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Muller, Jr. This book is protected by copyright. No part of this book may be reproduced in any form by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U. Fischer ; associate editors, Daniel B.
Jones, Frank B. Pomposelli, Gilbert R. Upchurch, Jr. Suzanne Klimberg, Steven D. Schwaitzberg, Kirby I. Mastery of surgery Rev. Fischer ; associate editor, Kirby I. Bland ; section editors, Mark P. ISBN hardback : alk. Fischer, Josef E. Mastery of surgery.
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It was not always so. My late father-in-law, Dr. Down, one of those to whom the book is dedicated, was born on a farm near Odebolt, Iowa in , one of ten children on acres of rich Missouri bottomland. All of the children survived into adulthood — a remarkable achievement. The family still holds five-year reunions on that farmland which is owned as an investment by Princeton University which generously allows the family visits.
While the older boys worked the fields, as a young boy my father-in-law was assigned to help out his sisters in the house. Working in the house allowed him ample opportunities to read and develop his desire for knowledge. All of the children were offered college as an option and all but one attended at least one year.
Howard decided to attend Morningside, a small Methodist college in Sioux City, then went on to medical school at Northwestern. He elected to train at the Mayo Clinic which he completed in In fact, he was the first well-trained and experienced surgeon in that vast area. On almost a weekly basis he, and later his partner, Martin Blackstone, and a nurse, rode circuit, operating in various towns; returning the following week to see how well the patients fared under the care of their general practitioner.
The practice expanded and eventually he established a general medical practice and a busy surgical practice in Sioux City, population 85,, which then and now serves as a catchment area for prosperous and relatively well-to-do farmers.
Patients checked in, went shopping downtown and returned at the appropriate time. When Dr. Down died at the age of 91 we found his account books. Many of the patients could not pay and later sent bushels of potatoes, wine, butter, etc.
Some did not pay at all. When he died in , Karen and I went through the house and found some of the most interesting gifts, and I might add, some of the worst liquor, obviously given as payment. For the most part he operated daily, came home for dinner with the family, and then returned to make rounds.
The only way Dr. Down could get away on vacation was to get out of town. It took me a long time before I could live up to the two trips Karen made with the family when she was eleven and thirteen traveling to a variety of states so that he could get away from his practice.
Down lived very modestly in a threebedroom, two-story house with one fullbath in a very nice neighborhood. He was highly respected and beloved. He sat on a number of boards while his wife was the president of a number of organizations including the YWCA and Planned Parenthood.
He loved music and was on the Board of the Sioux City Symphony. In this capacity as a board member, Karen and I were invited to dine with Dr. Down and soprano Victoria de Los Angeles. He continued to operate until late in life and then practiced as a general internist until he was 80 years old. He was a tall, attractive and quiet man who never said much yet dominated a room whether or not he spoke.
During his long career he served as governor of the College and President of the Iowa Surgical Society. He never told Karen whether he approved of me as a son-in-law.
Probably the closest he came to doing so was after I gave grand rounds at one of his hospitals in Sioux City. As he walked me out to the tarmac and just before I boarded the plane to return to Boston, without a word he stuffed a quart of Johnny Walker Black Label under my arm.
I must have done something right! Speaking at his memorial service I reflected that Dr. Down terrified colleagues, nurses and at least one son-in-law without saying much; everyone knew his standards were extremely high. On the day of his funeral his brother and best friend Charles, a lawyer, told me that Howard was indeed very proud of me and he asked if he could get copies of the articles I had written and that his brother had discussed with him.
As you can imagine, it was wonderful to hear this from his best friend but it would have been better to hear it while he was alive. This was a time when surgeons were revered for their daring, their inventiveness, their interest in patients and what they did to cure disease.
