John Colford Jr. MD, PhD, MPH

• Professor, Epidemiology

https://publichealth.berkeley.edu/people/john-colford/

Examination in intervals between recurrent internal herniation may be negative or may demonstrate mild degrees of dilatation gastritis diet butter gasex 100 caps order amex, stasis gastritis symptoms in tamil discount gasex online amex, and perhaps edematous mucosal folds that may be falsely attributed solely to adhesions gastritis diet of the stars discount gasex 100 caps otc. The herniated loops may depress the distal transverse colon and indent the posterior wall of the stomach gastritis baby buy discount gasex. Stasis of barium within the hernial contents and mild dilatation of the duodenum may be Clinical Features the clinical manifestations of paraduodenal hernias may range from chronic or intermittent mild digestive 384 17 gastritis diet ����� buy genuine gasex. Note the position of the inferior mesenteric vein and ascending left colic artery in the anterior margin of the neck of the sac. Lateral drawing of the mesentericoparietal fossa of Waldeyer showing its position behind the superior mesenteric artery and small bowel mesentery. Development of a right paraduodenal hernia via the fossa of Waldeyer toward the ascending mesocolon. Note the position of the superior mesenteric artery anterior to the hernia and in the leading edge of the sac. A circumscribed grouping of jejunal loops (arrows) has herniated in to the ascending mesocolon and the right portion of the transverse mesocolon. Not only the intestinal loops, but their mesentery and vessels are also incorporated in to the hernia. These vascular changes can be distinguished from volvulus superimposed upon malrotation. This characteristic reversal of their course indicates the posteromedial border of the hernial orifice, beyond which the intestinal loops herniate. These hernias are fixed to the extraperitoneum and are often adhered to the hernial sac. An abnormal collection of gas is seen in the lesser peritoneal sac between the liver (L) and the stomach (S). There is less gas in the small intestine and within the lesser sac owing to partial spontaneous reduction of the hernia. The foramen may open to some extent when the trunk is flexed, as in the sitting position. Herniation of bowel through the foramen of Winslow accounts for 8% of all internal hernias. Some relief of pain may be achieved with forward bending or the knee­chest position. The fluid levels do not conform precisely to the anatomic recesses of the lesser omental cavity. Compression at this site then leads to distention of the ascending colon and cecum as well. The entrance of the mesenteric vascular pedicle with mesenteric fat is seen at the widened foramen of Winslow (arrow) behind the duodenum (d). A barium enema study reveals obstruction with a tapered point near the hepatic flexure if the herniation contains the cecum and ascending colon. Two other similar, but rare, entities are (a) the intramesosigmoid hernia, which involves a defect of only one of the constituent mesenteric leaves, the separation of which forms the hernial sac15, and. At surgery, 60 cm of viable jejunum incarcerated behind the cecum was reduced, and the hernia orifice was sutured. A dilated inferior mesenteric vein (arrow) appears as a landmark on the edge of the sigmoid mesocolon. A sac-like mass of incarcerated jejunal loops (arrowhead) is located anterior to the left psoas muscle. Barium enema study with reflux shows constriction around the closely approximated afferent and efferent loops (arrows) of the ileum. Blurred and engorged mesenteric vessels converge toward the orifice of the hernial sac. Intrahepatic anastomoses between the biliary tree and bowel for hilar cholangiocarcinoma70,71 may mimic this appearance. These loops are tethered toward the site of volvulus to the left of the level of the falciform ligament; to the right, the thin-walled loops proximal to the obstructing hernia are air-filled and dilated (white asterisks). The heart functions primarily as a pump to circulate blood and supply the body with oxygen and nutrients. The heart is capable of adjusting its pump performance to meet the needs of the body. As needs increase, as with exercise, the heart responds by accelerating the heart rate to propel more blood to the body. As needs decrease, as with sleep, the heart responds by decreasing the heart rate, resulting in less blood flow to the body. The heart consists of: four chambers - two atria that receive incoming blood - two ventricles that pump blood out of the heart four valves that control the flow of blood through the heart an electrical conduction system that conducts electrical impulses to the heart, resulting in muscle contraction. The top of the heart (the base) is at approximately the level of the second intercostal space. The bottom of the heart (the apex) is formed by the tip of the left ventricle and is positioned just above the diaphragm to the left of the sternum at the fifth intercostal space, midclavicular line. The heart is tilted forward and to the left so that the right side of the heart lies toward the front. The average adult heart is approximately 5 (12 cm) long, 3½ (8 to 9 cm) wide, and 2½ (6 cm thick) - a little larger than a normal-sized fist. Heart size and weight are influenced by age, weight, body build, frequency of exercise, and heart disease. The heart surfaces are explained below: anterior - the front posterior - the back inferior - the bottom lateral - the side. Enclosing and protecting the heart is the pericardium, which consists of an outer fibrous sac (the fibrous pericardium) and an inner two-layered, fluid-secreting membrane (the serous pericardium). The outer fibrous pericardium comes in direct contact with the covering of the lung (the pleura) and is attached to the center of the diaphragm inferiorly, to the sternum anteriorly, and to the esophagus, trachea, and main bronchi posteriorly. The myocardium is the thick, middle, muscular layer that makes up the bulk of the heart wall. Chamber thickness is related to the amount of resistance the muscle must overcome to pump blood out of the chamber. The endocardium is a thin layer of tissue that lines the inner surface of the heart muscle and the heart chambers. The serous pericardium is a continuous membrane that forms two layers: the parietal layer lines the inner surface of the fibrous sac and the visceral layer (also called epicardium) lines the outer surface of the heart muscle. Between the two layers of the serous pericardium is the pericardial space, or cavity, which is usually filled with 10 to 30 mL of thin, clear fluid (the pericardial fluid) secreted by the serous layers. The primary function of the pericardial fluid is to provide lubrication, preventing the circulatory system is required to provide a continuous flow of blood to the body. The circulatory system is a closed system consisting of heart chambers and blood vessels. The circulatory system consists of two separate circuits, the systemic circuit and the pulmonary circuit. The systemic circuit is a large circuit and includes the left side of the heart and blood vessels, which carry oxygenated blood to the body and deoxygenated blood back to the right heart. The pulmonary circuit is a small circuit and includes the right side of the heart and blood vessels, which carry deoxygenated blood to the lungs and oxygenated blood back to the left heart. The two circuits are designed so that blood flow is pumped from one circuit to the other. The two upper chambers, the right atrium and the left atrium, are divided by a wall called the interatrial septum. The two lower chambers, the right ventricle and the left ventricle, are divided by a thicker wall called the interventricular septum. The two septa divide the heart in to two pumping systems - a right heart and a left heart. Oxygen and carbon dioxide exchange takes place in the alveoli and arterial (oxygenated) blood returns via the pulmonary veins to the left heart. The left heart then pumps arterial blood to the systemic circulation, where oxygen and carbon dioxide exchange takes place in the organs, tissues, and cells; then venous blood returns to the right heart. Blood flow within the body is designed so that arteries carry oxygen-rich blood away from the heart and veins carry oxygen-poor blood back to the heart. This role is reversed in pulmonary circulation: pulmonary arteries carry oxygen-poor blood in to the lungs, and pulmonary veins bring oxygen-rich blood back to the left heart. The thickness of the walls in each chamber is related to the workload performed by that chamber. Both atria are low-pressure chambers serving as blood-collecting reservoirs for the ventricles. The right ventricular wall is thicker than the walls of the atria, but much thinner than that of the left ventricle. The right ventricular chamber pumps blood a fairly short distance to the lungs against a relatively low resistance to flow. The left ventricle has the thickest wall, because it must eject blood through the aorta against a much greater resistance to flow (the arterial pressure in the systemic circulation). The tricuspid valve consists of three separate cusps or leaflets and is larger in diameter and thinner than the mitral valve. The tricuspid valve directs blood flow from the right atrium to the right ventricle. The chordae tendineae are then attached to papillary muscles, which arise from the walls and floor of the ventricles. As pressure