRI.
5 Contrast enhancement on delayed images (>10min).
There are four patterns of late contrast enhancement of
MI: First pattern is subendocardial enhancement with
sparing of the subepicardial region (. Fig. 5.1.4a ). Second
pattern is full-thickness myocardial wall enhancement
(. Fig. 5.1.4b ). Third pattern is full-thickness myocardial
5
wall enhancement, with subendocardial hypointense
a
area, representing a severe edema compressing the
intramural vessels (. Fig. 5.1.4c ). Fourth pattern is seen as
a dark hypointense area that represents the infracted
area surrounded by a rim enhancement (. Fig. 5.1.4d ).
The fourth pattern is seen in extensive MI with less viable
myocardium.
5 Stunned and hibernating myocardium is visualized as
wall motion abnormalities (akinesia or hypokinesia)
in cine MRI with no contrast enhancement on delayed
images (>10min).
b
c
. Fig. 5.1.4 Short-axis dark-blood T1W postcontrast cardiac MR illustrations show di erent pattern of myocardial enhancement after MI:
( a ) subendocardial enhancement with sparing of the subepicardial region; ( b ) full-thickness myocardial wall enhancement; ( c )
full-thickness myocardial wall enhancement, with subendocardial hypointense area; and ( d ) dark hypointense area represents the
infarction surrounded by a rim enhancement
d
5.1 · Acute Chest Pain
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Why does atherosclerosis not develop in the veins and is only seen
in the arteries, although the cholesterol circulates in the blood in
both veins and arteries?
is occurs because the arterial pulsation assists in the
deposition of the cholesterol molecules within the intima.
Normally, the pulmonary arteries do not pulsate, but when
pulmonary hypertension develops, the high pressure blood
within the arteries evokes the arterial wall to pulsate, resulting in developing atherosclerosis within the pulmonary
arteries.
Acute Pulmonary Embolism
Acute pulmonary embolism (PE) is an emergency situation
characterized by closure of a pulmonary artery by an embolus
causing pulmonary ventilation–perfusion mismatch or, in a
worse scenario, pulmonary infarction.
e bronchial circulation only supplies nutrients and
does not participate in gas exchange in normal situations.
However, in PE, the bronchial circulation responds with
enlargement and hypertrophy and participates in blood
oxygenation due to decreased pulmonary ow and
ischemia.
PE is categorized according to severity into two main
types: acute sub-massive and acute massive PE.Acute submassive PE is characterized by <50 % occlusion of the pulmonary vascular bed, whereas acute massive PE is characterized
by >50 % occlusion of the pulmonary vascular bed.
Patients with acute PE o en describe acute sudden chest
“gunshot-like” pain with progressive dyspnea, tachycardia,
and cyanosis. Many patients have a history of deep venous
thrombosis (DVT), varicose veins, immobilization, or recent
pelvic surgery. A dislodged part of the initial thrombus,
mostly from the lower limbs, travels through the venous circulation until it blocks an arterial pulmonary vessel in the
chest as an embolus, causing pulmonary vascular congestion. If this congestion persists, pulmonary infarction
occurs.
In small percentage of patients, the unresolved thrombus
a er treatment can be incorporated into the vessel wall and
covered by a layer of epithelium. is thrombus organization
causes intravascular stenosis of the a ected lumen, resulting
in the development of pulmonary hypertension and cor pulmonale.
Acute PE is best diagnosed by V/Q scan (ventilation–
perfusion nuclear scan study) in circulatory stabilized
patient. e scan typically shows pulmonary ventilation–
perfusion mismatch. In unstable acute PE patients, CT pulmonary angiography is the initial examination of choice.
197
Signs on Chest Radiograph
5 Radiographs are normal in 12 % of cases.
5 Pulmonary infarction can appear as a patchy
radio-opaque shadow on chest radiograph, which
cannot be differentiated from patchy pneumonia
or pulmonary contusions. Therefore, the
radiographic signs have to be correlated with the
history and the clinical data.
5 Hampton’s hump : is a wedge-shaped radio-opaque
patch that is round shaped, located at the lung
periphery, and directed from peripheral toward the
hilum (. Fi g. 5.1.5 ). This patch represents wedge-shaped
infarction of the peripheral lung parenchyma.
5 PE can be accompanied by Hemorrhagic pleural
effusion.
a
b
. Fig. 5.1.5 Posteroanterior chest radiograph ( a ) and chest
HRCT in two di erent patients with pulmonary infarction show
Hampton’s hump in ( a ) ( arrowhead ) and basal area of pulmonary
parenchymal consolidation due to infarction in ( b )
5
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