Francis D. They were feared but committed. They were respected. They were surgeons! One of my mentors, Dr. Edward D. Churchill, my firstyear chief and long time chair of the department of surgery at Massachusetts General Hospital MGH , believed in surgery and felt that surgery was the answer to disease. Claude Welch, Dean of Boston Surgeons and another one of my mentors believed that an exploratory laparotomy was merely an extension of the physical exam. Welch was a remarkable surgeon who performed the first 10 aneurysmectomies at the Massachusetts General Hospital and some of the first parathyroidectomies, in addition to being a superb and busy GI surgeon.
Robert Linton, another mentor and a giant in the field of vascular surgery, was a meticulous surgeon and taught me a great deal about the technique of surgery. He taught me to own my instruments. Churchill was one of the wisest men I have ever met. If you asked him about the chicken—and you could commit to the time to listen—he would begin with the creation of the egg at the birth of the world. He is not adequately credited for taking the daring stance that he could recognize an applicant at the beginning of the surgical program and commit to finish them five years later.
His rectangular program finally became the surviving form of the American Surgical Residency Program. This is not to take anything from Dr. Halsted was not interested in meeting the surgical needs of the United States. He was interested in producing elite professors. In Cincinnati, Dr. George Heuer, a direct descendent of the Hopkins system and the first Christian Holmes professor, Dr.
Mont Reed, Dr. Nolan Carter and Dr. Gunderson, who filled in during the war waiting for Dr. Carter to return - they were all giants and products of the Hopkins program. They made enormous contributions to surgery: Dr. Heuer to neurosurgery, Dr. Reed to wound healing and general physiology and, Dr. Carter to early cardiothoracic surgery and performing some of the first cardiac perfusion operations in the United States.
While I dedicate this volume in part to my late father-in-law, Dr. Howard Down, I dedicate it to all of those surgeons who dominated American medicine for a century — the century of the surgeon as Dr.
Thorwald put it. They were surgeons who believed in the discipline, they were at the top of their game and looked up to by all as being inventive, courageous and making American surgery the envy of the world as Germanic surgery was destroyed by World War II. I mourn the passing of that time. We are no longer at the top of the heap. We are no longer the adventurous and rigorous group that were simultaneously feared and admired, who did things under difficult conditions, but kept at it until they had perfected operations that have since saved thousands of lives.
Yet the diseases for which we operate are the same and most of our patients are older with a greater number of co-morbidities. Greater technical and analytical skills are required to ensure a live patient at the end of an operative procedure. When will our surgical residents learn these skills?
This the driving reason for this book. We need this book to teach how operations are performed — so that residents and young attendings can have some understanding of the intricasies of operative procedures. Much has changed in the past five years as evidence of our results leads to decreased mortality and morbidity and better outcomes for our patients.
Many changes in surgery have occurred since our work on the 5th edition began eight years ago. The Roux-en-y reconstruction following gastrectomy is generally agreed to be the best reconstruction, better than the gastroduodenostomy Billroth 1 and gastrojejunostomy Billroth 2.
Thyroid carcinoma is being treated as a malignancy and node dissection is part of the best practice. Cancer of the head and neck is being treated with chemotherapy and radiation even if nodes are negative — with a better outcome — and operations are less destructive. Patients with carcinoma of the lung can undergo less extensive resections with no sacrifice of outcome and with minimally invasive techniques less pain and disability.
In vascular disease, minimally invasive techniques done to a considerable extent by vascular surgeons are accompanied by less pain and disability. Eighty-five percent of vascular cases are done endovascularly.
I owe immense gratitude to too many people and undoubtedly will inadvertently miss mentioning all of them. To our children, Erich and Alexandra, of whom I am immensely proud and whose interests I share and I hope partially cultivated. And I must mention my daughter-in-law Hallie, and my son-in-law Peter, both of whom have enthusiastically been welcomed into our family. Thank you to Bob Baker who was kind enough to take me, along with Dr.
Lloyd Nyhus, in the 3rd edition; Dr. I hope we have succeeded in producing a textbook of surgery that is also an atlas reflecting the latest minimally invasive and other techniques as well as showcasing the views of many internationally known surgeons, and hopefully make up, at least partially, for the interference with adequate training.