increases during ventricular contraction (systole), the valve cusps close. Backflow of blood in to the atria is prevented by contraction of the papillary muscles and the tension in the chordae tendineae. This may result in a regurgitation of blood from the ventricle in to the atrium, leading to cardiac compromise. S1 is best heard at the apex of the heart located on the left side of the chest, fifth intercostal space, midclavicular line. The pulmonary valve directs blood flow from the right ventricle to the pulmonary artery. It is best heard over the second intercostal space on the left or right side of the sternum. When pressure in the right atrium exceeds that of the right ventricle, the tricuspid valve opens, allowing blood to flow in to the right ventricle. As the right ventricle fills with blood, the pressure in that chamber increases, forcing the tricuspid valve shut and the pulmonic valve open, ejecting blood in to the pulmonary arteries and on to the lungs. The left atrium receives arterial blood from the pulmonary circulation via the pulmonary veins. When pressure in the left atrium exceeds that of the left ventricle, the mitral valve opens, allowing blood to flow in to the left ventricle. As the left ventricle fills with blood, the pressure in that chamber increases, forcing the mitral valve shut and the aortic valve open, ejecting blood in to the aorta and systemic circuit, where the blood releases oxygen to the organs, tissues, and cells and picks up carbon dioxide. Although blood flow can be traced from the right side of the heart to the left side of the heart, it is important to realize that the heart works as two pumps (the right heart and the left heart) working simultaneously. As the right atrium receives venous blood from the systemic circulation, the left atrium receives arterial blood from the pulmonary circulation. Toward the end of ventricular filling, the two atria contract, pumping the remaining blood in to the ventricles. Contraction of the atria during the final phase of diastole to complete ventricular filling is called the atrial kick. In abnormal heart rhythms, the loss of the atrial kick results in incomplete filling of the ventricles, causing a reduction in cardiac output (the amount of blood pumped out of the heart). The ventricles contract simultaneously, ejecting blood through the pulmonary artery in to the lungs and through the aortic valve in to the aorta. There is some individual variation in the pattern of coronary artery branching, but in general, the right coronary artery supplies the right side of the heart and the left coronary artery supplies the left side of the heart. The right coronary artery arises from the right side of the aorta and consists of one long artery that travels downward and then posteriorly. Dominance is a term commonly used to describe coronary vasculature and refers to the distribution of the terminal portion of the arteries. The artery that gives rise to both the posterior descending artery with its septal branches and the posterior left ventricular arteries is considered to be a "dominant" system. The term can be confusing because in most people the left coronary artery is of wider caliber and perfuses the largest percentage of the myocardium. Thus, the dominant artery usually does not perfuse the largest proportion of the myocardium. The left coronary artery arises from the left side of the aorta and consists of the left main coronary artery, a short stem, which divides in to the left anterior descending artery and the circumflex artery. The circumflex artery travels along the lateral aspect of the left ventricle and ends posteriorly. In 10% of the population, the circumflex artery gives rise to the posterior descending artery with its septal branches, terminating as the posterior left ventricular arteries. A left coronary artery with a circumflex that gives rise to both the posterior descending artery and the posterior left ventricular arteries is considered a "dominant" left system. When the left coronary artery is dominant, the entire interventricular septum is supplied by this artery. Table 1-1 summarizes the coronary artery distribution to the myocardium and the conduction system. The right and left coronary artery branches are interconnected by an extensive network of small arteries that provide the potential for cross flow from one artery to the other. These small arteries are commonly called collateral vessels or collateral circulation. If a blockage occurs in a major coronary artery, the collateral vessels enlarge and provide additional blood flow to those areas of reduced blood supply. In other vascular beds of the body, arterial blood flow reaches a peak during ventricular contraction (systole).

Sixty percent of infantile hemangiomas occur in head and neck gastritis diet ������ 100 caps gasex order with mastercard, with superficial strawberry-colored lesions and facial swelling and/or deep lesions gastritis diet foods safe 100 caps gasex, often in parotid gastritis diet ����� order gasex 100 caps free shipping, masticator gastritis symptoms ie 100 caps gasex buy otc, and buccal spaces gastritis sore throat trusted gasex 100 caps. Retropharyngeal, sublingual, and submandibular spaces, along with oral mucosa, are other common locations. Venous vascular malformations are congenital low-flow, nontumorous vascular malformations, have an equal gender incidence, may not become clinically apparent until late infancy or childhood, virtually always grow in size with the patient during childhood, and do not involute spontaneously. Masticator space, sublingual space, tongue, orbit, and dorsal neck are other common locations. Frequently, venous malformations do not respect fascial boundaries and commonly involve more than one deep fascial space. Rapid enlargement of the lesion, areas of high attenuation values and fluid­fluid levels suggest prior hemorrhage. Comments Lymphatic malformations represent a spectrum of congenital low-flow vascular malformations, differentiated by size of dilated lymphatic channels. The parapharyngeal space may be compressed posteromedially by edematous medial pterygoid muscle. Overlying subcutaneous tissues often demonstrate linear stranding or mottled increased attenuation beneath thickened skin. Abscesses may present as uniloculated or multiloculated, ovoid to round mass with air or fluid attenuation centers. Masticator space infection may be accompanied by mandibular osteomyelitis and airway encroachment. Infection may spread in to the suprazygomatic and nasopharyngeal masticator spaces, causing osteomyelitis of the skull base, or extend inferiorly in to the floor of the mouth and upper neck. Masticator space infection originates most commonly from second or third molar tooth infection (parodontal or periapical abscess in the mandible that may demonstrate signs of osteomyelitis) or following dental procedure. Masticator space cellulitis and abscess formation may also occur as a complication of mandibular or zygomatic arch fractures, especially when treated with internal fixation. Infection may also extend to the masticator space from adjacent areas in the neck. Comments Acute osteomyelitis of the mandible most often results from tooth infection, less often from adjacent deep space infection, from dental manipulation, following surgical procedures or penetrating trauma. The lesion often demonstrates marked expansion with thinned or imperceptible cortical shell. Larger lesions with extraosseous extension show extensive soft tissue enhancement mixed with cystic low-density areas. Sharply and smoothly marginated, ovoid to fusiform, homogeneous soft tissue mass along the course of the mandibular division of the trigeminal nerve, isodense to hypodense relative to muscle, with variable, often intense contrast enhancement. Large tumors may undergo cystic degeneration and present with central unenhancing and peripheral enhancing areas. Smooth, corticated enlargement of the bony foramen and canal involved are typical of change from V3 schwannoma. Most commonly manifests from age 30 to 50 y (M F) with a slow-growing painless mass of the affected area. Other benign expansile mandibular masses include odontogenic keratocyst, dentigerous cyst, giant cell reparative granuloma, brown tumor, giant cell tumor, aneurysmal bone cyst, hemangioma, cystic fibrous dysplasia, and ossifying fibroma. Can be multifocal in patients with neurofibromatosis type 2; occurs in patients in their 30s to 40s. About 50% of all neurofibroma cases are sporadic, 50% are associated with neurofibromatosis type 1. Neurofibroma Solitary neurofibroma: Fusiform, ovoid or tubular sharply circumscribed mass, isodense to hypodense relative to cervical cord, smooth and surrounded by fat planes. Differs from schwannoma by an overall lower density that may approach water and conspicuous absence of contrast enhancement. Plexiform neurofibroma: Usually large, diffuse, ill-defined, lobulated, multinodular, low-density mass involving multiple cervical compartments (transspatial), including the masticator space. A typical sign is the target sign with central punctate enhancement surrounded by peripheral low attenuation within multiple tumor nodules. Aggressive fibromatosis (extra-abdominal desmoid fibromatosis, juvenile fibromatosis) Benign soft tissue tumor of fibroblastic origin arising from aponeurotic neck structures. Invasion of the masticator space is usually a late manifestation of carcinoma of the oral