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The involvement is usually unilateral and the affected bones are invariably shortened and often deformed generic 100 mg nizagara otc. In long bones order 25mg nizagara otc, columns of radiolucent cartilage may be separated by bony septa cheap 50mg nizagara otc, producing a striated appearance. In the hands and feet, the lesions are globular and expansile, often with stippled or mottled calcification. Multiple globular and expansile lucent filling defects involving virtually all the metacarpals and the proximal and distal phalanges. A combination of endo- steal and periosteal cortical thickening causes symmetric fusiform enlargement and undertu- bulation of long bones. Encroachment on the me- dullary canal may cause anemia and secondary hepatosplenomegaly. Amorphous increased den- sity at the base of the skull may lead to impinge- ment on the cranial nerves. Dense endosteal and periosteal cortical thickening causes fusiform enlargement of the midshaft of the femur. A dense, uniform, and symmetric increase in bone density is associated with undertubulation of long bones. Alternating dense and lucent trans- verse lines (probably reflecting the intermittent nature of the pathologic process) may develop in the metaphyses of long bones and vertebrae. Other characteristic findings include a miniature bone inset within each vertebral body (bone-within-a- bone appearance) and increased density at the end plates (sandwich vertebrae). Dense, uniform, symmetric increase in the density of the femur with failure of proper modeling. Osteogenesis imperfecta Inherited generalized disorder of connective tissue associated with blue sclerae, multiple fractures, and hypermobility of joints. The rarest “cystic” form is characterized by flared metaphyses that are hyperlucent and traversed by a honeycomb of coarse trabeculae. The shaft may be overconst- ricted and show severe bending deformities and healed fractures in addition to generalized os- teopenia. Metatropic dwarfism Very rare short-limbed dwarfism in which the patient is normal at birth. Progressive kyphoscolio- sis with characteristic trumpet-like expansion of multiple metaphyses, especially in the femurs and tibias. Healing fracture/ Common cause of localized undertubulation and metaphyseal injury deformity of a long bone. During the healing phase, an elevated solid periosteal reaction may simulate a “double cortex” (especially in infants and child- ren), but disappears with further bone remodeling. Biliary atresia Most common cause of persistent neonatal jaundice; usually fatal within 2 years unless corrected surgically. Metabolic and nutritional disorders Healing rickets and scurvy Widening of the diametaphyses with cortical (Fig B 22-10) thickening and undertubulation occurs in the healing phase of these diseases. Mucopolysaccharidoses Thickening and undertubulation of the shafts of long bones, often with irregular wavy contours, is common. Metaphyseal flaring may be seen in Morquio’s disease, whereas tapering of the ends of long bones suggests Hurler’s disease. Homocystinuria Inborn error of methionine metabolism in which there is usually widening of the metaphyses and enlargement of the ossification centers of long bones, most commonly at the knees. There is usually striking osteoporosis of the spine that is often associated with biconcave deformities of vertebral bodies. Congenital rubella Undertubulation of long bones with radiolucent (see Fig B 21-2) metaphyseal bands and characteristic alternating lucent and sclerotic longitudinal striations (celery stick pattern). Osseous changes regress in infants who grow normally, but may persist in those who fail to survive. Bone cysts, tumors, and Localized widening near the end of a long bone tumor-like conditions may be caused by a variety of benign expansile mass lesions (including Langerhans cell histio- cytosis). Lead poisoning Wide sclerotic bands of lead deposited in the metaphyses can prevent normal bone remodeling and lead to residual deformity. There is still some bony demineralization and residual cupping and fraying of the distal radius and ulna. Primarily involves the mandible, scapula, clavicle, ulna, and ribs and almost always develops before the age of 5 months. Chronic osteomyelitis Sclerosis and solid periosteal new bone formation may produce marked thickening of the affected area. Paralysis (infancy Poliomyelitis, birth palsies, and congenital malfor- and childhood) mations of the spinal cord and brain result in (Fig B 23-1) decreased peripheral muscle tone and secondary bone atrophy. In addition to overconstriction of the shafts, there is generalized osteoporosis and cortical thinning. Muscular disorders Generalized overconstriction of the shafts of long (Fig B 23-2) bones (similar to that in paralysis) develops in such conditions as muscular dystrophy, arthrogryposis, amyotonia congenita, and infantile muscular atrophy (Werdnig-Hoffmann disease). Replacement of muscle by fat produces a characteristic finely striated or striped appearance. The fascial sheaths may appear as thin shadows of increased density