Ebook Diagnostic imaging of infants and children: Part 1

(BQ) Part 1 book Diagnostic imaging of infants and children presents the following contents: Neonatal lung disease, pulmonary infection, the mediastinum, congenital heart disease, anomalies of the great vessels, the breast, developmental abnormalities of the lungs and diaphragm,...

Diagnostic Imaging of Infants and Children VOLUME I Notice Medicine is an ever-changing science As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required The author and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and gener­ ally in accord with the standards accepted at the time of publication However, in view of the possibility of human error or changes in medical sciences, nei­ ther the author nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work Readers are encouraged to confirm the information contained herein with other sources For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for adminis­ tration This recommendation is of particular importance in connection with new or infrequently used drugs Diagnostic Imaging of Infants and Children Robert G Wells, MD Pediatric Diagnostic Imaging, SC PDI Pediatric Teleradiology Milwaukee, Wisconsin Director, Pediatric Imaging Northwestern Lake Forest Hospital Lake Forest, Illinois Associate Clinical Professor of Radiology and Pediatrics Medical College of Wisconsin Milwaukee, Wisconsin VOLUME I edical New York Chicago Milan San Francisco New Delhi Lisbon San Juan Seoul London Madrid Singapore Mexico City Sydney Toronto � McGrow·H/1/ CompanieS Copyright© 2013 by The McGraw-Hill Companies, Inc AU rights reserved Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any fonn or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher ISBN: 978-0-07-180839-2 MHJD: 0-07-180839-6 The material in this eBook also appears in the print version of this title: ISBN: MHJD: 0-07-176966-8 978-0-07-176966-2, All trademarks are trademarks of their respective owners Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark Where such designations appear in this book, they have been printed with initial caps McGraw-Hill eBooks are available at special quantity discounts to use as premiums and sales promotions, or for use in corporate training programs To contact a representative please e-mail us at bulksales@mcgraw-biU.com TERMS OF USE This is a copyrighted work and The McGraw-Hill Companies, Inc ("McGraw-Hill") and its licensors reserve all rights in and to the work Use of this work is subject to these tenns Except as pennitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill's prior consent You may use the work for your own noncommercial and personal use; any otber use of the work is strictly prohibited Your right to use the work may be terminated if you fail to comply with these tenns THE W ORK JS PROVIDED "AS JS." McGRAW-HILL AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE W ORK VIA HYPERLJNK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NO T LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE McGraw-Hill and its licensors not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free Neither McGraw-Hill nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom McGraw-Hill has no responsibility for the content of any information accessed through the work Under no circumstances shall McGraw-Hill and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages This limitation of liability shall apply to any claim or cause whatsoever whetber such claim or cause arises in contract, tort or otherwise To Annie, my loving wife and best friend To my sons, Jack, Sam, and Joe, who have taught me much more than I will ever teach them And to Jack Sty, who one day said to me, "Bob, let's write another book " This page intentionally left blank Contents Foreword Preface Acknowledgments ix xi xiii VOLUME I PART Developmental Abnormalities of the Lungs and Diaphragm Neonatal Lung Disease Pulmonary Infection Abnormalities, and Systemic Disease Pulmonary Neoplasms and Masses PART 179 219 17 Autoimmune Disorders of the Brain THE CARDIOVASCULAR Heart and Pericardium 11 Congenital Heart Disease 13 The Vascular System 277 279 14 Congenital Abnormalities of the Brain 315 403 THE BRAIN 15 Hydrocephalus 267 12 Anomalies of the Great Vessels 251 433 485 625 18 Metabolic and Destructive Disorders of the Brain 21 Head Trauma PART 641 20 Intracranial Vascular Abnormalities 683 797 THE SPINE of the Spine 847 887 22 Developmental Abnormalities 889 23 Infection, Inflammation, and Degenerative Disorders of the Spine 24 Neoplasms and Masses of the Spine 25 Trauma and Surgery of the Spine 977 957 1007 VOLUME II PART THE HEAD AND NECK 26 The Skull and Face 10 Acquired Diseases of the PART 191 SYSTEM 75 The Chest Wall 139 Pulmonary Trauma, Surgery, The Mediastinum 45 Chronic Lung Disease, Genetic The Breast 597 ································· 19 Intracranial Neoplasms and Masses THE THORAX and Toxins 16 Intracranial Infections 27 The Orbit 1043 28 The Paranasal Sinuses 1045 1091 1137 29 The Nose, Nasal Cavity, and Nasopharynx 30 The Neck, Pharynx, and Trachea 31 The Salivary Glands 32 The Thyroid and Parathyroid Glands 33 The Temporal Bone and Ear 1153 1173 1249 1261 1293 487 575 vii viii Contents PART THE GASTROINTESTINAL SYSTEM 34 The Esophagus 35 The Stomach 323 1325 1357 50 Urinary Tract Calcifications and Stones 51 Urinary System Trauma, Surgery, and Therapy 36 The Smalllntestine 1379 52 Renal Vascular Abnormalities 37 The Colon 1447 53 The Female Genital System 38 The Omentum, Mesentery, and Peritoneal Cavity 39 The Anterior Abdominal Wall 1495 1503 40 Abdominal Trauma and Otherlntraabdominal Emergencies PART THE HEPATOBILIARY SYSTEM 41 The Hepatobiliary System PART THE PANCREAS 42 The Pancreas PART THE SPLEEN 43 The Spleen 1629 1631 653 1655 47 Urinary System lnfection 48 Vesicoureteral Reflux 49 Neoplasms and Masses of the Urinary System 1715 1741 1759 1777 1785 PART 11 THE ADRENAL CiLANDS 56 The Adrenal Glands SYSTEM 58 Dysostoses and Developmental Deformities 59 Metabolic Bone Diseases Go Systemic Arthritis 931 1933 57 Skeletal Dysplasias 1925 PART 12 THE M USCULOSKELETAL 1965 1967 202 2073 2113 61 Hematological and of the Extremity Soft Tissues 65 Musculoskeletal Trauma 2141 64 Nonneoplastic Abnormalities Index 2123 62 Musculoskeletal Infections 1855 1887 63 Musculoskeletal Tumors 46 Diseases of the Renal Parenchyma Affect Both Genders 1827 1841 55 Genital Abnormalities that Ischemic Bone Disease 44 Developmental Abnormalities 45 Renal Cysts 1523 1609 PART 10 THE GENITOURINARY of the Urinary System 1521 1607 SYSTEM 1511 54 The Male Genital System 1813 2161 2237 225 /-1 Fo rewo rd Diagnostic Imaging of Infants and Children by Robert Wells is a must-have text that I am sure you will