cavity, oropharynx, paranasal sinuses, nasopharynx, external auditory canal, or salivary gland. Squamous cell carcinoma and adenoid cystic carcinoma may enter the masticator space by direct extension from the faucial tonsil or retromolar trigone, by way of direct mandibular invasion from the floor of the mouth, or via perineural tumor spread along the mandibular and lingual nerves, which originate from the mandibular division of the trigeminal nerve. They include sarcomas of the mandible or surrounding soft tissues and malignant neurogenic lesions. Soft tissue extension of osteosarcomas involves the masticator space when the angle, ramus, or condyle is the primary site of involvement. The most common masticator space sarcoma in the pediatric population is a rhabdomyosarcoma (first and second decades, rare in adults). Sarcomas Sarcomas of the masticator space present as often large, poorly marginated, heterogeneous masses with intermediate attenuation values and variable, heterogeneous contrast enhancement. Bone production or calcifications are most commonly seen in osteosarcoma, chondrosarcoma, synovial sarcoma, and Ewing sarcoma. Bone fragments within tumors can be present in any masticator space sarcoma with extensive bone destruction of the mandibular, zygomatic arch, or pterygoid plate. Masticator space sarcomas can spread by direct extension in to the middle cranial fossa or in to the pterygopalatine fossa. Tubular mass along the course of the mandibular division of the trigeminal nerve and its primary branches within the masticator space. Extension through the enlarged foramen ovale to involve the gasserian ganglion is not uncommon with this lesion. Ill-defined and infiltrative masticator space mass, isolated or associated with nodal disease, extranodal lymphatic disease (Waldeyer ring), and/or involvement of other extranodal, extralymphatic sites. Metastases typically manifest as ill-defined mandibular destructive soft tissue attenuating masses, often with extension in to surrounding tissues. Malignant schwannoma Malignant nerve sheath tumors arising from the mandibular division of the trigeminal nerve are rare. Usually occurs as a multifocal disease in the setting of known primary tumor (breast, lung, renal, or prostate cancer). Other crystal-associated arthropathies are gout, calcium hydroxyapatite crystal deposition disease, and chronic renal failure. If infected, the wall may thicken and enhance, and the cyst content develops higher attenuation. Solitary, multifocal or transspatial, lobular soft tissue mass, homogeneous and isodense with muscle. Infantile hemangiomas can be well circumscribed, replacing the parotid gland, or can be infiltrative and might involve periparotid structures. First branchial cleft cysts are very rare (only 8% of all branchial cleft remnants). Most commonly seen in middle-aged women with recurrent abscesses around the ear or at the angle of the mandible; unresponsive to treatment. A cutaneous hemangioma may also be found overlying the parotid region as an associated finding. True capillary hemangiomas are neoplastic conditions; typically display a rapid proliferation phase during the first year of life followed by an involution phase with fatty replacement. Infantile hemangiomas are high-flow lesions during their proliferative phase, low-flow lesions in their involutional phase. Sixty-five percent are present at birth; 90% are clinically apparent by 3 y of age, with the remaining 10% present in young adults. In children, the most common location is the posterior cervical space, followed by the oral cavity. In adults, lymphatic malformations are rare, may be posttraumatic, and are more commonly seen in the sublingual, submandibular, and parotid spaces. Other cystic lesions of the parotid gland are sialoceles and dermoid, epidermoid, mucus retention and sebaceous cysts. Infantile hemangioma (capillary hemangioma) Lymphatic malformation (lymphangioma, cystic hygroma). Tend to appear as cystic masses filled with homogeneous low-attenuation material and without contrast enhancement. Cysts usually have thin walls, and most commonly there are multiple intercommunicating cystic components. Infected lesions show higher attenuation, an enhanced thickening of the cyst wall, and infiltration of the adjacent soft tissues. Polycystic disease of the parotid glands Bilateral, markedly enlarged parotid glands with small areas of decreased density producing a mildly inhomogeneous appearance. Inflammatory/infectious conditions Acute viral, bacterial, and calculus-induced parotitis are the most common salivary gland abnormalities. Diffuse swollen, enhancing parotid gland with focal area of rim-enhancing fluid attenuation. There are secondary inflammatory changes in the overlying subcutaneous fat and skin. Intraparotid and periparotid lymph nodes may be involved in the inflammatory reaction. The abscess may extend in to the masticator and parapharyngeal spaces or upper neck. Other viral etiologies are Coxsackie viruses, parainfluenza viruses, influenza virus type A, herpes virus, echovirus, and choriomeningitis virus. Most common bacterial organisms are Staphylococcus aureus (50%­90%), Streptococcus viridans, Haemophilus influenzae, Escherichia coli, anerobes, and Streptococcus pneumoniae. Acute suppurative parotitis and abscess (continues on page 319) Parotid Space Lesions 319 Table 8. Often with coexistent diffuse homogeneous cervical lymphadenopathy and adenoidal, faucial, and lingual tonsillar hypertrophy. Unilateral, diffusely enlarged parotid gland, often slightly denser than normal, with or without dystrophic calcifications. Cystic changes in the gland and dilated Stensen duct with or without calculi may be evident. Chronic inflammatory disease of the salivary glands can result in loss of parenchymal as well as fatty matrix and consequent shrinkage of the gland. Unilateral or, less commonly, bilateral diffuse enlargement of the parotid gland, with multiple small nodular "foamy" densities distributed throughout the gland or a solitary mass. Comments Lymphoepithelial cysts in the parotid gland may be secondary to incomplete ductal obstruction by periductal lymphocytic infiltration or arise within the intraparotid lymph nodes. Chronic recurrent sialadenitis is clinically characterized by recurrent diffuse or localized painful swelling of the salivary gland. These diseases may affect the intraparotid or juxtaglandular lymph nodes or the gland parenchyma directly. Parotid sialogram reveals a normal central duct system and numerous globular collections of contrast material, 1 to 3 mm in diameter, uniformly scattered throughout the gland. Comments Sjögren syndrome is an autoimmune disease with chronic inflammation of the exocrine glands that occurs either alone (primary Sjögren syndrome) or with any of several connective tissue diseases (secondary Sjögren syndrome). The adult form predominantly affects women over 40 y of age with keratoconjunctivitis sicca, xerostomia, and xerorhinia. Associated with clearly increased risk of developing non­Hodgkin lymphoma in intra- or extraparotid sites. Benign mixed tumors are the most common salivary tumors to have calcifications or ossifications in the tumor matrix. A large, deep, pear-shaped mass may widen the stylomandibular notch and displace the parapharyngeal space anteromedially. Usually located in the posterior aspect of the tail of the parotid gland; appear as round to ovoid, smoothly marginated, strong and homogeneously enhancing soft tissue masses, measuring 2 to 4 cm, that contain no calcification. Angiolipoma is similar to ordinary lipomas except for associated angiomatous proliferation. Tend to occur along the facial nerve as well-defined, fusiform soft tissue mass with varying degrees of contrast enhancement. Some of the parotid facial nerve tumors may be extensive, multilobulated, with areas of cystic formation and inhomogeneous enhancement. Intraparotid, most often ovoid, well-demarcated, heterogeneous, low-density mass, solitary or multiple. Plexiform neurofibroma shows a usually large, illdefined, more infiltrative, heterogeneous mass with a mixed density pattern. Benign mixed tumor follows the rule of 80s: 80% of parotid tumors are benign; 80% of benign parotid tumors are benign mixed tumors; 80% of parotid benign mixed tumors are in the superficial lobe; 80% of salivary gland benign mixed tumors are parotid; 80% of untreated benign mixed tumors remain benign. Most common in Caucasians, rare in African Americans (M:F 1:2; age range 30­60 y). Rare tumor that occurs in the major salivary glands, exclusively in adults older than 50 y. Lipomas represent 1% of all parotid tumors, invade deeply in to the intraglandular septa, and occur in all age groups. Oncocytoma Lipoma Facial schwannoma Facial schwannomas are usually solitary and manifest as a slowly enlarging, painless mass. These tumors can occur at any age, most commonly between 20 and 50 y, with a female predominance. Neurofibroma may arise from the facial nerve trunk or its branches and may therefore lie within the parotid gland. Multiple or plexiform neurofibromas are seen in patients with von Recklinghausen disease. High-grade carcinomas demonstrate infiltrating margins, particularly when associated with adjacent soft tissue or muscle invasion and an inhomogeneous aspect. Malignant adenopathy is often present (levels 2 and 5; intra- and periparotid nodes). It represents 10% of all salivary gland tumors and 30% of all salivary gland malignancies.

