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Surgery_Schwartz. procedures has become increasingly demonstrated.165,166Computed TomographyCT affords a high degree of resolution and detail of the splenic parenchyma, vasculature, and its relationship to neighboring structures, making it the preferred imaging modality for many surgeons. CT has become an invaluable tool in the evaluation and management of the blunt trauma patient, and standardized scoring systems for splenic trauma based on CT images now aid in management decisions.169 In the nontrauma setting, CT is extremely useful for assessment of splenomegaly, identification of solid and cystic lesions, and guidance of percutaneous pro-cedures.3 The use of iodinated contrast material adds diagnostic clarity to CT imaging of the spleen, although at the cost of, the small but real risks, possible renal impairment or allergic reac-tions. Three-dimensional reconstruction after CT scan may help to predict the difficulty of the procedure and to choose the best surgical approach.170,171The appearance of


Surgery_Schwartz

Surgery_Schwartz. impairment or allergic reac-tions. Three-dimensional reconstruction after CT scan may help to predict the difficulty of the procedure and to choose the best surgical approach.170,171The appearance of normal splenic tissue on a noncon-trast CT is uniform parenchymal attenuation with values ranging between 40 and 60 Hounsfield units (HU).172 On a contrast-enhanced CT, the appearance of the spleen depends largely on the timing of the intravenous bolus administration of contrast material. Due to the different rates of flow through the red and white pulp, the spleen appears heterogeneously enhanc-ing during the first minute after initiation of intravenous admin-istration of contrast material during the arterial and early portal venous phases.23 The frequency of these artifacts increases with advancing patient age. When evaluating for splenic abscess, a contrast-enhanced CT should be utilized.64,173Three-dimensional CT volumetry is a novel modality that measures the volume of the spleen.


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Surgery_Schwartz. advancing patient age. When evaluating for splenic abscess, a contrast-enhanced CT should be utilized.64,173Three-dimensional CT volumetry is a novel modality that measures the volume of the spleen. This tool may be of some benefit in planning technically challenging cases involving sple-nomegaly. A recent retrospective review of laparoscopic sple-nectomy patients who underwent CT volumetry preoperatively demonstrated a higher conversion rate when the spleen was measured to be greater than 2700 cc.170 This information may aid in proper informed consent as well as preoperative planning to assist in determination of which patients may benefit from a minimally invasive or open surgical approach.139Plain RadiographyRarely is plain radiography used for primary splenic imaging. Plain films can indirectly provide an outline of the spleen in the left upper quadrant or suggest splenomegaly by revealing dis-placement of adjacent air-filled structures (e.g., the stomach or splenic flexure of the


Surgery_Schwartz

Surgery_Schwartz. provide an outline of the spleen in the left upper quadrant or suggest splenomegaly by revealing dis-placement of adjacent air-filled structures (e.g., the stomach or splenic flexure of the colon). Plain films may also demonstrate splenic calcifications. Splenic calcifications often are found in association with splenomegaly but are otherwise a nonspe-cific finding. Splenic calcifications can indicate a number of benign, neoplastic, or infectious processes, including phlebo-lith, splenic artery aneurysm, sickle cell changes, tumors (e.g., hemangioma, hemangiosarcoma, lymphoma), echinococcosis, or tuberculosis.168Magnetic Resonance ImagingAlthough MRI offers excellent detail and versatility in abdomi-nal imaging, it is more expensive than CT scan or ultrasound and offers no obvious advantage for primary imaging of the spleen. MRI can be a valuable adjunct to the more commonly used imaging techniques when splenic disease is suspected but not definitively diagnosed.168,173Magnetic


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Surgery_Schwartz. for primary imaging of the spleen. MRI can be a valuable adjunct to the more commonly used imaging techniques when splenic disease is suspected but not definitively diagnosed.168,173Magnetic resonance (MR) signal characteristics of the spleen are related to the relative ratio of red and white pulp and the relationship of the timing of the intravenous (IV) contrast bolus and the time of image acquisition. The spleen will gener-ally have a homogeneous MR signal on noncontrast images. Table 34-5Laparoscopic splenectomy results by hematologic indicationITP (N = 151)TTP (N = 7)ANEMIA (N = 40)MALIGNANCY (N = 28)OR time (min)128146149165EBL (mL)13796116238LOS (days)2.23.02.22.6Conversions from LS to OS3 (2%)1 (14%)1 (3%)1 (4%)Complications14 (9%)01 (3%)3 (11%)EBL = estimated blood loss; ITP = idiopathic thrombocytopenic purpura; LOS = length of hospital stay; LS = laparoscopic splenectomy; OR = operating room; OS = open splenectomy; TTP = thrombotic thrombocytopenic purpura.Data from


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Surgery_Schwartz. = idiopathic thrombocytopenic purpura; LOS = length of hospital stay; LS = laparoscopic splenectomy; OR = operating room; OS = open splenectomy; TTP = thrombotic thrombocytopenic purpura.Data from Brunicardi FC, Andersen DK, Billiar TR, et al: Schwartz’s Principles of Surgery, 8th ed. New York, NY: McGraw-Hill; 2005.Brunicardi_Ch34_p1517-p1548.indd 154023/02/19 2:37 PM 1541THE SPLEENCHAPTER 34On contrast MRI, the spleen appears to have heterogeneous enhancement during the arterial phase of contrast enhancement.AngiographyAngiography of the spleen most commonly refers to inva-sive arterial imaging, and when it is combined with thera-peutic splenic arterial embolization (SAE), there are multiple applications for this procedure: localization and treatment of hemorrhage in select trauma patients; delivery of a variety of therapies in patients with cirrhosis or portal and sinistral hyper-tension and in transplant patients; and adjunct (or, more con-troversially, as an alternative) to


Surgery_Schwartz

Surgery_Schwartz. patients; delivery of a variety of therapies in patients with cirrhosis or portal and sinistral hyper-tension and in transplant patients; and adjunct (or, more con-troversially, as an alternative) to splenectomy for treatment of hematologic disorders such as ITP or hypersplenism.174-176 Preoperative or intraoperative SAE for elective splenectomy is also a common, although not universal, practice. Few pro-spective data have been published in the last 5 years on pre-operative SAE.177 Preoperative SAE is purported not only to facilitate less intraoperative blood loss but also possibly to allow a laparoscopic approach in patients whose spleens had previ-ously been considered too large for, or otherwise not amenable to, safe laparoscopic resection. Limited success in using partial SAE as an alternative to therapeutic splenectomy in chronic ITP has been previously reported.178 Its detractors argue that the need for increased analgesics and occasional extended hospital stay preoperatively,


Surgery_Schwartz

Surgery_Schwartz. to therapeutic splenectomy in chronic ITP has been previously reported.178 Its detractors argue that the need for increased analgesics and occasional extended hospital stay preoperatively, the possibility of pancreatitis, and the well-described risks of invasive arteriography associated with the passage of wires and catheters through the vasculature, may negate any presumed benefits of preoperative SAE.Nuclear ImagingRadioscintigraphy with technetium-99m sulfur colloid demon-strates splenic location and size. It may be especially helpful in locating accessory spleens after unsuccessful splenectomy for ITP and has recently proven useful in diagnosing splenosis.179,180 Unfortunately, no conclusive outcome benefit has been shown for preoperative technetium scanning before splenectomy.52,181 When dealing with diseases of platelet sequestration, indium-labeled autologous platelet scanning (ILAPS) demonstrates whether platelet sequestration is predominantly in the spleen, liver, or both.