surrounded by fat. The fascial sheaths appear as thin shadows of the leg with cortical thinning and diffuse osteoporo- increased density (arrows) surrounded by fatty infiltration sis. Most patients are tall and appear emaciated because of a decrease in subcutaneous fat. Bilateral dislocation of the lens of the eye often occurs because of weakness and redundancy of its sup- porting structures. Laxity of ligaments elsewhere leads to loose-jointedness, double-jointedness, and recurrent dislocations. Homocystinuria Inborn error of methionine metabolism that produces a Marfan-like appearance of thin and elongated tubular bones. In contrast to Marfan’s syndrome, the long tubular bones in homocys- tinuria have widened metaphyses and enlarged ossification centers and there is often striking osteoporosis (especially in the spine). Osteogenesis imperfecta Inherited generalized disorder of connective tissue (Fig B 23-4) in which long bones are slender and overcons- tricted. There is striking osteoporosis with thinning of the cortices and a marked susceptibility to frac- ture (from minimal trauma) that leads to bowing and other deformities. The bones of the lower extremity ges are unusually long and slender (arachnodactyly). Periosteal new bone formation is much more common and severe than in the adult form of the disease. Growth distur- bances are common and include overgrowth of the epiphyses of an affected joint (balloon epiphysis), initially accelerated bone growth because of local hyperemia, and then delayed bone growth due to early epiphyseal fusion or the administration of steroids. Conversely, overgrowth of bone may produce elephantoid soft-tissue and bony thicken- ing. Other major abnormalities include pseudoar- throses, “ribbon ribs,” posterior vertebral scalloping, and orbital dysplasia. Epidermolysis bullosa Thin, osteoporotic tubular bones may reflect chro- (see Fig B 11-7) nic muscle atrophy in this rare hereditary disorder in which the skin blisters spontaneously or with injury.
You will not be asked on the exam to provide the fine judgment call for the borderline case that might be managed that way (the experts are routinely doing it in burns under 20% and daring to include patients with as much as 40%) order nizagara without a prescription, but the vignette is a classic one in which the decision is easy: very small and clearly third-degree purchase nizagara online from canada. This is considered a provoked attack cheap nizagara 50 mg visa, and as far as rabies is concerned, only observation of the pet is required (for development of signs of rabies). Had the bite been to the face, and thus near the brain, treatment should be started and then discontinued if it is proven to be not necessary. But having the animal available will allow it to be killed and the brain examined for signs of rabies, thus hopefully sparing the hunter the necessity of getting vaccinated. Had the bite been to the face, and thus near the brain, treatment should be started and then discontinued if it is proven to be not necessary. While exploring caves in the Texas hill country, a young man is bitten by bats (that promptly fly away). His companion, who is an expert outdoorsman, reports that the snake had elliptical eyes, pits behind the nostrils, big fangs, and rattlers in the tail. Physical examination shows 2 fang marks about 2 cm apart, and there is no local pain, swelling, or discoloration. The description of the snake is indeed that of a poisonous rattlesnake, but even when bitten by a poisonous snake, up to 30% of patients are not envenomated. The most reliable signs of envenomation are excruciating local pain, swelling, and discoloration (usually fully developed within 30 minutes)—none of which this man has. Continued observation (about 12 hours) is all that is needed, plus the standard wound care (including tetanus prophylaxis). His companion, who is an expert outdoorsman, reports that the snake had elliptical eyes, pits behind the nostrils, big fangs, and rattlers in the tail. Physical examination shows two fang marks about 2 cm apart, as well as local edema and ecchymotic discoloration. Blood should be drawn for typing and crossmatch, coagulation studies, and renal and liver function. Surgical excision of the bite site and fasciotomy are only needed in extremely severe cases. While playing in the backyard of her south Texas home, a 6-year-old girl is bitten by a rattlesnake. The point of this vignette is to remind you that snake antivenin is one of the very few medicines for which the dose is not calculated on the basis of the size of the patient. The dose of antivenin depends on the amount of venom injected, regardless of the size and age of the victim. During a picnic outing, a young girl inadvertently bumps into a beehive and is stung repeatedly by angry bees. She is seen 20 minutes later and found to be wheezing, hypotensive, and madly scratching an urticarial rash. While rummaging around her attic, a woman is bitten by a spider that she describes as black, with a red hourglass mark in her belly. A patient seeks help for a very painful ulceration that he discovered in his