keep as a con­ stant friend It is a one-of-a-kind book, written in a style pathophysiology For clinicians, this text is a resource for reviewing the advantages and disadvantages of various imaging approaches and for understanding the signifi­ that is concise and informative Kudos to Dr Wells for the cance of imaging findings The easy-to-read style and the superlative work clear correlation of radiologic findings with disease patho­ This richly illustrated reference covers the gamut of pediatric diseases and injuries Extensive integration of physiology and clinical features make it an excellent choice for medical students, residents, and fellows clinical considerations and review of disease pathogenesis This text is a terrific source of information across the help to make sense of imaging patterns and provide the entire spectrum of pediatric radiology, and I strongly rec­ radiologist with tools to establish a confident diagnosis ommend this book to anyone interested in the subject Readers of various backgrounds will find this text use­ ful Radiologists can pull it off the shelf for a quick review Richard Towbin, MD of the imaging findings and differential diagnosis of a con­ Radiologist-in-Chief dition, with additional material available for those desiring Phoenix Children's Hospital a more in-depth review of the clinical presentation and Phoenix, Arizona ix 470 Part The Ca rd i ovascu l a r System The treatment of patients with suspected aortic injury includes the early administration of P-blockers Most patients with documented aortic injuries undergo emergent surgery Nonoperative treatment is appropriate for some injuries, such as minimal intimal abnormality or a small noncommunicating intramural hematoma Endovascular stent graft placement is an option for selected patients with thoracic aortic injuries.'37·'38 Cardiac injuries can occur in children suffering blunt thoracic trauma The most common injury to the heart is a cardiac contusion Other potential injuries include trau­ matic ventricular septal defect, cardiac pseudoaneurysm, and coronary artery occlusion or aneurysm.'39 Abdomen and Pelvis The renal arteries are susceptible to damage from blunt abdominal trauma or severe deceleration mechanisms Stretching or avulsion of the renal artery can occur as the mobile kidney moves relative to the fixed aorta Potential renal arterial injuries include intimal disruption, dissec­ tion, main renal artery avulsion, branch vessel transection, false aneurysm, and arteriovenous fistula CT is sufficient for the detection of many renal vascular injuries Absent or diminished contrast enhancement ofthe renal parenchyma is an important indicator of possible renal arterial injury CT angiography, MR angiography, and conventional angi­ ography provide detailed assessment of arterial injuries Chapter 51 has additional discussion of renal injuries.l4° Most liver and spleen injuries involve relatively small intraparenchymal vessels Active contrast extravasation on CT is an important indicator of a clinically significant vas­ cular injury Avulsion or thrombosis of the main hepatic artery or splenic artery is rare Tearing of the intrahepatic segment of the inferior vena cava can occur with deep liver lacerations caused by blunt trauma.'3 Trauma patients with unstable pelvic fractures often have associated disruption of pelvic arteries and veins For those patients with clinical evidence of traumatic pel­ vic hemorrhage, the strategy for treatment and diagnostic evaluation depends on the clinical stability of the patient and the availability of resources Unstable patients often proceed immediately to surgery Others can be evaluated with contrast-enhanced CT Emergent angiography and embolization are most appropriate for patients with active hemorrhage from the internal iliac artery.'4'·'42 N eck Cervical vascular injuries present challenges both in diag­ nosis and management These injuries may be clinically silent, and are probably underdiagnosed Patients with cer­ vical vascular injuries are at substantial risk for death or major permanent neurological deficits.l43-l44 Penetrating injuries of the neck that extend deep to the platysma muscle result in carotid or vertebral artery inju­ ries in approximately 20% to 35% of patients Penetrating injuries occur from gunshot wounds, stab wounds, and other lacerations Potential vascular injuries in these patients include pseudoaneurysm, arteriovenous fistula, vessel transection, intimal flap, dissection, and occlusion Stab wounds account for 20% to 40% of cervical vascular injuries in reports that include pediatric and adult patients The typical arterial injury in these patients is a tangential laceration or complete transection Penetrating injuries of the neck are classified as occur­ ring within three anatomic zones Zone is inferior to the cricoid cartilage Zone is between the cricoid cartilage and the angle of the mandible, and zone is superior to the angle of the mandible Zone and injuries are more difficult to assess clinically than those in zone 2, and imag­ ing studies are more often required The clinical presenta­ tion ofvascular injury caused by penetrating trauma ranges from an otherwise asymptomatic innocuous-appearing wound to exsanguinating hemorrhage Injuries to the pharynx, esophagus, and jugular veins are common in these patients Tracheal injury is rare The carotid arteries are involved in approximately 8o% of neck vessel injuries caused by penetrating wounds; the vertebral arteries are partially protected by the cervical spine Vascular neck injuries with blunt trauma are rare, but are potentially devastating The prevalence in children is unknown For individuals of all ages, cervical vascular injury is estimated to occur in less than 1% of instances of blunt trauma to the neck Many of these patients are asymptom­ atic or have delayed manifestations of the vascular injury Cervical vascular injury caused by blunt trauma carries a mortality rate of approximately 20%, and a permanent neurological sequelae rate of greater than 50% The most common arterial injuries in patients suffering blunt trauma are occlusion, intimal flap, and dissection Vertebral artery injuries are more common than carotid injuries with blunt trauma The vertebral arteries are susceptible to direct injury from a transverse foramen fracture, and to indirect injury from stretching across adjacent bones with facet dislocation or with whiplash, twisting, or hyperflexion of the neck The most common imaging findings of cervical vascu­ lar injury with both penetrating and blunt mechanisms are occlusion and stenosis Occlusion and stenosis can occur from a variety of mechanisms, such as dissection, throm­ bosis, transection, and extrinsic compression Complete