The dorsal mesogastrium continues to grow after the stomach completes its rotation gastritis bacteria 100 caps gasex purchase with visa. This ongoing growth forms a duplication of the dorsal mesogastrium folding upon itself anterior to the transverse colon and small intestine gastritis flare up diet gasex 100 caps order with amex. Later gastritis symptoms vs gallbladder buy gasex with a visa, the four leaves fuse and are suspended from the greater curvature of the stomach as the greater omentum gastritis omeprazole 100 caps gasex otc. A fusion also occurs as the dorsal mesogastrium courses over the transverse colon and continues posterior to the posterior abdominal wall gastritis foods generic gasex 100 caps buy. The portion from the transverse colon to the posterior abdominal wall fuses with the transverse mesocolon. The right portion of transverse mesocolon fuses and covers the duodenum forming the duodenocolic ligament. The mesentery of the small intestinal loop undergoes dramatic changes as the small intestine elongates faster than the coelomic cavity grows. The completed rotation and reentry of the small bowel and its mesentery occur by the 12th week. From its narrow origin, the mesentery of the intestine spreads out resembling a fan. The intestine is freely movable on the mesentery until the 14th week, when the secondary fusions affix portions of gut, forming new lines of attachment. The root of the small intestine mesentery is in continuity with the attachment of the transverse mesocolon in the left upper abdomen and the peritoneum overlying the ascending colon on the right side. Pelvic Specialization the genital system in its early development is the same for males and females. This enfolding eventually forms the fallopian tube, which is open to the greater peritoneal cavity cranially and fuses with the uterovaginal primordium distally to form the uterus and upper vagina. This elongates and becomes the suspending mesentery of the uterus, the broad ligament, which is in continuity with the pelvic side wall. The blood vessels, lymphatics, and nerves supplying the female pelvic organs course from the extraperitoneal space to organs within this ligament. Three-dimensional drawing of the peritoneal attachments of the ventral and dorsal mesenteries to the abdominal wall. The round ligament is embedded in the broad ligament and attaches to the superior corner of the uterus. The round ligament extends through the inguinal area to insert in to the labrum majus. The formation of the broad ligament and its specialized ligaments provides the abdominopelvic continuum of the subperitoneal space. This ligament forms as an extension of the lateral pelvic extraperitoneum to the suspended female organs providing the avenues for their blood, lymphatic, and nerve supply. Thus, the subperitoneal space provides continuity of the extraperitoneum with the female pelvic organs via the broad ligament as well as continuity of the pelvis and the abdomen. The suspending dorsal mesentery of the distal foregut and midgut undergoes considerable elongation as the stomach and duodenum go through their complex rotation. As the dorsal bulge of the stomach increases, it carries the mesentery along with it, to the left side of the abdomen. Eventually, the region is enclosed on the left by the surrounding organs and mesenteries, and the only normal aperture is on the right, the epiploic foramen (foramen of Winslow). The elongated dorsal mesogastrium doubles back on itself from the greater curvature of the stomach. Occasionally, this fusion does not take place, resulting in an extension of the lesser sac between these folds. Early in development, the gastrointestinal tract elongates and herniates in to the yolk sac. The ovaries are incorporated within the broad ligament as they are suspended in to the body cavity. The midgut is that segment elongating proximal to the vitelline duct, the prearterial limb. To accommodate the length of the small bowel, the small bowel forms a serpentine pattern, an appearance it maintains in to adulthood. When the body cavity has enlarged sufficiently, the herniated bowel returns (by the 12th week). The postarterial limb is forced to the periphery so that the right colon courses anterior to the superior mesenteric artery to the right upper quadrant. The suspending mesenteries of the ascending and descending colon then fuse with the posterior abdominal wall. Asymmetric cecal growth due to the ileocecal valve inhibiting growth on its side moves the appendix to the same side as the ileocecal valve. Hepatobiliary System the hepatobiliary structures develop from a diverticulum off the ventral aspect of the distal foregut. The anterior portion of the mesogastrium connects the spleen and stomach, the gastrosplenic ligament. This portion of the dorsal mesogastrium partially fuses with the posterior abdominal wall over the left kidney. It is formed by cells of neural crest origin arising from the sympathetic ganglionic masses that will form the celiac ganglion and mesenteric ganglion. As the liver enlarges, the majority is peritonealized (covered by visceral peritoneum), but the posterior aspect retains contiguity with the diaphragm as the bare area of the liver. The pronephros is formed by the end of the 3rd week and involutes by the 5th week. The mesonephros forms from the intermediate mesoderm and is the first functioning excreting duct of the fetus. Some segments persist (Wolffian duct) and develop in to portions of the genital system: in males to the vas deferens, epididymis, and efferent ductules of the testes and in females in to the epoophoron and paroophoron. The metanephros begins development in to the kidneys and ureters by the 5th week of gestation. The uncinate process and inferior portion of the pancreatic head are derived from the ventral bud. The body, tail, and superior portion of the head develop from the dorsal mesentery of the duodenum. The ventral pancreas rotates an additional 1808 and eventually lies in the concavity of the duodenum. The fusion of the dorsal mesoduodenum gives the pancreas its extraperitoneal location, within the pancreaticoduodenal compartment of 22 2. The development of the metanephros is accompanied by a change in its position and orientation. There is migration of the metanephrosis with fetal growth from L2­L3 at 3 months to T12­ L1 at birth. As the kidney migrates cephalad, more proximal portions of the aorta progressively supply it until the definitive renal arteries result in the renal arteries. These ventral ligaments of the pelvis and lower abdomen subdivide the ventral portion of the peritoneal cavity. The coelomic cavity is transformed in to the peritoneal cavity, the largest lumen in the human body, with its recesses and perivisceral spaces. Its discrete features of anatomy determining the spread and localization of disease processes are detailed and illustrated in Chapter 4. It is emphasized that the extraperitoneum is circumferential in the abdomen and pelvis. Thus, the classical extraperitoneal spaces and the suspended abdominal and pelvic organs are interconnected as they all reside within the single 23 the Fundamental Concept of the Subperitoneal Space the subperitoneal space is