forearm on arising this morning. Yesterday he spent several hours cleaning up the attic, and he thinks he may have been “bitten by a bug. No, nobody actually bit him—he did it by punching someone in the mouth and getting cut with the teeth that were smashed by his fist. The point of management is that human bites are bacteriologically the dirtiest that one can get and antibiotics are given. Rabies shots will not be needed, but surgical exploration by an orthopedic surgeon will be required as well as antibiotics. Physical examination of the hips reveals that one of them can be easily dislocated posteriorly with a jerk and a “click,” and returned to normal position with a “snapping. The physical examination should suffice, but if there is any doubt, do a sonogram. Abduction splinting with Pavlik harness A 6-year-old boy has insidious development of limping with decreased hip motion. In this age group, Legg-Calve-Perthes disease (avascular necrosis of the capital femoral epiphysis). A 13-year-old obese boy complains of pain in the groin (it could be the knee) and is noted by the family to be limping. He sits in the office with the sole of the foot on the affected side pointing toward the other foot. As the hip is flexed, the leg goes into external rotation and cannot be rotated internally. Forget the details: a bad hip in this age group is slipped capital femoral epiphysis, an orthopedic emergency. A young toddler has had the flu for several days, but until 2 days ago he was walking around normally. He is in pain and holds the leg with the hip flexed, in slight abduction and external rotation, and you cannot examine that hip—-he will not let you move it. Aspiration of the hip under general anesthesia to confirm the diagnosis, and open arthrotomy is performed for drainage. A child with a febrile illness but no history of trauma has persistent, severe localized pain in a bone. Although there is no swelling of the knee joint, he complains of persistent pain right over the tibial tubercle, which is aggravated by contraction of the quadriceps. This is another one with a fancy name: Osgood-Schlatter disease (osteochondrosis of the tibial tubercle). It is usually treated with immobilization of the knee in an extension or cylinder cast for 4–6 weeks, if more conservative management fails (rest, ice, compression, and elevation). Physical examination shows that there is plantar flexion of the ankle, inversion of the foot, adduction of the forefoot, and internal rotation of the tibia. This is the complex deformity known as club foot (fancy name: talipes equinovarus). The sequence of correction starts with the adducted forefoot, then the hindfoot varus, and finally the equinus. About 50% of patients respond completely and need no surgery; those who require surgery are operated on age >6–8 months, but <1–2 years. A 12-year-old girl is referred by the school nurse because of potential scoliosis. The thoracic spine is curved toward the right, and when the girl bends forward a “hump” is noted over her right thorax. This is too complicated for the exam, but the point is that scoliosis may progress until skeletal maturity is reached.
Sharply marginated lucency corre- of the kidney (most often the upper pole of a sponds to the dilated calyces filled with kidney with partial or complete duplication of the nonopacified urine seen during the nephrogram collecting system) cheap nizagara 25mg free shipping. The obstructed area slowly opacifies as pelvic duplication with an ectopic ureterocele or be contrast material passes into the dilated purchase nizagara 25mg otc, urine- the result of infection (especially tuberculosis) generic nizagara 50mg with visa. Ret- filled system (may require films as late as 24 to rograde or antegrade pyelography may be of value 36 hours after injection). Nonobstructed calyces to visualize precisely the point of obstruction (if not draining the remainder of the kidney opacify determined on delayed films). The overall radiographic appearance is indistinguishable from that of renal cell carcinoma. Differs from multicystic (dysgenetic) kidney in that it is unilateral, involves only a segment of an otherwise normal kidney, and has no associated abnor- malities of the ureter or renal artery. Congenital arteriovenous Unifocal mass, most commonly in a parapelvic Most commonly cirsoid (multiple coiled vascular malformation or medullary location, which impresses the channels grouped in a cluster). Cirsoid vascular channels ernous form is composed of a single well-defined occasionally produce multinodular impres- artery feeding into a single vein. Curvilinear with hematuria and may produce an abdominal calcification may form in the walls of the mass. Subcapsular hematoma Nonopacifying mass between opacified renal Post-traumatic or spontaneous (often associated parenchyma and the renal capsule that with neoplasm, arteriosclerosis, or polyarteritis no- flattens and compresses the underlying renal dosa). The cortical margin though septa sometimes divide the cyst into cham- appears as a very thin, smooth radiopaque bers that may or may not communicate with each rim about the