occlusion is detected with a high sensitivity by all vascular imaging techniques Doppler sonography shows no flow at the site of occlusion, and echogenic thrombus may be vis­ ible Proximal to the occlusion, there is a high impedance waveform, and absent or reversed diastolic flow CT angi­ ography shows lack of enhancement of the occluded seg­ ment On standard MR images, there is a lack of a flow void in the involved vessel, and thrombus may be identified as material of elevated signal intensity within the lumen M R angiography shows lack o f flow-related signal I t i s impor­ tant to recognize that the diminished flow velocity within the patent vessel distal and proximal to the occlusion may result in overestimation of the length of the occluded seg­ ment Contrast-enhanced MR angiography may increase Chapter 13 The Vascu l a r System 471 the diagnostic accuracy by allowing the differentiation of a true occlusion from patent segments of the vessel with slow flow.145 The imaging findings in the presence of a trauma­ related stenosis overlap those of complete obstruction Doppler sonography of the vessel proximal to the steno­ sis shows high impedance If the stenotic segment is in a location that can be evaluated with ultrasound, Doppler shows increased flow velocity at the narrowed portion of the vessel CT angiography is the best noninvasive tech­ nique to accurately characterize a high-grade stenosis, as the contrast allows visualization of the remaining patent lumen ("string sign") Contrast-enhanced M R angiography provides similar information Traumatic intimal flaps and dissections are usually caused by blunt injuries, and are rare with penetrating mechanisms The impact is most often to the neck, but cervical vascular injuries can also occur with thoracic or cranial trauma The mechanism often involves hyperexten­ sion of the neck with rotation, hyperflexion, or whiplash Motor vehicle-related injury is the overall most common cause of traumatic neck vessel dissection in patients of all ages Dissection can result from chiropractic manipula­ tion Dissection can also occur with athletic activities that involve abrupt turning or extension of the neck The verte­ bral arteries are most susceptible to stretching injury in the C1-C2 region Basilar skull fractures can be accompanied by dissection of the petrous portions of the carotid arter­ ies Most carotid artery dissections involve both the cervical and petrous portions; 20% are localized to the cervical seg­ ment only, and 10% to the petrous segment only In young children, intraoral trauma as a consequence of a fall while carrying an object in the mouth is the most common cause of traumatic carotid artery dissection Spontaneous dissec­ tions are rare in children; the risk is elevated in patients with a connective tissue disease or fibromuscular dysplasia.146 Patients with trauma-related cervical vascular dissec­ tion often have nonspecific clinical findings, and some patients are asymptomatic Potential findings include neurological symptoms from embolism or hypoperfusion (stroke, transient ischemic attack) , incomplete Horner syn­ drome (oculosympathetic paresis with preserved ipsilateral facial sweating) , neck bruit, headache, and neck pain Neck pain sometimes follows the course of the carotid artery (car­ otodynia) The clinical manifestations of the vascular injury are often masked by those of other injuries, such as direct head trauma In addition, the onset of symptoms from neck vessel dissection can be delayed In general, noninva­ sive evaluation of the neck vessels (CT angiography, sonog­ raphy, or MR angiography) is appropriate for blunt trauma patients in the following situations: neurological symptoms that are not accounted for by direct injury to the brain or spinal cord, suspicious findings on physical examination of the neck, a basilar skull fracture with mental status abnor­ malities, or evidence of a delayed infarct.'47-'4 Sonography is effective for the detection of dissection in those portions of the carotid and vertebral arteries that are not obscured by bone or other structures The common carotid arteries and the proximal aspects of the internal carotid arteries in particular are amenable to sonographic evaluation A vascular abnormality beyond the reach of the transducer can also be surmised if diminished antegrade flow results in dampened spectral waveforms CT angiography is an excellent noninvasive tech­ nique to screen trauma patients for possible injuries of the neck vessels Axial images typically show the contrast enhanced lumen to be eccentrically narrowed at the site The overall vessel diameter in the region of the dissection is usually enlarged because of an intramural hematoma An intimal flap is visualized as a thin filling defect in the vessel lumen CT is particularly well suited for the detec­ tion of a pseudoaneurysm CT angiography is superior to sonography for the depiction of abnormalities in the intraosseous segments of the carotid and vertebral arter­ ies , and avoids some of the flow-related artifacts of M R angiography MRI for the evaluation of a trauma patient with neu­ rological symptoms should include M R angiography sequences as well as conventional axial images of the neck to detect neck vessel abnormalities Obstruction or high­ grade stenosis is detected with a high sensitivity utilizing MR angiography; however, subtle arterial wall abnormali­ ties may be difficult to differentiate from artifactual irregu­ larity An inconclusive exam must be supplemented with additional imaging such as angiography, as even minor abnormalities of a major neck artery can lead to serious neurological consequences Angiography is the gold standard technique for the detection of trauma-related pathology of the neck vessels In general, the examination should include evaluation of the aortic arch, the carotid and vertebral arteries, and the intracranial vessels The potential findings include abnor­ mal flow characteristics of a vessel, obstruction, stenosis, intimal flap, dissection, aneurysm, and distal embolism Pseudoaneurysm is common after a penetrating injury of the neck, and nearly always involves the carotid artery This lesion is clinically silent in many patients The pseudo­ aneurysm sometimes produces a palpable mass, depending on the size and location Neurological symptoms occur in a substantial minority of patients, a result of distal migration of thrombus or vascular occlusion Imaging studies show a pseudoaneurysm as a focal widening or outpouching of the vessel Although angiography provides the greatest imag­ ing detail of the vessel lumen and the cavity of the pseu­ doaneurysm, sonography and CT show the relationship to adjacent structures in the neck and the thickness of clot within