conceptualized as one compartment lying deep to the peritoneal lining of the abdomen and pelvis. Drawing emphasizes the global continuity of the subperitoneal space (stippled area). The extraperitoneal space extends in to the ligaments and mesenteries of the abdomen and pelvis, thus defining the subperitoneal space. The peritoneum (thick, black inner line) covers the extraperitoneum in its entirety and reflects to encase the ligaments and mesenteries. Note the continuity of the subperitoneal space within the fascial planes formed by the renal fascia in the abdomen and the umbilicovesical fascia in the pelvis. Significantly, once disease enters the subperitoneal space, it can spread in any direction and extend in to any solid or hollow organ as it follows the blood vessels, lymphatics, and nerves. The ligaments and mesenteries of the abdomen and pelvis are identified by their adjacent organs and/or the vessels coursing within them. The gastrohepatic ligament extends between the left lobe of the liver and lesser curvature of the stomach and contains the left and right gastric arteries and veins. The free edge of the gastrohepatic ligament is the hepatoduodenal ligament, which contains the portal triad and parabiliary plexus. The gastrohepatic ligament extends cephalad as the falciform ligament to the anterior abdominal wall, separating the medial and lateral segments of the left the Subperitoneal Space 25. In this way, pathways are provided interconnecting the liver, gallbladder, duodenum, stomach, pancreas, and distal esophagus. Dorsal Mesogastric Derivatives the dorsal mesogastrium gives rise to a series of ligaments interconnecting the organs in the left upper abdomen. The splenorenal ligament extends laterally to the splenic hilum as the gastrosplenic ligament. The gastrosplenic ligament resides between the posterolateral wall of the stomach and spleen and contains the splenic vessels, short gastric arteries and veins, and proximal portion of the left gastroepiploic artery and vein as they course along the body of the stomach. This ligament is identified connecting the greater curvature of the stomach and anterior surface of the transverse colon. The portion of the gastrocolic ligament on the right is identified by the right gastroepiploic artery, which is a branch of the 26 3. Clinical Anatomy of the Abdomen gastroduodenal artery coursing anterior to the head of the pancreas. This artery continues cephalad in the fused portion of the gastrocolic ligament and transverse mesocolon and then along the greater curvature of the stomach within the gastrocolic ligament. The right gastroepiploic vein joins the middle colic vein forming the gastrocolic trunk. This network of ligaments in the left upper abdomen establishes local continuity between the stomach, spleen, pancreas, and transverse colon, and global continuity with the entire abdomen as extensions of the subperitoneal space. Modest amount of adipose tissue deep to the right and left crura establishes continuity of the extrapleural space of the thorax with the subperitoneal space of the abdomen via the esophageal hiatus. The small intestinal mesentery is fan shaped with its undulating ruffles suspending approximately 600­700 cm (20­22 ft) of small bowel (jejunum and ileum). The small intestine mesentery is an investment of the extraperitoneum that continues from its reflection from the posterior parietal peritoneum. The line of attachment of the root of the small intestine mesentery passes from the duodenojejunal junction, where it is in continuity with the root of the transverse mesocolon, over the third portion of the duodenum, obliquely across the aorta and inferior vena cava, the right ureter, and psoas muscle, to the right iliac region. The connective tissue within this region of the mesentery blends and connects with the subperitoneal tissue in the extraperitoneum of the right posterior lower abdomen. Continuity of the ventral mesogastrium as the lower portion of the gastrohepatic ligament continues in to the hepatoduodenal ligament (small arrowhead). The falciform ligament is in continuity with the hepatoduodenal ligament (large arrowhead). Continuity of dorsal mesogastrium as the splenorenal ligament (large arrow) continues in to the gastrosplenic ligament. The length of the intestinal border to an extent approximately 40 times that of its root is brought about by its unique frilled nature. Thus, the root of the small bowel mesentery interconnects the upper abdomen and the right lower abdomen, which in turn connects with the extraperitoneum of the abdomen and pelvis. The small intestinal arteries arise from the left side of the superior mesenteric artery. Those arising above the ileocolic artery course in the jejunal mesentery, those distal to the ileocolic artery in the ileal mesentery. The transverse mesocolon is identified by the branches of the middle colic artery and vein. The middle colic vein joins the right gastroepiploic vein in the fused transverse mesocolon and gastrocolic ligament, and drains in to the superior mesenteric vein anteriorly as the gastrocolic trunk. It is identified by its position between these organs and the contained middle colic vessels. On the left, lateral extension of the transverse mesocolon is to the side wall at T11, constituting the phrenicocolic ligament. The ileocolic vessels course near the base of the small intestine mesentery anterior to the third portion of the duodenum near the midline to the right iliac fossa. The right middle colic vessels branch from the superior mesenteric vessels to the right and course within the ascending mesocolon. The left colic artery and vein extend from the marginal vessels of the descending colon and identify the descending mesocolon. These portions of the subperitoneal space are depicted in continuity with the root of the small intestine mesentery identified by the superior mesenteric vein (V). Fluid within the peritoneal cavity outlines the small intestine mesentery (large arrow) and the transverse mesocolon (small arrow). Note the infiltrated greater omentum extending caudad from the transverse colon (T). The distal sigmoid mesocolon and upper mesorectum are identified by the superior rectal vessels. The subperitoneal space within the cardinal ligaments blends laterally beneath the parietal peritoneum overlying the pelvic muscles and continues to follow the course of the major pelvis vessels anteriorly. The broad ligament encloses the subperitoneal space that surrounds the suspended female pelvic organs and interconnects them with the lateral pelvic wall. Central and Lateral Continuity the lateral pathways of communication of the subperitoneal space between the abdomen and the pelvis are formed by the convergence of the pararenal spaces to form the infrarenal space, caudal to the perirenal space, which descends in to the extraperitoneum of the pelvis. On the right side, the junction of the root of the small intestine mesentery in the right lower quadrant with the subperitoneal space at the proximal ascending colon provides continuity with all the abovedescribed connections of the root of the small intestine mesentery in addition to the continuity with the right lateral abdomen and right lateral pelvis.