Josef E. Nyhus Selective vagotomy, antrectomy and gastroduodenostomy for the treatment of duodenal ulcer is an operation that is no longer done. Very frequently parietal cell vagotomy has largely supplanted selective vagotomy, but antrectomy and gastroduodenostomy are useful for carcinoma of the stomach with some slight modifications as pictured elsewhere in the book. This is a classic chapter, and it is included for historical reasons but also because Dr.
Nyhus, one of the originators of Mastery of Surgery wrote a superb chapter. It can be read with profit. Schwaitzberg, John L. Sawyers, and William O. Richards Dr. Steven Schwaitzberg has written an excellent chapter on selective vagotomy and pyloroplasty.
However, as Dr. Schwaitzberg pointed out to me himself, this is an operation that is no longer done very frequently, if at all. However, it is a chapter that elucidates some points concerning surgery of the stomach, unfortunately no longer carried out with any great degree of regularity. It is a chapter that can be read with significant profit. Salam The distal splenorenal shunt was advocated originally as an operation for portal hypertension which had a lower rate of hepatic encephalopathy as compared to the central splenorenal shunt which is useful in patients with significant ascites, patients on whom distal splenorenal is contraindicated , a claim which has not held up.
In addition, recent data from randomized prospective trials seem to conclude that the portacaval shunt is at least as good and perhaps better as in regard to long term outcomes.
Dozois and Roger R. However, as the pouch has become the standard operation for ulcerative colitis—and in some hands, familial polyposis—very few now perform this procedure.
Chapter Care of Stomas e Laurie Maidl and Jill Ohland The care of stomas has become a nursing subspecialty, and the presence of a stoma nurse is a very important part of most hospi- tals of any size. The stoma nurse helps with preoperative planning of the operation, siting of the ileostomy or colostomy, help with difficult stomas, and care of patients with gastrointestinal cutaneous fistulas. Dealing with the ureteropelvic junction in open fashion is an art form that will be applied to the minority of patients.
Nonetheless, it is important that one know how to do the operation if the occasion demands and the preservation of renal function is at stake. Veronikis The chapter on anterior and posterior colporrhaphy presented here is a rather detailed chapter and one which can be read with profit. However, the vaginal floor and its repair has become much more complicated and so anterior and posterior colporrhaphy, in and of itself, are used less frequently.
They may be used with operations for the prolapse of the rectum and they may be utilized in the more sophisticated approach to cystocele and urethracele. However, the anatomy which is described in the anatomical repair, is valuable and can shed light in other specialties to the necessity for having pelvic floor repair, for example, or come in useful as stated in my commentary for repair of rectal prolapse.
Terranova, DeSantis and Frigo, as they have in the past, have contributed to the classic operation which started all repairs of inguinal hernia by Dr. Edoardo Bassini. They come to the conclusion that while of historical interest and of interest as far as the anatomy of the inguinal canal, this operation as currently described in and of itself is no longer viable.
The Shouldice operation described elsewhere in this volume may actually disagree with that particular conclusion. But according to the authors, prosthetic material must be used in order to get a reasonable recurrence rate.
It is presented on the website for historical interest as it really started everything. One may differ as to whether or not Shouldice repair is useful or whether I use a variant of the Shouldice operation, sometimes with vicryl mesh and seem to have low recurrence rates. However, the reader will decide from all of the repairs which are made available in the hernia section. Rutledge Dr. Robb Ruttledge is an excellent practitioner who preceded me in the Massachusetts General Hospital residency by a number of years.
He is an exemplary gentleman and a superb surgeon who, despite being in private practice is highly academic in his approach. I consider him a friend. Ruttledge nicely describes it. The chapter appeared in the fourth edition. Nyhus Chapters and are two classic articles appearing from a golden age in surgery, the collaboration with Dr.
Robert Condon and Dr. Lloyd Nyhus. They deal with the anatomy first and foremost of the inguinal canal by two individuals who have made this a major focus of their long and distinguished academic careers. The anatomy is masterfully described and is well argued. Familiarity with this approach is essential because there are times when there is a hernia in the vicinity of the abdomen and anatomical knowledge of this area will enable a repair to be done with less difficulty, thus preventing another operative procedure.