the lesion Treatment approaches for cervical vascular injuries are varied, and somewhat controversial Complete occlusion of an artery can be treated with anticoagulation, thromboly­ sis, or surgical repair or bypass Because collateral flow via other neck vessels is often sufficient, definitive endovas­ cular embolization to prevent distal thrombus migration is one treatment option Nonocclusive dissection is often 472 Part The Ca rd iovascu l a r System treated with anticoagulation and observation alone; many heal spontaneously empties slowly, and has an irregular contour Unlike most congenital aneurysms , the traumatic variety does not have a neck, and is not usually located at a branching I ntracranial Intracranial vascular injuries are less common than are point in the vessel A large lesion can be visualized on CT or M R (Figure 3-33) I n addition to the carotid-cavernous fistula described those of the neck A similar pathological spectrum of inju­ above, traumatic arteriovenous fistulae can involve other ries occurs in these vessels Intracranial arterial injuries ves sels in the neck and head Most are a result of penetrat­ can occur with closed head trauma or penetrating injuries ing injuries , but blunt trauma is responsible for a sub­ Most traumatic intracranial dissections occur in the supraclinoid segments of the carotid arteries, the middle stantial minority of these lesions (Figure 3-34) Potential clinical manifestations of a traumatic arteriovenous fistula cerebral arteries , or the vertebrobasilar arteries Intracranial include pain, a palpable mass, a bruit, pulsatile tinnitus, and dissection can occur with either penetrating or blunt trauma venous distention Neurological manifestations can occur mechanisms Spontaneous intracranial dissections are rare as a consequence of intracranial hemorrhage, shunting of in children The supraclinoid segments ofthe internal carotid blood away from the brain and cord, intracranial venous arteries are prone to stretching during acceleration/decelera­ hypertension, or cord compres sion from enlarged veins tion events, as the vessels are tethered at the anterior clinoid processes and are mobile beyond this point Stretching and/ or a sudden increase in blood pressure because of trauma or ARTERIAL THROMBOSIS exertion may cause enlargement of, and dissection of blood Arterial thrombosis in children is typically associated with into, the normal small gaps in the honeycomb structure of a predisposing factor, such as an indwelling arterial cath­ the internal elastic lamina The intramural hematoma of an eter, hypercoagulable state, trauma, or arterial stenosis intracranial dissection is usually located between the inter­ I nfants with an umbilical arterial catheter have a risk of nal elastica and media, as compared to a location within about the media of most cervical dissections However, the media nal aorta or common iliac vein Potential clinical manifes­ 25% for the formation of thrombus in the abdomi­ and adventitia of intracranial arteries are relatively thin, and tations of aortoiliac thrombosis in neonates include signs there is a greater risk of aneurysmal dilation or rupture if of diminished lower extremity perfusion and hematuria the hematoma extends into the outer layers of the vessel '5° or hypertension due to renal artery involvement However, Traumatic intracranial aneurysms are quite rare Most signs and symptoms are lacking in many infants with are pseudoaneurysms in which there is complete disrup­ umbilical catheter-related thrombosis Complete sponta­ tion of the vessel wall; the cavity of the aneurysm represents neous resolution of thrombosis occurs in most affected excavation of a hematoma Closed head trauma is the most infants ; removal of the umbilical catheter speeds this common precipitating event, with vascular injury produced process Thrombosis in some infants , however, leads to by shearing forces, compression against an unyielding permanent stenosis or occlusion Potential long-term structure (bone, falx, tentorium) , or tearing at the site of a sequelae include hypertension and diminished lower­ fracture Other mechanisms include penetrating injury and extremity growth • 53 surgical procedures The most commonly involved vessels The appropriate position of an umbilical artery cath­ are the internal carotid arteries, the major carotid branch eter is with the tip either superior or inferior to the maj or vessels, and the vertebrobasilar vessels Traumatic aneu­ visceral branches of the abdominal aorta In general, tip rysms of the cavernous segments of the internal carotid positions between arteries are nearly always associated with a basal skull frac­ positions between T6 and Tw are acceptable, as are tip L3 and L5 An umbilical artery cath­ ture Traumatic aneurysms can also arise from peripheral eter follows a distinctive inferior loop as it courses from cerebral vessels and the middle meningeal arteries '5' the umbilicus to the internal iliac artery, before ascending Rupture of a traumatic intracranial aneurysm is associ­ to the left of the midline in the abdomen (see Chapter 6) ated with a high mortality rate Rupture often does not occur The maj or risk o f umbilical artery catheter malposition is until days or weeks after the injury; consequently, the lesion thrombosis of a mesenteric vessel.'54 may initially be clinically silent Some patients complain of Sonography is the imaging modality of choice for An aneurysm of the intracranial portion of the evaluation of the neonate with suspected aortoiliac throm­ headaches internal carotid artery because of a basal skull fracture can bosis, although overlying intestinal gas can interfere with produce a characteristic triad that includes the fracture, ipsi­ the examination Most often, the thrombus appears as lateral visual impairment, and epistaxis This type of aneu­ echogenic material in the lumen The character of the clot rysm can also rupture into the cavernous sinus to produce a varies between patients, and ranges from distention and carotid-cavernous fistula Clinical manifestations ofthis com­ complete occlusion of the lumen, to nonocclusive localized plication include proptosis, abducens and oculomotor nerve clot adherent to the vessel wall, to thin linear intraluminal palsies, facial numbness, a pulsatile bruit, and headache Angiography is the most sensitive technique for the material On Doppler studies , collateral vessels have con­ stant forward flow during diastole because of downstream detection and characterization of a traumatic intracra­ vasodilation; the normal triphasic high-resistance flow pat­ nial aneurysm The aneurysm cavity typically fills and tern is lacking.'55 Chapter The Vascu l a r System A c Figure 13-33 Traumatic intracranial