Disk herniation/extruded disk fragment­ herniation/extrusion: Herniated fragment of nucleus pulposus without connection to disk of origin gastritis or gallbladder quality 100 caps gasex. Disk herniations can be midline chronic gastritis remedies buy gasex 100 caps without prescription, off-midline in lateral recess gastritis diet 1200 purchase 100 caps gasex with amex, posterolateral within intervertebral foramen uremic gastritis symptoms order gasex 100 caps without prescription, lateral gastritis diet �� gasex 100 caps purchase otc, or anterior. Can extend superiorly, inferiorly, or both directions; with or without associated epidural hematoma, with or without compression or displacement of thecal sac and/or nerve roots in lateral recess and/or foramen. Disk herniations can occur in to the end plates of vertebral bodies, Schmorl nodes. Disk herniation/extrusion: Disk herniation in which the head of the disk herniation is larger than the neck on sagittal reconstructed images. Disk herniation/extruded disk fragment: Disk herniation that is not in contiguity with disk of origin. Sagittal image shows an osteosclerotic and osteolytic metastatic lesion, as well as a pathologic fracture involving the T1 vertebral body. Epithelial-lined tube extending internally from the dorsal skin of lower back, with or without extension in to spinal canal through the median raphe or spina bifida, with or without associated dermoid or epidermoid in spinal canal (50%). Well-circumscribed, spheroid or multilobulated, intradural extramedullary or intramedullary lesions, usually with low to intermediate attenuation. Well-circumscribed, spheroid or multilobulated, intradural or extramedullary lesion with low to intermediate attenuation No contrast enhancement. Tarlov cysts (perineural cysts) Dorsal dermal sinus Abnormality resulting from lack of normal developmental separation of superficial and neural ectoderm. Nonneoplastic congenital or acquired ectodermal inclusion cystic lesions filled with lipid material, cholesterol, desquamated cells, and keratinaceous debris; usually mild mass effect on adjacent spinal cord or nerve roots; adults: M F; with or without related clinical symptoms. Nonneoplastic extramedullary epithelial-inclusion lesions filled with desquamated cells and keratinaceous debris; usually mild mass effect on adjacent spinal cord and/or nerve roots. May be congenital (with or without associated with dorsal dermal sinus, spina bifida, and hemivertebrae) or acquired (late complication of lumbar puncture). Results from developmental failure of separation the notochord and foregut; observed in patients older than 40 y. Location: thoracic cervical posterior cranial fossa craniovertebral junction lumbar; usually midline in position and often ventral to the spinal cord. Neoplasm and other masses Ependymoma Intradural, circumscribed, lobulated lesions at conus medullaris and/or cauda equina/filum terminale, rarely in sacrococcygeal soft tissues; lesions usually have intermediate attenuation, with or without hemorrhage. Ependymomas at conus medullaris or cauda equina/filum terminale usually are myxopapillary type, thought to arise from ependymal glia of filum terminale. Usually are slow-growing neoplasms associated with long duration of back pain, sensory deficits, motor weakness, and bladder and bowel dysfunction; with or without chronic erosion of bone with scalloping of vertebral bodies and enlargement of intervertebral foramina. Encapsulated neoplasms arising asymmetrically from nerve sheath; most common type of intradural extramedullary neoplasms; usual presentation in adults with pain and radiculopathy, paresthesias, and lower extremity weakness. Meningioma Extra- or intradural extramedullary lesions, intermediate attenuation, with contrast enhancement, with or without calcifications. Spheroid or lobulated intradural-extramedullary lesion with intermediate attenuation, with or without tubular vessels, with contrast enhancement, with or without foci of hemorrhage; usually located in region of cauda equina and filum terminale. Single or multiple nodular lesions and/or focal or diffuse abnormal subarachnoid disease along pial surface of spinal cord. Comments Unencapsulated neoplasms involving nerve and nerve sheath; common type of intradural extramedullary neoplasms often with extradural extension; usual presentation in adults with pain and radiculopathy, paresthesias, and lower extremity weakness. Paragangliomas are neoplasms that arise from paraganglion cells of neural crest origin and usually occur at carotid body, jugular foramen, middle ear, and along vagus nerve. Disseminated tumor in the subarachnoid space (leptomeninges) usually is associated with significant pathology (neoplasm vs inflammation and/or infection). Primary neoplasms commonly associated with disseminated subarachnoid tumor include primitive neuroectodermal tumors. Teratoma Circumscribed lesions with variable low, intermediate, and/ or high attenuation; with or without contrast enhancement. May contain calcifications and cysts, as well as fatty components that can cause chemical meningitis if ruptured. Neurosarcoid results in granulomatous disease in the leptomeninges, producing similar patterns of subarachnoid enhancement. Adhesive arachnoiditis is a chronic disorder that results in aggregation of nerve roots within the thecal sac or adhesion of nerve roots to the inner margin of the thecal sac. Can result from prior surgery, hemorrhage, radiation treatment, meningitis, or myelography (pantopaque). Chronic inflammatory disorder that results in metaplastic ossification changes in the subarachnoid space; usually occurs in the thoracic and lumbar regions. Pyogenic arachnoiditis can result from surgical complication, extension of intracranial meningitis, epidural abscess, vertebral osteomyelitis, or immunocompromised status. Coronal image shows multiple paraspinal neurofibromas in a patient with neurofibromatosis type 1. Myelographic images show multiple intradural nodular lesions from drop metastases. Pathologic changes considered to be a combination of demyelination and arterial or venous ischemia. Other noninfectious inflammatory diseases involving the spinal cord Sarcoid Intramedullary lesion or multiple lesions in spinal cord. Organisms reported to result in spinal cord abscess or nonviral myelitis include Streptococcus milleri, Streptococcus pyogenes, Mycobacterium tuberculosis, atypical mycobacteria, syphilis, Schistosoma mansoni, and fungi (Cryptococcus, Candida, and Aspergillus); seen in immunocompromised patients. The most common type of parasite to involve the spinal cord is Toxoplasma gondii in immunocompromised patients. Associated with rapid decline in neurologic function related to site of lesion in spinal cord. Lesions with irregular margins that can be located in the spinal cord (white and/or gray matter), dura, or both locations. Not usually associated with mass effect unless there is recent hemorrhage or venous occlusion. Hydromyelia refers to distention of the central canal of the spinal cord (lined by ependymal cells). Sagittal (a), coronal (b), and axial (c) postmyelographic images show diffuse expansion of the spinal cord secondary to a syrinx. Anaplastic astrocytomas account for most of the rest, glioblastomas account for only 1%. Intramedullary ependymomas involving the upper spinal cord often are cellular or mixed histologic types, whereas ependymomas at the conus medullaris or cauda equina usually are myxopapillary. Usually are slow-growing neoplasms associated with long duration of neck or back pain, sensory deficits, motor weakness, bladder and bowel dysfunction. May extend inferiorly from lesion in cerebellum, ganglioglioma (contains glial and neuronal elements), ganglioneuroma (contains only ganglion cells), gangliocytoma (contains only neuronal elements). Usually intramedullary lesion but occasionally extends in to the intradural space or extradural location. Rare intramedullary lesions that can present with pain, bladder or bowel dysfunction, and paresthesias. Location: cervical spinal cord (45%), thoracic spinal cord (35%), lumbar region (8%). Usually solitary lesions, occasionally multiple; spread hematogenously via arteries or direct extension in to leptomeninges with invasion of pial surface or central canal of the spinal cord. Ependymoma Intramedullary circumscribed expansile lesion, often midline/central location in spinal cord. Intramedullary locations: cervical spinal cord (44%), both cervical and upper thoracic spinal cord (23%), thoracic spinal cord (26%). Intramedullary lesion or superficial lesions on the spinal cord, with or without leptomeningeal tumor nodules. Sagittal (a) and axial (b) postcontrast images show a tiny enhancing hemangioblastoma on the pial surface of the spinal cord in this patient with von Hippel­Lindau disease (arrows). Normal muscles are of soft tissue density and are separated from each other by fatty septa. In many muscle diseases, the muscle fibers become necrotic and degenerate or are replaced by fat and connective tissue. Fatty replacement of muscle may be complete and homogeneous or incomplete and inhomogeneous, but it is not characteristic for a specific disease. It is observed with muscular dystrophies, neuropathies, ischemias, and metabolic and systemic myopathies, as well as idiopathically. It allows definition of the exact dimensions of a lesion and its relationship to