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The continuously updated review of surgery

BASIC SCIENCE

Gastrointestinal physiology
John McLaughlin

225 231

Adult groin hernias: acute and elective


Michael Nelson Brian M Stephenson

255

Digestion and absorption


Anthony D Jackson John McLaughlin ABDOMINAL SURGERY

Investigation of abdominal masses


Quat Ullah Richard A Nakielny

262

Blunt and penetrating abdominal trauma 237


Adam Brooks JAD Simpson TEST YOURSELF

266

Abdominal access techniques (including laparoscopic access)


Ralph Smith Sukhpal Singh

Abdominal wound dehiscence and incisional hernia


David C Bartlett Andrew N Kingsnorth

243

MCQs

272

Anatomy of the anterior abdominal wall and groin


Vishy Mahadevan

251

Required Reading for The Royal College of Surgeons of England STEP Modules

2009 Elsevier Ltd

ISSN 0263-9319

Abdominal surgery

Volume 27:6 June 2009

Available online at www.surgeryjournal.co.uk

Basic science

Gastrointestinal physiology
John McLaughlin

pumps are rapidly recruited to the apical surface by fusion of a vast intracellular canalicular membrane network and actively extrude H+ into the lumen against a concentration gradient of 106 (the largest concentration gradient in human physiology). H+ derives from the action of the enzyme carbonic anhydrase, which is abundant in parietal cells (CO2+H2OH2CO3HCO3+H+). Chloride is secreted in parallel via cyclic AMP-dependent apical channels. Control secretion of gastric acid is intrinsic and extrinsic, and occurs in three phases. The cephalic phase accounts for about 40% of total acid secretion and is triggered by food in the mouth, although the sight, smell or thought of food can trigger this, as can any conditioned reflex (Pavlovs dogs secreted acid in response to a mealtime bell when food was not given). It is a vagal mechanism and is virtually abolished by vagotomy. This is the rationale for vagotomy in the historical management of acid peptic disease, particularly ulcers. It is mediated by post-ganglionic cholinergic fibres acting on muscarinic (M3) receptors on the parietal cell. The gastric phase is triggered by food in the stomach, particularly l-aromatic amino acids (l-tryptophan, l-phenylalanine) and small peptides liberated from initial digestion of protein, which directly stimulate the release of the hormone gastrin from antral G-cells. The sensory mechanism is not confirmed, but recent evidence suggests that the extracellular calcium receptor (originally cloned from parathyroid cells) acts as a polymodal nutrient sensor expressed by G-cells. Mechanical stretch also has a role via intrinsic neural reflexes and the vagal efferent nerves produce a gastrin-releasing peptide. Alcohol and caffeine further stimulate acid secretion. Intestinal phase food entering the intestine stimulates about 10% of acid secretion, which will persist with purely post-pyloric tube feeding. G-cells are also present in the duodenum, predominantly secreting gastrin-28 which has a longer circulating halflife than gastrin-14, the predominant antral G-cell product (see below). The intestinal phase is more complex because inhibitory hormones are also released, particularly in response to fat (cholecystokinin (CCK), peptide YY) and acid (secretin, gastric inhibitory polypeptide). These inhibitory effects constitute the so-called enterogastrone mechanism, and also contribute to slowing gastric emptying, particularly after fatty meals. The acid hypersecretion and hypergastrinaemia in surgical short bowel probably reflects the functional loss of enterogastrones because their tissue source has been removed surgically. Gastrin and the feedback control of secretion of gastric acid: gastrin is a regulatory peptide but is not a major direct regulator of acid secretion by parietal cells. Amidated gastrins, the active moiety at the CCK-2 (CCK, gastrin) receptor, are produced by cleavage and post-translational modification from the preprogastrin precursor, the initial translational product of the gastrin gene. There is increasing evidence the progastrin has biological activity, related to cell proliferation and differentiation. The main target is the gastrin/CCK-2 receptor on the histamine-secreting enterochromaffin-like cell, not the parietal cell as had been thought. Histamine is secreted to act in a paracrine manner on nearby parietal cells, operating at H2-receptors to stimulate acid secretion via the mechanisms discussed above. Gastrin is trophic
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Abstract
This contribution focuses on the gastrointestinal tract and its ability to absorb nutrients, water and electrolytes, and also how it forms an effective barrier against potentially harmful contents, such as bacteria. its structure and function are also discussed.

Keywords gastrointestinal; physiology

The gastrointestinal tract must not only absorb nutrients, water and electrolytes, but must also form an effective barrier against the ingress of potentially harmful contents, such as bacteria. Its structure and function are highly adapted to serve these conflicting roles.

Secretion of gastric acid


The primary reason for secreting gastric acid is to kill ingested microorganisms. This appears less important in the developed world and acid secretion is pharmacologically stopped with impunity in millions of individuals. Acid denatures proteins, but gastric enzymes and defence molecules are pH-adapted to allow digestion to begin. At a pH of about 1 after a meal, gastric acid is injurious to tissues except the highly adapted gastric mucosa. A gel of mucus coats the epithelium, and bicarbonate is secreted locally so that the pH adjacent to the cell surface is 67. A surface coating of mucus also provides defence against autoproteolysis, serving as a gel with a progressive pH gradient occurring from the cell surface to the lumen. The epithelium is further protected by a variety of factors including: prostaglandins (PGE2 in particular; its synthesis is blocked by non-steroidal anti-inflammatory drugs, majorly contributing to their ulcerogenicity) epidermal growth factors (e.g. heparin-binding epidermal growth factors, amphiregulin) trefoil peptides which are secreted into the lumen and may monitor for damage and protect the mucosa. Hydrochloric acid is secreted by parietal cells in the gastric body (oxyntic mucosa), which express the H+K+ ATPase or proton pump. When stimulated, particularly by histamine, proton

John McLaughlin FRCP is a Senior Lecturer in Medicine at Manchester University, Manchester and Honorary Consultant in Gastroenterology at Hope Hospital, Salford, UK. He is Clinical Director of the Gastrointestinal Physiology service. Conflicts of interest: none declared.

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Basic science

to the oxyntic mucosa indirectly via epidermal growth factors, which leads to the thickened folds found in ZollingerEllison syndrome. The enterochromaffin-like cell also operates under vagus nerve control, probably via pituitary adenylate cyclaseactivating peptide. There is also an epithelial inhibitory mechanism in which a fall in pH leads to an increase in the secretion of somatostatin from D-cells, which inhibit both G-cells and enterochromaffin-like cells. Hence, proton-pump inhibitors induce hypergastrinaemia. It is usually recommended that inhibitors of acid secretion should be stopped to measure and evaluate an elevated concentration of gastrin in plasma. The utility of measuring intragastric pH is often overlooked; hypergastrinaemia cannot be due to the medication if gastric acid secretion is not suppressed. The D-cell is also an intermediary in the enterogastrone mechanisms, and expression of the somatostatin gene appears to be downregulated in Helicobacter pylori antritis. Proton-pump inhibitors: given that only the proton pump is common to acid secretion, it is not surprising that its inhibitors have transformed the management of acid-related disease. Anticholinergics are readily bypassed and not of value clinically, whereas H2-receptor antagonists and even vagotomy leave a substantial proportion of acid secretion intact. Gastrin receptor antagonists are in development. Acid is secreted with an osmotically appropriate volume of water, and so proton-pump inhibitors also reduce the volume of gastric juices, not just their acidity. This contributes to their effectiveness in gastro-oesophageal reflux disease and also their adjunctive use in short bowel with gastric hypersecretion.

Enterochromaffin-like cell hyperplasia


In addition to its role in secretion of gastric acid, gastrin is also a direct growth factor for the enterochromaffin-like cell, which explains the presence of enterochromaffin-like hyperplasia seen in some chronically hypochlorhydric and consequently hypergastrinaemic patients (e.g. in pernicious anaemia, in which there is autoimmune destruction of parietal cells). This can progress to small carcinoid nodules in a minority, and invasion and metastasis can occur in a very small minority. This underlies the rationale for antrectomy rather than total gastrectomy for corpus carcinoids, removing the anatomical source of gastrin. The risk of surgery appears higher than the risk of invasiveness and surveillance is adequate initially. The risk of aggressive neoplasia is higher in non-hypochlorhydric hypergastrinaemia (Zollinger Ellison syndrome and/or multiple endocrine neoplasia (MEN1). Measuring intragastric pH is very helpful.

Biology of the intestinal epithelium


Gastrointestinal epithelial cells originate from a stem cell population in the crypt zone. There are four cell types resulting from differentiation pathways controlled by a complex array of transcription and differentiation factors. The key lineage commitment decision is whether to adopt the dominant pathway to an absorptive phenotype (enterocyte/colonocyte) or a secretory phenotype. This includes mucus-secreting goblet cells, hormone-secreting enteroendocrine cells (EECs) (Figure 1), and defence peptidesecreting Paneth cells. Progenitor cells originating from the stem cell population differentiate along an absorptive (enterocyte) or

Conceptual model: transepithelial signalling by EECs


Nutrients Lumen Apical

Basolateral

Neurones Paracrine/endocrine factors Epithelia

Muscle

Immune cells
EEC, enteroendocrine cell

Figure 1

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secretory (EEC, Paneth cell, goblet cell) cell pathway under the control of specific differentiation and transcription factors. In the small intestine, the cell types, except Paneth cells, ascend the cryptvillus axis, moving over a period of 35 days to be shed by apoptosis. Paneth cells move to the base of the crypts, and appear to have a longer lifespan. Increasing evidence implicates Paneth cells in the pathogenesis of inflammatory bowel disease, given their key role in epithelial recognition and defence against microorganisms. The Crohns gene, CARD15, encodes a Paneth cell protein. Abnormal epithelial structure in disease reflects changes in the regulation of epithelial turnover. Some of this may be adaptive; for example, increased turnover and goblet cell hyperplasia in response to nematode infection may contribute to parasite expulsion (weep and sweep hypothesis).

The epithelium as a barrier


The gut prevents the passage of bacteria and other undesirable substances (dietary contaminants, bacterial products) from the lumen into the organism. The colon contains tenfold more bacteria than cells in the host body. This is mainly achieved by tight junctions between cells (Figure 2). These are complex structures comprising multiple proteins that constitute a pore close to the apical surface of the cells that filters molecules according to size. Key members are ZO-1, occludin and the claudin family. This constitutes the paracellular pathway, and is a minor route for the absorption of some small ions (e.g. calcium). Water also passes this way, with some movement occurring transcellularly. Increasing interest has focused on the regulation of tight junctions, and whether they contribute to the increase in intestinal permeability seen in injury and inflammation in the gut. Current research aims to identify factors that protect or restore the barrier, for example antioxidants and nutrients (e.g. glutamine). The gut microflora has an active symbiotic role in maintaining the barrier. Using probiotic bacteria to alter bacterial flora and enhance the barrier has

generated interest. Another approach is to give these with bacterial nutrients (prebiotics); the combination is termed a synbiotic. A class of dietary fibre substances, fructo-oligosaccharides, has also been shown to modulate permeability, an effect also observed in germ-free (gnotobiotic) states. Changes in inflammatory signalling by epithelial cells occur in response to probiotic bacteria, suggesting an active intrinsic effect of fibre (previously thought to be inert and solely the target of bacterial fermentation). There is also evidence that psychological stress increases gut permeability via these or other structures. Increased permeability leads to inappropriate fluxes of fluids and electrolytes, and may underpin bacterial translocation, prequelling sepsis. The mucosa is immunologically active. Defence against injury is provided by secretory immunoglobin and various cellmediated mechanisms, and sampling antigenic content via specialized dendritic cells scattered throughout the gut. These can open tight junctions, passing processes between epithelial cells to sample luminal contents.

Enteroendocrinology
The gut is the largest endocrine, with up to 20 types of EEC scattered throughout the gastrointestinal epithelium. As noted above, EECs are derived by selective terminal differentiation from a common stem cell niche. EECs serve a variety of physiological roles, but their key function is to operate as transepithelial signal transduction conduits. The apical surface of most EECs is open to the lumen, projecting microvillus processes that are believed to operate as chemosensors. Variables sensed intraluminally include nutrients, pH and osmolarity. Each EEC produces one or more regulatory peptide (or biogenic amines, principally histamine and 5-hydroxtryptamine) which are secreted predominantly basolaterally by exocytosis. The released mediators were thought to act as true hormones (via the circulation to act at a distance) but many of their actions occur locally (paracrine effects). The epithelium is a target, for example, in the regulation

Absorption of glucose, galactose, salt and water


Glucose and galactose absorbed from the lumen via SGLT-1 Lumen SGLT-1 H2O Cholera toxin cAMP VIP Cl- transported via a Cl- channel activated by cAMP and VIP

Tight junction Na+ Glucose Galactose GLUT-2 Glucose and galactose exported through the basolateral membrane via GLUT-2 Na+ H2O K+ Basolateral membrane Enterocyte Na+ K+

Na+ 2Cl K+

Sodium is required for the transportation of monosaccharides into both the cytosol of the enterocyte and into the basolateral space before entering the portal circulation

Na-K ATPase

SGLT-1, sodium-dependent glucose and galactose transporters; GLUT 2, glucose transporters; cAMP, cyclic AMP; VIP, vasoactive intestinal peptide. Figure 2

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of local secretomotor events, but afferent nerve fibre terminals, particularly fibres of vagal origin, appear to be the major site of action for many enteroendocrine factors. The key difference between EECs and other endocrine organs (e.g. pituitary gland, islets of Langerhans) is that the former exist as individual cells scattered throughout the epithelium. This has posed a major hurdle in studying these cells because there is no method for isolating EECs and studying their function. The key endocrine cells of the stomach have been discussed in relation to acid secretion, but two other hormones from the stomach have major roles. Leptin, the fat controller originally isolated from adipocytes, is also secreted by the pepsinogensecreting chief cells of the stomach (which were not previously thought to have an endocrine nature), and to activate vagal afferent nerves to contribute to satiety. Ghrelin is secreted by a population of endocrine cells. This was originally identified as a growth hormone-releasing (GH-Relin) factor, not an effect believed to be mediated from the stomach. Ghrelin is unusual in being the first gut hormone described that rises in the plasma during fasting and falls upon feeding: it is unclear whether the rising level pre-prandially is a signal to eat, or whether the falling value after a meal constitutes a satiety signal. Ghrelin accelerates gastric emptying, and is being studied in models of gastroparesis (e.g. diabetes). Reports that altered concentrations of ghrelin after gastric bariatric and bypass surgery contribute to the value of the procedure have been very inconsistent. Ghrelin and leptin may also contribute to gastric mucosal protection. The duodenum is a major enteroendocrine territory, with immediate sampling of just-emptied gastric contents serving to modulate the secretory and motility patterns controlling digestion and absorption with maximal efficiency. Secretion of lipid-induced CCK by the I-cell subtype of EECs triggers pancreatobiliary secretions. CCK also delays the emptying of lipid-rich chyme from the stomach, in addition to limiting further food intake by inducing satiety (Figure 3). These effects of CCK are mediated largely by vagal reflexes. The CCK-1 receptor is expressed by vagal afferent neurones. The cell bodies lie in the nodose ganglion in the neck, and the synthesized receptors are transported down the axonoplasm to peripheral terminals where they are activated by CCK. Recent work suggests that the vagal circuitry responds to several factors inducing satiety (CCK, leptin, possibly cytokines) and hunger (endocannabinoids, ghrelin), and integrates these positive and negative signals in the short-term control of food intake. CCK has also been implicated in the hypophagic state associated with intestinal inflammation; CCK cell hyperplasia and hypersecretion appear to contribute to the reduction in food intake observed. Free fatty acids rather than intact triglyceride induce secretion of CCK (hence lipase inhibitors such as orlistat may blunt the satiating effects of meals). Secretion of CCK is also impaired in pancreatic insufficiency. The molecular basis of fatty acid sensing by EECs is unclear, but the recent identification of four fatty acid receptors (G protein-coupled receptor (GPR) 40, 41, 43 and 120) has yielded candidate mechanisms and potential pharmacological targets. The best characterized is GPR40, responsible for fatty acid-induced secretion of insulin by pancreatic -cells. Secretin cells respond to acidic pH and fatty acids to induce pancreatic alkaline secretions. Another key cell type, the L-cell, secretes glucagon-like peptides-1 and -2 and peptide YY. Glucagonlike peptide-1 also mediates delayed gastric and intestinal transit,
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Response to a fatty meal


Fatty acids

Mucosal

EEC

Basolateral CCK Pancretic exocrine secretion GI motility Gallbladder emptying Satiety

In response to a fatty meal, cholecystokinin (CCK) release coordinates responses including regulation of pancreatic exocrine secretion and control of gastrointestinal (GI) motility, in particular gallbladder emptying and gastric emptying; it has now been recognized as an important satiety factor. EEC, enteroendocrine cell

Figure 3

whereas glucagon-like peptide-2 is implicated in epithelial trophism and repair (this underpins its evaluation in the therapy of intestinal failure and short bowel). Glucagon-like peptide also has an incretin effect, signalling to the pancreas to induce insulin secretion in the absence (but anticipation) of a rise in blood glucose. Peptide YY responds to nutrients, particularly fat, arriving in the terminal ileum; this heralds imminent malabsorption and hence nutrient wastage, and triggers the ileal brake mechanism, further delaying gastrointestinal transit. The other key endocrine cell of the gut is the enterochromaffin cell, whose major product is the amine 5-hydroxytryptamine. About 97% of the 5-hydroxtryptamine in the body is in the gut, and its release regulates motility and secretion throughout the intestine. Increased numbers of enterochromaffin cells and secretion of 5-hydroxtryptamine have been reported in gut infection, but this appears to persist after resolution of infection, and may be a component of the functional gut symptoms frequently observed following enteritic episodes. Increased numbers of enterochromaffin cells have been reported in post-infectious irritable bowel syndrome. There is little other evidence of disorders of the enterochromaffin system, other than rare tumours.

Gastrointestinal motility
Motility is the term used to describe the orderly processes that move the luminal contents from the mouth to the anus. The dominant process in the oesophagus and small bowel is peristalsis, in which a bolus is propagated by a wave of contraction. Peristalsis is an intrinsic property controlled by the neural plexus, and persists in extrinsically denervated gut (Figure 4).