Surgery_Schwartz

Surgery_Schwartz. When dealing with diseases of platelet sequestration, indium-labeled autologous platelet scanning (ILAPS) demonstrates whether platelet sequestration is predominantly in the spleen, liver, or both. This becomes important in deciding whether or not a patient will benefit from a splenectomy. ILAPS is a nuclear imaging modality in which autologous platelets are reinfused into the patient after ex vivo labeling. Subsequent scintigraphy demonstrates the site(s) of platelet sequestration and clearance. It has been proposed that patients with purely or predominantly splenic sequestration determined by ILAPS may be more likely to respond to splenectomy than those exhibiting hepatic, mixed, or diffuse patterns.176An emerging and novel application for spleen scintigraphy may be as a noninvasive method to diagnose nonalcoholic ste-atohepatitis (NASH). Conventional imaging methods are reli-able for the detection of moderate to severe fatty changes in the liver, though they are not reliable for


Surgery_Schwartz

Surgery_Schwartz. to diagnose nonalcoholic ste-atohepatitis (NASH). Conventional imaging methods are reli-able for the detection of moderate to severe fatty changes in the liver, though they are not reliable for detecting NASH or hepatic fibrosis. NASH, which may lead to cirrhosis, can result from nonalcoholic fatty liver disease (NAFLD), the most common cause of steatosis. With the alarming rise of obesity worldwide, NAFLD is also increasingly common with prevalence rang-ing from 6.3% to 33%.15,182 The diagnosis of progression from NAFLD to NASH has been dependent on histologic assessment of tissue obtained from liver biopsy. Characteristics unique to NASH have been reported, among them the association of splenic enlargement, not seen to a similar degree in NAFLD.13In addition, the ratio of liver-to-spleen uptake determined by scintigraphy has been found to be predictably altered in NASH patients. The liver-to-spleen uptake ratio is significantly decreased in NASH patients, but not NAFLD patients,


Surgery_Schwartz

Surgery_Schwartz. uptake determined by scintigraphy has been found to be predictably altered in NASH patients. The liver-to-spleen uptake ratio is significantly decreased in NASH patients, but not NAFLD patients, leading some to conclude that technetium-99m-phytate scintigraphy is a reliable tool to differentiate NASH from NAFLD.183 Although additional studies are needed to identify the role of these nuclear medicine studies in prognostication and monitoring of those patients at high risk for the development of NASH, recent stud-ies show promise in this regard.184Microbiology and Pathogenesis. Life-threatening infec-tion in the asplenic patient is attributable to four main factors: loss of splenic macrophages, diminished tuftsin production, loss of the spleen’s reticuloendothelial screening function, and dysregulated coagulation.187 In the normal host, these factors work in concert to eliminate opsonized bacteria from the blood-stream. This system is particularly suited for the removal of encapsulated


Surgery_Schwartz

Surgery_Schwartz. coagulation.187 In the normal host, these factors work in concert to eliminate opsonized bacteria from the blood-stream. This system is particularly suited for the removal of encapsulated bacteria, whose polysaccharide coating is a natu-ral defense against opsonization (S pneumoniae, H influenzae, and N meningitidis are the classic examples). Infections with protozoa that invade the red blood cell, such as Babesia microti (transmitted by tick bites), Ehrlichia, and Plasmodium, occur more frequently in splenectomized individuals than in normal hosts. Other potential infectious bacterial sources include group A streptococci, C canimorsus (transmitted by dog bites), group B streptococci, Enterococcus species, Bacteroides species, Salmonella species, and Bartonella species.124 In the absence of the spleen, elimination of these pathogens from the bloodstream falls solely to the liver, a process that has been demonstrated to be less effective.12,126 Further, the pathophysiology of infection


Surgery_Schwartz

Surgery_Schwartz. the spleen, elimination of these pathogens from the bloodstream falls solely to the liver, a process that has been demonstrated to be less effective.12,126 Further, the pathophysiology of infection in asplenic patients has also been implicated in their increased risk of thrombosis and pulmonary hypertension.187More recently, the bacterial patterns of splenectomy sepsis have been changing. After the introduction of vaccinations and new oral antibiotics, postsplenectomy patients can suffer from diverse strains of bacterial infection, which are not strictly cor-related with the splenic function. In recent cohort series, gram negative bacteria are prevalent, representing 45% to 50% of infections in asplenic patients.193,194 In vaccinated patients, the rate of sepsis by pneumococcus is very low. In fact, encapsulated bacteria, such as S pneumoniae, N meningitidis, and H influenzae, were rarely encountered in those series in whom vaccination was routinely adopted.193-196Sepsis by uncommon


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Surgery_Schwartz. In fact, encapsulated bacteria, such as S pneumoniae, N meningitidis, and H influenzae, were rarely encountered in those series in whom vaccination was routinely adopted.193-196Sepsis by uncommon bacteria as well by protozoa infec-tions such as malaria and babesiosis are also known to affect asplenic patients.196-200Clinical Features. OPSI is uniformly fatal without treat-ment, and thus sepsis in a splenectomized patient is a medical emergency.21,187,192 Therefore, any clinical suggestion of infec-tion, including seemingly isolated fevers, must be viewed with a high index of suspicion and treated empirically as thorough investigation proceeds. OPSI may begin with a relatively mild-appearing prodrome of symptoms. In addition to fever, nonspe-cific symptoms such as malaise, myalgias, headache, vomiting, diarrhea, abdominal pain, and others should be viewed with alarm in the asplenic patient. This process can progress rapidly to fulminant bacteremic septic shock, with hypotension,


Surgery_Schwartz

Surgery_Schwartz. headache, vomiting, diarrhea, abdominal pain, and others should be viewed with alarm in the asplenic patient. This process can progress rapidly to fulminant bacteremic septic shock, with hypotension, anuria, and disseminated intravascular coagulation.The true incidence of OPSI is not precisely known because defining criteria vary among published series. Overall lifetime risk remains low, ranging from <1% to 5%.12,21,126,201 Among 9Brunicardi_Ch34_p1517-p1548.indd 154123/02/19 2:37 PM 1542SPECIFIC CONSIDERATIONSPART IIthose who develop OPSI, some characteristics can be identified that impart greater risk. Reason for splenectomy is the single most influential determinant of OPSI risk. Case series demon-strate that those who undergo splenectomy for hematologic dis-ease (malignancy, myelodysplasia, or hemoglobinopathy) are far more susceptible to OPSI than patients who undergo sple-nectomy for trauma or iatrogenic reasons. Age is also an impor-tant consideration, with children 5 years


Surgery_Schwartz

Surgery_Schwartz. or hemoglobinopathy) are far more susceptible to OPSI than patients who undergo sple-nectomy for trauma or iatrogenic reasons. Age is also an impor-tant consideration, with children 5 years of age or less and adults 50 years or older being at elevated risk. Finally, time interval from spleen removal must be considered. A large number of OPSI cases occur many years to decades after splenectomy.186,189 This observation underscores both the threat of this lethal dis-ease and the need for lifelong vigilance.Antibiotics and the Asplenic Patient. Antibiotic therapy for the asplenic patient can be considered in three contexts: therapy for established or presumed infections, prophylaxis in anticipation of invasive procedures (e.g., dental procedures), and general prophylaxis. The most critical action in the treat-ment of established or presumed OPSI is the immediate use of broad-spectrum intravenous antibiotics, ideally after the collec-tion of blood cultures. Vancomycin provides


Surgery_Schwartz

Surgery_Schwartz. critical action in the treat-ment of established or presumed OPSI is the immediate use of broad-spectrum intravenous antibiotics, ideally after the collec-tion of blood cultures. Vancomycin provides broad-spectrum Gram-positive coverage, including coverage against penicillin-resistant S pneumonia.190 Ceftriaxone should be added to include Gram-negative coverage for N meningitidis and H influenza.190 Early implementation of antibiotics and goal-directed therapy for sepsis can significant reduce mortality rates.21,191 For the lat-ter two indications, unfortunately, evidence supporting efficacy is scant, and guidelines for antibiotic prophylaxis are not uni-form. Optimal duration of chemoprophylaxis in children also remains unclear; however, a daily dose of antibiotics until 5 years of age or at least 5 years after splenectomy are commonly recommended, although some advocate continuation into at least early adulthood.121,122,192 Concerns regarding compliance and bacterial resistance have


Surgery_Schwartz

Surgery_Schwartz. at least 5 years after splenectomy are commonly recommended, although some advocate continuation into at least early adulthood.121,122,192 Concerns regarding compliance and bacterial resistance have been raised, which have led some authors to suggest that lifelong daily antibiotic prophylaxis be recommended only for those patients whose antibody titers fail to respond appropriately to vaccination or, alternately, that asplenic patients be advised to carry at all times a reserve sup-ply of antibiotic to be self-administered at the earliest sign of infection.122 Considering the grave consequences of OPSI and its relatively low incidence, controlled trials resulting in mean-ingful data on this issue seem unlikely to be performed.Education. Several risk management strategies are com-monly recommended to patients following splenectomy, including wearing a medical bracelet, carrying a laminated medical alert card, possessing a medical letter with specific empiric therapy instructions


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Surgery_Schwartz. recommended to patients following splenectomy, including wearing a medical bracelet, carrying a laminated medical alert card, possessing a medical letter with specific empiric therapy instructions (including drug names and dos-ages), and keeping a 5-day supply of standby antibiotics, par-ticularly when travel is anticipated.187,189 The need for a high index of suspicion, prompt action, and aggressive education of the patient, family, and medical providers cannot be overstated in asplenic patients.REFERENCESEntries highlighted in bright blue are key references. 1. Moynihan B. The surgery of the spleen. Br J Surg. 1921 Jan 22; 1(3134):114-6. 2. McClusky DA, 3rd, Skandalakis LJ, Colborn GL, Skandalakis JE. Tribute to a triad: history of splenic anatomy, physiology, and surgery—part 1. World J Surg. 1999;23(3):311-325. 3. McClusky DA, 3rd, Skandalakis LJ, Colborn GL, Skandalakis JE. Tribute to a triad: history of splenic anatomy, physiology, and surgery-part 2. World J Surg.