bulging lucent cyst (beak sign). Cysts vary in size and may occur at single or A thickened wall suggests bleeding into the multiple sites in one or both kidneys. Cyst puncture is necessary if there is an 3% of cases (not pathognomonic of a benign atypical appearance or a strong clinical suspicion process, as 20% of masses with this appearance of an abscess or if the patient has hematuria or hy- are malignant). Parapelvic cyst Hilar mass displacing the kidney laterally and Extraparenchymal cyst occurring in the region rotating it on its anteroposterior axis. Most parapelvic cysts lie lateral sionally compresses hilar fat to produce a thin, to the renal pelvis and can spread, elongate, and lucent fat line separating the cyst from the adja- compress adjacent calyces (may even cause ob- cent renal parenchyma. Adult polycystic kidney Bilateral large kidneys with a multilobulated Inherited disorder in which many progressively disease contour. The pelvic and infundibular structures growing cysts cause lobulated enlargement of are elongated, effaced, and often displaced the kidneys and progressive renal impairment. Ap- around larger cysts to produce a crescentic proximately 35% of patients have associated cysts outline. The characteristic mottled, “Swiss of the liver (they do not interfere with hepatic func- cheese” nephrogram is due to the presence tions). About 10% have one or more saccular of innumerable lucent cysts of various sizes (berry) aneurysms of the cerebral arteries (may rup- throughout the kidneys. Plaques of calcification ture and produce fatal subarachnoid hemor- occasionally occur in cyst walls. Smooth cortical kidneys, renal failure, and maldevelopment of in- margins (unlike the adult form). In the childhood form, renal cient renal function, urography results in a abnormality is usually milder but is associated nephrogram with a streaky pattern of alter- with severe congenital hepatic fibrosis and portal nating dense and lucent bands reflecting contrast hypertension. Renal function demonstrate small, smoothly rounded calculi is preserved, though tubular stasis predisposes to occurring in clusters or in a fan-like arrange- calculus formation and pyelonephritis. Generally ment in the papillary tip of one or more renal asymptomatic, except when medullary calculi pyramids. Most common cause individual cysts may become slightly opaque of an abdominal mass in the newborn. Other man- during urography to produce the cluster- ifestations include an atretic ureter with a blind of-grapes sign (round lucent cysts separated proximal end (on retrograde pyelography) and from each other by slightly opacified septa). Ultra- Usually there is compensatory hypertrophy of sound can differentiate the disorganized pattern the contralateral kidney. Excretory urogram in a young boy with large, palpable abdominal masses demon- strates renal enlargement with characteristic streaky densities leading to the calyceal tips. Possible causes include a parenchymal cyst drain- (pyelogenic cyst) Delayed urographic opacification occurs by ret- ing into a calyx, a ruptured cortical abscess, and di- rograde filling through a narrow channel that latation of a renal tubule or the blind end of a typically arises from a calyceal fornix. A number of cysts (often very small) in the corti- large medullary cyst may produce a sharply de- comedullary junction and medulla. Multilocular cyst Unifocal mass that is usually in a polar Uncommon unilateral mass composed of multiple location. Sharply defined lucent nephro- cysts of various sizes and adjoining primitive cellu- graphic defect. Differs from multicystic (dysgenetic) kidney in that a mul- tilocular cyst is unilateral, involves only a segment of an otherwise normal kidney, and has no associ- ated abnormality of the ureter or renal artery. Perinephric cyst (pararenal Elliptical soft-tissue mass in the flank with up- Most cases result from accidents, operative trauma, pseudocyst, urinoma) ward and lateral displacement of the lower pole or renal transplantation. In infants and children, of the kidney, medial displacement of the ureter, congenital obstruction of the urinary tract may and often obstructive hydronephrosis. Most common clinical finding is a pal- reduced or absent excretion of contrast mate- pable flank mass (usually a normal urinalysis and rial. Echinococcal cyst Thick-walled cyst with nonhomogeneous lu- Usually a solitary cyst, predominantly in the cency. Often produces narrowing or even ob- polar region, that may have a calcified wall. There may be a munication with the collecting system almost al- permanent or intermittent communication be- ways occurs through the calyx rather than directly tween the cyst and the calyceal system. A large cortical In young infants with congenital heart disease and disease cyst may cause a focal contour bulge or calyceal the trisomy syndromes, numerous small cysts may distortion. In tuberous sclerosis, the cysts are of tubular origin, and severe involvement may lead to hypertension and renal failure. Cystic dysplasia (associated Rarely detected on excretory urography (accom- Rarely recognized as a clinical