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Peristalsis in the small intestine


The muscles behind the bolus of food contract, while the ones in front relax, which moves the bolus along in the direction of the arrow. Peristalsis is controlled by the intrinsic neural plexus network. Excitatory motor fibres releasing ACh and substance P cause contractions, while inhibitory motor fibres release VIP and NO. Mucosal wall receptors detect the food bolus and interact with the excitatory and inhibitory fibres to either increase or decrease contraction

Contraction

Relaxation

ACh Substance P

Mucosal and wall receptors + Myenteric plexus +

VIP NO

ACh, acetylcholine; VIP, vasoactive intestinal peptide; NO, nitric oxide. Figure 4

Excitatory motor fibre

Inhibitory motor fibre

The intrinsic rhythm appears to be generated by specialized neurones called the interstitial cells of Cajal, which govern the activity of local smooth muscle. These neurones express the protein c-kit, and are therefore the likely cell of origin of gastrointestinal stromal tumours which are characterized immunohistochemically by c-kit positivity. Recent supporting data have suggested that gastrointestinal stromal tumour cells retain some of the electrophysiological properties and ion channels typical of the interstitial cells of Cajal. Data also are accumulating for loss of interstitial cells of Cajal in disorders of gastrointestinal motility, particularly slow transit constipation with acquired megacolon, but also in acute obstruction, Chagasic megacolon and diabetic gastroenteropathy. It is however possible that interstitial cells of Cajal are lost as a secondary consequence of the motility disorder. Gastrointestinal motility is largely an intrinsic property of the gut, but is subject to external influences. In general, the parasympathetic (vagal and sacral) pathways increase motility via postganglionic fibres utilizing acetylcholine, substance P and ATP. Sympathetic noradrenergic spinal fibres tend to inhibit motility; inhibitory 2-receptors are expressed on post-ganglionic vagal fibres and reduce cholinergic transmission. Hormones also affect motility. CCK inhibits gastric and small bowel motility, but stimulates the colon, and may be responsible for the gastrocolic reflex (in which eating can trigger an urge to defaecate). Thyroid hormones are stimulatory. Glucagon and opioids have strong antimotility effects in the gut. Electrolyte disturbances (particularly K+ and Ca2+) can also have profound effects on neuromuscular function. Congenital or acquired abnormalities of visceral muscle or the enteric nervous system are likely to underlie the pseudoobstructive syndromes. A wide range of common drugs is also able to influence motility. Gastric motility: the pattern of motility is quiescent initially (phase I) in the fasting state. After about 40 minutes, activity restarts (phase II), with a gradual increase in contractions that
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begin in the stomach and reach a peak of intensity (phase III) lasting about 10 minutes, before returning to phase I quiescence. This phase III pattern starts in the stomach (hunger contractions) and travels along the small bowel over about 90 minutes; it is termed the migrating motor complex. This acts as an intestinal housekeeper, sweeping out the small bowel to prevent stagnation and bacterial contamination. Gastric, biliary and pancreatic secretions are also triggered by the migrating motor complex, which is coincident with a peak in circulating motilin. This hormone is mimicked by erythromycin, a prokinetic antibiotic. Feeding interrupts this pattern. The proximal stomach undergoes tonic relaxation via a vagal reflex, with further phasic relaxations. This allows the intragastric volume to rise without a commensurate increase in pressure. The loss of such adaptive relaxation may partly contribute to the early fullness and rapid gastric emptying seen after vagotomy. In the fed state, rhythmical contraction of the antrum at a rate of 3 contractions per minute acts as a mechanical pump to emulsify food and, in coordination with the pylorus, propel food into the duodenum. The pylorus also acts as a sieve and relatively little food of greater than 3 mm in diameter passes through. Foods rich in lipids markedly slow gastric emptying. They exert an inhibitory effect on the antral pump, stimulate pyloric contractions and maximally relax the proximal stomach. These effects are mainly mediated by CCK acting on CCK-1 receptors on vagal afferent fibres. The time taken for gastric emptying is highly variable and can be up to 5 hours, depending on the type of nutrient, osmolality and temperature. Meals light in nutrients, and liquids, can be emptied within 1 hour. Attempts to define normality must be interpreted cautiously, but many patients with functional dyspepsia and early satiety lie outside the apparent norms. Intestinal motility: the small intestine propagates waves at a higher frequency than the antrum (about 12 contractions/ minute) although peristalsis is also regulated by intrinsic reflexes

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to distension (Figure 4). Small intestinal transit to the caecum takes about 90 minutes. The main function of the colon is water absorption, and movement of the contents slows down. Bacteria are present and the migrating motor complex dissipates at the ileocaecal valve. Reflux of colonic contents into the terminal ileum triggers expulsive contractions to maintain relative sterility. Colonic transit may take 2448 hours, and occurs by haustration and mass movement. Haustration comprises slow, segmental contractions over several centimetres, and is responsible for the gross appearance of the colon. Haustration mixes the colonic contents to facilitate water absorption. Mass movement involves episodic muscle contractions over a longer segment of colon and occurs only a few times daily. It resembles peristalsis in that the distal segment of colon relaxes in anticipation, producing a wave that propagates at a rate of

about 1 cm/second to move the colonic contents distally. Their arrival in the sigmoid colon leads to an urge to defaecate, and an increase in amplitude has been noted in some patients with irritable bowel syndrome.

FurThEr rEAdinG aziz Q, Thompson DG. Brain-gut axis in health and disease. Gastroenterology 1998; 114: 55978. champion Mc, Orr Wc, eds. evolving concepts in gastrointestinal motility. Oxford: Blackwell science, 1996. Dockray GJ. Gastrin and gastric epithelial physiology. J Physiol 1999; 15: 31524. smout aJMP, akkermans LMa. normal and disturbed motility of the Gi tract. stroud: Wrightson Biomedical, 1992.

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BASIC SCIENCE

Digestion and absorption


Anthony D Jackson John McLaughlin

water must also be absorbed, leaving insoluble carbohydrates for excretion. Discrete mechanisms are in place for digestion and absorption for each nutrient, highlighting the complexity of the digestive process. Protective measures are in place to guard against the absorption of toxins and antigenic material in ingested food. Neural, hormonal and local inputs converge to provide an elaborate network of control over the numerous processes that accompany passage of food through the alimentary canal, signifying how finely and intricately adapted the gastrointestinal tract is for its function. Digestive process The digestive process begins during mastication (i.e. food is mechanically broken into smaller physical particles) which generates a larger surface area for the digestive enzymes in subsequent sections of the gastrointestinal tract. Enzymes are also present in the oral secretions and mixed with food to carry out the preliminary steps in the breakdown of fats (lingual lipase) and carbohydrates (salivary amylase). Further physical processing and mixing (by triturative antral contractions) with the strongly acidic secretions of the stomach lead to the formation of a semi-solid paste (chyme) which is gradually released, when sufficiently fluid, into the small intestine. Gastric emptying is delayed by duodenal and ileal sensory braking mechanisms in response to nutrient sensing and endocrine reflexes, which are most potently triggered by fat. The duodenum serves as a mixing pot where chyme meets the pancreatic digestive enzymes, and gastric acidity is neutralized by bicarbonate (secreted by pancreatic ductal cells and duodenal Brunners glands) before contact is made with the more defenceless absorptive surfaces of the jejunum. Profuse secretion of mucus is also paramount in providing a protective surface coating. The alkaline pancreatic secretions containing the key digestive enzymes are released into the duodenum in anticipation of the acidic chyme, providing the optimum pH for the enzymatic processes of digestion to operate. Digestion of the liquefied food continues during the two-metre journey through the jejunum, which is also the major site of nutrient absorption. Extensive folding in the jejunum vastly increases surface area to maximize absorption: transverse foldings of the jejunal submucosa (plicae circulares) are carpeted by fields of finger-like villi, whose epithelial cells express microvilli, multiplying the total absorptive surface available by a factor of >500. Epithelial cells of the villi (enterocytes) absorb the end products of digestion and express membrane-bound enzymes in their microvilli (brush-border enzymes) that contribute to the final digestive process. Stem cells in the intestinal crypts divide to produce epithelial cells that move up and along the lining of the villi over 46 days, displacing older cells further along, eventually causing them to be shed by apoptosis into the lumen. Once shed, brush-border enzymes remain active and continue to have a role in ongoing digestion. Final absorption of nutrients and solutes from the gut lumen is not a simple diffusive process. More than 350 solute-specific channels and transporters have been identified, subdivided into 46 families of solute carriers. They represent the gateway to all cells and are crucial to the cellular absorption of all macronutrients, micronutrients, vitamins and minerals.
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Abstract
The gastrointestinal tract exists to support nutrition, digesting and assimilating nutrients including water and salts. Disorders of the gut readily impair nutritional status, although there is considerable functional reserve. Many macronutrients are structural components of animals and plants, and therefore ingested in complex molecular forms that cannot be readily absorbed. They must be digested to simpler components in the gastrointestinal tract before absorption and assimilation can occur. For the major complex macronutrients, (fat, carbohydrate, protein), the gut secretes specific enzymes that catalyse the hydrolysis of these nutrients to their basic oligomeric subunits, which are then taken up by specific transport proteins expressed in the epithelial membrane for optimal transport from the lumen into enterocytes. The digestive process is progressive, beginning in the oral cavity and continuing during passage to the small intestine, the key site of most nutrient absorption. The colonic bacterial flora salvages nutrients from otherwise indigestible fibre. Micronutrients (vitamins, minerals), electrolytes and water must be absorbed; specific transport mechanisms exist for each. The magnitude of specialized processes that act in conjunction to enable effective digestion and absorption (along with the regulatory inputs that converge to coordinate these events) demonstrate how finely adapted the gastrointestinal tract is to its function.

Keywords absorption; basic science; carbohydrate; digestion; enterocytes; fat; minerals; nutrient transport; protein; vitamins

A typical meal comprises a complex mixture of nutritive substances that the gastrointestinal system must separate and break down into its basic molecular subunits to permit systemic absorption and assimilation. This contribution begins with an overview of the entire process, then focuses upon specific classes of nutrients.

Overview of the progress of nutrients through the gut


Carbohydrate, protein and fat are the macronutrients that constitute the bulk of a meal. Dietary vitamins, mineral ions and

Anthony D Jackson BSc(Hons)PhD Faculty of Life Sciences, Manchester University, Manchester, UK. Conflicts of interest: none declared. John McLaughlin FRCP is a Senior Lecturer in Medicine at Manchester University, Manchester and Honorary Consultant in Gastroenterology at Hope Hospital, Salford, UK. He is Clinical Director of the Gastrointestinal Physiology service. Conflicts of interest: none declared.

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Digestion and absorption of lipids


Dietary fat is an important source of energy and daily consumption may be 90100 g, contributing about 30% of energy intake. The hydrophobic nature of fat presents the gut with particular difficulty in digestion and absorption: it can be argued that much of the anatomical and regulatory sophistication of the gut is adapted to maximize lipid absorption, a valuable energy store and thermal insulator supporting survival in evolutionary conditions, principally privation. Most fats are ingested as structured triglycerides, although a small proportion (5%) are composed from phospholipids. In health, the gastrointestinal tract absorbs ingested fat with 95% efficiency, the remainder being excreted in the faeces. Absorbing <95% is categorized as malabsorption and presents clinically as steatorrhoea in more severe situations. Triglycerides must be split into free fatty acids and monoglycerides (Figure 1) to be absorbed. Lingual lipases begin breaking down triglycerides during chewing, although very little digestion of bulk lipids occurs until fats are emulsified with bile salts in the duodenum. Gastric lipases are secreted in the stomach, but their contribution to lipid digestion is ancillary to the enzymatic events that occur in conjunction with bile salts in the small intestine. The family of lipases are water-soluble enzymes and can act only at the surface of fat droplets. The formation of

large lipid droplets prevents lipases full access to their substrate until emulsification occurs with bile salts. Release of chyme into the duodenum is sensed by enteroendocrine cells in the duodenal epithelium, triggering the release of important hormones that coordinate events leading to lipid breakdown. Two key examples of duodenal enteroendocrine cells follow. The acidity of chyme stimulates the release of the peptide secretin from enteroendocrine S-cells. Secretin exerts its effects on the pancreatic ducts, causing the release of bicarbonate-rich secretions that neutralize the duodenal pH. (This is why proton pump inhibitors are valuable adjuncts in pancreatic replacement therapy because alkaline pancreatic secretions are also lost in pancreatic insufficiency, and the endogenous or supplementary enzymes are poorly active in an acidic microenvironment.) Lipids in the lumen trigger release of cholecystokinin from enteroendocrine I-cells into the bloodstream. Cholecystokinin is the major stimulus for pancreatic acinar cells to secrete their digestive enzymes via the cholecystokinin-1 receptor. The gallbladder responds to cholecystokinin by contracting, liberating bile salts into the lumen. Cholecystokinin contributes to the potent effect of lipids in delaying gastric emptying to maximize efficient digestion and absorption. Cholecystokinin mediates its effects via paracrine activation of cholecystokinin-1 receptors on vagal afferent neurons, rather than acting solely as a classical hormone.

Breakdown of triglycerides
a Lipid emulsion TG BS BS Monoglyceride Mixed micelle Triglycerides (TG) in the duodenum are emulsified with bile salts (BS) released from the gallbladder. Lipase, in concert with co-lipase, liberates free fatty acids and monoglycerides from TG, which form mixed micelles with BS.

BS BS

Lipase + Co-lipase

Fatty acid

b Enterocyte Mixed micelles fuse with the jejunal epithelium and lipid digestion products access the cytosol. FATP4 and CD36 are transporters for free fatty acids. TG are resynthesized in the cytosol and complexed with apolipoproteins (APO) to form chylomicrons, which enter the lymphatics.

FATP4/CD36

Chylomicron APO + + Lymphatics

Figure 1

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Pancreatic lipase is the principal enzyme involved in triglyceride digestion, responsible for up to 70% of hydrolysis, though gastric and lingual lipases retain their activity in the small intestine, thereby acting synergistically. Bile salts act as detergents due to their amphipathic structure, breaking up large, hydrophobic lipid droplets, giving increased exposure to the digestive lipases. The cofactor co-lipase is required for pancreatic lipase to be effective in attacking the lipidbile salt mixture. This binds to the surface of emulsified droplets and stabilizes the interactions between pancreatic lipase and lipids, facilitating cleavage. As free fatty acids are released, they complex with available bile salts, forming micelles that are about 2 nm in diameter. Phospholipids are broken down by phospholipase-A2, which is also secreted in the pancreatic fluids. The formation of micelles is as important to absorption as digestion. Bile salts have amphipathic qualities and therefore have increased solubility in the aqueous environment of the lumen compared to free fatty acids and monoglycerides. To access the epithelium of the jejunal mucosa, lipids must pass through the still (or unstirred) water layer between villi, which does not mix with the bulk contents of the lumen. Passage relies on simple diffusion along concentration gradients. Lipid micelles diffuse across more readily than free fatty acids because they are more soluble in the aqueous phase, and fuse with the enterocytes of the villi upon contact with the cell membrane. Proteins known to transport fatty acids are expressed apically by jejunal enterocytes (FATP4, CD36), suggesting that facilitated transport of fatty acids into the epithelium from the lumen may also occur. From here, fatty acids can diffuse (in association with fatty acid-binding proteins in the cytoplasm) into the cytoplasm to be resynthesized into triglycerides. Triglycerides are resynthesized from fatty acids and monoglycerides within the enterocytes. Triglycerides are packaged with apolipoproteins to form chylomicrons and leave the cell by exocytosis. As with bile, the amphipathic apolipoprotein component solubilizes chylomicrons, but their size prevents them from entering capillaries, hence they enter the systemic circulation via the lymphatics. Lipids with shorter chains are soluble without apolipoprotein and are exported directly into the capillaries. Bile salts are predominantly reabsorbed in the terminal ileum and returned to the liver (enterohepatic recirculation). Several disease processes impair absorption of fat; pancreatic insufficiency and loss of surface area of the gut (short bowel, villus atrophy) are the most common. Faecal fat collection is a widely used method to assess the efficiency of fat absorption, but has serious flaws. It is increasingly replaced with more specific and patient-friendly tests (e.g. isotopically labelled triglyceride (triolein) breath testing, faecal elastase).

Carbohydrate digestion is initiated by salivary amylase secreted from the parotid and submandibular glands, which begins to break down starches and glycogens into simpler disaccharides and trisaccharides. Salivary amylase is inactive in the acidic pH of the stomach. The remaining polysaccharides are hydrolysed by pancreatic -amylase upon entry into the duodenum, yielding disaccharides and trisaccharides. Unlike lipids, sugars are freely soluble in water and emulsification is not required. Sugar absorption occurs principally in the jejunum (Figure 2). Disaccharides and trisaccharides diffuse freely to the epithelium of jejunal villi but require further digestion by enzymes in the brush-border membrane before absorption can proceed. Only monosaccharides in the form of glucose, galactose and fructose are taken up by epithelial cells and they gain entry via two main transporter proteins. Glucose and galactose enter the cell by the same transporter: sodium-glucose transport protein-1. Transport is driven by the energy of a high extracellular Na+ gradient; two Na+ are transported per molecule of glucose or galactose. The gradient is maintained by Na+/K+-ATPase pumps in the membrane of enterocytes, which pump Na+ back out from the cell. Fructose has its own, selective carrier protein, GLUT5, which transports fructose without the requirement of the sodium gradient. Monosaccharides pass through intestinal enterocytes without further

Sugar absorption in the jejunum

Na+

SGLT1

GLUT5

Na+ Na+/K+ ATPase K+

Glucose Galactose Fructose

GLUT2

Digestion and absorption of carbohydrate


Dietary carbohydrates are ingested as simple sugars, such as monosaccharides (e.g. glucose) and disaccharides (sucrose) and complex polysaccharides (starches, glycogen). The energy intake from these types of carbohydrates can constitute up to 70% of daily intake of energy from all nutrients. Other polysaccharides such as cellulose (the predominant structural component of plants) cannot be broken down because humans do not possess the requisite enzymes.
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Blood

Glucose and galactose are cotransported with Na+ into jejunal enterocytes by the Na+/glucose cotransporter-1 (SGLT1). Fructose is transported separately by the fructose transporter (GLUT5). All three monosaccharides are transported out of the enterocyte by the glucose transporter gene-2 (GLUT2).