These two classics have appeared in every previous edition and they are included here on the website. At a time when most surgical residents never learn the anatomy of the inguinal canal, which I find unfortunate, these two chapters are superb in how the knowledge of surgical anatomy can lead not only to a concept but also to performance of an excellent clinical operation at that time.
Stoppa The Shouldice Clinic declined to bring the operation up to date. It is still useful to review this procedure because it is, in its best sense, the descendent of the Bassini repair. It has largely been supplanted by the various mesh repairs and the Lichtenstein tension free repairs. Condon A classic article on the standard repair of Inguinal Hernia. Hubbard, and Irshad H.
In the last decade, an enormous amount of data has been published, which describes the wide spectrum of illnesses that can result following trauma or infection—from a minor, local reaction to surgery, to a systemic stress response, to sepsis, to systemic inflammatory response syndrome SIRS , and, finally, to multi-organ failure MOF.
This information has provided the basis for many new concepts and techniques, which are now used daily in modern surgery. Having a thorough understanding of the mechanisms leading to illness following trauma and infection is crucial for any practicing surgeon. This understanding is the very hallmark of transferring knowledge gained in research to innovative surgical care at the bedside.
The systemic alternations are mediated by a complex signaling system, including afferent and efferent nervous signals, immunological and hormonal adaptations, and a systemic washout of locally produced substances like cytokines and other mediators. The first reference to the stress response resulted from keen observations by Sir David Cuthbertson in the s who described a biphasic immune, inflammatory, and metabolic response to injury. This was further modified by Francis Moore in the s.
It starts with the activation of local coagulation and innate immune system factors. While evidence of a systemic response may be minimal in subjects with mild injury, in an insult of sufficient magnitude, the local activation is followed by systemic inflammatory and endocrine responses.
These can present as surges in plasma catecholamine, cortisol and aldosterone levels inflicting tachycardia, tachypnea, vasoconstriction, lower cardiac output, lower oxygen consumption, lower basal metabolic rate, sodium and water retention, translocation of blood from the peripheral to the central vital organs, and acute-phase protein APP production.
The flow phase of the stress response is characterized by explosive metabolic activity, increasing immune activity, enhanced enzymatic activity, and tissue repair. This response is mediated by a massive neuroendocrine flux involving the production and secretion of catecholamines, antidiuretic hormone ADH , cortisol, insulin, glucagon, and growth hormone GH.
The increased adrenergic stimulation causes an increase in the ratio of glucagon to insulin and, combined with the increased cortisol and cytokines, induces the state of enhanced proteolysis and lipolysis. The supply of amino acids comes from catabolism of mostly skeletal muscle and visceral organs. Some of these amino acids are taken up by the liver as substrates for gluconeogenesis and protein synthesis.
Others are reserved for enzyme synthesis and collagen deposition at the site of injury. The energy needs of most other tissues are met by the availability of free fatty acids FFA and ketone bodies. These are made available via enhanced lipolysis with released glycerol acting as a glucose precursor. The hepatic glucose production supplies the glucose obligatory tissues. Clearly, this process of catabolism requires an enhancement of blood flow to the muscle, the liver, and the areas of injury.
Individuals present with tachycardia and tachypnea, peripheral edema, fever, hyperglycemia, leukocytosis, increased O2 consumption, increased CO2 production, increased minute ventilation, elevated resting energy expenditure and negative nitrogen balance. Consequently, the liver provides substrates through gluconeogenesis and synthesis of ketone bodies, detoxifies nitrogenous waste via the synthesis of urea and elaborates a series of APPs that bind metabolic by-products or limit the activity of proteolytic enzymes secreted by activated leukocytes.