nearby neurovascular structures and bone. Besides lipomas and cysts, other lesions may contain adipose tissue or fluid, respectively. The poorly defined border on the posteroinferior border (arrowheads) indicates that the cyst is ruptured. Differentiation of actual invasion of neighboring structures such as the neurovascular bundle and bone from simple distortion and pressure defects by the adjacent mass is not always feasible. Metabolic (metastatic) calcifications are associated with a disturbance in calcium/phosphorous metabolism, resulting in the deposition of calcium in normal tissues. Such conditions include renal osteodystrophy (less commonly, primary hyperparathyroidism), hypoparathyroidism, hypervitaminosis D, milk­alkali syndrome (prolonged excessive intake of milk and alkali for heartburn in peptic ulcer disease, often associated with renal insufficiency), sarcoidosis, and processes associated with massive bone destruction. Dystrophic calcifications represent calcium deposits in damaged tissue without metabolic derangement. They are associated with traumatic, ischemic, neuropathic, infectious, and neoplastic conditions. Besides calcification of a hematoma, other traumatic causes include sequelae of previous surgery, irradiation, and thermal injuries. Subcutaneous fat necrosis resulting in calcification of the subcutaneous adipose tissue is found with pancreatic disorders, Weber­Christian disease (nonsuppurative nodular panniculitis with subsequent necrosis and fibrosis in the subcutaneous fat and all visceral adipose tissues), and vascular insufficiency, in which calcified varicose veins or arteriosclerotic arteries are frequently also present. Soft tissue calcifications are also found in a variety of parasitic infestations, such as cysticercosis and echinococcosis. In malignant neoplasms, such as synovial sarcoma, and less commonly in other soft tissue sarcomas, such as malignant fibrous histiocytoma, leiomyosarcoma, and rhabdomyosarcoma, both necrosis and hemorrhage may lead to secondary calcifications. Extraskeletal chondrosarcomas and osteosarcomas may demonstrate irregular, poorly marginated calcific deposits, whereas calcifications in their benign counterparts (chondromas and osteomas) tend to be well defined. Irregular calcifications about the trochanter Phleboliths are dystrophic calcifications in organizing thrombi. They present as circular or elliptical calcifications with radiolucent centers measuring 1 cm in their longest diameter. They are quite characteristic but may occasionally be simulated by extraarticular (tenosynovial) chondromatosis, cysticercosis, and the calcified fatty deposits in Ehlers­Danlos syndrome (connective tissue disease with joint hyperextensibility and multiple musculoskeletal and other anomalies). Idiopathic soft tissue calcifications are limited to the connective tissue disorders. In the latter conditions, the calcifications Metabolic (metastatic) calcifications Hyperparathyroidism (primary; more commonly secondary, due to chronic renal disease; and, rarely, ectopic, caused by lung or kidney tumors) Hypoparathyroidism Hypervitaminosis D Williams syndrome (idiopathic hypercalcemia of infancy) Milk­alkali syndrome Sarcoidosis Conditions associated with massive bone destruction. In tumoral and circumscript calcinosis, calcium­fluid levels are sometimes observed. Soft tissue ossification is diagnosed when cancellous bone is surrounded by cortical bone. Because only a limited number of diseases presenting initially with soft tissue calcification may eventually progress to soft tissue ossification, the differential diagnosis of the latter is accordingly smaller. It is characterized by a peripheral ring of ossification ("eggshell" calcification) surrounding a more lucent center. In the absence of a history of trauma, the same lesion is often referred to as a pseudomalignant osseous tumor of soft tissue. A parosteal osteosarcoma presents as a radiodense lesion attached in a sessile fashion to the external cortex. In contrast to myositis ossificans, ossification of the tumor proceeds from the base of the lesion to its periphery. An osteochondroma is composed of a medullary cavity that is contiguous with the bone from which it arose and is surrounded by sharply defined cortical bone and a thin cartilaginous cap with varying degrees of calcifications. Soft tissue ossifications with a predilection for the para-articular regions are found in melorheostosis, a condition in which the bony alterations are diagnostic. Heterotopic bone formation occurs commonly after surgery, especially after insertion of hip prostheses and in a variety of neurologic disorders, especially paraplegia. Venous insufficiency and thermal injuries may lead to soft tissue ossification in the extremities. Myositis ossificans progressiva (fibrodysplasia ossificans progressiva) is a rare cause of soft tissue ossification associated with anomalies and hypoplasias of the great toes and thumbs, exostoses, and progressive fusion of primarily the axial skeleton. Gas in this life-threatening condition is commonly produced by a mixture of both aerobic and anaerobic bacteria. An ossified parosteal sarcoma (a) is attached in sessile fashion to the outer table of the skull. The medullary cavity of an osteochondroma (b, arrow) is contiguous with the femur from which it arose and surrounded by sharply defined cortical bone. Cellulitis, a streptococcal or, less commonly, a staphylococcal infection, can be differentiated from necrotizing fasciitis by the predominant involvement of the subcutaneous fat and superficial fascial tissues and the absence of soft tissue gas. Pyomyositis typically affects otherwise healthy children and young adults, especially in tropical regions, but it is also recognized with increasing frequency in malnourished and immunodeficient patients. Gas bubbles are occasionally seen in this intramuscular abscess caused by a Staphylococcus aureus infection in about 90% and by a streptococcal infection in the remaining cases. Soft tissue contamination with gas gangrene occurs in devitalized tissues in which the arterial blood supply has been compromised.

Normal axillary lymph nodes are oval shaped gastritis diet education purchase genuine gasex line, measure 10 mm in size gastritis diet india cheap 100 caps gasex free shipping, and contain a central fatty hilus gastritis foods cheap gasex 100 caps mastercard. Lymph nodes exceeding 2 cm in diameter are indicative of metastatic or lymphomatous disease gastritis symptoms hunger buy discount gasex 100 caps online. A common origin of axillary and parasternal (internal mammary) lymph node metastases is breast carcinoma gastritis diet ������� generic 100 caps gasex visa. As a general rule, the ratio between smallest and largest lymph node diameter should be 0. Any ratio approaching 1-and thus corresponding to a rounding of the node-is highly suspicious of inflammatory, infectious, or metastatic affection. Lack of central fat is likewise pathognomonic, but it may be observed in asymptomatic persons. The diaphragm is a large, dome-shaped muscle that incompletely divides the thorax from the abdomen. The diaphragmatic crura are tendinous structures arising from the anterolateral surface of the upper lumbar spine. The right crus is larger and longer than the left crus and originates from the first three lumbar vertebral bodies, whereas the left crus arises from the first two lumbar vertebrae. The nodular appearance of the diaphragmatic crura should not be mistaken for enlarged retrocrural lymph nodes, which normally are small (6 mm in diameter). They tend to be rather large and may contain omental or retroperitoneal fat, bowel, spleen, liver, kidney, stomach, and pancreas. Morgagni hernias are rare and usually right-sided; tend to be small; occur through an anteromedial parasternal defect; may contain liver, omentum, or bowel; and are often associated with a pericardial defect. Over 90% of these hernias are located on the left side, usually in the central or posterior portion of the diaphragm. Omentum, stomach, bowel, spleen, and kidney may herniate through the ruptured diaphragm; thus, strangulation is a common complication. A diaphragmatic eventration is caused by a congenitally weak diaphragm with cephalad displacement of the corresponding abdominal content. The eventration occurs more frequently on the right side, where it involves the anteromedial portion of the diaphragm. In this situation, the liver is displaced superiorly and should not be confused with a peripheral pulmonary or pleural mass. On the left side, the eventration usually involves the entire hemidiaphragm and mimics diaphragmatic paralysis. Concomitant pneumopericardium (arrow), pneumothorax, and soft tissue emphysema are seen in the left lateral chest wall. Pericardial fluid may occasionally also be seen around the right cardiac auricles and in the vicinity of the apex of the heart. Serous transudates are observed in congestive heart failure, hypoalbuminemia, or after irradiation: Lymph fluid may be secondary to neoplasm, cardiothoracic surgery, or obstruction of the hilum or superior vena cava. Fibrinous exudates occur in the presence of infections, uremia, collagen diseases, and hypersensitivity conditions. This strategy not only is robust in relation to cardiac motion artifacts, but also gives way for assessment of myocardial function. However, in arrhythmic or noncompliant