Figure 2

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processing; they leave the cell basolaterally to enter the blood stream via the GLUT2 transporter (which is a cotransporter for all three monosaccharides). Complex carbohydrates making up dietary fibre are not digested by intestinal enzymes, so pass into the colon intact. They are a source of nutrition for colonic bacteria and are broken down, yielding short-chain fatty acids that are relatively soluble in water, and are readily absorbed and locally metabolized by colonocytes.

Digestion and absorption of protein


Virtually all ingested protein is absorbed by healthy humans; faecally excreted protein is derived from colonic bacteria and shed epithelial cells, chiefly colonic cells. Proteolytic enzymes are not present in salivary secretions. Inactive proteases (pepsinogens) are secreted in abundance by the stomach chief cells. They are converted to active pepsins by the low pH of the stomach, cleaving proteins and polypeptides into amino acids and smaller peptides. Gastric pepsins become inactive in the neutral pH environment of the small intestine, where pancreatic acinar proteases are the key enzymes in proteolysis. These powerful proteolytic enzymes are secreted in the pancreatic juices as inactive precursor enzymes (e.g. trypsinogen), essentially to prevent autodigestion of the pancreas. Trypsin, chymotrypsin, elastase and carboxypeptidases represent the fundamental activated enzymes in proteolysis. Trypsinogen is activated by the brush-border enzyme enterokinase. Once active, trypsin can act in an autocatalytic manner to convert trypsinogen to trypsin, and is responsible for converting the other proenzymes to their active form. In the duodenal and jejunal lumen, protein is rapidly converted to small polypeptide chains and single amino acids, which are suitable for absorption. For the small polypeptide chains that remain, a number of brush-border enzymes are expressed, completing hydrolysis upon their diffusion to the villus epithelium. Dipeptides, tripeptides and single amino acids are cleaved from the polypeptide chains and are readily absorbed by a large family of transporters. For amino acids, transport into enterocytes is facilitated by electrochemical gradients involving Na+ and, in some cases, Cl. Dipeptide and tripeptide transport is driven by a H+ concentration gradient that is generated by Na+/H+ exchanger expressed on the luminal enterocyte membrane. Only single amino acids can leave enterocytes basolaterally to enter the circulation so additional enzymes are present in the enterocytic cytosol to cleave dipeptides and tripeptides into amino acids. Basolateral exit into the mucosal capillaries is also via amino acid-specific transport proteins.

absorbed in the jejunum and ileum by passive diffusion across a concentration gradient. The Na+/K+-ATPase pump on the basolateral membrane of intestinal epithelial cells exports Na+ into the interstitial fluid and pumps K+ back into the cell in exchange. The concentration gradient generated causes K+ to diffuse back into the interstitial fluid before entering local capillaries with Na+. HCO3 and Cl released in pancreatic fluids are actively reabsorbed, mainly in the jejunum, but secondarily in the ileum and colon. About two litres of water may be consumed per day, yet only approximately 100 ml are lost to the faeces. Ingested water is added to by about seven litres of water in saliva, gastric, pancreatic, biliary and intestinal secretions that require reabsorption. The gastrointestinal tract must therefore be highly efficient at taking up water from the intestinal lumen. Transport of intestinal water is principally driven by osmotic pressure gradients and is thought to occur mainly by a paracellular route. Several isoforms of specific water channels (aquaporins) are expressed along the length of the gastrointestinal tract and could be crucial to the transport of epithelial water, particularly in alleviating osmotic pressure generated by solute absorption. The jejunum is more prominent than the ileum in water absorption but, in combination, these sites are responsible for the reabsorption of 8.5 litres of water per day. The colon is involved in only a small fraction of total reuptake of water. It receives about 10001500 ml per day, of which it manages to take up 8090%. Loss of function of the small intestine or colon can lead to significant diarrhoea via failure of water absorption, but disease states can lead to increased secretion which can exceed absorption, most dramatically in cholera and vasoactive intestinal polypeptide-secreting tumours via activation of guanyl cyclases. Increased cellular concentrations of cyclic guanosine monophosphate trigger net secretion of water and electrolytes.

Minerals and vitamins


Essential dietary mineral ions include calcium, iron, magnesium and copper. Calcium is absorbed at all sections of the intestine, although uptake is greater proximally. Entry into epithelial cells is mainly via calcium channels driven by electrochemical gradients (although some transport occurs paracellularly across tight junctions). Upon entry into epithelial cells, calcium is bound to a cytosolic protein, calbindin, which delivers calcium to the basolateral membrane. Calcium is also transported through the cytosol in vesicles which are released by exocytosis at the basolateral membrane. Vitamin D is crucial to normal absorption of calcium in the intestine. It upregulates the expression of cellular proteins that are essential for calcium absorption (e.g. calbindin) by acting on nuclear receptors in epithelial cells and promoting gene expression. Iron: in general, iron absorption is <5% of daily intake. Iron is present in food as Fe2+ (ferrous), Fe3+ (ferric) and in haem (in protein complexes). Fe2+ is the favoured state for absorption into duodenal epithelial cells (Figure 3). Fe3+ has a greater tendency than Fe2+ to form insoluble complexes with other ions in the lumen, hindering its absorption. Ascorbate aids iron absorption by reducing
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Absorption of electrolytes and water


Virtually all of the electrolytes that are ingested are absorbed at some point along the gastrointestinal tract, the major sites for which are the jejunum, ileum and colon. Regulation of electrolyte uptake is complex and is controlled by circulating hormones, luminal factors and neural inputs. Predominant absorption of Na+ occurs in the jejunum in cotransport with sugars (although active absorption occurs additionally in the ileum and colon without the prerequisite sugars). K+ is

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Absorption of iron into duodenal epithelial cells


++ Fe2+ +++ Fe3+ ++ DMT1 H+ +++ +++ +++ IREG1 Blood +++
DMT1: Divalent metal transporter-1; IREG1: Iron-regulated transporter-1.

++

Ferroxidase Entry of Fe2+ into duodenal epithelial cells is driven by an H+ gradient. Fe2+ is oxidized intracellularly to Fe 3+ by the enzyme ferroxidase and iron-binding protein complexes with available Fe3+ . IREG1 is responsible for exporting Fe 3+ from the cell and into local capillaries, where it binds to transferrin to travel in the blood.

Iron-binding protein

TransferrinFe 3+ complex Figure 3

it to the Fe2+ state. Iron reductases in the brush border of the duodenum also carry out this role. Fe2+ is taken up into epithelial cells by the divalent metal cation transporter DMT1, which cotransports H+ along with Fe2+(Fe3+ is not transported). Intracellularly, Fe2+ is converted to Fe3+ by ferroxidase, whereupon it is bound to iron-binding proteins that aid passage through the cytosol and, as a result, prevent the formation of insoluble complexes with available anions. Basolateral transport occurs by the transporter protein IREG1 and Fe3+ enters the circulation chaperoned by its plasma carrier protein, transferrin. In iron deficiency, the expression of iron transport mechanisms is appropriately increased in enterocytes, enhancing the efficiency of iron absorption; this also occurs in pregnancy. The defect in hereditary haemochromatosis leads to the same enterocyte status, with a now inappropriate overexpression of iron transporters progressively leading to the overload state. Conversely, the hepatic antimicrobial peptide hepcidin downregulates iron transport in the intestine, probably by inhibiting the function of the exit protein IREG1. This may be appropriate acutely in depriving bacteria of iron, but may contribute to the iron-deficiency state common in chronic inflammatory conditions. Copper and magnesium: about one-half of the daily intake of copper and magnesium is absorbed at sites in the small intestine. Comparatively less is known about the cellular mechanisms underlying epithelial transport, although DMT1 may also play a role. Vitamins are readily absorbed at all sites in the small intestine. Fat-soluble vitamins (A, D, E, K) are absorbed along with the digestion products of lipids in the micellar process. Watersoluble vitamins (e.g. B-complex, ascorbic acid, folic acid), are easily absorbed by intestinal epitheliauptake is via simple diffusion, following concentration gradients, although specific transporter proteins enhance uptake of most water-soluble vitamins (e.g. thiamine, folic acid). Absorption of vitamin-B12 is more complex (Figure 4). This water-soluble vitamin requires the chaperone protein, intrinsic
235

factor, which is secreted by gastric parietal cells and is necessary for absorption. Pernicious anaemia, an autoimmune gastritis with loss of parietal cells, culminates in achlorhydria and malabsorption of B12. Gastrectomy also disables absorption

Absorption of vitamin-B12
IF TCB12 B12 Blood IFB12 Internalization ?

Vitamin-B12 combines with intrinsic factor (IF) in the lumen which in turn dimerizes. IFB12 dimers bind to membrane receptors on terminal ileal enterocytes which internalizes, importing the IFB12 complex into the cytosol. It is thought that, after passage through the cytosol, extracellular transport is mediated by transport proteins and appears in the systemic blood flow bound to transcobalamin-II (TC). Figure 4

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of B12. Intrinsic factor dimerizes in the intestinal lumen, each dimer binding two molecules of vitamin-B12. Receptor proteins in the brush-border membrane recognize the intrinsic factorB12 complex which is then internalized by endocytosis exclusively in the terminal ileum. B12 deficiency also follows terminal ileal

resection or disease (e.g. Crohns disease). Basolateral exit from ileal epithelial cells is largely uncharacterized, though potentially involves active or facilitated transport by a carrier protein. B12 appears in the blood bound to transcobalamin-II, another chaperone protein.

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Abdominal access techniques (including laparoscopic access)


Ralph Smith Sukhpal Singh

Preoperative removal of hair Hair should be removed preoperatively if necessary, ideally with electric clippers. Premature (>6 hours before surgery), inappropriate or unskilled hair removal may traumatize the skin and allow colonization with potentially pathogenic micro-organisms at the surgical site.

Abstract
This contribution discusses safe exposure of intra-abdominal organs using laparoscopy and laparotomy; extraperitoneal access is not considered in detail. The techniques of Single Port Access (SPA) laparoscopy and Natural Orice Transluminal Endoscopic Surgery (NOTES) will also be described. This review should be read in conjunction with Anatomy of the anterior abdominal wall and groin, in this issue. Common abdominal incisions are shown in Figure 1.

Cleaning The surgical site and surrounding area are cleaned with an antiseptic agent, alcoholic or aqueous povidone-iodine or chlorhexidine, progressing from the incision site to the periphery. Areas of high microbial counts (groin, axilla, pubis, open wounds) should be prepared last and stoma sites isolated from the prepared area. The antiseptic agent must remain on the skin for sufcient time to achieve maximum effectiveness. This is the time taken to air-dry for alcoholic agents; at least 30 seconds is needed for non-alcoholic agents. Alcoholic agents should not be used on mucous membranes. Care must be taken to prevent alcoholic antiseptic agents from pooling beneath the patient or around diathermy pads to reduce the risk of burns.

Keywords laparoscopy; laparotomy; natural orice transluminal endoscopic surgery; NOTES; single port access; SPA

Preparation in the operating theatre


The abdomen of the anaesthetized patient should be examined because further information regarding intra-abdominal disease may be elicited when the musculature of the abdominal wall is relaxed, inuencing the surgical approach. Positioning The patient is positioned to allow optimal access to the area of interest; this is usually supine, but the LloydeDavies or lithotomy positions provide better access to the pelvis. In the latter positions, the patient is supine with the buttocks placed at the lower break in the table and the legs exed at the hips and knees, with sufcient abduction to allow access to the perineum. In the lithotomy position, the ankles are then placed in stirrups. In the LloydeDavies position, the legs are supported at the calf and ankle in pneumatic stirrups. Compression of the lateral popliteal nerve must be avoided; prolonged placement in this position increases the risk of deep venous thrombosis or compartment syndrome. The position may be further adjusted to facilitate different steps of the operation, for example:  Trendelenberg (head-down, to facilitate access to the pelvis)  reverse Trendelenberg (for better access to the upper abdomen)  left or right tilt.

Drapes The prepared area of skin and the drape fenestration should be sufciently large to accommodate extension of the incision, the need for additional incisions, and all potential drain or stoma sites. The passage of bacteria through surgical drapes is a potential cause of wound infection, so the drape type should be appropriate for that procedure. Drapes may be permeable linen or impermeable (disposable or non-disposable). Impermeable drapes result in signicantly fewer bacteria in the operative eld and wound compared with permeable linen drapes (through which bacteria can easily penetrate). Adhesive plastic incision drapes have previously been used if the risk of wound infection is high to reduce surgical site infection. However a recent review of over 4000 patients indicated an increased rate of infection in patients when such drapes were used (relative risk 1.23, p 0.03).

Laparoscopy
Laparoscopy provides:  the least traumatic access to all parts of the abdominal cavity  superb views of the anatomy  excellent cosmetic result  an attenuated stress response to surgery. The pneumoperitoneum may be achieved via open (Hasson) or closed (Veress needle, see below) methods; the incision for both is identical. It may be infra- or supra-umbilical, longitudinal or transverse, depending on:  preference  the intended procedure  surface anatomy (the relative length of their upper or lower abdomen)  previous scars. Important adjuncts to optimizing access at laparoscopy are catheterizing the bladder to allow better views of the pelvis, and decompressing a distended stomach with a naso/orogastric tube.

Ralph Smith MRCS is a Specialty Registrar in General Surgery, South West Thames Rotation, London Deanery, UK. Conicts of interest: none declared. Sukhpal Singh MS FRCS (Gen) is a Consultant General Surgeon at Frimley Park Hospital, Frimley, UK. Conicts of interest: none declared.

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Closed method The closed method uses a springloaded Veress needle. The anterior abdominal wall is manually elevated, and the needle introduced into the peritoneal cavity (Figure 2). Two clicks/ points of resistance should be noted as the needle passes through the linea alba and enters the peritoneal cavity. The needle position may be checked by instilling and aspirating normal saline:  aspiration should not be possible if the needle is intraperitoneal  saline may be aspirated if the needle is placed extraperitoneally  bowel content or blood may be aspirated if the needle is within an intra-abdominal viscus or vessel. A satisfactory drop test (whereby a drop of saline placed in the hub of the needle is sucked into the peritoneal cavity by negative intra-abdominal pressure when the anterior abdominal wall is manually elevated) indicates correct placement. When the gas is connected, the gas ow and intra-abdominal pressure gauges on the insufator should be carefully observed to ensure that the:  gas ows freely  initial intra-abdominal pressure is low and increases gradually with the volume of gas insufated. The rst port is introduced blindly (Figure 3). Most complications of laparoscopy (Table 1) are related to blind insertion of the Veress needle or of the rst port. A recent review of 17 randomised controlled trails containing 3040 patients concluded there is no increase in major complications

Figure 2 Insertion of the Veress needle. The anterior abdominal wall is elevated and the Veress needle held halfway down the shaft with the tap open. The ring and little nger stabilize the needle as it is advanced. Air is sucked in as the needle enters the peritoneal cavity, allowing the small bowel to fall away.

compared with the open methods described below. Extraperitoneal or failed insufation was reportedly higher when using the Veress needle. However, safety shields and retracting trocars do not prevent injury, and the potential complications associated with blind insertion of the Veress needle and primary port make the open technique the rst-choice method for many surgeons. Open methods The rst method is essentially a mini-laparotomy, whereby the linea alba is identied, incised, the peritoneum identied, elevated with two clips, and incised. The main problem with this method is that there is often a gas leak, which may be minimized by using a threaded Hasson cannula or a balloon-tip cannula.

Common abdominal incisions

e d f h i l j

b a

The second semi-open method involves incising the umbilical ligament: the central part of the umbilicus is elevated with a towel clip and a 1 cm transverse or longitudinal skin incision made. The umbilical ligament is identied, grasped, and a 0.5 cm incision made along its length (Figure 4). The abdominal cavity is

c g k

Name of incision a Lanz b RutherfordMorrison c Gridiron d Right upper quadrant transverse e Right subcostal f Upper midline laparotomy g Lower midline laparotomy h Midline laparotomy i Medial paramedian j Lateral paramedian k Pfannensteil l Palmers point

Incision used for Appendicectomy Right hemicolectomy Appendicectomy Cholecystectomy Cholecystectomy (left subcostal splenectomy)

General access to peritoneum

Urological and gynaecological procedures Laparoscopy

Figure 1

Figure 3 Insertion of the rst trocar. The index nger prevents the trocar from being fully inserted.