Renal blood flow and glomerular filtration increase and facilitate excretion of the nitrogenous by-products. Cytokines released from macrophages and adipokines released from adipose tissue result in disruption of capillary tight junctions, leading to vascular leak allowing fluid and substrates to flow toward the avascular area of injury, as well as to the interstitium in other body parts. Manifestations of this hypermetabolic phase can be seen clinically in every postoperative patient.
Patients retain fluid and sodium via concentrated urine, and redistribute blood flow to the vital organs, as well as compensate for the intravascular depletion secondary to capillary leak and possible external losses. If allowed to go unchecked, this catabolic response would deplete endogenous resources and become maladaptive.
Systemic inflammatory response, severe metabolic depletion, and possible secondary infection can all cause damage to vital organs that were not initially compromised by the injury. Adult respiratory distress syndrome ARDS , renal insufficiency, hepatic dysfunction, loss of gut epithelial barrier function, immunoparalysis, and sepsis may develop and the multi-organ dysfunction can be fatal. Fortunately, with appropriate support measures, the stress response nearly always resolves itself without complications.
The intensity and duration of the flow phase roughly correlate to the extent and type of injury. The catabolic process usually peaks at about 48 to 72 hours post-injury. If the insult is resolved, it can lead to an anabolic state, dominated by insulin, GH, and insulin-like growth factor I IGF-I within 5—10 days of injury.
The change is associated with a flux of protein, fluid, and electrolytes returning to depleted intracellular space, particularly the muscle.
Interstitial edema fluid is reabsorbed and the excess fluid is eliminated with a brisk diuresis. Serum levels of these ions decrease and require repletion. Anorexia and fatigue gradually resolve, and heart rate, respirations, and plasma glucose normalize. Nitrogen balance becomes positive and homeostasis is restored.
The immune and inflammatory responses to injury are predictable and well-orchestrated, and adaptive series of events evolve leading to maximize healing potential. A normal, balanced, and well-controlled inflammatory response in previously healthy patients almost always results in an uneventful recovery. Innate Immune System The immune response can be divided into an early innate and a later adaptive responses.
The innate immune system is the first line of defense and its principal components are the epithelial barriers, immune cells phagocytes such as neutrophils, macrophages and dendritic cells, and natural killer [NK] cells. Tissue damage, or microorganisms invading one or more of the epithelial barriers, is immediately recognized by the multiple components of innate immunity.
The mechanisms used by the innate immune system to recognize nonself entities have been elucidated only recently. The innate immune response derives from preexisting recognition of pathogen-associated molecular patterns PAMPs or microorganism-associated molecular patterns MAMPs.
The best known examples of PAMPs are lipopolysaccharides LPS in gram-negative bacteria, lipoteichoic acids in gram-positive bacteria, mannose-rich oligosaccharides in microbial glycoproteins, mannans, unmethylated CpG sequences in bacteria, double-stranded RNA in replicating viruses, glucans, and N-formylmethionine bacterial eukaryotic protein.
The receptors that have evolved to recognize these PAMPs are called patternrecognition receptors, and these can functionally be divided into endocytic receptors, which mediate internalization and phagocytosis of microbes, and signaling receptors, which activate cellular signaling pathways that induce the expression of a variety of immune-response genes.
The most important receptors that mediate endocytosis are the mannose receptors of the calciumdependent lectin family, which recognize terminal mannose and fucose residues of glucoproteins and glycolipids that are characteristic of microorganisms, as well as the scavenger receptors that bind to bacterial cell walls.
Toll-like Receptors The Toll signaling pathway was initially described in Drosophila in , with the human homologue identified in This family of type I transmembrane receptors is characterized by an extracellular domain with leucine-rich repeats and a cytoplasmic domain.
At least 11 human TLRs have been identified, and each is known to detect a specific PAMP and has a specific intracellular signaling pathway. TLR-1, 2, 4, 5, and 6 mainly recognize bacterial products, of which TLR2 has been implicated in the signaling process of gram-positive bacteria. TLRs seem to play a bridging role between the innate and the adaptive immune systems.