pseudoaneurysm This -year-old child was struck in the head by a falling television A There is a basilar skull fracture (arrows) of the body and right greater wing of the sphenoid bone and the petrous portion of the left temporal bone B Two days later, an unenhanced CT shows an oval suprasellar lesion surrounded POPLITEAL ARTERY ENTRAPMENT SYNDROME Popliteal artery entrapment syndrome is the most com­ mon cause of lower-extremity claudication in young athletic individuals This refers to a developmental abnor­ mality in which the popliteal artery courses between the medial head of the gastrocnemius muscle and the femur, rather than in a normal location lateral to the muscle 473 B D by high-attenuation subarachnoid blood C Imaging with IV contrast confirms that this is a result of an aneurysm D An anterior three-dimensional volume-rendering shows the aneurysm to arise from the left internal carotid artery (Images courtesy Dr Smita Bailey, Phoenix Children's Hospital.) Chronic vascular microtraurna because of the compres­ sion can lead to thrombosis, stenosis, or aneurysm for­ mation Occasionally, there are manifestations of acute lower-leg ischemia as a consequence of thrombosis or embolism Arteriography with the leg in neutral position is often normal in patients with popliteal artery entrapment syn­ drome, unless there is stenosis, thrombosis, or aneurysm Stenosis caused by compression by the gastrocnemius 474 Part The Ca rd iovascu l a r System approximately 30% of these patients, the left innominate vein is present These developmental variables influence the dynamics of blood flow, and are important in determin­ ing the severity of right-to-left shunting when there is an anomalous connection to the left atrium Rarely, a right superior vena cava drains anomalously into the left atrium in conjunction with a normal draining (via the coronary sinus) left superior vena cava.'5 9-' ' A left superior vena cava usually is not detectable on standard chest radiographs unless traversed by an IV cath­ eter In this situation, the catheter descends lateral to the aortic arch, courses obliquely across the midportion of the heart, and enters the right atrium Occasionally, there is slight focal prominence of the left upper mediastinal con­ tour, just above the aortic knob Imaging with CT or M R shows a n enlarged coronary sinus There i s preferential flow though the anomalous vessel if IV contrast is injected via the left arm ( Figure -35) ' 62 Right Superior Vena Cava Anomalies Figure 13-34 Traumatic arteriovenous fistula This 8-year-old child suffered severe multisystem trauma in a motor vehicle incident A lateral image from a vertebral an giogram shows an atrioventricular fistula from the basilar artery muscle is present on arteriographic images obtained with the ankle in active dorsiflexion or plantarflexion M RI allows accurate depiction of the relationship between the popliteal artery and the gastrocnemius muscle in these patients The differential diagnosis of lower extremity clau­ dication in a teenager includes popliteal artery entrapment syndrome, arterial compression by a mass (e.g., osteochon­ droma) , cystic adventitial disease, fibromuscular dysplasia, and arteritis.'s ,ts7 VENOUS DISEASE Rare isolated anomalies of the right superior vena cava include absence, congenital aneurysmal dilation, and anomalous insertion Anomalous insertion of the left bra­ chiocephalic vein into the right superior vena cava inferior to the azygous vein is an occasional finding in children with congenital heart disease The anomalous vein crosses the midline dorsal to the ascending aorta Congenital Interruption ofthe Inferior Vena Cava Interruption of the inferior vena cava with azygous con­ tinuation occurs in approximately half of patients with polysplenia This anomaly occurs only rarely in otherwise normal individuals On standard radiographs, there is dila­ tion of the azygous vein as it enters the superior vena cava Cross-sectional imaging shows lack of the intrahepatic segment of the inferior vena cava, and enlargement of the azygous vein Venous Anomalies Su perior Vena Cava Obstruction Persistent Left Superior Vena Cava Superior vena cava syndrome i s caused b y extrinsic com­ pression or intraluminal occlusion ofthe superior vena cava The most common mechanism is catheter-related thrombo­ sis, often related to malposition of a central venous catheter Another potential cause of vena cava occlusion is compres­ sion by a mediastinal neoplasm, abscess, or hematoma The clinical syndrome consists of edema of the face, neck, upper extremities, and upper portion of the thorax Dilated chest wall veins are usually visible The pericardiophrenic veins serve as important collateral pathways, and become distended in response to superior vena cava obstruction The pericardiophrenic veins may be single or multiple, and drain into the left superior intercostal vein or the brachioce­ phalic veins opposite the jugular vein insertions Inferiorly, they anastomose with the inferior phrenic veins, which drain into the inferior vena cava or renal vein.'63 Persistent left superior vena cava occurs in approximately 0.3% of individuals without heart disease, and in 4.3% of individuals with congenital heart disease.'s8 A left-sided superior vena cava represents a persistent left anterior car­ dinal vein The persistent left superior vena cava most often drains through the oblique vein of Marshall, dorsal to the left atrium, and into the coronary sinus of the right atrium In approximately 8% of patients with a left superior vena cava, drainage occurs into the left atrium; this results in a right-to-left shunt With a large shunt, cyanosis occurs 99rn'fc-MAA scintigraphy provides documentation of the degree of right-to-left shunting in these patients A right superior vena cava is present in 8o% to 90% of individuals with a persistent left superior vena cava In Chapter 13 The Vascu l a r System 475 Figure 3-36 I nferior vena cava thrombosis Figure 13-35 Left superior vena cava There is dense opacification of a persistent left superior vena cava on this coronal reformatted CT image The contrast injection was via a left arm vein Standard chest radiographs of children with superior vena cava syndrome may show enlargement of the azy­ gos vein Underlying pathology in the mediastinum may produce widening A specific diagnosis can be achieved with venography, contrast enhanced CT, or MR Superior vena cava syndrome as a result of acute thrombosis can be treated with catheter directed thrombolysis In some instances, an underlying stenosis is identified on venogra­ phy after recanalization; treatment with angioplasty in this situation may improve venous blood flow and decrease the risk for recurrent thrombosis I