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Surgery_Schwartz. 1. World J Surg. 1999;23(3):311-325. 3. McClusky DA, 3rd, Skandalakis LJ, Colborn GL, Skandalakis JE. Tribute to a triad: history of splenic anatomy, physiology, and surgery-part 2. World J Surg. 1999;23(5):514-526. 4. Aristotle. De Paribus Animalium [On the Parts of Animals]. Cambridge: Harvard University Press; 1961. 5. Garfield E. Citation indexes for science; a new dimension in documentation through association of ideas. Science. 1955;122(3159):108-111. 6. Cameron BD. Trends in the usage of ISI bibliometric data: uses, abuses, and implications. Libraries and the Academy. 2005;5(1):105-125. 7. Foster M. Lectures on the History of Physiology During the Sixteenth, Seventeenth, and Eighteenth Centuries. Vol 164. Cambridge: Cambridge University Press; 1901. 8. Wilkins BS. The spleen. Br J Haematol. 2002;117(2):265-274. 9. Morgenstern L. A history of splenectomy. In: Hiatt JR, Phillips EH, Morgenstern L, eds. Surgical Disease of the Spleen. New York: Springer; 1997. 10. Gray H. On the


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Surgery_Schwartz. Haematol. 2002;117(2):265-274. 9. Morgenstern L. A history of splenectomy. In: Hiatt JR, Phillips EH, Morgenstern L, eds. Surgical Disease of the Spleen. New York: Springer; 1997. 10. Gray H. On the Structure and Use of the Spleen. London: J.W. Parker and Son; 1854. 11. Bryant T. Case of excision of the spleen for an enlargement of the organ, attended with leucocythaemia, with remarks. Guys Hosp Rep. 1867;13(412). 12. Bickenbach KA, Gonen M, Labow DM, et al. Indications for and efficacy of splenectomy for haematological disorders. Br J Surg. 2013;100(6):794-800. 13. Musallam KM, Khalife M, Sfeir PM, et al. Postoperative out-comes after laparoscopic splenectomy compared with open splenectomy. Ann Surg. 2013;257(6):1116-1123. 14. Mebius RE, Kraal G. Structure and function of the spleen. Nat Rev Immunol. 2005;5(8):606-616. 15. Tarantino G, Savastano S, Capone D, Colao A. Spleen: a new role for an old player? World J Gastroenterol. 2011;17(33):3776-3784. 16. Morgenstern L, Skandalakis


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Surgery_Schwartz. Nat Rev Immunol. 2005;5(8):606-616. 15. Tarantino G, Savastano S, Capone D, Colao A. Spleen: a new role for an old player? World J Gastroenterol. 2011;17(33):3776-3784. 16. Morgenstern L, Skandalakis JE. Anatomy and embryology of the spleen. In: Hiatt JR, Phillips EH, Morgenstern L, eds. Surgical Diseases of the Spleen. Vol 15. Berlin/Heidelberg: Springer-Verlag; 1997. 17. Magowska A. Wandering spleen: a medical enigma, its natural history and rationalization. World J Surg. 2013;37(3):545-550. 18. Bratosin D, Mazurier J, Tissier JP, et al. Cellular and molecular mechanisms of senescent erythrocyte phagocytosis by macro-phages. A review. Biochimie. 1998;80(2):173-195. 19. Knutson M, Wessling-Resnick M. Iron metabolism in the reticuloendothelial system. Crit Rev Biochem Mol Biol. 2003;38(1):61-88. 20. Nolte MA, Belien JA, Schadee-Eestermans I, et al. A con-duit system distributes chemokines and small blood-borne molecules through the splenic white pulp. J Exp Med.


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Surgery_Schwartz. Mol Biol. 2003;38(1):61-88. 20. Nolte MA, Belien JA, Schadee-Eestermans I, et al. A con-duit system distributes chemokines and small blood-borne molecules through the splenic white pulp. J Exp Med. 2003;198(3):505-512. 21. Di Sabatino A, Carsetti R, Corazza GR. Post-splenectomy and hyposplenic states. Lancet. 2011;378(9785):86-97. 22. Spelman D, Buttery J, Daley A, et al. Guidelines for the pre-vention of sepsis in asplenic and hyposplenic patients. Intern Med J. 2008;38(5):349-356. 23. Davies JM, Lewis MP, Wimperis J, et al. Review of guidelines for the prevention and treatment of infection in patients with an absent or dysfunctional spleen: prepared on behalf of the British Committee for Standards in Haematology by a work-ing party of the Haemato-Oncology task force. Br J Haematol. 2011;155(3):308-317. 24. Habermalz B, Sauerland S, Decker G, et al. Laparoscopic splenectomy: the clinical practice guidelines of the European Association for Endoscopic Surgery (EAES). Surg Endosc.


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Surgery_Schwartz. 2011;155(3):308-317. 24. Habermalz B, Sauerland S, Decker G, et al. Laparoscopic splenectomy: the clinical practice guidelines of the European Association for Endoscopic Surgery (EAES). Surg Endosc. 2008;22(4):821-848. 25. Pozo AL, Godfrey EM, Bowles KM. Splenomegaly: investigation, diagnosis and management. Blood Rev. 2009;23(3):105-111.Brunicardi_Ch34_p1517-p1548.indd 154223/02/19 2:37 PM 1543THE SPLEENCHAPTER 34 26. Iolascon A, Andolfo I, Barcellini W, et al. Recommendations regarding splenectomy in hereditary hemolytic anemias. Haematologica. 2017;102(8):1304-1313. 27. Schilling RF. Risks and benefits of splenectomy versus no splenectomy for hereditary spherocytosis—a personal view. Br J Haematol. 2009;145(6):728-732. 28. Barcellini W, Bianchi P, Fermo E, et al. Hereditary red cell membrane defects: diagnostic and clinical aspects. Blood Transfus. 2011;9(3):274-277. 29. Casale M, Perrotta S. Splenectomy for hereditary spherocy-tosis: complete, partial or not at all? Expert Rev


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Surgery_Schwartz. membrane defects: diagnostic and clinical aspects. Blood Transfus. 2011;9(3):274-277. 29. Casale M, Perrotta S. Splenectomy for hereditary spherocy-tosis: complete, partial or not at all? Expert Rev Hematol. 2011;4(6):627-635. 30. Prchal JT, Gregg XT. Red cell enzymopathies. In: Hoffman R, ed. Hematology: Basic Principles and Practice. Vol 561. 3rd ed. New York: Churchill Livingstone; 2001. 31. Grace RF, Zanella A, Neufeld EJ, et al. Erythrocyte pyru-vate kinase deficiency: 2015 status report. Am J Hematol. 2015;90(9):825-830. 32. Beutler E, Gelbart T. Estimating the prevalence of pyruvate kinase deficiency from the gene frequency in the general white population. Blood. 2000;95(11):3585-3588. 33. Carey PJ, Chandler J, Hendrick A, et al. Prevalence of pyru-vate kinase deficiency in northern European population in the north of England. Northern Region Haematologists Group. Blood. 2000;96(12):4005-4006. 34. Hamilton JW, Jones FG, McMullin MF. Glucose-6phosphate dehydrogenase


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Surgery_Schwartz. in northern European population in the north of England. Northern Region Haematologists Group. Blood. 2000;96(12):4005-4006. 34. Hamilton JW, Jones FG, McMullin MF. Glucose-6phosphate dehydrogenase Guadalajara—a case of chronic non-spherocytic haemolytic anaemia responding to splenec-tomy and the role of splenectomy in this disorder. Hematology. 2004;9(4):307-309. 35. Michel M. Classification and therapeutic approaches in auto-immune hemolytic anemia: an update. Expert Rev Hematol. 2011;4(6):607-618. 36. Giudice V, Rosamilio R, Ferrara I, Seneca E, Serio B, Selleri C. Efficacy and safety of splenectomy in adult autoimmune hemolytic anemia. Open Med (Wars). 2016;11(1):374-380. 37. Hill J, Walsh RM, McHam S, Brody F, Kalaycio M. Lapa-roscopic splenectomy for autoimmune hemolytic anemia in patients with chronic lymphocytic leukemia: a case series and review of the literature. Am J Hematol. 2004;75(3):134-138. 38. Plikat K, Rogler G, Scholmerich J. Coombs-positive autoim-mune hemolytic


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Surgery_Schwartz. patients with chronic lymphocytic leukemia: a case series and review of the literature. Am J Hematol. 2004;75(3):134-138. 38. Plikat K, Rogler G, Scholmerich J. Coombs-positive autoim-mune hemolytic anemia in Crohn’s disease. Eur J Gastroen-terol Hepatol. 2005;17(6):661-666. 39. Rigal D, Meyer F. Autoimmune haemolytic anemia: diagnosis strategy and new treatments (in French). Transfus Clin Biol. 2011;18(2):277-285. 40. Rees DC, Williams TN, Gladwin MT. Sickle-cell disease. Lancet. 2010;376(9757):2018-2031. 41. Rice HE, Englum BR, Rothman J, et al. Clinical outcomes of splenectomy in children: report of the splenectomy in congenital hemolytic anemia registry. Am J Hematol. 2015;90(3):187-192. 42. Al-Salem AH. Indications and complications of splenec-tomy for children with sickle cell disease. J Pediatr Surg. 2006;41(11):1909-1915. 43. Rachmilewitz EA, Giardina PJ. How I treat thalassemia. Blood. 2011;118(13):3479-3488. 44. Phrommintikul A, Sukonthasarn A, Kanjanavanit R, Nawarawong W.