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Complications of laparoscopy
Specic Immediate: extra-peritoneal insufation, injury to intra-abdominal viscera or vessels, injury to blood vessels either of the anterior abdominal wall, or in the retroperitoneum Early: pain in shoulder tip Late: incisional hernia, metastases at port site General Immediate: bradycardia, inadequate oxygenation secondary to diaphragmatic splinting by excessive peritoneal insufation or extreme head-down position in an obese patient, pneumothorax, pneumomediastinum, gas embolism Early: deep vein thrombosis/pulmonary embolism, hypothermia, nausea and vomiting Table 1

Figure 5 Semi-open technique II. The peritoneal cavity is entered with an artery clip.

probed using a clip (Figure 5) and the rst port introduced over a graduated bougie. A gas leak is less likely with this method. The procedure may not be appropriate if a patient has had multiple previous operations because the abdomen is not entered under direct vision. Under such circumstances, the pneumoperitoneum may be created by placing the Veress needle in the right or left upper quadrant (Palmers point, Figure 1) and the rst port introduced under direct vision using an optical trocar (e.g. Visiport, Optiview). Ports and trocars A wide range of port and trocar designs have been developed. Each have their own specialist indications, advantages, disadvantages and surgeon preference. Some examples include;  Radially expanding trocars reportedly reduce the incidence of port site herniation and may avoid the need for closure of the fascial defect (important for obesity surgery).  Ports inserted using cutting trocars have reduced xity to the abdominal wall and may dislodge more frequently than blunt tipped trocars during laparoscopic procedures

 Extra-long trocars and ports for bariatric procedures  Blunt tipped balloon ports reduce gas leak throughout the insufation period  Optical trocars (e.g. Visiport) allow safer access into the peritoneal cavity with visualisation of all abdominal wall layers during insertion (particularly useful in patients who have had previous abdominal surgery with increased risk of adhesions and visceral injury) (Figure 6). Hand-assisted laparoscopic surgery Hand-assisted laparoscopic surgery is being used increasingly, particularly in laparoscopic colonic surgery. A sleeve and cuff are introduced into the peritoneum via a small incision that allows the intra-abdominal placement of a hand during laparoscopy, to:  facilitate tumour assessment  facilitate colonic mobilization  allow the ends of bowel to be exteriorized and an extracorporeal anastomosis done  reduce operation time  allow more complex procedures to be performed laparoscopically. Gasless laparoscopy In gasless laparoscopy, the operative eld is created with abdominal wall lift devices. However, poor exposure and technical difculty have led to gasless laparoscopy being of historical interest only. Minimal access to the retroperitoneum or extraperitoneal space Retroperitoneoscopy, with dissection of the retroperitoneal space via a balloon catheter, balloon trocar or nger dissection, allows excellent access to:  the kidneys  the adrenal glands  blood vessels  lymph nodes  the lumbar spine. Access to the extraperitoneal space for mesh repair of bilateral or recurrent inguinal herniae is achieved via a subumbilical

Figure 4 Semi-open technique I. The fat of the umbilical ligament bulges through the vertical incision.

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Ports and Trocars. a radially expanding, b retractable bladed, c balloon and d optical (reproduced with permission from Covidien Autosuture). Figure 6

transverse incision, starting in the midline and extended 2 cm laterally. The anterior rectus sheath is dissected out, incised in the line of the incision, and the rectus muscle retracted laterally to reveal the posterior rectus sheath. The extraperitoneal space is developed manually with the laparoscope or with a balloon dissector. Single port access laparoscopy (SPA) Appendicectomy, cholecystectomy and inguinal hernia repair have recently been successfully perfomed via a single transumbilical port. A multi-instrument access port (e.g. SILS Port, Tri-Port) is inserted to allow passage of commonly used laparoscopic instruments. Most procedures using SPA laparoscopy are performed using a 5 mm camera and two 5 mm operating ports via a single peri-umbilical incision. SPA laparoscopy offers potential improvements in post operative pain, wound infection, cosmesis and post-operative recovery. Loss of triangulation using a single port creates a technically challenging dissection. Improvements of existing rotational or curvilinear laparoscopic instruments will help widen the application of SPA laparoscopy (Figure 7). Natural orice transluminal endoscopic surgery (NOTES) NOTES may allow common laparoscopic procedures such as cholecystectomy and appendicectomy to be performed without visible surgical incisions. Access to the peritoneal cavity is gained by a viscerotomy through the stomach, colon, vagina or bladder. An operating endoscope is inserted to allow a peritoneoscopy and exible instruments are used to perform the surgical procedure. The majority of NOTES has been performed in a research setting and is considered experimental in humans. Particular concerns exist regarding potential complications

associated with the viscerotomy and the failure to achieve secure closure, as leakage of gastric or colonic content into the peritoneal cavity is usually associated with signicant morbidity. Operative access and the range of achievable dissection is currently limited by the quality of suitable endosurgical instruments, the surgeons learning curve and patient safety concerns.

Laparotomy
Exposure There must be sufcient exposure to allow the procedure to be done efciently and safely. The required exposure depends on:  the diagnosis (if known) and the planned surgery  whether surgery is elective or emergency  the speed at which exposure must be achieved  whether exposure can be increased if required by extending the incision  previous surgical history and scars. Classication of laparotomy incisions Laparotomy wounds can be classied as:  vertical  transverse or complex  muscle splitting  muscle cutting. Midline vertical incisions allow rapid access, with minimal blood loss, and are easily extended. The paramedian incisions take longer, are associated with more blood loss, but a right paramedian incision offers excellent access to all parts of the abdomen. Incisions placed more transversely in Langers lines offer comparable

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access to most intra-abdominal structures as vertical incisions, with fewer complications (pain, pulmonary comorbidity, dehiscence) and an excellent cosmetic result, but are more difcult to extend. More complex incisions offer access to specic sites for certain operations (e.g. rooftop incision for pancreatic surgery; MercedeseBenz incision (an inverted Y) for liver transplant). The incision: diathermy or knife? Traditionally, a knife has been used for the skin incision, but recent data suggest that the diathermy blade allows the incision to be done more quickly, with less blood loss, less postoperative pain and no adverse effects on wound healing or cosmetic effect. The incision: pointers and pitfalls Much has been written on whether to incise around or through the umbilicus when carrying out a midline laparotomy. Either method is acceptable if appropriate care is taken, although incising around the umbilicus provides less risk of damage to the hernia contents if an umbilical hernia is present. The easiest place to enter the peritoneum with a midline laparotomy wound (having incised skin, subcutaneous fat, and the linea alba) is the umbilicus. The peritoneum is grasped between two clips, elevated and incised, and the peritoneal contents fall away as air enters the abdominal cavity. The inner aspect of the incision line is palpated to ensure that there are no adherent structures, and the incision completed. The falciform ligament will be encountered in midline incisions that extend above the umbilicus. Rather than incising the falciform (which increases the risk of bleeding) it is more elegant to dissect to one side or other in the extraperitoneal plane and enter the peritoneal cavity lateral to the falciform ligament. The peritoneal cavity should be entered on the left of the falciform for surgery in the left upper quadrant, and conversely for surgery in the right upper quadrant. Injury to the bladder must be avoided for midline incisions that extend towards the symphysis pubis; the incision may need to be extended to one or other side of it. The potential requirement and site for a stoma should also be considered. One must avoid inadvertent enterotomy when entering the distended abdomen, or where there have been multiple previous laparotomies. For this latter group, it is preferable to extend the incision onto the unscarred abdominal wall and enter the peritoneal cavity there because there is less risk of damaging adherent bowel. The incidence of inadvertent enterotomy in patients with previous laparotomies is unknown, but one paper suggests a rate of 19%. The authors found that age, and three or more previous laparotomies were independent risk factors. They also showed that patients with inadvertent enterotomy during adhesiolysis had signicantly more:  postoperative complications  urgent relaparotomies  ICU admissions  use of parenteral nutrition  days spent in hospital. Postoperative pain, wound healing and cosmetic effect The complications of laparotomy are shown in Table 2. Obtaining adequate exposure must be balanced with minimizing postoperative pain. The size and location of the incision is

Single incision laparoscopic surgery (SILS) ports and TriPort in use (reproduced with permission from Covidien Autosuture and Olympus KeyMed). Figure 7

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Complications of laparotomy
Specic Immediate: injury to adherent intra-abdominal structures Early: wound infection, wound dehiscence Late: incisional hernia, poor cosmetic result, adhesions General Early: cardiovascular (deep vein thrombosis/pulmonary embolism, bleeding), respiratory (basal atelectasis, pneumonia), renal (renal failure) Table 2

during dressing changes and VAC may accelerate wound healing. However there is the risk of promoting or delaying healing of established entero-cutaneous stulae.2 A number of prospective randomized clinical trials have questioned whether there is a signicant increase in the frequency of wound dehiscence or incisional herniae with slowly absorbable suture compared to a non-absorbable suture. No difference in wound dehiscence has been reported, but some clinical trials suggest an increased risk of incisional herniae with absorbable sutures. Other predisposing factors to incisional herniae include:  poor surgical technique  wound infection  conditions associated with impaired healing of wounds (e.g. diabetes mellitus, corticosteroid therapy, malnutrition, morbid obesity, advanced age, pulmonary disease, malignancy). Optimizing access at laparotomy Access is optimized and maintained by skilled assistance and retraction. Retractors vary from the assistants hand to:  hand-held retractors (Deavers, Morris, St Marks)  self-retaining retractors (Golighers, Balfour)  ring retractors (TurnereWarwick)  xed retractors (Thompson, Omnitract). Strategies to control unwanted viscera from entering the operative eld include systematic packing with swabs, or using a bowel bag, which also limits loss of heat and uid from externalized bowel. Ceiling-mounted overhead lighting, which is moved and focused on the operative eld, is an essential adjunct for optimizing access. This may not be sufcient in certain circumstances and headlights, or a light mounted on a retractor (e.g. St Marks), may improve access. Good access is fundamental to successful surgery, but optimizing access requires careful planning. This is relatively straightforward for elective surgery but, for emergencies, careful preoperative examination, patient positioning and an appropriately sited incision allows the operation to proceed smoothly and successfully. A

paramount, but the strategy for relief of postoperative pain must be considered preoperatively. This may include:  an epidural catheter  local anaesthetic blockade at time of surgery  patient-controlled analgesia  intermittent opiates (i.v. or i.m.)  NSAIDs  combinations of oral paracetamol and opiate. Careful closure of wounds avoids the complications of wound dehiscence (see below), infection or incisional herniae. Continuous mass closure is recommended for closure of a midline laparotomy wound, using number 1 absorbable (polydioxanone) or non-absorbable (nylon) monolament suture, taking 1 cm bites of tissue, 1 cm apart, at least 1 cm from the wound edge (which pass through all layers of the incision apart from the skin), using four times as much suture as the wound length (Jenkins rule). The skin is closed with clips, interrupted non-absorbable sutures, or a subcuticular absorbable suture (the rst two options are more appropriate if infection is present). Care must be taken to achieve a good cosmetic appearance. Wound dehiscence, which classically occurs at 8e10 days postoperatively, signies technical failure. It is recognized by a serosanguinous ooze arising from the wound and, on further inspection, intra-abdominal contents (usually small bowel) are seen in the wound. The patient will be systemically unwell. The management of wound dehiscence involves:  reassurance  analgesia  appropriate cardiovascular support  covering the wound with warm saline dressings  resuturing of the wound under general anaesthesia, with deep-tension sutures if required. Recently, vacuum assisted closure devices (VAC) have been used to accelerate wound healing following supercial abdominal wound dehiscence and laparostomy. An occlusive low negative pressure continuous suction dressing is applied to the abdominal wound to generate improved blood ow and formation of granulation tissue.1 Benets include reduced frequency and pain

REFERENCES 1 Lambert KV, Hayes P, McCarthy M. Vacuum assisted closure: a review of development and current applications. Eur J Vasc Endovasc Surg 2005; 29(3): 219e26. 2 Heller L, Levin S, Butler C. Management of abdominal wound dehiscence using vacuum assisted closure in patients with compromised healing. Am J Surg 2006; 191(2): 165e72. FURTHER READING Grantcharov TP, Rosenberg J. Vertical compared with transverse incisions in abdominal surgery. Eur J Surg 2001; 167: 260e7. Kearns SR, Connolly EM, McNally S, McNamara DA, Deasy J. Randomised clinical trial of diathermy versus scalpel incision in elective midline laparotomy. Br J Surg 2001; 88: 41e4.

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Abdominal wound dehiscence and incisional hernia


David C Bartlett Andrew N Kingsnorth

failure of the entire wound with evisceration, or burst abdomen. The incidence of abdominal wound dehiscence ranges from 0.25e3% with an associated mortality of up to 25%2,3 and is most often seen at around 1 week post surgery.2,4 Incisional hernia (Figure 1) is a chronic wound failure and presents some time after surgery, often at follow-up clinics or as a new referral. The incidence varies between 5% and 15% following vertical midline incisions at one year follow up. More than 50% of incisional hernias occur in the rst year postoperatively and 90% of incisional hernias occur within three years of surgery.5e7

Abstract
Abdominal wound dehiscence and incisional hernias are common problems facing the general surgeon. Both can be thought of as forms of wound failure and the risk factors are similar for both. Some of these may be avoided by sound surgical technique and correct patient preparation. The management of wound dehiscence ranges from simple dressings to emergency surgery to close a burst abdomen followed by a period of intensive care. The management of incisional hernias is a much bigger topic and encompasses various surgical techniques. This review will describe the aetiology of wound failure and the management of acute wound dehiscence. It will then go on to cover in more detail the assessment of patients presenting with incisional hernia as well as outlining the main surgical options available and some of the auxiliary techniques that are used to aid repair. Lastly the topic of laparostomy closure, an increasing problem due to the increasing numbers of patients undergoing major surgery, and the use of Vacuum Assisted Closure devices are briey reviewed.

Cause and prevention


The causes of acute and chronic wound failure are similar. Poor surgical technique and wound infection can cause acute dehiscence; acute dehiscence is the commonest cause of incisional hernia which is preceded by wound infection in nearly 50%.5 There are a number of other risk factors that predispose to wound failure. These can be divided into preoperative (patient related) factors, operative (surgical) factors and postoperative factors (Table 1). There is evidence that, in many cases, wound failure after abdominal wall closure is dependent on the surgeon. Many of these risk factors are not readily avoidable, but sound surgical technique with appropriate suture material, good bites of tissue (>1 cm), properly laid knots with sufcient throws and avoidance of excessive tension is important. If possible, the restoration of normal anatomy during the closure of abdominal wounds should be attempted. In the midline, this means apposition of the linea alba and, in lateral or horizontal incisions, closure of tendinous, aponeurotic and fascial structures (e.g. posterior and anterior rectus sheath) in layers. The optimal technique for closing a midline incision is mass closure with a continuous slowly absorbable monolament suture.8e10 The use of a slowly absorbable material, such as PDS, appears to provide sufcient strength for a long enough period to allow the wound to heal, whilst reducing other complications such as persistent wound pain and suture sinus. Whilst there is little evidence of its superiority over interrupted sutures in randomised trials,11 a continuous suture ensures that tension is distributed evenly along the length of the wound and is a popular technique because of its safety, efcacy and speed. A suture length to wound length ratio of at least 4:1 should be used, allowing a minimum of 1 cm bites at 1 cm intervals, and is associated with a lower rate of incisional hernia.12 The choice of incision is a further consideration. There has been a growing interest in transverse incisions which provide excellent access to most parts of the abdomen. This approach has been found to have a lower incidence of both early and late complications including wound dehiscence and incisional hernia.13 Incisional hernia at port sites following laparoscopic surgery is also a recognised complication with an incidence of up to 3.6%.14 These usually remain unreported until a complication occurs. The midline supra- or subumbilical port site used during many procedures should be closed with a slowly absorbable monolament suture. Consideration should also be given to closing port sites of 10 mm or more elsewhere, especially when they have been stretched, for example, to remove a gallbladder.

Keywords dehiscence; hernia; hernia repair; incisional hernia; incisional


hernia repair; laparostomy; VAC therapy; vacuum assisted closure; ventral hernia; wound dehiscence; wound failure

Introduction
Abdominal wound dehiscence and incisional hernia can both be thought of as forms of wound failure, which may be dened as the failure of the incision to heal and to maintain the normal anatomy of the abdominal wall. Wound dehiscence is an acute wound failure1 and can be dened as the partial or complete disruption of any or all layers of a surgical wound. This can range from a relatively minor breakdown of the skin and subcutaneous tissue to a complete

David C Bartlett MRCS is a Clinical Research Fellow/SpR in HPB and Liver Transplant Surgery at the University of Birmingham and Queen Elizabeth Hospital Birmingham. He graduated from Bristol University in 2001 and completed Basic Surgical Training at Derriford Hospital, Plymouth before obtaining a NTN in the West Midlands. His main interest is Hepatobiliary surgery but is also undertaking research in hernia surgery. Conicts of interest: none declared. Andrew N Kingsnorth FRCS FACS is Professor of Surgery at Derriford Hospital, Plymouth, UK. He qualied at the Royal Free Hospital School of Medicine, London, and trained in General Surgery at Oxford, Harvard University, Edinburgh and Cape Town. His research interests include pancreatic disease and hernia. Conicts of interest: none declared.

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Minimal dissection of tissue, good haemostasis and the selective use of drains can reduce postoperative formation of a seroma or haematoma and subsequent infection that could lead to dehiscence.

Management of wound dehiscence


Supercial wound dehiscence can often be managed conservatively. This involves regular inspection and dressing of the wound. If the dehiscence has been caused by an infected collection then the opening of the wound and the resulting drainage may allow subsequent healing by secondary intention. Remaining sutures or skin clips that prevent the wound from opening sufciently to allow drainage should be removed. If there is ongoing infection or surrounding cellulitis then antibiotics will be required. Large supercial dehiscences may require debridement of infected and necrotic tissue as well as careful selection of appropriate packing and dressing materials. More advanced techniques such as vacuum dressings may also be required. Specialist tissue viability nurses often have a lot to offer and should be involved in difcult cases. A t patient with a clean, non-infected wound may benet from delayed primary closure which usually results in a superior cosmetic outcome. The management plan should be discussed with the patient and reassurance offered. Many patients nd the sudden opening-up of their wound distressing. A complete dehiscence, or burst abdomen, due to disruption of the fascial layers with exposure of the viscera will require emergency surgery. This involves debridement of the wound edges as necessary with removal of previous suture material and re-suturing, often with retention sutures. Interrupted heavy 1/0 non-absorbable suture is used taking large bites from the wound edge (>3 cm) and including all layers. A plastic sleeve may be used over the suture where it overlies the skin to prevent it from cutting into the skin (Figure 2). However, whilst retention sutures may allow satisfactory closure of the abdomen, there is evidence that this technique does not reduce the incidence of later incisional hernia.16 Occasionally it becomes clear that such a closure will have serious effects on the patient, such as compromising ventilation or risking abdominal compartment syndrome. In such cases it will be necessary to leave the patient with a laparostomy. Such patients may become seriously ill with sepsis and organ failure, and are best managed in a HDU or ICU.

Figure 1 A large incisional hernia.

It is particularly important to identify the existence of a preexisting umbilical hernia when using an umbilical port, and to ensure that the defect is properly dened and repaired at the end of the procedure.15 In addition to sound surgical technique, the risk of infection must also be minimised. This can be achieved through:  Ensuring that the skin is shaved as late as possible  Adequate skin preparation  Appropriate use of prophylactic antibiotics for high-risk patients and procedures.