entity but relatively with lower urinary tract panying hydronephrosis obscures evidence of common on pathologic examination of the kidneys obstruction) the multiple cortical cysts). The increased pressure presumably results in malformation of the renal parenchyma and the development of numerous cortical cysts, espe- cially beneath the capsule. The nephrogram is composed of many streaky collections of contrast material radiating from the calyces to the periphery. May be multifo- points at which the centrilobar cortex of one lobe cal or bilateral. Splenic impression Flattening of the upper lateral margin of the left The impression on the renal contour is probably kidney. There is often an associated bulge lower on the lateral margin of the kidney (dromedary hump). May be multifocal or sis and atrial fibrillation, infective endocarditis, or bilateral. Chronic atrophic Cortical depression overlying a retracted papilla, Related to chronic pyelonephritis and vesico- pyelonephritis whose calyx is secondarily smoothly dilated. Focal areas of parenchymal loss and calyceal clubbing in the upper pole of the right kidney. Note the tortuosity and rapid tapering of inter- lobar arteries and their branches that is characteristic of arteriolar nephrosclerosis.
For this reason buy nizagara 100mg on line, perform a Stamm gastros- avascular portion just to the left of the middle colic vessels cost of nizagara. Be absolutely certain the inci- pyloroplasty during this type of operation because it is sion in the mesentery does not constrict the veins of the vas- assumed that the vagus nerves have been interrupted during cular pedicle buy nizagara american express. Pass the course of dissecting a heavily scarred esophagus out of the proximal portion of the jejunal segment through the hia- the mediastinum. Closure Esophagojejunostomy Repair the diaphragm and close the thoracoabdominal Establish an end-to-side esophagojejunal anastomosis on the incision as illustrated in Figs. No distal to the staple line on the proximal closed end of the abdominal drains are utilized. Jejunal interposition for reﬂux esophagitis and esopha- managing-your-practice/coding-billing-insurance/cpt. Colon interposition of esophageal replacement: current indications and long-term func- benign esophageal disease. Colon interposition for esophageal replacement: an alternative technique based on the use of the right colon. Esophagogastroduodenoscopy with brushing and biopsies of Identify the gastrophrenic ligament by passing the left hand any abnormal mucosa behind the stomach so the ﬁngertips can identify this avascu- Esophageal manometry or pH studies in selected patients lar ligament, which attaches the greater curvature to the dia- phragm. The ligament extends from the gastroesophageal junction down to the ﬁrst short gastric vessel. It is simple to Pitfalls and Danger Points divide once it has been stretched by the surgeon’s left hand behind the stomach. Although in a few cases no short gastric Inadequate mobilization of gastric fundus and abdominal vessels must be divided, there should be no hesitation to esophagus divide one to three proximal short gastric vessels to create a Injury to spleen or to vagus nerves loose fundoplication. Fundoplication wrap too tight or too long On the lesser curvature aspect of the gastroesophageal Inadequate fundoplication suturing junction, it is necessary to divide the proximal portion of the Undiagnosed esophageal motility disorders, such as gastrohepatic ligament. This ligament often contains an achalasia, diffuse spasm, aperistalsis, or scleroderma accessory left hepatic artery arising from the left gastric artery Hiatal closure too tight, causing esophageal obstruction and going to the left lobe of the liver and the hepatic branch Hiatal closure too loose, permitting postoperative parae- of the left vagus nerve. Division of the accessory left hepatic sophageal herniation artery has, in our experience, not proved harmful. Do not Injury to left hepatic vein or vena cava when incising trian- divide the left gastric artery itself. Preserving the left gastric gular ligament to liberate left lobe of liver artery and the hepatic branch of the vagus nerve helps prevent the fundoplication from slipping in a caudal direction. Chassin Preventing Splenic Injury rather than by the tightness of the wrap itself. Splenic trauma is a common but preventable complication of Therefore the fundoplication should be made loose, rather the Nissen operation. Many surgeons hand retractor, there is no reason for any retractor to come use an indwelling esophageal bougie to avoid creating a into contact with the spleen. Regardless of whether the indwelling injury is usually traction on the body of the stomach toward bougie is used, it is possible to judge the tightness of the the patient’s right, which avulses that portion of the splenic wrap by applying Babcock clamps to each side of the gastric capsule attached to the omentum or to the gastrosplenic liga- fundus and tentatively bringing them together in front of the ment. Note where the omentum geon should be able to pass one or two ﬁngers between the