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Surgery_Schwartz. J Pediatr Surg. 2006;41(11):1909-1915. 43. Rachmilewitz EA, Giardina PJ. How I treat thalassemia. Blood. 2011;118(13):3479-3488. 44. Phrommintikul A, Sukonthasarn A, Kanjanavanit R, Nawarawong W. Splenectomy: a strong risk factor for pul-monary hypertension in patients with thalassaemia. Heart. 2006;92(10):1467-1472. 45. Sheikha AK, Salih ZT, Kasnazan KH, et al. Prevention of overwhelming postsplenectomy infection in thalassemia patients by partial rather than total splenectomy. Can J Surg. 2007;50(5):382-386. 46. Dedeoglu S, Bornaun H. Pulmonary hypertension in chil-dren with beta thalassemia major, are splenectomy and high-ferritin levels related or not? J Pediatr Hematol Oncol. 2017;39(4):259-265. 47. Cines DB, Blanchette VS. Immune thrombocytopenic purpura. N Engl J Med. 2002;346(13):995-1008. 48. George JN. Sequence of treatments for adults with primary immune thrombocytopenia. Am J Hematol. 2012;87(suppl 1): S12-S15. 49. Rodeghiero F, Besalduch J, Michel M, Provan D, Grotzinger


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Surgery_Schwartz. JN. Sequence of treatments for adults with primary immune thrombocytopenia. Am J Hematol. 2012;87(suppl 1): S12-S15. 49. Rodeghiero F, Besalduch J, Michel M, Provan D, Grotzinger K, Thompson G. Treatment practices in adults with chronic immune thrombocytopenia—a European perspective. Eur J Haematol. 2010;84(2):160-168. 50. Auger S, Duny Y, Rossi JF, Quittet P. Rituximab before splenectomy in adults with primary idiopathic thrombo-cytopenic purpura: a meta-analysis. Br J Haematol. 2012; 158(3):386-398. 51. Kojouri K, Vesely SK, Terrell DR, George JN. Splenectomy for adult patients with idiopathic thrombocytopenic purpura: a systematic review to assess long-term platelet count responses, prediction of response, and surgical complications. Blood. 2004;104(9):2623-2634. 52. Mikhael J, Northridge K, Lindquist K, Kessler C, Deuson R, Danese M. Short-term and long-term failure of laparoscopic splenectomy in adult immune thrombocyto-penic purpura patients: a systematic review. Am J Hematol.


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Surgery_Schwartz. for splenomegaly: retrospective clinical study. World J Surg. 2013;37(1):52-58. 171. Berindoague R, Targarona EM, Balague C, et al. Can we pre-dict immediate outcome after laparoscopic splenectomy for splenomegaly? Multivariate analysis of clinical, anatomic, and pathologic features after 3D reconstruction of the spleen. Surgical innovation. 2007;14(4):243-251. 172. Vancauwenberghe T, Snoeckx A, Vanbeckevoort D, Dymarkowski S, Vanhoenacker FM. Imaging of the spleen: what the clinician needs to know. Singapore Med J. 2015;56(3):133-144. 173. Karakas HM, Tuncbilek N, Okten OO. Splenic abnormali-ties: an overview on sectional images. Diagn Interv Radiol. 2005;11(3):152-158. 174. Dent D, Alsabrook G, Erickson BA, et al. Blunt splenic injuries: high nonoperative management rate can be achieved with selective embolization. J Trauma. 2004;56(5): 1063-1067. 175. Koconis KG, Singh H, Soares G. Partial splenic emboliza-tion in the treatment of patients with portal hypertension: a review of the


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Surgery_Schwartz. with selective embolization. J Trauma. 2004;56(5): 1063-1067. 175. Koconis KG, Singh H, Soares G. Partial splenic emboliza-tion in the treatment of patients with portal hypertension: a review of the english language literature. J Vasc Interv Radiol. 2007;18(4):463-481. 176. Cuker A, Cines DB. Evidence-based mini-review: is indium-labeled autologous platelet scanning predictive of response to splenectomy in patients with chronic immune thrombo-cytopenia? Hematology Am Soc Hematol Educ Program. 2010;2010:385-386. 177. Wu Z, Zhou J, Pankaj P, Peng B. Comparative treatment and literature review for laparoscopic splenectomy alone versus preoperative splenic artery embolization splenectomy. Surg Endosc. 2012;26(10):2758-2766. 178. Mousa A, Armbruster J, Adongay J, AbuRahma AF. Splenic artery embolization as a treatment option for chronic pancyto-penia secondary to hypersplenism: a case report and review of literature. Vasc Endovascular Surg. 2012;46(6):501-503. 179. Williams G, Rosen MP,


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Surgery_Schwartz. embolization as a treatment option for chronic pancyto-penia secondary to hypersplenism: a case report and review of literature. Vasc Endovascular Surg. 2012;46(6):501-503. 179. Williams G, Rosen MP, Parker JA, Kolodny GM. Splenic implants detected by SPECT images of Tc-99m labeled damaged red blood cells. Clin Nucl Med. 2006;31(8): 467-469. 180. Lui EH, Lau KK. Intra-abdominal splenosis: how clinical his-tory and imaging features averted an invasive procedure for tissue diagnosis. Australas Radiol. 2005;49(4):342-344. 181. Balague C, Vela S, Targarona EM, et al. Predictive factors for successful laparoscopic splenectomy in immune thrombocy-topenic purpura: study of clinical and laboratory data. Surg Endosc. 2006;20(8):1208-1213. 182. Sweet PH, Khoo T, Nguyen S. Nonalcoholic fatty liver dis-ease. Prim Care. 2017;44(4):599-607. 183. Bolton-Maggs PH, Langer JC, Iolascon A, Tittensor P, King MJ; General Haematology Task Force of the British Committee for Standards in Haematology.


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Surgery_Schwartz. liver dis-ease. Prim Care. 2017;44(4):599-607. 183. Bolton-Maggs PH, Langer JC, Iolascon A, Tittensor P, King MJ; General Haematology Task Force of the British Committee for Standards in Haematology. Guidelines for the diagnosis and management of hereditary spherocytosis—2011 update. Br J Haematol. 2012;156(1):37-49. 184. Tovo CV, de Mattos AZ, Coral GP, Branco FS, Suwa E, de Mattos AA. Noninvasive imaging assessment of non-alcoholic fatty liver disease: focus on liver scintigraphy. World J Gastro-enterol. 2015;21(15):4432-4439. 185. Rubin LG, Schaffner W. Clinical practice. Care of the asplenic patient. N Engl J Med. 2014;371(4):349-356. 186. Theilacker C, Ludewig K, Serr A, et al. Overwhelming post-splenectomy infection: a prospective multicenter cohort study. Clin Infect Dis. 2016;62(7):871-878. 187. O’Neal HR, Jr, Niven AS, Karam GH. Critical illness in patients with asplenia. Chest. 2016;150(6):1394-1402. 188. Chong J, Jones P, Spelman D, Leder K, Cheng AC. Over-whelming


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Surgery_Schwartz. HR, Jr, Niven AS, Karam GH. Critical illness in patients with asplenia. Chest. 2016;150(6):1394-1402. 188. Chong J, Jones P, Spelman D, Leder K, Cheng AC. Over-whelming post-splenectomy sepsis in patients with asplenia and hyposplenia: a retrospective cohort study. Epidemiol Infect. 2017;145(2):397-400. 189. Sinwar PD. Overwhelming post splenectomy infection syndrome—review study. Int J Surg. 2014;12(12):1314-1316. 190. Lynch AM, Kapila R. Overwhelming postsplenectomy infec-tion. Infect Dis Clin North Am. 1996;10(4):693-707.Brunicardi_Ch34_p1517-p1548.indd 154623/02/19 2:37 PM 1547THE SPLEENCHAPTER 34 191. Brigden ML. Overwhelming postsplenectomy infection still a problem. West J Med. 1992;157(4):440-443. 192. Dionne B, Dehority W, Brett M, Howdieshell TR. The asplenic patient: post-insult immunocompetence, infection, and vacci-nation. Surg Infect (Larchmt). 2017;18(5):536-544. 193. Dendle C, Sundararajan V, Spelman T, Jolley D, Woolley I. Splenectomy sequelae: an analysis of