nferior Vena Cava Obstruction Occlusion o f the inferior vena cava can b e caused by extrinsic compression or intraluminal thrombus The most common cause of thrombosis is the presence of a catheter Other causes of thrombosis include dehydration, trauma, sepsis, and thrombophilic disorders Although there is effective collateralization in children who suffer vena cava occlusion, various long-term and acute compli­ cations can occur These include pulmonary embolism, renal vein thrombosis, lower extremity edema, hepatic vein thrombosis, and chronic lower-extremity venous hypertension Neoplasms , most commonly Wilms tumor, can extend into the vena cava as tumor thrombus The azygos and hemiazygous systems are important collateral pathways for blood flow in the presence of inferior vena cava obstruction.'55·' 64 A longitudinal sonographic image of a 6-month-old infant with congenital heart disease shows echogenic thrombus completely filling the intrahepatic portion of the inferior vena cava (arrows) The superior aspect of the cava in the region of hepatic vein inflow is patent Sonography of thrombotic inferior vena cava obstruc­ tion usually allows visualization of the intraluminal clot, if there is no intervening intestinal air ( Figure 3-36) Doppler studies, particularly i n infants , provide a n accu­ rate assessment of flow or the lack thereof in the pres­ ence of thrombosis or extrinsic narrowing Doppler evaluation of patent veins below the obstruction shows dampening of normal waveforms Vena cava obstruction is also effectively diagnosed with CT and M R These tech­ niques are particularly useful in older patients with an intraabdominal or retroperitoneal mass Contrast venog­ raphy is the gold standard test for the depiction of the luminal integrity of the vena cava and its major tributar­ ies Dilated paraspinal collateral vessels fill with contrast if there is substantial vena cava stenosis or occlusion Lower- Extrem ity Deep Venous Th rombosis Deep venous thrombosis and pulmonary embolism con­ stitute the clinically important manifestations of venous thromboembolic disease In the pediatric age group the annual incidence is approximately per 1oo,ooo children '6 The pathophysiology of deep venous thrombosis most often involves the formation ofvenous thrombi along valve cusps within the soleal sinuses Typically, the precipitat­ ing event is endothelial injury, which allows exposure of the subendothelium to platelets that bind to the vein wall Subsequently, there is adhesion of fibrin, erythrocytes, and leukocytes, thereby creating a thrombus Slowing or turbu­ lence of blood flow may contribute to endothelial damage and thrombus formation After approximately week, the thrombus becomes increasingly adherent to the vein wall 476 Part The Ca rd i ovascu l a r System Fibroblast infiltration and neovascularization of the throm­ bus lead to scarring and venous valve damage Although eventual recanalization usually occurs, some degree of per­ manent damage to the vein is typical Hypercoagulability is an important precipitating or exacerbating factor in some patients with venous throm­ bosis The possibility of an inherited hypercoagulable condition should be considered in any child who devel­ ops extensive venous thrombosis or thromboembolism A positive family history of venous thromboembolic dis­ ease is also an important indicator in these patients The most common inherited cause of hypercoagulability in the United States is factor V Leiden mutation; this is pres­ ent in nearly 5% of the white American population This mutation is rare among individuals of Asian or African descent Antithrombin deficiency, protein C deficiency, and protein S deficiency are additional causes of hyper­ coagulability, but are much less common Homozygous homocystinuria and dysfibrinogenemia are rare causes of hypercoagulability.'66 The factor V Leiden mutation causes resistance to acti­ vated protein C, thereby leading to increased conversion of prothrombin to thrombin The risk for thromboembolic disease in patients who are homozygous for this mutation is 50 to 100 times that of the general population; heterozy­ gotes have to 10 times the risk Other factors that place individuals at elevated risk for venous thrombosis include trauma, surgery, prolonged immobilization, malignancy, myeloproliferative disorders, the use of oral contraceptives, and pregnancy Antiphospholipid syndrome refers to vascular throm­ bosis in association with the presence of of antiphospho­ lipid antibodies These antibodies are lupus anticoagulant, anticardiolipin, and anti-j3-glycoprotein I Up to half of patients with antiphospholipid syndrome suffer at least episode of venous thrombosis Other potential clinical manifestations include arterial thrombosis, cardiac isch­ emia, renal vein thrombosis , and hematological abnor­ malities such as thrombocytopenia The prevalence of antiphospholipid antibodies increases with patient age.' 67 Deep venous thrombosis of the lower extremities typi­ cally begins in the deep calfveins and propagates superiorly It is associated with symptomatic pulmonary embolism in approximately one-third of untreated patients The usual clinical findings include pain, swelling, and warmth of the affected lower extremity The pain may be exacerbated by dorsiflexion of the foot (the Homan sign) A positive D-dimer assay is a sensitive, but nonspecific, marker for venous thrombosis In most patients with deep venous thrombosis, the clinical findings are nonspecific, and the differential diagnosis includes various other lesions such as cellulitis, lymphedema, and venous insufficiency The most important acute complication of deep venous thrombosis is pulmonary embolism, although approxi­ mately one-half of patients with proven pulmonary embo­ lism not have detectable deep venous thrombosis with sonography.'68 The major long-term sequela of deep venous thrombosis is chronic venous insufficiency, which occurs in approximately 90% of these patients Chronic venous insufficiency may lead to the "postthrombotic syndrome" : chronic limb pain, edema, skin hyperpigmentation, claudi­ cation, and venous stasis ulcers Postthrombotic syndrome is rare in children, but can occur as an adult manifestation of venous disease that began in childhood Sonography is usually the initial imaging study for the evaluation of a patient with suspected deep venous thrombosis A noncompressible, thrombus-filled vein on sonography is diagnostic of venous thrombosis There is temporal variation in the echogenicity of the clot Acute thrombosis is often hypoechoic; lack of compressibility and absence of flow on Doppler are crucial findings for proper diagnosis ( Figu re 3-37) Within a few days, the clot becomes moderately hyperechoic (Figure 