may be adherent to the splenic capsule. If necessary, divide wrap and the esophagus without difﬁculty with an 18 F naso- these attachments under direct vision. Otherwise readjust the fundoplication apply a moist gauze pad over the spleen and avoid lateral so it is loose enough for this maneuver to be accomplished. Traction on the gastroesophageal junction in a caudal direction along the lesser curve of the stomach generally does not cause injury to the spleen. If a portion of the splenic capsule has been avulsed, it can almost always be managed by applying topical hemostatic Another cause of postoperative dysphagia is making the fun- agents followed by 10 min of pressure. For the usual Nissen operation, do can be repaired by suturing with 2-0 chromic catgut (see not wrap more than 2–3 cm of esophagus. Extensive disruption of the spleen at its hilus may may be appropriate when esophageal dysmotility and gastro- necessitate splenectomy. Avoiding Postoperative Dysphagia Avoiding Fundoplication Suture Probably secondary to local edema, transient mild dysphagia Line Disruption is common during the ﬁrst 2–3 weeks following operation, although some patients have difﬁculty swallowing for many Polk and others have noted that an important cause of failure months after a hiatus hernia operation. There are several pos- after Nissen fundoplication has been disruption of the plica- sible causes for this dysphagia. For this reason, use 2-0 fundoplication wrap so tight or so wide that permanent dys- sutures. We have used 2-0 Tevdek because it retains its ten- may be sutured so tightly the hiatus impinges on the lumen of sile strength for many years, whereas silk gradually degener- the esophagus and prevents passage of food. It is also important not to pass the suture nasogastric tube in place, after the crural sutures have been into the lumen of the stomach or esophagus. If this error is tied to repair the defect in the hiatus, it should still be possible committed, tying the suture too tight causes strangulation and to insert an index ﬁnger without difﬁculty between the esopha- possibly leakage. There is no virtue in closing tion is to turn in the major fundoplication sutures with a layer the hiatus snugly around the esophagus. Patients who Failure to Bring the Esophagogastric present to the surgeon with reﬂux esophagitis and who also Junction into the Abdomen complain of dysphagia should undergo preoperative esopha- geal manometry to rule out motility disorders that may require If it is not possible to mobilize the esophagogastric junction surgery in addition to the antireﬂux procedure or instead of it. Such a situation can generally be suspected prior to opera- tion when the lower esophagus is strictured. In our opinion, The Nissen operation produces a high pressure zone in the these patients require a transthoracic Collis-Nissen opera- lower esophagus by transmitted gastric pressure in the wrap, tion (see Chap. Although it is possible to perform a 19 Transabdominal Nissen Fundoplication 195 Collis-Nissen procedure in the abdomen, it is difﬁcult. In most cases it is not necessary to free the left lobe of the liver; simply elevate the left lobe with a Weinberg retractor to expose the Keeping the Fundoplication from Slipping diaphragmatic hiatus. Various methods have been advocated to keep the fundopli- cation from sliding in a caudal direction, where it constricts Mobilizing the Esophagus and Gastric Fundus the middle of the stomach instead of the esophagus and pro- duces an “hourglass” stomach with partial obstruction. The Make a transverse incision in the peritoneum overlying the most important means of preventing this caudal displace- abdominal esophagus (Fig. Also, catch the wall of the Then divide the peritoneum overlying the left margin of the stomach just below the gastroesophageal junction within the diaphragmatic hiatus. This suture anchors the lower portion of the esophagus using a peanut dissector until most of the the wrap (see Fig. Then pass the index ﬁnger gently behind the esophagus and encircle it with a latex drain (Fig. Enclose both the Documentation Basic right and left vagus nerves in the latex drain and divide all the phrenoesophageal attachments behind the esophagus. If • Findings the right (posterior) vagus trunk courses at a distance from • Placement of wrap relative to vagus nerves the esophagus, it is easier to dissect the nerve away from • Closure of hiatus? Some exclude both vagus trunks from the wrap, but we prefer to include them inside the loose Operative Technique wrap. Before the complete circumference of the hiatus can be visualized, it is necessary to divide not only the phreno- Incision esophageal ligaments but also the cephalad portion of the gastrohepatic ligament, which often contains an accessory Elevate the head of the operating table 10–15°. The midline incision beginning at the xiphoid and continue exposure at the conclusion of this maneuver is seen in about 2–3 cm beyond the umbilicus (Fig. Insert a Thompson or Upper Hand retractor to behind the gastric fundus to identify the gastrophrenic liga- elevate the lower portion of the sternum.