They are expressed on dendritic cells and T-lymphocytes, as well as on a variety of parenchymal cells e. The adrenal-expressed TLRs influence the systemic inflammatory response by their effect on cortisol secretion. TLRs are also involved in the recognition of endogenous ligands, which are released from damaged or dying cells, or come from a depredated extracellular matrix. These molecules include lipids, carbohydrates, proteins, and nucleic acids. Extensive research has been conducted on whether genetic variations can be used to identify patients at high risk of developing sepsis and organ dysfunction during severe infection.
Although septic patients with TLR-4 polymorphism have been shown to have reduced levels of circulating inflammatory cytokines and an increased risk of bacterial infection, the associations of mortality with polymorphism in TLRs during sepsis are still controversial.
New research suggests that manipulation of TLR signaling pathways offers significant therapeutic potential, particularly in the treatment of organ injury accompanying sepsis, but this concept requires further exploration. These receptors are activated by chemokines, proteolytic products of complement proteins e. Complement The complement system consists of more than 30 proteins, including serum, serosal, and cell membrane proteins.
Being part of the innate immune system, the complement system does not require prior immunization for activation; it is rapidly activated in a nonspecific manner in one of three main pathways: classic, alternative, and mannan-binding lectin pathways.
In the classical pathway, it is activated by an IgM or IgG antibody—antigen complex. The alternative pathway does not rely on an antibody—antigen complex; it is activated directly by bacterial cell wall components. The mannan-binding lectin pathway is homologous to the classical pathway, except that the cascade is initiated by a mannanbinding lectin protein, produced by the liver that can activate complement cleavage when binding to a pathogen surface.
Activation of the complement cascade results in the formation of products that act to lyse microbes, activate platelets, stimulate histamine release, recruit neutrophils by chemotactic action, and facilitate both phagocytosis and bacterial killing through opsonization of bacteria and stimulation of neutrophil degranulation. Complement activation pathways are regulated by a large number of regulatory complement-control proteins, preventing over-activation of the whole system; systemic overwhelming activation of the system can result in changes in hemodynamic parameters, leading to shock.
HMGB1 plays a critical role in stabilizing nucleosome formation and in regulating transcription; it also plays an important role in signaling following tissue damage. When present in an extracellular location, HMGB1 can activate the innate immune system and promote inflammation. It is passively released by necrotic, but not apoptotic cells as well as actively secreted by immune cells, macrophages, and NK cells upon activation with TNF.
HMBG1 acts as a chemokine and is a chemoattractant for macrophages, neutrophils, and dendritic cells and causes the secretion of several proinflammatory cytokines e. The role of HMGB1 in multi-organ damage in severe sepsis was demonstrated in an animal model.
Inhibition of HMGB1 by specific antibodies protected mice from mortality in both LPS-induced and cecal ligation and puncture-induced sepsis. Furthermore, administration of recombinant HMGB1 protein recapitulated severe sepsis by inducing lethal organ dysfunction. Several techniques have been developed to inhibit the biological activity of HMGB1 in sepsis. A protein fragment A-box, which contains the DNA-binding domain of HMGB1, competes with intact HMGB1 for binding to its cell surface receptor, and exhibited a therapeutic effect in sepsis models even when administered after the onset of the diseases.
Ethyl pyruvate, a stable and nontoxic derivative of pyruvic acid, has been shown to suppress HMGB1 release from macrophages in vitro, reduce serum HMGB1 levels, and improve survival in sepsis models in mice.
Adaptive Immune System Fig. The proinflammatory signal transduction pathway. Modified from Baeuerle PA. Pro-inflammatory signaling last pieces in the NF-kappaB puzzle? Curr Biol ;8:R19, with permission. Neutralization of C5a, using a monoclonal antibody, resulted in improved survival and decreased organ damage in animal models. Alarmins Activation of the immune system is triggered by injury or trauma without evidence of a bacterial focus.
This is mediated by alarmins or PAMPs. New full-color design throughout the text, including many new color images, help readers visualize and remember key anatomic features and surgical techniques.
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