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Surgery_Schwartz. immunocompetence, infection, and vacci-nation. Surg Infect (Larchmt). 2017;18(5):536-544. 193. Dendle C, Sundararajan V, Spelman T, Jolley D, Woolley I. Splenectomy sequelae: an analysis of infectious outcomes among adults in Victoria. Med J Aust. 2012;196(9):582-586. 194. Ejstrud P, Kristensen B, Hansen JB, Madsen KM, Schonhey-der HC, Sorensen HT. Risk and patterns of bacteraemia after splenectomy: a population-based study. Scand J Infect Dis. 2000;32(5):521-525. 195. Edgren G, Almqvist R, Hartman M, Utter GH. Splenectomy and the risk of sepsis: a population-based cohort study. Ann Surg. 2014;260(6):1081-1087. 196. Leone G, Pizzigallo E. Bacterial infections following splenec-tomy for malignant and nonmalignant hematologic diseases. Mediterr J Hematol Infect Dis. 2015;7(1):e2015057. 197. Yu RK, Shepherd LE, Rapson DA. Capnocytophaga canimor-sus, a potential emerging microorganism in splenectomized patients. Br J Haematol. 2000;109(4):679. 198. Sica S, Di Mario A, Salutari P, et al.


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Surgery_Schwartz. RK, Shepherd LE, Rapson DA. Capnocytophaga canimor-sus, a potential emerging microorganism in splenectomized patients. Br J Haematol. 2000;109(4):679. 198. Sica S, Di Mario A, Salutari P, et al. Morganella morganii pericarditis after resolvent splenectomy for immune pan-cytopenia following allogeneic bone marrow transplanta-tion for acute lymphoblastic leukemia. Clin Infect Dis. 1995;21(4):1052-1053. 199. Demar M, Legrand E, Hommel D, Esterre P, Carme B. Plas-modium falciparum malaria in splenectomized patients: two case reports in French Guiana and a literature review. Am J Trop Med Hyg. 2004;71(3):290-293. 200. Rosner F, Zarrabi MH, Benach JL, Habicht GS. Babesiosis in splenectomized adults. Review of 22 reported cases. Am J Med. 1984;76(4):696-701. 201. Okabayashi T, Hanazaki K. Overwhelming postsplenectomy infection syndrome in adults—a clinically preventable disease. World J Gastroenterol. 2008;14(2):176-179.Brunicardi_Ch34_p1517-p1548.indd 154723/02/19 2:37 PM


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Surgery_Schwartz. Abdominal Wall, Omentum, Mesentery, and RetroperitoneumScott Kizy and Sayeed Ikramuddin 35chapterABDOMINAL WALLGeneral ConsiderationsIncision and closure of the abdominal wall is among the most common surgical procedures performed. Knowledge of its lay-ered anatomy is critical in the management of surgical patients. Cranially defined by the costal margin and xiphoid process and caudally ending over the pubic bones of the pelvis, the abdomi-nal wall provides support and protection to the peritoneal and retroperitoneal organs.Surgical AnatomyEmbryologically, the abdominal wall is derived from the meso-derm and envelops the future abdominal contents as bilateral migrating layers originating from the paravertebral area. The leading bars of these sheets fuse in the midline as the linea alba at 7 weeks after gestation and reach the umbilicus at 8 weeks.The abdominal wall consists of nine distinct layers: skin, subcutaneous tissue, superficial fascia, external oblique muscle, internal


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Surgery_Schwartz. at 7 weeks after gestation and reach the umbilicus at 8 weeks.The abdominal wall consists of nine distinct layers: skin, subcutaneous tissue, superficial fascia, external oblique muscle, internal oblique muscles, transversus abdominus muscle, trans-versalis fascia, preperitoneal adipose tissue, and peritoneum. The subcutaneous tissue is composed of superficial adipose tis-sue that is contiguous with Camper’s fascia anteriorly. Deep to this, Scarpa’s fascia consists of a fibrous matrix of tissue that fuses with the anterior layer of fascia of the flank and back.The muscles of the abdominal wall consist of the rectus abdominus medially and the external oblique, internal oblique, and transversus abdominis laterally. The rectus abdominus is a paired longitudinal muscle spanning the length of the abdomen. Divided by the linea alba, both rectus muscles originate at the pubic symphysis and crest and insert on the xiphoid process, the fifth and sixth ribs, and the seventh costal cartilage.


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Surgery_Schwartz. the abdomen. Divided by the linea alba, both rectus muscles originate at the pubic symphysis and crest and insert on the xiphoid process, the fifth and sixth ribs, and the seventh costal cartilage. Three ten-dinous insertions cross the rectus muscle along its length. The muscle is contained within an aponeurotic sheath formed from the fusion of differing components of the lateral fascial layers.Laterally, the three muscular layers (external oblique, internal oblique, and transversus abdominis) have obliquely oriented fibers relative to one another. The external oblique arises from the eighth rib and inserts medially into the linea alba and anterior iliac crests. The fibers of this muscular layer travel medial and caudal from its insertion. The internal oblique originates from the thoracolumbar fascia. Its fibers travels cra-nially and anteriorly, inserting on the lower costal margin and the xiphoid process. The deep muscular layer, the transversus abdominis muscle, begins at the


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Surgery_Schwartz. fascia. Its fibers travels cra-nially and anteriorly, inserting on the lower costal margin and the xiphoid process. The deep muscular layer, the transversus abdominis muscle, begins at the costal margin and lumbar fas-cia, runs horizontally and anteriorly, and inserts on the linea alba, xiphoid process, and pubis symphysis (Fig. 35-1).Altogether, these muscular layers provide fascial aponeu-rotic sheaths anteriorly. These fascial layers provide variable contributions to the separate layers of the rectus sheath and ultimately fuse in the midline as the linea alba. The rectus sheath that encloses the rectus muscles has differing composi-tions above and below the arcuate line. The anterior rectus sheath is composed of the external oblique aponeurosis through-out its length. The internal oblique aponeurosis is bilaminar and contributes to the anterior and posterior rectus sheaths above the arcuate line. Below this line, the internal aponeurosis contrib-utes only to the anterior rectus


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Surgery_Schwartz. aponeurosis is bilaminar and contributes to the anterior and posterior rectus sheaths above the arcuate line. Below this line, the internal aponeurosis contrib-utes only to the anterior rectus sheath. The transversus abdomi-nis aponeurosis contributes the posterior rectus sheath above the arcuate line and the anterior rectus sheath below the arcuate line. Therefore, below the arcuate line, all the aponeurotic layers of the lateral musculature form the anterior sheath, leaving the transversalis fascia as the only posterior fascial covering. This layer is a weak fibrous layer separated from the peritoneum by preperitoneal fat (Fig. 35-2).Along the posterior abdominal wall are folds correspond-ing to underlying vasculature and embryologic remnants. The median umbilical fold is formed by the obliterated urachus trav-eling from the dome of the bladder to the umbilicus in the mid-line. The bilateral medial folds are formed by remnants of the umbilical arteries. Lastly, the lateral folds are


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Surgery_Schwartz. urachus trav-eling from the dome of the bladder to the umbilicus in the mid-line. The bilateral medial folds are formed by remnants of the umbilical arteries. Lastly, the lateral folds are associated with the inferior epigastric vessels.The deep blood supply of the abdominal wall is supplied mostly from the inferior and superior epigastric arteries. The superior epigastric artery is the final branch of the internal tho-racic artery. It enters the rectus sheath below the costal margin 1Abdominal Wall 1549General Considerations / 1549Surgical Anatomy / 1549Physiology / 1550Abdominal Surgical Incisions and Closure / 1550Congenital Abnormalities / 1553Acquired Abnormalities / 1554Omentum 1557Surgical Anatomy / 1557Physiology / 1558Acquired Disorders / 1558Mesentery 1559Surgical Anatomy / 1559Sclerosing Mesenteritis / 1559Mesenteric Cysts / 1560Mesenteric Tumors / 1561Retroperitoneum 1561Surgical Anatomy / 1561Retroperitoneal Infections / 1561Retroperitoneal Fibrosis /