Risk factors for wound dehiscence after laparotomy


Preoperative/patient factors Age (>65) C Male C Smoker C Obesity C Diabetes C Hypoalbuminaemia/malnutrition C Sepsis C Anaemia C Uraemia C Malignancy C Chemotherapy/radiotherapy C Steroid use
C

Operative factors C Emergency surgery C Re-operation C Bowel (dirty) surgery C Suture type and technique Postoperative factors C Mechanical ventilation C Haemodynamic instability C Increased intraabdominal pressure C Ascites C Wound infection Table 1

Management of incisional hernias


Most patients with incisional hernias, at least initially, have few symptoms. At presentation up to 25% of patients are asymptomatic.17 If symptoms occur, they commonly consist of:  Restriction of movement or of wearing certain clothes  Embarrassment due to disgurement  Discomfort or pain. Such patients usually present to the general surgical outpatient clinic. Less commonly they may present as an emergency with:  Bowel obstruction  Ischaemic bowel  Spontaneous rupture of the contents of the hernia (rare).

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the contents into the remaining peritoneal cavity are likely to result in abdominal compartment syndrome if signicant loss of domain (about 20%) is present.21 Surgical repair of incisional hernia Only the smallest hernias (<3e4 cm) should be repaired with a suture technique.22,23 A suitable technique for such a hernia is the Mayo repair, whereby the fascial edges are closed with a 2 cm overlap using interrupted monolament suture, and reinforced with a continuous running suture (Figure 3). However, attempts at repairing larger hernias with such a technique are associated with an increased risk or recurrence.24 Most incisional hernias are therefore repaired using one of several techniques that employ mesh. The down side to the use of mesh, however, is an increased rate of infection.25 Choice of mesh The ideal mesh should be non-absorbable, biocompatible, preserve the physiological elasticity of the abdominal wall and allow proper integration with the surrounding tissue.26 Polypropylene (Prolene, Marlex etc) and polyethylene (e.g. Mersilene) meshes are commonly used; they are exible and easily cut to size. They allow excellent tissue ingrowth, but they become anchored to adjacent tissues and are not suitable for techniques that allow the mesh to come into contact with abdominal contents. If this happens, extensive adhesions to the viscera form and erosion of the mesh into the intestines may occur. Traditional polypropylene meshes with a small pore size cause a relatively long lasting inammatory reaction with a stiff scar plate. Newer lightweight meshes (e.g. Vypro) with a larger pore size (3e5 mm) and a corresponding reduction in the amount of polypropylene result in better tissue integration, a more exible scar net, and a reduced inammatory response.27,28 The number of meshes available for intraperitoneal use has increased signicantly over recent years with the advent of laparoscopic hernia repair. These fall into three categories:

Figure 2 A burst abdomen resutured using retention sutures. Source: D J Leaper, Cardiff University, Cardiff, UK.

Assessment Clinical examination should be in the standing and supine positions to allow easy identication of the hernia, which may not be initially obvious if small. It may be necessary to ask the patient to cough or carry out a Valsalva manoeuvre to exaggerate the hernia. The edges of the defect can usually be palpated and the size of the defect should be noted because it may inuence surgical technique. The reducibility of the hernia should be assessed. Imaging Radiological investigation may be required in obese patients with small hernias that are difcult to show clinically, and those with very large complicated hernias. Ultrasound examination may show a fascial defect and provide a measurement of the size and identication of the contents of the hernial sac. However, this modality is highly operator dependent and time-consuming. MRI is increasingly used in selected patients, and may be particularly useful in the assessment of recurrent hernias where it allows visualisation of the existing mesh and identication of adhesions.18 CT is particularly helpful to fully assess large complex hernias, recurrent hernias or hernias with multiple defects, and is the modality of choice.19,20 Occult defects are identied, the contents of the sac are more clearly dened and estimation of the loss of domain of the abdominal contents can be made. Loss of domain is where large hernia sacs develop with abdominal contents permanently residing outside of the abdominal cavity and retraction of the normal musculature of the abdominal wall. A proportion of the abdominal contents have therefore lost domain within the abdomen. Attempts to reduce

Figure 3

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expanded polytetrauoroethylene (ePTFE), composite meshes and biological meshes. ePTFE meshes (Goretex, Dualmesh etc) have been shown to cause few adhesions and can be used safely in direct contact with the abdominal contents.29 Composite meshes comprise a polypropylene (Proceed, Sepramesh, Composix etc) or polyethylene (e.g. Parietex Composite) mesh layer with some form of barrier layer. The traditional mesh provides strength and allows incorporation into the abdominal wall while the barrier layer prevents adhesion of the underlying viscera. It is important to ensure that such meshes are inserted the correct way up. Biological meshes are acellular extracellular matrix materials derived from humans or animals. In theory such meshes become vascularised and colonised by host cells leading to partial or complete remodelling. There is therefore great interest in the use of such materials in contaminated environments as there is a theoretical possibility that infections can be cleared.30 Examples of such materials include porcine dermal collagen (Permacol) and human dermis (AlloDerm, FlexHD). Cost and a lack of long term evidence currently limit the routine use of biological meshes. There is currently insufcient evidence from randomised controlled trials to form generalised recommendations about which mesh should be used for incisional hernia repair.31,32 The choice will ultimately depend largely on surgeon preference and cost, taking into account the general principles outlined above. Open repair Three general techniques may be used during open mesh repair of incisional hernias e onlay, inlay and sublay (Figure 4). The initial approach is identical regardless of the technique of mesh placement. The old scar and redundant skin are excised and the underlying hernia sac dened by careful dissection from the surrounding tissues. The hernia sac is opened, adhesions between the contents and the sac are divided and the sac is excised. For an onlay repair, a border of at least 5 cm around the fascial edge is exposed by raising skin aps. The fascial edges are brought together using continuous non-absorbable monolament suture, applying the rule of 1 cm bites at 1 cm intervals. A mesh is placed to cover the suture line and overlap by at least 5 cm in all directions. The mesh must lie at, with no folds and no tension, and is secured with further non-absorbable suture to the underlying fascia. The skin is closed over the mesh.33 Tissue glue may be sprayed beneath the aps to reduce seroma formation if the skin aps are particularly large. Suction drains should be placed beneath the aps. The onlay technique is versatile and lends itself to repair of hernias in all quadrants of the abdomen. It gives excellent results for the repair of major incisional hernias when combined with components separation and brin sealant.34 The inlay technique involves suturing a mesh to the fascial edges without initially closing the defect. This requires the correct choice of mesh (as outlined above) because it will lie in contact with the viscera. One series of 350 patients reported excellent results with an inlay technique,35 although other groups have had less success with recurrence rates of up to 44% (higher than those for onlay and sublay repairs) and enterocutaneous stulas developing at the edges of the mesh where

Figure 4

constant friction caused bowel damage.36 Inlay techniques are not recommended unless there is a substantial defect that cannot be bridged or closed using other procedures. For the sublay technique, the posterior rectus sheath and peritoneum (the peritoneum only below the arcuate line) is closed and the mesh is placed above this.37 The rectus muscles are allowed to return to their natural position and cover the mesh. The anterior rectus sheath is closed. This can be a complex operation and is only really useful in the midline. Variations on the technique can be used away from the midline with the mesh positioned, for example, between the internal and external oblique muscle layers.38 Laparoscopic repair With the increasing popularity of laparoscopic surgery, the laparoscopic repair of incisional hernias is becoming the technique of choice for many surgeons. This technique has the potential to offer all the benets of other laparoscopic techniques such as a reduction in postoperative pain, early mobilisation and shorter hospital stay. However the learning curve is probably longer than that for open repair, and there is the potential for problems such as bowel injury, which may go unnoticed, and

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signicant bleeding, which may be difcult to control, leading to open conversion or reoperation in a number of cases. However, recent studies suggest the overall conversion and complication rates are low.39e41 In terms of recurrence, outcomes do not seem to differ signicantly between open and laparoscopic repair.42,43 Laparoscopic repair is particularly useful for the repair of recurrent hernias following a previous open repair, when a repeat open procedure may be difcult due to the distorted anatomy and existing mesh/scar tissue. Port placement requires some consideration for laparoscopic hernia repair. A pneumoperitoneum is created and appropriate ports (usually at least one 10 mm camera port and two 5 mm operating ports) are inserted. For large, complex hernias, multiple ports on both sides of the abdomen may be required. Great care is needed during initial port insertion as this will often be away from the midline and umbilicus, and there may be adherent bowel below the abdominal wall; an open insertion technique or the use of an optical trocar are appropriate methods. The insertion of subsequent ports under vision may also be difcult if the view is obscured by adherent bowel. The intraperitoneal onlay mesh (IPOM) is the most common technique used for laparoscopic repair (Figure 5). Adhesions between the hernia contents and anterior abdominal wall/hernia sac are divided so that the contents may be reduced. This is the most time-consuming part of the operation, and requires a careful mix of electrocautery or ultrasonic scalpel to prevent excessive bleeding, as well as sharp dissection with scissors in proximity to bowel to avoid thermal injury. The size of the defect is measured, following release of the pneumoperitoneum, and a mesh is shaped to cover and overlap the defect by 3e5 cm.44 The mesh may be labelled (left, right, top, bottom) to aid positioning and is then carefully rolled up and introduced via one of the ports. Once inside the abdominal cavity, the mesh is unrolled and positioned over the defect. This is aided by the placement of four or more sutures on the mesh, prior to inserting it into the abdomen, which can be grasped using a suture passer, such as the Endoclaw, and used to pull the mesh up onto the abdominal wall. The mesh is then secured in place with a double crown of metal tacks. These may be reinforced with slowly absorbable monolament transfascial sutures passed from outside, through the abdominal wall and mesh and back outside with the aid of the suture passer using small stab incisions. However, there is

evidence that tacks alone are sufcient, and some surgeons believe the use of transfascial sutures leads to increased postoperative pain.41 The port sites are closed in the standard manner, and stab incisions closed with glue or steristrips. Some surgeons believe that the hernial defect should be closed with re-approximation of the linea alba during laparoscopic repair, and several techniques have been described to achieve this; this is not a routine part of the procedure and because of this, as well as the fact that excess skin is not removed, there is often a persistent bulge following the repair of a large hernia. This should be explained to the patient prior to surgery, who may otherwise assume that the repair has failed. Despite the increasing tendency to laparoscopic repair, there is little evidence of a signicant benet over open repair in terms of recurrence rates and there remain a number of patients in whom laparoscopic repair is not possible. Relative contraindications to laparoscopic repair include:  Multiple recurrent hernias or extensive previous abdominal surgery where adhesions are likely to be too dense  Hernias presenting acutely with possible ischaemic bowel  Hernias where there is loss of domain and therefore the contents cannot be easily returned into the abdominal cavity  If other gastrointestinal surgery (e.g. bowel resection) is indicated. Components separation The Ramirez components separation technique allows enlargement of the abdominal wall surface by separating muscle layers without damaging the innervation or blood supply to the muscles. The technique allows advancement of the rectus abdominis muscle, anterior rectus sheath and internal oblique up to 10 cm towards the midline. This can cover a defect of up to 20 cm if performed on each side.45 It involves the detachment of the external oblique aponeurosis from the rectus muscle and the development of a plane between the external and internal oblique aponeuroses. An additional procedure is the further mobilisation of the rectus by incising the posterior rectus sheath at its medial border (sliding door technique).46 The components separation technique is particularly useful when supplemented with an onlay mesh repair. The fascial edges are closed in the midline. The repair is then covered with a mesh, which can be sutured to the divided edges of the external oblique with a continuous suture (Figure 6).34 Auxiliary techniques A number of other techniques can be used to aid the repair of large incisional hernias, particularly when there is loss of domain. Relaxing techniques involve multiple small incisions in fascial layers or at muscular attachments. Care must be taken to preserve the blood supply and innervation of the abdominal wall and sufcient fascia must be preserved to maintain the overall strength of the abdominal wall. Preoperative measures to increase the volume of the abdominal cavity have also been described. Progressive pneumoperitoneum may be achieved by placement of a catheter in the peritoneal cavity under local anaesthesia followed by gradual insufations of air or carbon dioxide.47,48 The

Figure 5

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Special cases of incisional hernia


C C C C C

Parastomal hernias Lumbar hernias Iliac crest hernias after harvest of bone for grafting Subxiphoid hernias following median sternotomy Incisional hernias after nephrectomy

Table 2

Figure 6 Onlay mesh repair, in this case combined with a Ramirez Component Separation. The mesh has been secured to the underlying fascia and, at its lateral borders, to the divided external oblique aponeuroses. A continuous suture has also been placed in the midline overlying the closure of the fascial layer beneath.

size of the peritoneal cavity is increased and adhesions elongated resulting in:  Easier dissection  Reduction of oedema  Improved diaphragmatic tone  Cardiorespiratory adaptation. Pneumoperitoneum is rarely used due to the complexity of the procedure and the availability of other procedures (e.g. components separation). Tissue expanders placed in the subcutaneous or submuscular space for a few months before surgery is another option.49 This technique is particularly useful when the anatomy of the abdominal wall is severely distorted due to:  Trauma  After removal of large tumours/congenital abnormalities. Special cases Women of childbearing age with symptomatic hernias of the anterior abdominal wall may undergo surgery before further pregnancies. The hernia sac is freed and the hernia reduced as described above for open mesh repair. Mesh should be avoided because it will severely limit the elasticity and expansion of the abdominal wall. The defect is repaired using a suture method such as the shoelace or onlay darn techniques, the descriptions of which are beyond the scope of this review.50 There are a number of other special cases in which incisional hernias may develop and which require modied repair techniques (Table 2). The underlying principles of dening the anatomy, reducing the hernia and carrying out a tension-free repair still hold. Mesh is often used and in some cases may be anchored to bone (e.g. during the repair of hernias occurring at the iliac crest after its use as a donor site for bone graft).

to bowel ischaemia and respiratory compromise or to facilitate re-exploration.51 The closure of a laparostomy is one of the most challenging procedures facing the hernia surgeon. The procedure must be carefully planned, starting from the moment the decision is made to leave an abdomen open, and may require input from intensivists, respiratory physicians and plastic surgeons. The aims of the procedure are to provide adequate soft tissue coverage of the viscera and restoration of function of the abdominal wall. It may be possible to close a laparostomy soon after it is formed following an initial period of resuscitation and recovery in an ICU. The likelihood of fascial closure correlates with the cause of the laparostomy.52 Closure is most likely after laparotomy for trauma. Laparotomies for gastrointestinal sepsis are more likely to be closed using supplementary mesh, and denitive closure is least likely if the underlying condition is pancreatitis. Different techniques are required if closure is not achieved within 1e3 weeks. By this time, the exposed viscera are covered with a layer of granulation tissue and the options are skin grafting or the placement of a temporary absorbable mesh. This effectively produces a planned incisional hernia that may be repaired subsequently. If primary fascial closure is not possible, denitive closure must be undertaken at a later stage once the patient is well and other complications (e.g. sepsis, stulas) have been managed. A variety of techniques and auxiliary procedures, similar to those described for incisional hernia repair, may be used.

Vacuum assisted closure


The use of topical negative pressure therapy (Vacuum Assisted Closure or VAC therapy) to promote wound debridement and healing was rst described for the treatment of open fractures.53 It has since been successfully applied to a wide variety of wounds and its use is now commonplace. There are, however, a number of contraindications (Table 3). Care also needs to be taken when

Contraindications to VAC therapy


C C

Closure of a laparostomy
A laparostomy may be performed after a wide range of surgical procedures where closure of the abdomen is not possible, where closure would cause abdominal compartment syndrome leading

C C

Malignancy in the wound Untreated osteomyelitis Non-enteric and unexplored stulae Necrotic tissue with eschar (prior debridement required)

Table 3

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Figure 7 VAC dressing applied to a laparostomy.

there are exposed blood vessels or organs as these will need to be protected before the dressing is applied. The application of a VAC dressing can be quite complex and is best achieved with the aid of someone experienced in the technique. Basically, the dressing consists of a piece of foam which is cut to the size of the wound and inserted into it to ll any cavity or space between the wound edges. This is then covered by an occlusive dressing. It is important that a good seal is obtained to prevent the loss of the vacuum. A specially designed suction tube is then placed over a hole in the inclusive dressing and connected to the vacuum pump. Various theories about the mode of action exist, including the removal of interstitial uid and decreased oedema, the alteration of factors such as proinammatory cytokines and matrix metalloproteinases, the promotion of blood ow and the stimulation of protein and matrix synthesis and angiogenesis.54 VAC therapy can be used successfully in the management of wound dehiscence to aid healing and is increasingly used in the management of laparostomy (Figure 7). The bowel loops are separated from the fascia and the constant negative pressure helps to prevent the fascial edges from retracting. The result is that primary fascial closure can be achieved in signicantly more patients, even several days following the initial laparotomy.55A

REFERENCES 1 Carlson MA. Acute wound failure. Surg Clin North Am 1997 Jun; 77(3): 607e36. 2 Spiliotis J, Tsiveriotis K, Datsis AD, et al. Wound dehiscence: is still a problem in the 21th century: a retrospective study. World J Emerg Surg 2009 Apr 3; 4(1): 12. 3 Waqar SH, Malik ZI, Razzaq A, Abdullah MT, Shaima A, Zahid MA. Frequency and risk factors for wound dehiscence/burst abdomen in midline laparotomies. J Ayub Med Coll Abbottabad 2005 Oct; 17(4): 70e3. 4 Rodriguez-Hermosa JI, Codina-Cazador A, Ruiz B, et al. [Risk factors for acute abdominal wall dehiscence after laparotomy in adults]. Cir Esp 2005 May; 77(5): 280e6. 5 Bucknall TE, Cox PJ, Ellis H. Burst abdomen and incisional hernia: a prospective study of 1129 major laparotomies. Br Med J (Clin Res Ed) 1982 Mar 27; 284(6320): 931e3.