patients, additional scanning may be required. Semimanual evaluation programs allow the calcium load to be quantified either according to the method described by Agatston or by simply determining total calcium volume. It is important to always consider the normal distribution of calcified plaques in patients of similar age and gender. Mediastinum describes a space that extends between the thoracic inlet and the diaphragm and may be divided in to an anterior, middle, and posterior compartment. Anterior refers to the space between the sternum and ventral pericardium, posterior to the space between the dorsal pericardium and posterior thoracic wall and middle to the remaining space in between, excluding the pericardium and pleural space. Although this subdivision is consistent in the lower mediastinum, it becomes arbitrary in the upper mediastinum. A typical, though most often nonvisible, mediastinal structure is the thymus, which lies ventrally to the anterior aortic arch. Being isodense to musculature in young children and adolescents, its density becomes fat equivalent after the age of 20 y. Thymic enlargement in adults commonly is observed along with hyperthyroidism, but it may also occur as a rebound phenomenon following steroid treatment and chemotherapy. The right and left lobes may be separate structures or be fused together; thus, the shape of the thymus is highly variable. The pulmonary hilum is anatomically ill-defined and represents a depression on the mediastinal pulmonary surface where bronchus, blood vessels, and nerves enter the lung. The left and right pulmonary hila are asymmetrical and thus, because of vessel opacification, it is necessary to systematically analyze both to differentiate between vasculature, lymph nodes, and hilar masses. Differentiation may be difficult, as masses and hilar or mediastinal lymph nodes often coexist. If visible, they appear as small oval structures, with a smallest to longest diameter ratio of 1. Any cross-sectional diameter 1 cm, nodal rounding, or diminishing of central fat is suspicious. Although this approach usually allows for screening of pulmonary artery embolism, bolus triggering on the pulmonary artery is preferable in these patients. Structures at the level of the left pulmonary artery, below the tracheal bifurcation (e). Diagnostic pearls: On precontrast scans, welldefined hypodense mediastinal cystic lesion is seen. Lymph node hyperplasia in association with a variety of pulmonary or generalized infections. Diagnostic pearls: Slightly enlarged, sharply marginated lymph nodes with homogeneous contrast attenuation. Symmetric mediastinal and hilar lympadenopathy in patients with suspected sarcoidosis. Diagnostic pearls: Enlargement of the paratracheal and preaortic lymph nodes in the upper mediastinum and symmetrical hilar lymphadenopathy are characteristic. Lympadenopathy may occur with or without micronodular lung opacities, involving preferentially the middle and upper portions of the lung. Diagnostic pearls: Lung manifestations often with associated minor enlargement of hilar and mediastinal lymph nodes. In patients with chronic exposition setting, lymph nodes show centripetal ringlike calcifications. Separate ends of a spectrum of chronic granulomatous inflammation of the mediastinum. Diagnostic pearls: Lobulated, elongated soft tissue mass may be detected in any part of the mediastinum. In the absence of characteristic pulmonary parenchymal changes, malignant lymphoma is an important differential diagnosis. Pneumoconiosis Lymph node changes are nonspecific, but pulmonary parenchymal findings are usually diagnostic. Chronic granulomatous or sclerosing mediastinitis Caused by a long-standing inflammation of the mediastinum leading to growth of acellular collagen and fibrous tissue within the chest and around the central vessels and airways. Has a different cause, treatment, and prognosis than acute infectious mediastinitis. Underlying cause of megaesophagus is chronic or recurrent inflammation, such as achalasia, Chagas disease, scleroderma, and candidiasis in immunocompromised patients. Tracheomalacia has a variety of etiologies, including polychondritis, complication of tracheal intubation, tumors, foreign bodies, and congenital tracheal stenosis. Physiologically, the trachea slightly dilates during inspiration and narrows during expiration. These processes are exaggerated in tracheomalacia, leading to airway collapse on expiration. Flaccidity of the tracheal support cartilage leading to focal tracheal collapse and concomitant cranial widening, especially when increased airflow is demanded. Diagnostic pearls: Focal narrowing of the medial and distal trachea with dilation cranially to it; sometimes thickened walls within dilated tracheal segment. The esophagus appears as a small, compressed slit ventrally to the pseudocyst (arrow). Enlarged hilar lymph nodes on the right side with concomitant perilymphatic noduli in the lung parenchyma. Periesophageal fibrosis due to chronic ulcerating esophagitis appears as a subtle fibrosis in the region of the distal esophagus (arrows). Diagnostic pearls: Round or oval, well-defined, very thin-walled, nonenhancing near-water-density mass. Also referred to as bronchial cyst and usually asymptomatic unless it becomes infected. Can potentially be life-threatening, as cysts can lead to compression, hemorrhage, rupture, or infection. Most common in the middle mediastinum; may occur in the posterior and occasionally in the anterior mediastinum. Occurs most frequently in the third or fourth decade of life and equally among men and women. Other cysts in the mediastinum are bronchogenic (34%), enteric (12%), thymic and others (21%). Pericardial and bronchogenic cysts share the second most common etiology after lymphomas. Diagnostic pearls: Round, smooth, thin-walled, nonenhancing mass of near-water density, most commonly located in the right cardiophrenic angle (middle or anterior mediastinum). Near-water attenuation differentiates pericardial cysts from lipomas and fat pads. Diagnostic pearls: Smooth, thin-walled, nonenhancing mass of near-water density in the posterior mediastinum. May contain viscous material and have a density near soft tissue but does not enhance. A closing disorder of the neural tube with herniation of the meninges through a vertebral column defect. Diagnostic pearls: Well-defined, solitary or multiple, water-density paravertebral posterior mediastinal lesion. Diagnostic pearls: Anterosuperior mediastinal mass usually adjunctive with a larger component in the neck; multiloculated, homogeneous, smooth mass near-water density; often appears cystic. Diagnostic pearls: A low left-sided, rarely bilateral, posterior mediastinal mass is seen at a paravertebral location; enters in to the chest between the chest wall and the spleen (see also. Lymphangioma Histologically, lymphatic sacs lined with endothelial cells, cavernous or cystic. Cystic hygroma occurs in children and may be clinically apparent at birth or within 2 y. A hernia occurs in the presence of an incomplete closure of the pericardioperitoneal canals by the pleuroperitoneal membrane. A large Bochdalek hernia may be a rare cause of acute respiratory distress in neonates. Diagnostic pearls: Mediastinal streaks or bubbles of air, often extending from/ to the neck. May be associated with subcutaneous or pulmonary interstitial emphysema and/or pneumothorax. Diagnostic pearls: Similar findings as in mediastinal hemorrhage or hematoma but usually confined to the posterior mediastinum. Well-defined, round, very thin-walled, nonenhancing mass of near-water density outpouching ventrally of the trachea. Round, smooth, thin-walled, nonenhancing mass of near-water density located in the right cardiophrenic angle. Water-density, thin-walled, nonattenuating mass in the upper posterior mediastinum near the neural foramen (arrow). Mediastinal streaks of air, extending from/ to the neck (a) throughout the complete mediastinum (b). Diagnostic pearls: Asymmetrically enlarged paratracheal and tracheobronchial lymph nodes in the acute phase. On postcontrast scans, lymph nodes often show peripheral enhancement and central areas of necrosis-related hypodensity. Acute mediastinitis is usually caused by bacterial overgrowth following a rupture of either the trachea or esophagus. Diagnostic pearls: Hypoattenuating diffuse, mediastinal widening associated with small gas bubbles. Diagnostic pearls: Symmetric widening of the anterior and middle mediastinum resulting from hemorrhagic, diffuse edema of lymph nodes. Either an inflammation or infection of the vertebrae depending on the underlying cause. Erosion or destruction of vertebral bodies at the level of the mass; usually in the inferior thoracic spine. After sternotomy, gas bubbles and fluid in the anterior mediastinum are indicative of an infection. Involvement of multiple disk spaces and large calcified paraspinal masses suggest spinal tuberculosis (Pott disease), marked by stiffness of the vertebral column, pain on motion, tenderness on pressure, prominence of certain vertebral spines, and occasionally abdominal pain, abscess formation, and paralysis. Spondylitis Neoplastic/thymic tumors Thymic hyperplasia, thymic rebound hyperplasia. Diagnostic pearls: Particularly the anteroposterior thickness of the gland is increased with preservation of the normal shape.

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