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Surgery_Schwartz. Anatomy / 1559Sclerosing Mesenteritis / 1559Mesenteric Cysts / 1560Mesenteric Tumors / 1561Retroperitoneum 1561Surgical Anatomy / 1561Retroperitoneal Infections / 1561Retroperitoneal Fibrosis / 1562Brunicardi_Ch35_p1549-p1566.indd 154912/02/19 9:58 AM 1550Key Points1 There are differences in the anatomic structure in the rectus sheath above and below the arcuate line. Below the arcuate line, all the lateral fascial layers combine and travel anteriorly forming the anterior rectus sheath and leaving the posterior aspect of the lower portion of the rectus muscles without an aponeurotic covering. Above the arcuate line, the posterior rectus sheath is formed by a portion of the internal oblique aponeurosis and the transversus abdominus sheath, and the anterior rectus sheath is formed by the remaining fibers of the internal oblique and the external oblique aponeuroses.2 Two randomized trials have found that closure of midline incisions with small fascial stitches of five to eight mm


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Surgery_Schwartz. the remaining fibers of the internal oblique and the external oblique aponeuroses.2 Two randomized trials have found that closure of midline incisions with small fascial stitches of five to eight mm length and five mm width is beneficial in preventing inci-sional hernias of the abdominal wall.3 Primary repair of ventral incisional hernias results in high recurrence rates, and repair utilizing other methods, includ-ing prosthetic mesh and component separation, are preferred techniques of repair.4 Laparoscopic incisional hernia repair results in similar recur-rence rates and wound infections, compared to open repair. Laparoscopic repair may result in a faster recovery and shorter hospitalization; however, there may be an increase in bowel injury when compared to an open repair.5 Desmoid tumors should be monitored for asymptomatic patients as there is a possibility of spontaneous regression. For patients with rapidly growing or symptomatic tumors resection is recommended. If complete


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Surgery_Schwartz. tumors should be monitored for asymptomatic patients as there is a possibility of spontaneous regression. For patients with rapidly growing or symptomatic tumors resection is recommended. If complete pathologic resection is not achievable without significant morbidity, more modest resection is recommended along with treatment with adju-vant therapies.6 The omentum provides an immunogenic and fibrotic response to foreign stimuli, allowing the abdomen to wall off infections preventing diffuse peritonitis.7 The role of surgery in the treatment of sclerosing mesenteri-tis is minimal and is most often undertaken to obtain tissue for diagnosis. Most cases should be treated medically with surgical interventions reserved for cases of bowel obstruc-tion and ischemia.8 Surgical interventions for retroperitoneal fibrosis include obtaining tissue for pathologic diagnosis, relieving ureteral obstructions via ureterolysis or ureteral stenting, and reliev-ing vascular obstructions via endovascular


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Surgery_Schwartz. fibrosis include obtaining tissue for pathologic diagnosis, relieving ureteral obstructions via ureterolysis or ureteral stenting, and reliev-ing vascular obstructions via endovascular stenting of affected vessels. Most cases are treated successfully with the use of steroids.and travels along the posterior surface of the anterior sheath and forms an anastomosis with the inferior epigastric artery at the umbilicus. The inferior epigastric artery arises from the external iliac artery. These arteries provide a collateral circula-tion between the vasculature of the upper and lower extremities (Fig. 35-3). The abdominal wall is also supplied by branches of the subcostal and lumbar arteries. Superficially, the abdominal wall subcutaneous and skin tissue is supplied by branches of the superficial epigastric arteries, femoral arteries, superficial exter-nal pudendal, and superficial circumflex arteries. Venous drain-age of the abdominal wall is variable but typically follows the


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Surgery_Schwartz. superficial epigastric arteries, femoral arteries, superficial exter-nal pudendal, and superficial circumflex arteries. Venous drain-age of the abdominal wall is variable but typically follows the aforementioned arteries. Above the umbilicus, the lymphatics of the abdominal wall drain into the superficial axillary nodes. Below the umbilicus, these drain into the inguinal nodes. Lym-phatics near the umbilicus can drain along the falciform liga-ment toward the hepatic nodes.Innervation of the abdominal wall is segmental, leading to a dermatomal sensory pattern. Afferent branches of the T4 to L1 nerve roots provide sensation of the abdominal wall (see Fig. 35-3). The muscles of the abdominal wall are inner-vated by the efferent branches of spinal nerves T6 to T12.PhysiologyAside from providing protection of the intraabdominal and retroperitoneal organs, the abdominal wall muscles assist with flexion, extension, and rotation of the torso along with the muscles of the back and trunk.


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Surgery_Schwartz. protection of the intraabdominal and retroperitoneal organs, the abdominal wall muscles assist with flexion, extension, and rotation of the torso along with the muscles of the back and trunk. Working as a unit, the rectus muscles and external/internal obliques activate to flex the trunk anteriorly and laterally. Rotation of the torso is performed by simultaneous stimulation of the contralateral external oblique and ipsilateral internal oblique. To rotate the torso to the right requires simultaneous contraction of the right internal oblique muscle and left external oblique muscle, and vice versa for leftward rotation. Altogether, the muscles of the abdominal wall can act to raise intraabdominal pressure providing assistance with respiration, coughs, defecation, uri-nation, and parturition.Abdominal Surgical Incisions and ClosureKnowledge of the abdominal wall anatomy is an important aspect of safe entry into the abdomen. The goal of an efficacious incision is to provide adequate


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Surgery_Schwartz. Surgical Incisions and ClosureKnowledge of the abdominal wall anatomy is an important aspect of safe entry into the abdomen. The goal of an efficacious incision is to provide adequate exposure to perform the proce-dure with minimal perturbation of the abdominal wall function.Incisions for open abdominal surgery are generally located in proximity to operative targets. There are two general types of incisions: longitudinal or transverse/oblique (Fig. 35-4). There does not appear to be differences in early or late postoperative complications or recovery time between these two types of inci-sions. However, transverse incisions may be associated with lower incisional hernia rates but higher rates of wound infec-tions. Overall, without clear evidence of superiority the choice of incision remains a surgeon-dependent decision. Several retractor systems can be used to provide exposure using these open incisions. Examples include the Bookwalter, Omni-Tract, and Thompson retractors (Fig.


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Surgery_Schwartz. remains a surgeon-dependent decision. Several retractor systems can be used to provide exposure using these open incisions. Examples include the Bookwalter, Omni-Tract, and Thompson retractors (Fig. 35-5).The most common longitudinal incision is the midline incision. Providing access to most intraabdominal organs and some retroperitoneal structures, the midline incision is carried down to the linea alba to allow access to the abdomen with mini-mal injury to skeletal muscles, nerves, and vessels. Paramedian longitudinal incisions are made lateral to the midline through the rectus sheath or in the pararectus location. These incisions restrict access to the contralateral abdomen and pelvis and risk damage to the musculature, vessels, and nerves.Closure of the midline incision requires reapproximation without undue tension or strangulation of the tissue to prevent Brunicardi_Ch35_p1549-p1566.indd 155012/02/19 9:58 AM 1551ABDOMINAL WALL, OMENTUM, MESENTERY, AND RETROPERITONEUMCHAPTER


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Surgery_Schwartz. without undue tension or strangulation of the tissue to prevent Brunicardi_Ch35_p1549-p1566.indd 155012/02/19 9:58 AM 1551ABDOMINAL WALL, OMENTUM, MESENTERY, AND RETROPERITONEUMCHAPTER 35perioperative dehiscence or incisional hernia formation. Clas-sically, the midline fascia of the incision is closed using sutures placed 1 cm from the edge and a width of 1 cm apart. Two European randomized controlled trials demonstrated reduced rates of incisional hernia with shorter stitch width (5–8 mm) compared to the standard 1 cm stitches. Studies are ongoing in the United States at this time. Several studies have evaluated the use of prophylactic mesh implanta-tion in the closure of the midline incision. While these studies demonstrate reduced incisional hernia formation in the short-term, more long-term data is needed to determine the inci-dence of mesh-related complications. Furthermore, the optimal location of mesh implantation and type of mesh used are still being evaluated.When


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Surgery_Schwartz. more long-term data is needed to determine the inci-dence of mesh-related complications. Furthermore, the optimal location of mesh implantation and type of mesh used are still being evaluated.When performing a transverse or oblique incision, a sur-geon can either divide or separate the muscle fibers of the abdom-inal wall. The classic McBurney’s incision for appendectomy, an oblique incision performed one-third of the way from the iliac spine to the umbilicus, is an example of a muscle-splitting approach. A subcostal incision can be used to access the upper abdomen, liver, gallbladder, spleen, pancreas, or adrenals. On closure of these incisions, two layers must be approximated. The deep layer includes the internal oblique, transversus abdominus muscle, and the transversalis fascia. The superficial layer includes the anterior aponeurotic tissue of the rectus sheath medially and the external muscle/aponeurosis laterally. A bilateral subcostal incision, or a chevron incision, can be