6 ODwyer PJ, Courtney CA. Factors involved in abdominal wall closure and subsequent incisional hernia. Surgeon 2003 Feb; 1(1): 17e22. 7 Mudge M, Hughes LE. Incisional hernia: a 10 year prospective study of incidence and attitudes. Br J Surg 1985 Jan; 72(1): 70e1. 8 vant Riet M, Burger JW, van Muiswinkel JM, Kazemier G, Schipperus MR, Bonjer HJ. Diagnosis and treatment of portal vein thrombosis following splenectomy. Br J Surg 2000 Sep; 87(9): 1229e33. 9 Rucinski J, Margolis M, Panagopoulos G, Wise L. Closure of the abdominal midline fascia: meta-analysis delineates the optimal technique. Am Surg 2001 May; 67(5): 421e6. 10 Weiland DE, Bay RC, Del SS. Choosing the best abdominal closure by meta-analysis. Am J Surg 1998 Dec; 176(6): 666e70. 11 Fagniez PL, Hay JM, Lacaine F, Thomsen C. Abdominal midline incision closure. A multicentric randomized prospective trial of 3,135 patients, comparing continuous vs interrupted polyglycolic acid sutures. Arch Surg 1985 Dec; 120(12): 1351e3. 12 Israelsson LA, Jonsson T, Knutsson A. Suture technique and wound healing in midline laparotomy incisions. Eur J Surg 1996 Aug; 162(8): 605e9. 13 Grantcharov TP, Rosenberg J. Vertical compared with transverse incisions in abdominal surgery. Eur J Surg 2001 Apr; 167(4): 260e7. 14 Bergemann JL, Hibbert ML, Harkins G, Narvaez J, Asato A. Omental herniation through a 3-mm umbilical trocar site: unmasking a hidden umbilical hernia. J Laparoendosc Adv Surg Tech A 2001 Jun; 11(3): 171e3. 15 Azurin DJ, Go LS, Arroyo LR, Kirkland ML. Trocar site herniation following laparoscopic cholecystectomy and the signicance of an incidental preexisting umbilical hernia. Am Surg 1995 Aug; 61(8): 718e20. 16 Gislason H, Viste A. Closure of burst abdomen after major gastrointestinal operationsecomparison of different surgical techniques and later development of incisional hernia. Eur J Surg 1999 Oct; 165(10): 958e61. 17 Nieuwenhuizen J, Kleinrensink GJ, Hop WC, Jeekel J, Lange JF. Indications for incisional hernia repair: an international questionnaire among hernia surgeons. Hernia 2008 Jun; 12(3): 223e5. 18 Kirchhoff S, Ladurner R, Kirchhoff C, Mussack T, Reiser MF, Lienemann A. Detection of recurrent hernia and intraabdominal adhesions following incisional hernia repair: a functional cine MRIstudy. Abdom Imaging 2009 Mar 21. 19 Toms AP, Dixon AK, Murphy JM, Jamieson NV. Illustrated review of new imaging techniques in the diagnosis of abdominal wall hernias. Br J Surg 1999 Oct; 86(10): 1243e9. 20 Ianora AA, Midiri M, Vinci R, Rotondo A, Angelelli G. Abdominal wall hernias: imaging with spiral CT. Eur Radiol 2000; 10(6): 914e9. 21 Kingsnorth AN, Sivarajasingham N, Wong S, Butler M. Open mesh repair of incisional hernias with signicant loss of domain. Ann R Coll Surg Engl 2004 Sep; 86(5): 363e6. 22 Kingsnorth A, LeBlanc K. Hernias: inguinal and incisional. Lancet 2003 Nov 8; 362(9395): 1561e71. 23 Hesselink VJ, Luijendijk RW, de Wilt JH, Heide R, Jeekel J. An evaluation of risk factors in incisional hernia recurrence. Surg Gynecol Obstet 1993 Mar; 176(3): 228e34. 24 Mittermair RP, Klingler A, Wykypiel H, Gadenstatter M. Vertical Mayo repair of midline incisional hernia: suggested guidelines for selection of patients. Eur J Surg 2002; 168(6): 334e8. 25 Burger JW, Luijendijk RW, Hop WC, Halm JA, Verdaasdonk EG, Jeekel J. Long-term follow-up of a randomized controlled trial of suture versus mesh repair of incisional hernia. Ann Surg 2004 Oct; 240(4): 578e83.

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26 Schumpelick V, Klinge U, Junge K, Stumpf M. Incisional abdominal hernia: the open mesh repair. Langenbecks Arch Surg 2004 Feb; 389(1): 1e5. 27 Klinge U, Klosterhalfen B, Birkenhauer V, Junge K, Conze J, Schumpelick V. Impact of polymer pore size on the interface scar formation in a rat model. J Surg Res 2002 Apr; 103(2): 208e14. 28 Klinge U, Junge K, Stumpf M, Ap AP, Klosterhalfen B. Functional and morphological evaluation of a low-weight, monolament polypropylene mesh for hernia repair. J Biomed Mater Res 2002; 63(2): 129e36. 29 Koehler RH, Begos D, Berger D, et al. Minimal adhesions to ePTFE mesh after laparoscopic ventral incisional hernia repair: reoperative ndings in 65 cases. JSLS 2003 Oct; 7(4): 335e40. 30 Campanelli G, Catena F, Ansaloni L. Prosthetic abdominal wall hernia repair in emergency surgery: from polypropylene to biological meshes. World J Emerg Surg 2008; 3: 33. 31 Eriksen JR, Gogenur I, Rosenberg J. Choice of mesh for laparoscopic ventral hernia repair. Hernia 2007 Dec; 11(6): 481e92. 32 den HD, Dur AH, Tuinebreijer WE, Kreis RW. Open surgical procedures for incisional hernias. Cochrane Database Syst Rev 2008;(3): CD006438. 33 Chevrel JP. [The treatment of large midline incisional hernias by overcoat plasty and prothesis (authors transl)]. Nouv Presse Med 1979 Feb 24; 8(9): 695e6. 34 Kingsnorth AN, Shahid MK, Valliattu AJ, Hadden RA, Porter CS. Open onlay mesh repair for major abdominal wall hernias with selective use of components separation and brin sealant. World J Surg 2008 Jan; 32(1): 26e30. 35 Hamy A, Pessaux P, Mucci-Hennekinne S, Radriamananjo S, Regenet N, Arnaud JP. Surgical treatment of large incisional hernias by an intraperitoneal Dacron mesh and an aponeurotic graft. J Am Coll Surg 2003 Apr; 196(4): 531e4. 36 de Vries Reilingh TS, van GD, Langenhorst B, et al. Repair of large midline incisional hernias with polypropylene mesh: comparison of three operative techniques. Hernia 2004 Feb; 8(1): 56e9. 37 Rives J, Lardennois B, Pire JC, Hibon J. [Large incisional hernias. The importance of ail abdomen and of subsequent respiratory disorders]. Chirurgie 1973 Jun; 99(8): 547e63. 38 Stumpf M, Conze J, Prescher A, et al. The lateral incisional hernia: anatomical considerations for a standardized retromuscular sublay repair. Hernia 2009 Feb 12. 39 Carlsen CG, Gaarden M, Lundhus E, Nielsen J. [Initial experiences with laparoscopic incisional hernial repair]. Ugeskr Laeger 2009 Mar 30; 171(14): 1182e5.

40 Heniford BT, Park A, Ramshaw BJ, Voeller G. Laparoscopic ventral and incisional hernia repair in 407 patients. J Am Coll Surg 2000 Jun; 190(6): 645e50. 41 Baccari P, Nifosi J, Ghirardelli L, Staudacher C. Laparoscopic incisional and ventral hernia repair without sutures: a single-center experience with 200 cases. J Laparoendosc Adv Surg Tech A 2009 Feb 13. 42 Bingener J, Buck L, Richards M, Michalek J, Schwesinger W, Sirinek K. Long-term outcomes in laparoscopic vs open ventral hernia repair. Arch Surg 2007 Jun; 142(6): 562e7. 43 Ballem N, Parikh R, Berber E, Siperstein A. Laparoscopic versus open ventral hernia repairs: 5 year recurrence rates. Surg Endosc 2008 Sep; 22(9): 1935e40. 44 LeBlanc KA. Incisional hernia repair: laparoscopic techniques. World J Surg 2005 Aug; 29(8): 1073e9. 45 Ramirez OM, Ruas E, Dellon AL. Components separation method for closure of abdominal-wall defects: an anatomic and clinical study. Plast Reconstr Surg 1990 Sep; 86(3): 519e26. 46 Kuzbari R, Worseg AP, Tairych G, et al. Sliding door technique for the repair of midline incisional hernias. Plast Reconstr Surg 1998 Apr; 101(5): 1235e42. 47 Mason EE. Pneumoperitoneum in the management of giant hernia. Surgery 1956 Jan; 39(1): 143e51. 48 Dumont F, Fuks D, Verhaeghe P, et al. Progressive pneumoperitoneum increases the length of abdominal muscles. Hernia 2009 Apr; 13(2): 183e7. 49 Tran NV, Petty PM, Bite U, Clay RP, Johnson CH, Arnold PG. Tissue expansion-assisted closure of massive ventral hernias. J Am Coll Surg 2003 Mar; 196(3): 484e8. 50 Abrahamson J, Gorman J. Pregnancy and ventral hernia repair. Hernia 2000 Dec; 4(4): 187e91. 51 Schachtrupp A, Fackeldey V, Klinge U, et al. Temporary closure of the abdominal wall (laparostomy). Hernia 2002 Dec; 6(4): 155e62. 52 Tsuei BJ, Skinner JC, Bernard AC, Kearney PA, Boulanger BR. The open peritoneal cavity: etiology correlates with the likelihood of fascial closure. Am Surg 2004 Jul; 70(7): 652e6. 53 Fleischmann W, Strecker W, Bombelli M, Kinzl L. [Vacuum sealing as treatment of soft tissue damage in open fractures]. Unfallchirurgie 1993 Sep; 96(9): 488e92. 54 Parrett B, Bayer L, Orgill D. Use of microdeformational wound therapy in difcult wounds. Operat Tech Gen Surg 2006 Dec; 8(4): 192e6. 55 Subramonia S, Pankhurst S, Rowlands BJ, Lobo DN. Vacuum-assisted closure of postoperative abdominal wounds: a prospective study. World J Surg 2009 Feb 23.

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Anatomy of the anterior abdominal wall and groin


Vishy mahadevan

Abstract
This contribution discusses the anatomy of the anterior abdominal wall and groin with regard to abdominal surgery.

Keywords anatomy; external oblique muscle; internal oblique muscle;


inguinal region; linea alba; musculo-aponeurotic layer; rectus sheath; skin; superficial fascia; transversalis fascia

The superficial fascia comprises two distinct layers. An outer, adipose layer immediately subjacent to the dermis and similar to superficial fascia elsewhere in the body. An inner fibroelastic layer termed Scarpas fascia (the membranous layer of superficial fascia). Scarpas fascia is more prominent and better defined in the lower half of the anterior abdominal wall. Also, it is more prominent in children (particularly infants) than in adults. Superiorly, Scarpas fascia crosses superficial to the costal margin and becomes continuous with the retromammary fascia. Laterally it fades out at the mid-axillary line. Inferiorly, it crosses superficial to the inguinal ligament and blends with the deep fascia of the thigh about 1 cm distal to the inguinal ligament. Below the level of the pubic symphysis, in the male, Scarpas fascia is prolonged quite distinctly into the scrotum and around the penile shaft. This prolongation of Scarpas fascia into the perineum is known as the superficial perineal fascia or Colles fascia. A similar, but much less distinct, extension of Scarpas fascia exists in the female perineum. Musculo-aponeurotic layer (Figure 1): a long, strap-like rectus abdominis muscle lies on either side of the vertical midline. Each muscle arises by two tendons; a lateral tendon from the pubic crest, and a medial tendon from the upper and anterior surfaces of the pubic symphysis. The two tendons unite a short distance above the pubis to give rise to a single muscle belly which runs upwards to attach to the anterior surfaces of the 7th, 6th and 5th costal cartilages. The upper part of the muscle usually shows three transverse tendinous intersections; one at the level of the umbilicus, one at the level of the xiphoid tip and one halfway between the two. On either side of the rectus abdominis, the musculo-aponeurotic plane is made up of a three-ply (overlapping) arrangement of flat muscular sheets. The outermost of these is the external oblique muscle, the innermost is the transversus abdominis muscle and the intermediate layer is the internal oblique muscle. Of these, only the external oblique has an attachment above the level of the costal margin. Followed anteromedially, each of these muscles becomes aponeurotic. These aponeuroses, between them, enclose the rectus abdominis muscle; the envelope is termed the rectus sheath. The external oblique muscle arises by fleshy digitations from the outer aspect of each of the lower eight ribs near their costochondral junctions. From this origin the muscle fibres fan downwards and forwards. The fibres that arise from the lower two ribs run downwards to insert onto the anterior half of the outer lip of the iliac crest; the posterior edge of this mass of fibres constitutes the free posterior border of the muscle. The remainder of the muscle ends in a broad aponeurosis. The lower edge of this aponeurosis extends between the anterior superior iliac spine and the pubic tubercle. It is rolled inwards to form a narrow and shallow gutter, and constitutes the inguinal ligament. The fascia lata (deep fascia of the thigh) attaches to the distal surface of the inguinal ligament. The rest of the external oblique aponeurosis runs in front of the rectus abdominis muscle of its side and interdigitates with the contralateral aponeurosis along the vertical midline. Below the level of the xiphoid process this interdigitation helps to form a raphe, the linea alba.
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The outline of the anterior abdominal wall is approximately hexagonal. It is bounded superiorly by the arched costal margin (with the xiphisternal junction at the summit of the arch). The lateral boundary on either side is, arbitrarily, the mid-axillary line (between the lateral part of the costal margin and the summit of the iliac crest). Inferiorly, on each side, the anterior abdominal wall is bounded in continuity, by the anterior half of the iliac crest, inguinal ligament, pubic crest and pubic symphysis.

Layers of the anterior abdominal wall


The anterior abdominal wall is a many-layered structure (Figure 1). From the surface inwards, the successive layers are: skin superficial fascia (comprising two layers) a musculo-aponeurotic layer (which is architecturally complex and composed of several layers) transversalis fascia a properitoneal adipose layer parietal peritoneum. Skin: the skin covering the anterior abdominal wall is thin compared with that of the back, and is relatively mobile over the underlying layers except at the umbilical region, where it is fixed. Natural elastic traction lines of the skin (also known as skin tension lines or Kraissls lines) of the anterior abdominal wall are disposed transversely. Above the level of the umbilicus these tension lines run almost horizontally, while below this level they run with a slight inferomedial obliquity. Incisions made along, or parallel to, these lines tend to heal without much scarring, whereas incisions that cut across these lines tend to result in wide or heaped-up scars.

Vishy Mahadevan FRCS(Ed) FRCS is a Professor of Surgical Anatomy at University College London, and a Barbers Company Reader in Anatomy at Royal College of Surgeons of England, London, UK. Conflicts of interest: none declared.

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Rectus abdominis muscle and rectus sheath


a b Tendinous intersections Linea alba

Rectus abdominis

Aponeurosis of external oblique Aponeurosis of internal oblique Skin Superficial fascia External oblique Internal oblique Transverse abdominis

Linea semilunaris

Aponeurosis of transversus abdominis c

Peritoneum

Anterior superior iliac spine Inguinal ligament

Rectus abdominis Pubic tubercle Peritoneum Extraperitoneal fat Transversalis fascia

a Right rectus abdominis after removal of the anterior layer of its sheath. b and c Transverse sections of the anterior abdominal wall showing the interlacing fibres of the aponeuroses of the right and left oblique and transversus abdominis muscles, above b and below c the arcuate line.
Source: Moore K L. Clinically oriented anatomy. Baltimore: Williams and Wilkins, 1992.

Figure 1

The internal oblique muscle lies immediately deep to the external oblique. It arises, in continuity, from the lateral two-thirds of the guttered inguinal ligament, from a central strip along the anterior two-thirds of the iliac crest, and from the lateral margin of the lumbar fascia along the lateral border of the quadratus lumborum muscle (a muscle of the posterior abdominal wall). The muscle fibres arising from the lumbar fascia run upwards to attach along the length of the costal margin. The remainder of the muscle fibres run upwards and medially from their origin, becoming aponeurotic lateral to the outer border of the rectus abdominis. At the outer edge of the latter, the aponeurosis of the internal oblique splits into two laminae (anterior and posterior), which run medially, respectively, in front of, and behind the rectus abdominis muscle, to interdigitate with their counterparts in the vertical midline, at the linea alba. The anterior lamina of the internal oblique is thus immediately deep to the external oblique aponeurosis. The posterior lamina running behind the rectus abdominis muscle is immediately in front of the transversus abdominis aponeurosis, down to the arcuate line (see below: rectus sheath). Transversus abdominis arises in continuity from the lateral half of the guttered surface of the inguinal ligament (immediately deep to the origin of the internal oblique), from the inner lip of the anterior two-thirds of the iliac crest, from the lateral margin of the lumbar fascia and from the inner surfaces of the cartilages of the lower six ribs. From this origin, the muscle fibres run forwards and medially, closely applied to the inner surface of the internal oblique. The fibres become aponeurotic at the lateral edge of the rectus abdominis, and the aponeurosis continues medially behind the posterior lamina of the internal oblique aponeurosis (and therefore behind the rectus abdominis) to meet its counterpart at the linea alba. A few finger-breadths below the level of the umbilicus, however, the aponeuroses of all three muscles run in front of rectus abdominis (see below: rectus sheath).
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The linea alba is a longitudinally disposed, midline interdigitation of the aponeuroses of the three-ply muscles (external oblique, internal oblique and transversus abdominis) of one side with those of the other side. The linea alba extends from the xiphoid process above, to the pubic symphysis below. Lying between the medial edges of the recti, the linea alba is a pale band of fibro-aponeurotic tissue, considerably wider and thicker above the level of the umbilicus than below. The rectus sheath (Figure 1b and c) is the aponeurotic envelope that ensheathes the rectus abdominis muscle. Thus, the rectus sheath may be said to possess an anterior wall and a posterior wall. The anterior wall of the rectus sheath is composed of two adherent layers; a superficial layer made up of the external oblique aponeurosis and a deep layer made up of the anterior lamina of the internal oblique aponeurosis. The posterior wall of the rectus sheath is, likewise, composed of two adherent layers. The anterior layer of the posterior wall is the posterior lamina of the internal oblique aponeurosis, while the posterior layer is the transversus abdominis aponeurosis. This arrangement holds true only from the level of the costal margin down to a level about three finger-breadths below the umbilicus. Below this level, all three aponeuroses run in front of the rectus abdominis muscle, with the result that below this level, there is no aponeurotic posterior wall to the rectus sheath. This abrupt change in the relationship of the aponeuroses to the rectus abdominis, results in the posterior wall of the rectus sheath having a sharp, free border, a short distance below the level of the umbilicus. This border is called the arcuate line. Thus, below the arcuate line the posterior surface of the rectus abdominis muscle is in direct relationship to the fascia transversalis. Above the level of the costal margin, the rectus abdominis is covered on its anterior surface only, by the external oblique aponeurosis alone. The transverse tendinous intersections in the

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rectus abdominis muscle blend with the anterior wall of the rectus sheath.