3-38) Contrast venography is generally considered the gold standard for the diagnosis of deep venous thrombosis, but is not com­ monly performed because of the availability ofless-invasive diagnostic techniques The American College of Radiology Practice Guide­ lines recommend that the sonographic evaluation for deep venous thrombosis include duplex color and spec­ tral Doppler studies, with compression and augmentation maneuverers The major veins of the leg are sequentially imaged in transverse orientation and inspected for echo­ genic thrombus With real-time observation, the transducer is utilized to intermittently compress the underlying vein With pressure applied, the walls of a normal vein coapt, thereby showing that no clot is present Longitudinal images of the vein using color and spectral Doppler evalu­ ations are then used to evaluate the blood flow characteris­ tics (Figu re 3-39) '6 The evaluation of respiratory phasicity and augmenta­ tion on Doppler studies provides indirect assessment of adjacent vein segments that are not in the field of view Venous occlusion cranial to the level of Doppler evalu­ ation is suggested by a lack of normal respiratory pha­ sicity Assessment of flow augmentation is performed by squeezing the leg (e.g , the calf or distal thigh) at a level below the area of Doppler observation If the tran­ sient increased venous flow is transmitted to the level of evaluation, it suggests that no occlusive thrombus exists between the level of compression and the transducer The augmentation portion of the examination is usually of limited usefulness as it rarely detects clot that has not already been demonstrated by standard images and com­ pression images.'7° CT venography is an additional option for the detec­ tion of deep venous thrombosis, and can be performed in conjunction with CT pulmonary angiography.'7' For the combined study, standard CT pulmonary angiography is performed followed by 5- or 10-mm axial CT images obtained at 4-cm intervals from the diaphragm to the ankles Imaging should be delayed at least minutes after the intravenous inj ection; most investigators con­ sider a 3- to 5-minute delay to be optimal Contiguous Chapter 13 The Vascu l a r System 477 A B Figure 13-37 Deep venous thrombosis A Transverse images without and with compression show distention of the common femoral vein with faintly echogenic thrombus (arrow) B There is no detectable blood flow with color c Doppler Note the hypoechoic appearance of the acute thrombus C A color Doppler image shows lack of flow in the popliteal vein (arrow) The adjacent artery has normal Doppler signal helical acquisition is an option, but results in a higher warfarin Low-molecular-weight heparin is frequently used radiation expo sure than the discontinuous axial tech­ in lieu of unfractionated heparin Anticoagulation with nique The combined CT venography and CT pulmonary oral warfarin is usually continued for at least months angiography examination has high sensitivity for the Longer therapy may be indicated in certain clinical situa­ detection o f l ower-extremity venous thrombosis and pro­ tions, such as the presence of a nonreversible risk factor vides superior evaluation of abdominal and pelvic veins or recurrent disease Anticoagulation therapy is effective in comparison to sonography.'72 The technique offers in preventing recurrence of deep venous thrombosis, advantages over sonography in obese patients or those but it does not directly promote clot lysis and is relatively with severe pain or swelling ineffective in preventing the future development of post­ Treatment goals in patients with acute deep venous thrombotic syndrome There are various treatment tech­ thrombosis include mitigation of acute symptoms, preven­ niques that involve clot lysis or direct thrombus removal, tion of pulmonary embolization, prevention of thrombus with the goals of speeding symptom resolution, diminish­ propagation and recurrence, and the prompt restoration of ing the near-term risk for pulmonary embolism, preserv­ venous patency to help prevent long-term manifestations ing venous valve function, and decreasing the likelihood of venous insufficiency The current standard of care indi­ or severity of chronic venous insufficiency These meth­ cates the use of heparin, usually supplemented with oral ods include surgical thrombectomy, catheter-directed 478 Part The Ca rd iovascu l a r System Patients with excessive extrinsic compression ofan iliac vein may be at an increased risk for deep venous thrombosis The most common form of iliac vein narrowing is com­ pression of the left iliac vein against the fifth lumbar ver­ tebra by the right iliac artery as it crosses anteriorly; this is termed May-Thurner syndrome or Cockett syndrome The involved segment of the vein wall may develop intimal hypertrophy with time, resulting in a propensity for throm­ bosis However, compression of the left common iliac vein by the right common iliac artery is common in asymptom­ atic individuals , and the risk associated with substantial compression for the eventual development of symptoms is unknown This is borne out by a study of asymptomatic adults undergoing helical CT for other indications, dem­ onstrating greater than so% compression in approximately 25% of the patients.'75-'77 Patients with symptomatic left iliac vein compression are usually female Symptoms typically develop during the second through fourth decades of life, often in association with prolonged immobilization or pregnancy Most com­ monly, patients report persistent left-leg edema, with or without other clinical signs of unilateral lower-extremity venous hypertension The clinical presentation is often related to acute deep venous thrombosis in the iliac vein These patients not necessarily suffer extension of thrombosis into the leg veins, and therefore lower-extrem­ ity sonography may be normal or show Doppler manifes­ tations of upstream obstruction A specific diagnosis is achieved with helical CT or MR venography There is focal narrowing of the proximal aspect of the left common iliac vein at the level of the right common iliac artery When present, thrombus is identified as intraluminal material Typically, there are dilated pelvic and lower abdominal col­ lateral veins because of chronic obstruction Treatment A B Figure 13-38 Subacute venous thrombosis There is a mixed echogenic pattern of clot in the greater saphenous vein in this patient with days of symptoms The vessel did not collapse with compression, and there was no visible flow on color Doppler (not shown) thrombolysis (e.g., alteplase) , and percutaneous mechani­ cal thrombectomy.'7J.l74 M ay-Th u rner Syndrome Figure 3-39 Normal duplex Doppler evaluation of the femoral vein A The