Surgery_Schwartz

Surgery_Schwartz. superficial layer includes the anterior aponeurotic tissue of the rectus sheath medially and the external muscle/aponeurosis laterally. A bilateral subcostal incision, or a chevron incision, can be used to access organs of the upper abdomen and diaphragm. A Mercedes-Benz modification includes a midline incision superiorly, providing further access to the upper abdomen or the lower mediastinum.Pelvic procedures are commonly performed through a Pfannenstiel incision. This incision is performed via a trans-verse skin incision carried down to the anterior rectus sheath. The sheath is also transversely incised and dissected off the underlying rectus muscle. The rectus muscles are separated, and access through the transversalis fascia is performed lon-gitudinally. Closure of this incision requires approximation of the peritoneum and rectus muscles and closure of the anterior rectus sheath.Laparoscopic port site incision placement must be care-fully planned based on approach angles and


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Surgery_Schwartz. requires approximation of the peritoneum and rectus muscles and closure of the anterior rectus sheath.Laparoscopic port site incision placement must be care-fully planned based on approach angles and working distances both to the operative site and between ports. Placement of a 278910789106511L1L2L31010(A) Anterior view(B) Rectus abdominis (RA)(C) External oblique (EO) (layer 1)(D) Internal oblique (IO) (layer 2)(E) Transversus abdominis (layer 3)Lateral viewsEOIliac crestIntertendinousband (IT)RAIOTARSRSRSEOEOEORAITRAITRAITRALinea albaPyramidalisITITFigure 35-1. Muscles of the anterior abdominal wall. A. The anterior abdominal wall musculature is shown with the rectus sheath reflected on the left side. B. Rectus abdominis. C. External oblique. D. Internal oblique. E. Transversus abdominus. (Reproduced with permission from Moore KL, Agur AM: Essential Clinical Anatomy, 5th edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2014.)Brunicardi_Ch35_p1549-p1566.indd


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Surgery_Schwartz. abdominus. (Reproduced with permission from Moore KL, Agur AM: Essential Clinical Anatomy, 5th edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2014.)Brunicardi_Ch35_p1549-p1566.indd 155112/02/19 9:58 AM 1552SPECIFIC CONSIDERATIONSPART IInasogastric tube and Foley catheter may help to decompress the stomach and bladder reducing injury to these structures on entry. Initial entry into the abdomen may be completed using the open Hasson or closed Veress needle techniques. The Hasson tech-nique involves direct visualization and systematic opening of each fascial layer encountered on entry. The closed technique utilizes the Veress needle to access the abdomen in a controlled fashion. Access to the peritoneum is confirmed using one or a combination of several techniques (saline drop method or measurement of intraabdominal pressure), and gas insuffla-tion is begun. The abdomen can then be accessed using either a visual entry port or a nonvisualized entry port at the site of the


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Surgery_Schwartz. method or measurement of intraabdominal pressure), and gas insuffla-tion is begun. The abdomen can then be accessed using either a visual entry port or a nonvisualized entry port at the site of the needle track or an alternative site. Choice of entry method is still controversial and based on surgeon preference. Retrospec-tive reviews suggest that complications may be lower using the Hasson technique, but randomized trials (although small) have not found significant differences in techniques.Abdominal incisions can lead to significant patient mor-bidity. Complications include hematomas/seromas, surgical site infections, fascial dehiscence, incisional hernias, and nerve injuries among others. In general, minimizing opera-tive incision lengths to only that which is necessary for a safe operation is prudent to reduce these complications and morbidity.Right externaloblique muscleFibers of rightexternal obliqueaponeurosisFibers of leftinternal obliqueaponeurosisFibers passing from


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Surgery_Schwartz. operation is prudent to reduce these complications and morbidity.Right externaloblique muscleFibers of rightexternal obliqueaponeurosisFibers of leftinternal obliqueaponeurosisFibers passing from superficial to deep(and vice versa) at linea albaLeft internaloblique muscleIntermuscular exchange of fibers between aponeuroses ofcontralateral external and internal oblique muscles.Fibers of left externaloblique aponeurosis,which run deep on theright side and runningsuperficially on the leftsideDeep fibers of left external oblique aponeurosisUmbilical ringDeep fibers of right external oblique aponeurosisIntramuscular exchange of superficial and deepfibers within aponeuroses of contralateralexternal oblique muscles. Transverse sections(B) Anterior view(A) Anterior viewsLineaalbaRectus abdominisAponeurosisof externalobliqueAponeurosisof internalobliqueAponeurosisof transversusabdominisParietal peritoneumSkinTransversus abdominisInternal obliqueExternal obliqueDeep membranous layerof


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Surgery_Schwartz. externalobliqueAponeurosisof internalobliqueAponeurosisof transversusabdominisParietal peritoneumSkinTransversus abdominisInternal obliqueExternal obliqueDeep membranous layerof subcutaneoustissueTransversalis fasciaExtraperitoneal fatRectussheathLinea alba(note fibers passingfrom superficial to deep,and vice versa, as inright side of figure A)Superficial fatty layer ofsubcutaneoustissueInvesting (deep) fascia:SuperficialIntermediateDeepFigure 35-2. Fiber direction and cross-sectional anatomy of the abdominal wall. A. Muscular and aponeurosis fiber direction of external and internal obliques. B. Cross-sectional anatomy of the anterior abdominal wall above and below the arcuate line. The posterior leaf of the rectus sheath exists above the arcuate line. Below this line, all aponeurotic sheaths converge and travel anterior to the rectus muscles, leaving the posterior rectus uncovered by a fascial layer. (Reproduced with permission from Moore KL, Agur AM: Essential Clinical Anatomy,


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Surgery_Schwartz. converge and travel anterior to the rectus muscles, leaving the posterior rectus uncovered by a fascial layer. (Reproduced with permission from Moore KL, Agur AM: Essential Clinical Anatomy, 5th edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2014.)Brunicardi_Ch35_p1549-p1566.indd 155212/02/19 9:58 AM 1553ABDOMINAL WALL, OMENTUM, MESENTERY, AND RETROPERITONEUMCHAPTER 35Congenital AbnormalitiesThe folds of mesodermal cells that form the abdominal wall lay-ers begin to form in the early weeks after gestation. The folds develop in the cephalic, caudal, and right/left lateral directions and converge at the umbilicus around 8 weeks. At around 6 weeks of development the contents of the abdominal cavity outgrow the space allowed by the surrounding layers of the Thoraco-abdominalnerves (T7-T11)Lateral cutaneous branchof subcostal nerve (T12)Anterior cutaneous branchof subcostal nerve (T12)Iliohypogastric nerve (L1)Ilio-inguinal nerve (L1)Xiphoid processAnterior superior iliac


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Surgery_Schwartz. (T7-T11)Lateral cutaneous branchof subcostal nerve (T12)Anterior cutaneous branchof subcostal nerve (T12)Iliohypogastric nerve (L1)Ilio-inguinal nerve (L1)Xiphoid processAnterior superior iliac spine (ASIS)AnteriorcutaneousbranchesLateralcutaneousbranchesInguinal ligamentSuperiorepigastric a.External obliqueInternal oblique TransversusabdominisInferior epigastric a.Deep circumflexiliac a.Superficialepigastric a.Superficialcircumflex iliac a.External iliac a.Femoral a.Transversalis fasciaMusculophrenic a.11th posteriorintercostal a.10th posteriorintercostal a.Subcostal a.Internal thoracic a.Anterior viewFigure 35-3. Neurovascular anatomy of the anterior abdominal wall. The right image demonstrates the arteries of the deep abdominal wall. The superior epigastric and inferior epigastric form an anastomosis along the posterior aspect of the rectus muscle. The image on the left demonstrates the dermatomal distribution of cutaneous nerves of the abdominal wall. (Reproduced with permission


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Surgery_Schwartz. an anastomosis along the posterior aspect of the rectus muscle. The image on the left demonstrates the dermatomal distribution of cutaneous nerves of the abdominal wall. (Reproduced with permission from Moore KL, Agur AM: Essential Clinical Anatomy, 5th edition. Philadelphia, PA: Lippincott Williams & Wilkins; 2014.)CDEFHGABFigure 35-4. Various open abdominal wall incisions. A. Mid-line incision. B. Paramedian incision. C. Right subcostal incision and “saber slash” extension (dashed line). D. Bilateral subcostal incision (also chevron incision) with “Mercedes Benz” extension (dashed line). E. Rocky-Davis incision and Weir extension (dashed line). F. McBurney incision. G. Transverse incision. H. Pfannen-stiel incision.Figure 35-5. Thompson retractor for exposure of intra-abdominal structures utilizing an upper midline incision.Brunicardi_Ch35_p1549-p1566.indd 155312/02/19 9:58 AM 1554SPECIFIC CONSIDERATIONSPART IIabdominal wall, resulting in temporary herniation of the abdom-inal