Inguinal region
The groin or inguinal region denotes the area adjoining the junctional crease between the front of the thigh and the lower part of the anterior abdominal wall, and includes the inguinal and femoral canals. The inguinal canal (Figure 2) is an obliquely placed slit-like space within the lower part of the anterior abdominal wall. It may be represented on the surface by a 1.5 cm-wide band, above and parallel to the medial half of the inguinal ligament. The inguinal canal starts laterally at the deep (internal) inguinal ring (a defect in the fascia transversalis), and runs downwards and medially to open at the superficial (external) inguinal ring (a triangular defect in the external oblique aponeurosis). In adults, the inguinal canal is about 56 cm long. In males, the inguinal canal contains the spermatic cord and the ilioinguinal nerve; in females, it contains the round ligament of the uterus and the ilioinguinal nerve. The inguinal canal consists of a floor, a roof, an anterior wall and a posterior wall. The floor of the inguinal canal is the upper surface of the in-rolled inguinal ligament; the floor being completed medially by the upper surface of the lacunar ligament (a curved extension of the medial end of the inguinal ligament). The anterior wall of the inguinal canal is the external oblique aponeurosis, reinforced on the lateral part of its inner surface by those fibres of internal oblique which arise from the inguinal ligament. The roof of the canal is formed by those fibres of internal oblique and transversus abdominis which, originating

Innervation and blood supply of the muscles of the anterior abdominal wall
The muscles of the anterior abdominal wall are supplied segmentally by the 7th to 11th intercostal nerves and the subcostal nerve. These nerves (accompanied by their corresponding posterior intercostal vessels) cross the costal margin obliquely to run in the neurovascular plane of the anterior abdominal wall, between the internal oblique and transversus abdominis muscles. The nerves supply these muscles and divide into lateral and an-terior branches. The former penetrate the overlying internal oblique to supply the external oblique muscle, while the anterior branches run medially, before entering the rectus abdominis through its posterior surface. Having supplied the muscles, these nerve branches eventually supply the overlying skin. Cutaneous innervation of the anterior abdominal wall by the 7th to 11th intercostal nerves and subcostal nerve is represented by a series of oblique band-shaped dermatomes. The dermatome corresponding to the 10th intercostal nerve is at the level of the umbilicus; that of the 7th intercostal nerve is at the epigastric level. The 11th intercostal and subcostal nerves supply strips of skin below the umbilical level, while the iliohypogastric nerve (L1) and the ilioinguinal nerve (also L1) supply a strip of skin immediately above the inguinal ligament and pubic symphysis. Because there is considerable overlap in the dermal territories of adjacent cutaneous nerves, damage to one or two of these nerves will usually not produce detectable anaesthesia. The posterior intercostal arteries (which accompany the intercostal nerves) supply the three-ply muscles in the lateral part of the anterior abdominal wall, and in this function are reinforced by the lumbar arteries, which are branches of the abdominal aorta. The rectus abdominis has a different blood supply. The upper half of the muscle is supplied by the superior epigastric artery (a branch of the internal thoracic artery). The artery enters the rectus abdominis alongside the xiphisternal junction with its companion veins. The lower half of the rectus abdominis is supplied by the inferior epigastric artery, a branch of the external iliac artery. Myocutaneous rotation flaps may be fashioned using the upper or lower halves of the rectus abdominis muscle; the former being based on the superior epigastric vascular pedicle and the latter being based on the inferior epigastric vascular pedicle. Transversalis fascia: the transversalis fascia is the anterior part of the general endo-abdominal fibrous layer that envelops the peritoneum. It is thicker and less expansile in the lower part of the anterior abdominal wall. The transversalis fascia is closely applied to the deep surface of the transversus abdominis muscle but is easily separable from the latter. Properitoneal adipose layer: the properitoneal adipose layer (also known as fascia propria) is interposed between the transversalis fascia and the parietal peritoneum. This layer offers little resistance to the spread of infection and, consequently, cellulitis secondary to surgical wound infections may spread rapidly within it.
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Right inguinal canal


a

Inguinal ligament Artery Vein Canal Spermatic cord

External oblique aponeurosis External ring llioinguinal nerve

Femoral

Inferior epigastric vessels b Internal oblique

Internal ring Transversalis fascia

Conjoint tendon Ilioinguinal nerve

a With the external oblique aponeurosis intact b With the aponeurosis removed
Source: Ellis H. Clinical anatomy. 10th edition. Oxford: Blackwell Science, 2002.

Figure 2

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from the inguinal ligament, run superomedially arching above the spermatic cord (or round ligament), before fusing to form the conjoint tendon. The posterior wall of the inguinal canal is the fascia transversalis, reinforced on its anterior surface medially by the conjoint tendon. The deep inguinal ring is thus a natural defect in the posterior wall of the canal, while the superficial ring is a natural defect in the anterior wall. Running obliquely in a superomedial direction behind the posterior wall of the inguinal canal, medial to the deep inguinal ring, are the inferior epigastric vessels.

Inguinal hernia is an abnormal protrusion of the peritoneal cavity into the inguinal canal. When this protrusion enters the inguinal canal through the deep inguinal ring, it is termed an indirect inguinal hernia. Such a hernia has the potential to enlarge and emerge through the superficial inguinal ring and, in men, the hernia may enter the scrotum. The neck of an indirect inguinal hernial sac is lateral to the origin of the inferior epigastric artery. By contrast, when the peritoneum protrudes into the inguinal canal, medial to the origin of the inferior epigastric artery, through an attenuated and weakened posterior wall, it is termed a direct inguinal hernia.

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Adult groin hernias: acute and elective


michael nelson brian m Stephenson

Abstract
The science of groin herniorrhaphy has evolved greatly over the last twenty years. There have been many developments by surgeons such as Halsted, mcVay, maloney and Shouldice since bassinis pioneering work in 1887. Their aim was to teach the principles of repair so that the average surgeon may attain acceptable recurrence rates. This review discusses crucial features of adult groin hernias, including anatomical considerations, prosthetic material, anaesthesia, inguinal hernias, femoral hernias, and complications of groin hernia repair.

Keywords abdominal surgery; bilayer repair; hernioplasty; inguinal


hernia; laparoscopic repair; lichtenstein repair; plug and patch repair; prosthetic material; scrotal problems; tension-free repair; totally extraperitoneal approach; transabdominal preperitoneal repair; transinguinal repair; wound problems

The anterior abdominal wall is formed by three flat muscles (external and internal obliques and the transversus abdominis) and their aponeuroses. The transversalis fascia covers the deepest surface of the transversus muscle, separating it from the underlying peritoneum. Between these two lies the preperitoneal (synonymous with properitoneal) space, which can be recognized by the glistening yellow fat that it contains. To allow the transmission from the abdominal cavity of the spermatic cord in men and the round ligament in women and the vessels of the lower limb, there must be a window for their passage; inguinofemoral herniation occurs through such an aperture. The aperture is an oval-shaped portalthe myopectineal orificein the lower anterior abdominal wall at its junction with the pelvis. The upper portion of the myopectineal orifice allows the passage of the spermatic cord from the deep inguinal ring to the superficial inguinal ring along the inguinal canal. Inguinal hernias occur in this upper portion either as an indirect or direct hernia. The lower portion of the myopectineal orifice allows the passage of the femoral vessels laterally and, in the case of herniation, a femoral hernia. As the embryological testicle descends towards the scrotum, an outpouching (sac) of peritoneum extends downwards anteriorly: the processus vaginalis. This usually becomes obliterated at the deep inguinal ring with its remnant covering the testicle as the tunica vaginalis. A communication exists between the sac and the peritoneal cavity if the process of obliteration is incomplete along this line of descent: this can lead to a primary indirect inguinal hernia.

About 105,000 people develop inguinal hernias each year in England and Wales; 10 elective repairs per 10,000 population are carried out in the UK. The number of inguinal hernia repairs done in NHS hospitals in England and Wales in 1998/9 was 76,087, of which about 8% were for recurrence. The science of groin herniorrhaphy has evolved greatly over the last twenty years. There have been many developments by surgeons such as Halsted, McVay, Moloney and Shouldice since Bassinis pioneering work in 1887. Their aim was to teach the principles of repair so that the average surgeon might attain acceptable recurrence rates.

Why use prosthetic material in groin hernia repair?


Surgeons have sought to bridge the gap through which hernias occur since Bassinis contribution to our understanding of the transversalis fascia. Silver wire coils and filigrees were used over one hundred years ago, followed by stainless steel and tantalum meshes. In 1948, Maloney described the darn using nylon suture material as a weave to create a tension-free lattice. More recently, preformed meshes composed of polyester (Dacron/ Mersilene) and polyethylene have been used, but the most suitable non-absorbable mesh is made of polypropylene. The chosen synthetic material must have a number of requisite features because tension-free hernia repair is the ideal. The mesh must: be well tolerated, with little chance of rejection be of a monofilament nature to avoid infection and sinus formation show a degree of fixity to the tissues after a prompt fibroblastic response (subsequent host incorporation forms a strong fibrous wall).

Anatomical considerations
The groin is one of the weakest points of the anterior abdominal wall and is the commonest site for hernias. Before the widespread use of laparoscopy, some hernia specialists stated that the anatomy of the inguinal region was misunderstood because many surgeons appreciated the anatomy only from an anterior view. The anatomy of the posterior aspect is now better understood with the detail afforded by laparoscopy.

Anaesthesia for hernia repair


Michael Nelson MBBCh FRCS is a Consultant in General Surgery at St Marys Hospital, Newport, Isle of Wight, UK. Conflicts of interest: none declared. Brian M Stephenson MS FRCS is a Consultant General and Colorectal Surgeon at the Royal Gwent Hospital, Newport, UK. Conflicts of interest: none declared.

Groin hernias can be repaired under general anaesthesia, but must we subject all our patients to this approach? General anaesthesia is necessary in some emergency cases, particularly if bowel resection is likely. A spinal anaesthetic is an easy option in the elective situation but the incidence of urinary retention is relatively high and a spinal headache is a side effect. The incidence of urinary retention is virtually zero with an epidural.
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Given the increasing elderly population with comorbidity, surgeons should offer repair under local anaesthesia. Advantages include: safety simplicity on-table assessment of the repair earlier mobilization shorter stay in hospital. Local anaesthesia may not be suitable in the obese. The points discussed below are important when repairing inguinal hernias under a local anaesthesia. An appropriate solution is a mixture of 1% lignocaine (rapid onset) and 0.5% bupivacaine (long duration) with adrenaline (1:100,000). Draw-up two 20 ml syringes, each containing 10 ml of each. The average usage is 3035 ml. Mark line of proposed incision with medial end over pubic tubercle. Give intracutaneous and subcutaneous injections along this line. Make deep vertical injections (12 ml) at right angles every 12 cm along the incision into the deeper subcutaneous tissues. When the external oblique aponeurosis is exposed, inject about 10 ml deep to this to flood and anaesthetize the three nerves contained within the canal. Add more local solution when the patient complains of discomfort (e.g. when dissecting over the pubis or at the base of an indirect sac). Splash remaining local anaesthetic into the wound as you close.

Inguinal hernias and their repair


Adult inguinal hernias appear as a lump in the groin and have a cough impulse unless they are irreducible. Indirect hernias can be asymptomatic, but usually cause some discomfort. Direct hernias are rarely painful and patients may notice only a small swelling. The incidence of occult, bilateral (often direct) inguinal hernias may be 2030%. The differential diagnosis includes inguinal lymphadenopathy (primary or secondary), a muscle haematoma and a lipoma or cystic hydrocele of the cord. A definitive diagnosis of these last two possibilities is often made only at surgery. Pure tissue repairs (Bassini, Shouldice, McVay, Maloney) give rise to tension along the suture lines. Hernia specialists obtained excellent results with these repairs, but general surgeons did not. Prosthetic mesh has gained in popularity in recent years and these repairs are described below. Open repair Lichtenstein repair: Lichtenstein et al (Los Angeles, USA) were the first to popularize mesh because sutured repairs (Bassini and Shouldice) led to unavoidable tension on the suture line. An oblique 68 cm incision is deepened down to the external oblique aponeurosis and this is opened in the direction of its fibres with care to expose and avoid injuring the underlying ilioinguinal nerve. The external oblique aponeurosis is opened from the pubic tubercle to the deep inguinal ring as two leaves. The spermatic cord is gently freed, avoiding damage to the external spermatic or cremasteric vessels which are very friable. The upper leaf of the
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external oblique aponeurosis is cleared from the underlying internal oblique muscle to identify the iliohypogastric nerve. An indirect sac is identified by thinning the cremasteric muscle fibres at the lateral end of the cord. The sac should be separated from the cord structures and be replaced into the peritoneal cavity. The sac should not be ligated or excised because this leads to further pain. It is often better to avoid opening the sac at all when dealing with a sliding hernia because the underlying bowel or bladder is liable to damage. In an inguinoscrotal hernia, the sac can be transected and the distal portion left in situ to minimize damage to the cord structures. With a direct hernia, particularly if the defect is wide and occupies most of the posterior wall, it should be held reduced with a pursestring or inverting suture. The mesh prosthesis is supplied as a flat piece (about 8 15 cm), so it must be prepared by trimming and later creating lateral tails. The cord is retracted, allowing placement of the first non-absorbable suture above and medial to the pubic tubercle (Figure 1). One must ensure adequate mesh coverage medial to the pubic tubercle and that the stitch bites into tissue over the pubic bone rather than the periosteum. The stitch is then continued laterally along the lower edge of the mesh and the inguinal ligament to just beyond the deep ring. At this stage the lateral end of the mesh is cut to create two tails and the larger upper one is pulled beneath the cord and then placed lateral to the cord. The upper portion of the mesh is sutured to the internal oblique muscle with three or four loose absorbable sutures. The upper tail is sutured to the lower tail and to the inguinal ligament creating a new deep ring for the spermatic cord. The mesh must be applied loosely (rather than tight and smooth-looking) because this pulls when the patient strains, coughs or stands. Recurrent inguinal hernia repair is challenging. Also, the anatomy is often distorted even if the operative notes of the previous repair are available. For recurrent inguinal hernias, two approaches are recommended by Lichtenstein et al. Fortunately most recurrences (>80%) are small (<3 cm) direct hernias or an indirect recurrence (possibly missed at the earlier repair). Dissection is aimed directly at the hernial sac and defect to minimize the chance of damage to the nerves and cord structures of the inguinal canal. Once the margins of the defect are defined and the sac reduced, the defect is filled with a solid plug of mesh, anchored with several non-absorbable sutures to its edges. Further action is not required unless the defect is very large, when the repair progresses as for a primary inguinal hernioplasty.

Figure 1 A trimmed mesh is held in place with a continuous suture along the inguinal ligament and its lateral tails accommodate the spermatic cord. The orange area represents the pubic tubercle.

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Plug and patch repair: the Lichtenstein hernia repair relies on the strength and correct placement of the prosthetic mesh. The hernial defect per se in primary hernias (indirect or direct) is not addressed as the underlying problem. The dissection could be described as minimalist when dealing with a recurrent hernia. This minimalist approach was further exploited by Rutkow (New Jersey, USA), who was the first to describe the plug and patch technique which, from an anatomical viewpoint, is a preperitoneal repair via an anterior incision. The dissection is aimed directly at the hernial defect in this repair. In an indirect hernia, the sac is dissected free from the cord until preperitoneal fat is seen, indicating that a relatively high dissection has been achieved, and the sac can be replaced through the deep ring. This allows the edges of the defect to be defined and the aperture to be plugged with a preformed mesh plug that comes in four sizes. The periphery of the plug is sutured to the edges of the ring with three or four loose absorbable sutures. In general, indirect hernias require a medium or large plug. In a direct hernia (Figure 2ac), the sac is separated from the cord, and the thin, attenuated transversalis fascia circumscribed just short of its base until the glistening preperitoneal fat is reached. A plug (usually large) is located in the defect and held in place with absorbable sutures placed around its circumference.