transverse image without compression shows a normal hypoechoic appearance of the vein ( arrow) The vessel ( arrow) collapses appropriately with compression The adjacent femoral artery remains patent B A longitudinal image with Doppler interrogation of the femoral vein shows normal respiratory phasicity and augmentation Chapter 13 The Vascu l a r System 479 consists of catheter directed thrombolysis (when there is substantial thrombosis) and endovascular stenting.'78 Primary Axillosu bclavian Venous Throm bosis Primary thrombosis of the subclavian andfor axillary veins is distinct from thrombosis associated with venous cath­ eters, trauma, or instrumentation Primary thrombosis at this site is also termed effort thrombosis or Paget-Schroetter syndrome Most patients are young adults or teenagers who develop acute symptoms after strenuous upper extremity exercise Symptoms include upper-extremity pain, swell­ ing, weakness, and limitation of motion The pathophysiology of primary axillosubclavian thrombosis involves venous compression in the upper por­ tion of the thorax The most common site of thrombosis is in the medial aspect of the subclavian vein, where the vessel is compressed as it passes between the clavicle and the subclavius muscle anteriorly and the scalenus muscle posteriorly, or between the costocoracoid ligament and the first rib The axillary vein can be compressed between the pectoralis muscle and the anterior rig cage Some cases appear to be related to hyperabduction of the arm , leading to stretching of the vessel and endothelial injury Primary subclavian vein thrombosis can also result from extrinsic compression by anomalous structures such as a cervical rib, aberrant transverse cervical artery, persistent axillopec­ toral muscle, or anteriorly positioned phrenic nerve '79 This is termed thoracic outlet compression syndrome Venography is usually the best method to diagnose axillosubclavian thrombosis This allows an unequivocal diagnosis, and also provides venous access and a roadmap for therapy Sonography and CT venography represent alternative diagnostic methods Because these patients present acutely, imaging studies show findings of fresh thrombosis Collateral pathways are poorly developed The length of the clot and the severity of obstruction vary between patients The standard therapy for acute primary thrombosis of the axillary or subclavian veins is thrombolysis '8 o This can be accomplished via peripheral IV infusion or, more effectively, by catheter-directed thrombolysis Any residual stenosis after restoration of venous patency can be treated with transluminal angioplasty An underlying extrinsic compression of the vein is sometimes best detected with venography performed with the arm elevated Surgical resection of the first rib or the proximal aspect of the clavi­ cle is often recommended for these patients, particularly if venography shows evidence of extrinsic compression '8' ·1 Anticoagulation can be maintained after successful thrombolysis until surgery is performed Urschel and Razzuk have reported that the best long-term results are achieved with an early diagnosis (less than month), expe­ ditious thrombolytic therapy, and prompt first rib resec­ tion.'8 Other surgical therapies that are occasionally used for these patients include patch angioplasty and venous bypass Central Venous Catheter- Related Central Venous Stenosis The most common cause of central venous thrombosis and stenosis is the presence of a central venous catheter Various factors, some of which are preventable, increase the risk for this complication Improper tip position is probably the most common preventable risk factor; the tip is optimally oriented away from the sidewall and located at the junction of the superior vena cava and the right atrium The use of an internal jugular entry site has a lower throm­ bosis risk than does a subclavian site The risk is dimin­ ished by selecting a catheter with as small a diameter as possible, and with as few lumens as possible Some studies show a lower complication rate for central venous catheters placed by interventional radiological techniques than with surgical cut-downs Standard radiographs serve to assess catheter posi­ tion The detection of thrombus or a stenosis requires venography or sonography (Figure 3-40) Thrombus appears as a filling defect in the vessel, whereas fibrotic stenosis usually has a tapered character Catheter-related central venous thrombosis and stenosis can be treated with catheter-directed thrombolysis and transluminal angioplasty Therapy is indicated for symptomatic indi­ viduals and those patients with an expected need for long­ term or repeated access (chronic total parenteral nutrition or hemodialysis) Figure 3-40 Catheter-related venous thrombosis A right arm venogram shows thrombosis of the medial aspect of the right subclavian vein (arrow) adjacent to a hemodialysis catheter that enters via the internal jugular vein 480 Part The Ca rd iovas cu l a r System Neonates can suffer a variety of complications related to umbilical venous catheters Optimal positioning of an umbilical venous catheter is such that the tip is located at the junction of the inferior vena cava and the right atrium On a properly positioned anteroposterior radiograph, the catheter projects just to the right of the spine and has a slight bend as it courses through the umbilical vein Malposition of the catheter into a portal vein is indicated by an abrupt angulation of the catheter within the liver, usually with the tip directed medially or laterally Extension into a portal vein can be confirmed with sonography Malposition in a portal vein carries the risk of thrombosis Malposition of an umbilical venous catheter in the pulmonary arteries or heart can lead to arrhythmias, thrombosis, perforation, and cardiac tamponade A catheter that has been advanced too far will frequently cross the atrial septum into the left atrium or a pulmonary vein; potential pulmonary com­ plications in this situation include thrombosis, pulmo­ nary edema, and pulmonary infarction Catheter-related thrombosis in the inferior vena cava can lead to renal vein thrombosis.'84-t8 13- Rosenbaum DM, Blumhagen J D Sonographic recognition o f idiopathic arterial calcification of infancy AJR Am J Roentgenol 1986;14 (2):249-25014- Greene J F Jr, Fitzwater JE, Burgess J Arterial lesions associated with neurofibromatosis Am ] Clin Pathol 1974;62(4) :481-487 15 Hoop R, Steinmann B, Valsangiacomo Buechel ER Cardiovasrular findings in 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Systemic Arthritis 9 31 1933 57 Skeletal Dysplasias 19 25 PART 12 THE M USCULOSKELETAL 19 65 19 67 202 2073 211 3 61 Hematological and of the Extremity Soft Tissues 65 Musculoskeletal