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Surgery_Schwartz. utilizing an upper midline incision.Brunicardi_Ch35_p1549-p1566.indd 155312/02/19 9:58 AM 1554SPECIFIC CONSIDERATIONSPART IIabdominal wall, resulting in temporary herniation of the abdom-inal contents through a central defect. At this time, the vitelline duct (omphalomesenteric duct) and allantois also pass through the central defect. The vitelline duct serves as a conduit to the embryologic midgut and the yolk sac. As the midgut develops outside of the abdomen, it undergoes a 270° counterclockwise rotation and reenters the abdomen at around 12 weeks. Failure of the midgut to reenter the abdomen leads to the congenital abdominal wall defect known as an omphalocele, in which the contents of the defect protrude through an open umbilicus and are covered by an amniotic/peritoneal membrane. Gastroschisis, on the other hand, results from either malformation or disrup-tion of the abdominal wall, either from genetic defects or vas-cular compromise. Gastroschisis presents as protruding


Surgery_Schwartz

Surgery_Schwartz. Gastroschisis, on the other hand, results from either malformation or disrup-tion of the abdominal wall, either from genetic defects or vas-cular compromise. Gastroschisis presents as protruding viscera through a defect lateral to the umbilicus (usually along the right side) without the amniotic sac covering.The vitelline duct usually involutes at around the eighth to ninth week after gestation. Failure of vitelline duct regression can lead to several abnormalities depending on the spectrum of involution. This spectrum includes total persistence of the vitel-line duct leading to omphalomesenteric fistula causing drainage of intestinal contents at the umbilicus, to partial closure leading to omphalomesenteric cyst. If the vitelline remnant persists at the ileal border, a Meckel’s diverticulum forms. The vitelline duct may also persist as a fibrous attachment of the intestine to the abdominal wall predisposing the patient to bowel obstruc-tions. Fistulas, cysts, and fibrous attachments


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Surgery_Schwartz. forms. The vitelline duct may also persist as a fibrous attachment of the intestine to the abdominal wall predisposing the patient to bowel obstruc-tions. Fistulas, cysts, and fibrous attachments should be resected when diagnosed.The urachus is the proximal portion of the allantois form-ing as the bladder descends into its pelvic position. The urachus closes and forms the median umbilical ligament of the abdomi-nal wall as previously described. Failure of the urachus to close results in urinary fistula or cyst. These are treated by urachal excision and closure of the bladder defect.Acquired AbnormalitiesAbdominal Wall Hernias. A protrusion or bulge of abdomi-nal contents through the abdominal wall muscle/fascia repre-sents an abdominal wall hernia. This may be present at birth or acquired from weakening or disruption of the overlying fascia, or from failed healing of a surgical incision. Hernias may present as asymptomatic bulges that increase with Val-salva maneuvers, or with


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Surgery_Schwartz. from weakening or disruption of the overlying fascia, or from failed healing of a surgical incision. Hernias may present as asymptomatic bulges that increase with Val-salva maneuvers, or with significant discomfort. On physical exam, the patient’s abdominal wall should be evaluated with the patient both standing and in the recumbent position. Her-nias may reduce spontaneously or with manual pressure. If a hernia is incarcerated, it cannot be reduced and generally requires surgical correction. If intestine is incarcerated in the hernia defect, bowel obstruction may ensue, which represents a surgical emergency. Incarcerated hernias present with sig-nificant pain, nausea, and vomiting. A hernia is considered strangulated if blood supply to its contents is compromised. Localized ischemia may lead to infarction and eventual perfo-ration if left untreated.Nonincisional hernias are named based on their location on the abdominal wall. Epigastric hernias are defects in the abdominal wall


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Surgery_Schwartz. may lead to infarction and eventual perfo-ration if left untreated.Nonincisional hernias are named based on their location on the abdominal wall. Epigastric hernias are defects in the abdominal wall located between the umbilicus and the xiphoid process. These hernias are usually small but may be associ-ated with multiple defects. They result from multiple factors, including muscle weakness, congenitally weakened epigastric fascia, or increases in intra-abdominal pressure. Epigastric hernias rarely contain bowel and usually contain portions of the omentum or falciform ligament. Given the rarity of incarcera-tion, repair of an epigastric hernia is indicated for symptomatic patients only. Laparoscopic repair can be attempted, but this type of hernia usually can be managed with a small incision where the defect is closed with interrupted sutures.Umbilical hernias may be congenital or acquired. Umbili-cal hernias are common in newborns, especially in premature infants. Closure of an


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Surgery_Schwartz. incision where the defect is closed with interrupted sutures.Umbilical hernias may be congenital or acquired. Umbili-cal hernias are common in newborns, especially in premature infants. Closure of an umbilical defect occurs after birth as the muscles of the rectus abdominis grow toward one another. Most umbilical hernias close spontaneously by 5 years of age and can be monitored as they will spontaneously resolve. Indications for repair include incarceration, symptomatic hernia, failure to decrease in size or if the defect fails to close by the age of 5 years.In adults, umbilical hernias form because of increased abdominal pressure due to pregnancy, obesity, or ascites. Females are at higher risk for this type of hernia than men. Small, asymptomatic hernias may be followed clinically. How-ever, if an umbilical hernia enlarges in size, causes symptoms, or incarcerates surgical treatment should be offered. Hernias can be repaired laparoscopically or with an open procedure. Mesh should


Surgery_Schwartz

Surgery_Schwartz. if an umbilical hernia enlarges in size, causes symptoms, or incarcerates surgical treatment should be offered. Hernias can be repaired laparoscopically or with an open procedure. Mesh should be employed for large defects where the fascial edges cannot be approximated without tension. In this case, mesh should be placed as a sublay technique (below the fascia) and sutured in place to prevent migration.Patients with cirrhosis and associated ascites with an umbilical hernia pose a significant clinical dilemma. Umbilical defects enlarge in these patients because of high intra-abdominal pressure associated with uncontrolled ascites. With severe liver disease, these patients are at high risk of operative complica-tions. Most hernias contain ascites; however, omentum and bowel may also enter the defect. Given the high pressure, skin breakdown may ensue leading to hernia rupture or weeping as well as risk of spontaneous bacterial peritonitis. All attempts should be made to control the


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Surgery_Schwartz. the defect. Given the high pressure, skin breakdown may ensue leading to hernia rupture or weeping as well as risk of spontaneous bacterial peritonitis. All attempts should be made to control the patient’s ascites prior to repair. Therefore, asymptomatic patients should be managed conserva-tively with aggressive management of ascites. Liver transplant candidates should undergo repair at the time of transplanta-tion as pretransplant repair has high morbidity and mortality. Patients with incarcerated hernias or with thinning or ruptured skin overlying the hernia should be treated emergently.Hernias that occur along the arcuate line are known as Spigelian hernias. While rare, these hernias form due to the anatomic weakness of lack of a posterior rectus sheath below the arcuate line. As the hernia develops, peritoneum that passes through the arcuate line will pass laterally toward the external oblique muscle given the overlying aponeurosis (Fig. 35-6). Most patients present with pain and


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Surgery_Schwartz. develops, peritoneum that passes through the arcuate line will pass laterally toward the external oblique muscle given the overlying aponeurosis (Fig. 35-6). Most patients present with pain and swelling in the mid to lower abdomen. Incarceration is common as up to 20% of patients present with a nonreducible hernia. Given the high rate of incar-ceration, surgical repair is usually recommended. Either open or laparoscopic repair can be performed. The defect is closed by approximating the medial and lateral edges of the transversalis fascia to the rectus sheath.Incisional Hernias. Hernias that develop at sites of pre-vious abdominal incisions are known as incisional hernias. Hernias can develop at the site of any previous abdominal incision. Up to 20% of midline incisions will develop her-nias eventually. Vertical incisions may have a higher risk of hernia formation than transverse or oblique incisions. Upper Brunicardi_Ch35_p1549-p1566.indd 155412/02/19 9:58 AM 1555ABDOMINAL WALL,


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Surgery_Schwartz. eventually. Vertical incisions may have a higher risk of hernia formation than transverse or oblique incisions. Upper Brunicardi_Ch35_p1549-p1566.indd 155412/02/19 9:58 AM 1555ABDOMINAL WALL, OMENTUM, MESENTERY, AND RETROPERITONEUMCHAPTER 35abdominal incisions are also at higher risk than lower inci-sions. Laparoscopic port sites may also develop hernias. The etiology of incisional hernias is complex. Several patient-derived factors increase the risk of hernia, including diabe-tes, immunosuppressant use, obesity, smoking, malnutrition, and connective tissue disorders. Local operative factors may also be implicated, including technique, wound infection, or high tension at the time of closure. Hernias can develop up to 10 years after surgery but normally occur in the early postop-erative period. Incisional hernias can present as asymptom-atic bulges or with severe discomfort. Multiple hernias can be present along the length of the incision. Elective surgery should be recommended in