Thus, the defect of an indirect or direct (or recurrent) hernia is addressed in a similar fashion. In addition to plugging the defect, an onlay patch (about 4 9 cm) is placed (but not sutured) to cover the posterior wall of the canal. The onlay patch is not an integral part of the repair, but acts as a form of prophylaxis,and, as such, need not be sutured. It is intended to strengthen the posterior wall in an indirect repair and strengthen the area of the deep ring in a direct repair. The repair is completed with closure of the lateral tails over the cord. The dissection using this approach is technically simple and leads to less postoperative discomfort and fewer complications. The plug can be used in femoral hernia repair (see below). Bilayer repair: Gilbert (Miami, USA) believes that the inguinal canal deserves to be protected with mesh placed over both sides of the myopectineal orifice. The Prolene Hernia System comprises a circular underlay portion of mesh connected with an oval onlay (Figure 3) patch and comes in three sizes. The dissection for indirect inguinal hernias is as before, but the surgeon is encouraged to bluntly dissect in the preperitoneal plane at the level of the deep ring to enlarge this space so that the underlay patch can be positioned behind the posterior wall. In direct hernias, as for the plug and patch repair, the defect is circumscribed at its base to allow positioning of the underlay patch. In both types of hernia repair, the onlay patch is slit (centrally or laterally) to accommodate the spermatic cord and then anchored at numerous points with sutures to ensure immobility. The authors have used this device, but feel that this approach involves a fair amount of blunt dissection. This technique probably has a place in the management of large direct and recurrent inguinal hernias, but the size of the connector (about 2 cm) makes it difficult to place in the smaller primary indirect hernias. Closure of open repairs The wound is closed in layers (continuous absorbable to EOA, interrupted to subcutaneous tissues); once the patient is comfortable and has passed urine, he can be discharged. The patient should be encouraged to take physical activity and return to work as soon as possible. Return to normality does not lead to recurrence, but the use of mesh per se does not guarantee a permanently secure repair. How the individual operation is performed is much more important. Lararoscopic repairs Laparoscopic techniques allow groin hernia repair to be undertaken without opening the anterior abdominal wall, but general

a The size of the direct hernia is appreciated when b the patient coughs c The defect in the transversalis fascia has been plugged. Figure 2 Figure 3 The bilayer Prolene Hernia System.

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anaesthesia is required. As with open repairs, a piece of mesh is used to cover the hernial defect in the preperitoneal plane after dealing with the sac and its contents. Laparoscopic hernia repair was first described in 1982, and there are two main approaches. The transabdominal preperitoneal repair involves entry into the abdominal cavity in the usual fashion and the hernia reduced under direct vision. The neck of the hernial sac is then excised, allowing entry to the preperitoneal plane, where further dissection creates a pocket in which the mesh is placed. In indirect hernias, the internal (deep) ring is closed with sutures, and in a direct defect, the transversalis fascia is plicated with a continous suture. In both types, a large sheet of polypropylene mesh (about 11 11 cm) is used to cover the site of the hernia and the back wall of the inguinal canal. The mesh is stapled or sutured in place, and the overlying previously created peritoneal defect must be closed meticulously to avoid internal herniation (a complication that has relegated this repair to second-best when compared to the totally extraperitoneal technique). In the totally extraperitoneal approach, insufflation, repair and mesh placement are done in the preperitoneal plane, with or without a balloon dissection device (Figure 4). Totally extraperitoneal repairs are technically much more challenging than transabdominal preperitoneal repairs (particularly when dealing with large indirect hernias), but major complications are less common and small bowel obstruction very unlikely because the peritoneal cavity is not violated. Despite this hurdle, recent data suggest that totally extraperitoneal repairs are now more common than transabdominal preperitoneal repairs.

Plane of dissection for totally extraperitoneal (TEP) repairs

Femoral hernias and their repair


Femoral hernias account for <10% of groin hernias, but may account for up to one-third of strangulated hernias. Anatomical considerations and diagnosis: the border of the femoral canal is about 2 cm in length and runs from the femoral ring to femoral orifice, and can be easily identified. The peritoneal sac of a femoral hernia enlarges and pushes its way through the normally closed distal end of the canal and becomes trapped. The canal is bound anteriorly by the inguinal liagament, with its lacunar extension forming the medial wall, and posteriorly is the pectineus muscle/fascia and superior ramus of the pubis. The lateral border of the canal is formed by the femoral vein. Rarely, instead of passing down the femoral canal, the hernia lies more laterally, superficial (prevascular) or deep to the vessels entering the leg. On clinical examination, a femoral hernia is below and lateral to the pubic tubercle and only rarely is there a cough impulse. In the elective situation, the differential diagnosis of femoral herniation includes a lymph node and saphena varix, but femoral hernias should be considered as the cause of intestinal (small bowel) obstruction when present. A femoral hernia can be repaired in several ways and each approach has its merits. Low approach: the hernial sac is exposed via a low 5 cm groin incision, cleared of the overlying preperitoneal fat, and opened (Figure 5a). The sac is opened to inspect the contents and, in the
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Figure 4

emergency situation, to check for bloodstained fluid which may indicate bowel ischaemia. The sac is excised, transfixed and the edges of the defect clarified further (Figure 5b). Traditionally, the defect was closed by loosely approximating the undersurface of the inguinal ligament to Coopers ligament with a non-absorbable stitch in an X or N fashion to form a lattice. This repair can be further reinforced by mobilizing a strip of pectineus fascia, folding it upwards on itself, and stitching it to the inguinal ligament. The femoral vein must be protected. Femoral hernias can also be plugged with mesh as a solid plug

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defect can be repaired with sutures, or a flat piece of mesh to cover the lower portions of the myopectineal orifice (MPO) as in a totally extraperitoneal repair. This approach, while giving good access, seems excessive in elective cases and the authors reserve it for acute cases in which we consider resection highly likely. An incarcerated hernia can be explored under local anaesthesia, and the operation subsequently converted to a preperitoneal approach, with a general anaesthetic, if the operative findings dictate it. Laparoscopic approach: the repair of femoral hernias, elective and acute, has been done laparoscopically. The operation is similar to that for inguinal hernia repair in that a transabdominal preperitoneal or totally extraperitoneal approach is feasible. The latter is preferred, but it is hard to justify the risk and expense when far less complex alternatives are readily available and can be done under locoregional anaesthesia.

The incarcerated/strangulated groin hernia


The incidence of strangulation is important given the accompanying postoperative mortality, particularly in the elderly. The Confidential Enquiry into Perioperative Deaths suggested an overall mortality of about 7% when emergency surgery was done for strangulation. The diagnosis is rarely in doubt because the hernia is tender and there are local signs (e.g. inflammation) and there may be systemic upset (e.g. tachycardia). Gentle taxis may allow an incarcerated inguinal hernia hernia to be reduced. This should not be attempted in a femoral hernia because it may cause further damage to the bowel. There may be symptoms and signs of intestinal obstruction and careful attention needs to be paid to the resuscitation of the patient with intravenous fluids and antibiotics. Not all inguinal hernias are at equal risk of strangulation and, while irreducible hernias are at higher risk, only 10% of patients operated on for strangulation give a history of preceding herniation. In general, indirect hernias are 10 times more likely to strangulate than direct hernias. Overall, the annual probability of strangulation appears to be between 0.3% and 3%. Recurrent inguinal hernias are probably also at increased risk of strangulation, but the magnitude of the problem is much more difficult to quantify. The anatomy of the femoral canal, with its narrow neck and unyielding boundaries, accounts for the fact that the proportion of femoral hernias presenting with strangulation may be as high as 50%, although audits have reported much lower figures. The need for resection for irreversible bowel ischaemia is twice as high in strangulated femoral hernias than for inguinal hernias.

Femoral hernia: a the sac is opened and b the defect defined. Figure 5

or with a preformed mesh plug. These plugs are secured to the adjacent tissues with four or five interrupted non-absorbable sutures. This approach is safe and quite satisfactory for most femoral hernias, but the exposure obtained makes the situation difficult to deal with if ischaemic bowel is encountered (e.g. Richters hernia). Transinguinal approach: the floor of the inguinal canal (transversalis fascia) can be opened to allow reduction of the sac of the femoral hernia. When the margins are clearly defined, Coopers ligament is then directly sutured to the iliopubic tract. Another technique is to obliterate the space with a portion of mesh that can then be continued as an inguinal hernioplasty. This technique has few merits and predisposes to a later direct inguinal hernia. High/preperitoneal approach: bowel resection can be readily performed when the hernial sac is uncovered via the preperitoneal approach. The abdominal incision can be a midline (Henry), pararectus (McEvedy), Pfannenstiel or transverse suprainguinal muscle-splitting (Nyhus), but the sac is exposed only when the peritoneum is reflected from the posterior lower abdominal wall. The peritoneal cavity can be conveniently entered above the incarcerated hernia if the hernia is difficult to reduce. The hernial
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Complications of groin hernia repair


Wound problems: postoperative problems (e.g. bruising, haematoma) are not uncommon if repairs are done under local anaesthesia and patients should be warned. Careful attention to technique and meticulous haemostasis are important. Wound infection, which predisposes to recurrence, may occur in 12% of patients and, although there is no firm evidence for routine antibiotic prophylaxis, the authors give adults a single dose of amoxicillin.

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The inplantation of mesh in hernia repairs leads to an inflammatory process and the development of a seroma which can be detected by ultrasound within a few days of surgery. This is usually a self-limiting process, but large seromas may have to be aspirated. Underlying mesh sepsis must be considered if repeated aspirations are necessary, but this is uncommon. Scrotal problems: penile and scrotal oedema is not uncommon and certainly more common after repair of large or bilateral hernias. Ischaemic orchitis and testicular atrophy occurs in 0.53% of men, and is possibly due to venous congestion (from surgical trauma) rather than from primary arterial damage. Gentle dissection and cord mobilization can minimize its incidence. The temptation to deliver the testicle into the wound when operating on an inguinoscrotal hernia must be avoided. The formation of a hydrocele can also occur when the distal sac of a large hernia is left in situ. The accumulation of this fluid can be prevented by dividing the sac anteriorly along its length. Specific problems: there is a great deal of overlap in the cutaneous areas supplied by the iliohypogastric (L1) and ilioinguinal (L1) nerves and the sensory branches of the genitofemoral nerve (L2). Patients may have a variable area of skin anaesthesia after surgery but, in general, it returns to normal within a few months and is of little functional consequence. This is in contrast to persistent postoperative pain that is an increasingly recognized problem. Causes include adductor strain, osteitis pubis and neuralgia, with or without neuroma formation. Such patients should be cared for using a multidisciplinary approach including specialist pain teams. The femoral artery may be more superficial than imagined and be at increased risk in thin patients. The vein may be damaged in femoral hernia repair, but oedema and deep vein thrombosis may not be apparent for some time after surgery, particularly if a sutured repair was overly tight. Complications of laparoscopic hernioplasty: the complications seen after open groin hernia repair are also seen after laparoscopic hernioplasty, but some are unique and specific to this approach. Apart from the complications from general anaesthesia, vascular, bowel and bladder injury may occur during the creation of the pneumoperitoneum, as required in transabdominal preperitoneal repairs. Small bowel obstruction, due to entrapment in peritoneal defects (after transabdominal preperitoneal

repairs) and trocar site herniation is seen in 12% of repairs. Neural injuries are observed after open repair, but damage to the lateral femoral cutaneous nerve (L2, L3) is unique to laparoscopic repairs. Wound seromas can occur in up to 7% of preperitoneal (totally extraperitoneal) repairs, but most resolve within 68 weeks of surgery.

Results of inguinal hernia repair in the modern era


When considering recurrence, a long period of follow-up is required because 50% of recurrences do not appear for five or

Glossary
Inguinal canal passes obliquely through the anterior abdominal wall from the deep to the superficial ring. The posterior wall of the canal is the transversalis fascia. it contains the structures which comprise the spermatic cord: three arteries (testicular, cremasteric and to the vas), three nerves (ilioinguinal, genital branch of genitofemoral and sympathetics) and three other structures (vas deferens, pampiniform plexus of veins and remnants of the processus vaginalis). Indirect inguinal hernia passes through the deep inguinal ring and extends down the canal towards the scrotum. The sac is lateral to the inferior epigastric vessels. it is described as inguinoscrotal if it passes into the scrotum. indirect hernias are twice as common as direct ones. Sliding hernia occurs when a viscus (often sigmoid colon or caecum), or its mesentery forms one of the walls of the hernial sac. occurs in about 5% of hernias and more common in the elderly. A sliding component in direct or femoral hernias is very rare. Direct inguinal hernia is one that is due to a weakened transversalis fascia in Hesselbachs triangle. it is very unusual for the sac to pass into the scrotum. They are common in the obese and elderly and are often bilateral, but rarely incarcerate because the neck is wide. Femoral hernia is one that comes through the femoral canal medial to the femoral vein. it is more likely to strangulate than an inguinal hernia because its neck is narrow. Incarcerated hernia: the hernia is said to be irreducible or incarcerated if the contents of a hernial sac become entrapped. Strangulated hernia: the hernia is described as strangulated if the blood flow to the viscus in an incarcerated hernia becomes compromised; necrosis and perforation will follow if it is not reduced or repaired. Herniotomy: excision of the hernial sac. Herniorrhaphy: repair of the hernia using locally available tissue (e.g. sutured repair). Hernioplasty: repair of the hernia using synthetic material (e.g. mesh repair). Table 2

Guidelines for the urgency of groin hernia repair


indirect and symptomatic direct inguinal hernias should be repaired to relieve symptoms and eliminate the small risk of strangulation Small, easily reducible, direct inguinal hernias can be safely left alone because the risk of strangulation is very small irreducible hernias and those with a short history should be repaired sooner rather than later Femoral hernias should be repaired urgently Table 1

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more years after initial surgery, and 20% may not be apparent for 1525 years! Recurrence in the first few years is probably due to technical failure (technique, tension, missed hernia, infection). Thereafter, tissue weakness or failure, and a later, acquired hernia are more likely causes for the recurrence. Follow-up of ten years seems the minimum required to quote the true recurrence rate of a repair. It appears that general surgeons may have recurrence rates of 510%, while more dedicated surgeons have rates of 12%, and published hernia zealots have rates of <1%. All the repairs described have published series with recurrence rates of <1%. The challenge is for the general surgeon to attain rates of <12% and the surgeon must choose the repair he/she is most comfortable with. When comparing recurrence rates, it is prudent to recall the thoughts of Kirk who, in 1983, wrote: In my experience, outstanding and thoughtful surgeons who devise new techniques attribute their success to the method. They are too modest. Their colleagues know that it is not the particular method that brings success, but the enthusiasm for perfection and painstaking skill with which it is accomplished.

has been estimated that a laparoscopic repair has an additional UK NHS cost of about 300 per procedure. Given the higher intraoperative risks (after transabdominal preperitoneal repairs), and probable higher rates of recurrence with longer follow-up, there seems little to recommend its widespread use. Many experienced surgeons find the repair awkward and time-consuming. If the difference in outcome was real, the last decade would have seen the numbers of laparoscopic repairs rising but, to date, <510% of repairs in the UK are done this way. The UK NHS National Institute for Health and Clinical Excellence has appraised the role of laparoscopic surgery in inguinal hernia repair and has suggested the following tailored approach: primary inguinal hernias should be repaired with an open mesh technique recurrent and bilateral hernias may be repaired laparoscopically (totally extraperitoneal approach) in units with appropriately trained teams who regularly undertake these procedures. Guidelines for the urgency of groin hernia repair and a glossary of terms are described in Table 1 and 2, respectively.

Open tension-free or laparoscopic groin hernia repair?


Laparoscopic cholecystectomy has many advantages for the patient, hospital and employer when compared to the open procedure. However, is this true when comparing laparoscopic and open tension-free inguinal hernioplasty? Laparoscopic surgeons claim there is less postoperative pain and earlier return to full activity, but the overall picture is not so simple because we know these endpoints are quite subjective, irrespective of whether the patient is motivated or not. Laparoscopic repair is not suitable for all patients with a symptomatic hernia. In a recent MRC randomized trial, >40% of identified patients were excluded because they were unfit, had large or difficult hernias, or had had previous abdominal surgery. Laparoscopy incurs extra costs (theatre time, laparoscopic equipment), and it
FuRTHeR ReADInG bay-nielsen m, Kehlet H, Strand l, et al. Quality assessment of 26,304 herniorrhaphies in denmark: a prospective nationwide study. Lancet 2001; 358: 11248. nHS national institute for Clinical excellence. guidance on the use of laparoscopic surgery for inguinal hernia. london: nHS national institute for Clinical excellence, 2001. The mrC laparoscopic groin Hernia Trial group. laparoscopic versus open repair of groin hernia: a randomised comparison. Lancet 1999; 354: 18590. Vrijland WW, van den Tol mP, luijendijk rW, et al. randomized clinical trial of non-mesh versus mesh repair of primary inguinal hernia. Br J Surg 2002; 89: 2937.

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Investigation of abdominal masses


Quat ullah richard A nakielny

Abstract
due to the rapid advances in diagnostic imaging methods, clinicians must be constantly updated about the indications, contraindications and limitations of each method. such advances do not obviate the need for history-taking, clinical examination and laboratory investigations. The relevant information and findings, along with suspected diagnosis, must be included on the request card for the radiologist to organize the most appropriate test; one must consider if imaging is necessary and whether the results will affect management before such requests are made.

Keywords abdominal surgery; intraluminal contrast studies; mri; multislice CT; PeT-CT; radiograph; radioisotope imaging; ultrasound

The primary aim of imaging a suspected abdominal mass is to: determine the origin and site of the mass characterize the mass determine other relevant features (e.g. invasion, metastasis, comorbidity). No imaging method is completely tissue-specific; biopsy (usually image-guided) is required if doubt exists about the tissue diagnosis.

Ultrasound In diagnostic ultrasound examinations, very-high-frequency sound waves (typically 35 MHz) are directed into the body from a transducer placed on the skin. Sound travelling through the body is reflected by the tissue interfaces to produce echoes, which are collected by the transducer and converted into electrical signals and seen on the monitor as shades of grey. Ultrasound is one of the most commonly requested diagnostic examinations. It is relatively harmless, easily available and inexpensive. Ultrasound machines are portable and can be used in ITU, HDU and ward settings if the patient cannot visit the Ultrasound Department. It is also being used increasingly in guided procedures (e.g. biopsies, drainage of collections, gaining access for procedures such as nephrostomy and percutaneous transhepatic cholangiography). Successful diagnosis depends upon many factors, including operator skill and body habitus (limited value in obese patients). Ultrasound cannot penetrate bone or air. Postoperatively, excessive bowel gas due to paralytic ileus can limit the diagnostic value. For ultrasound of the upper abdomen (particularly liver and biliary tract), the patient must fast for four hours to allow proper visualization of the gallbladder. A full bladder is needed to act as a window for seeing pelvic structures. Gynaecological conditions can be further assessed by transvaginal ultrasound, for which the patient must empty the bladder before imaging. Indications: ultrasound is very useful in differentiating between solid and cystic masses (Figure 1). It can also differentiate a simple from a complicated cyst by showing wall irregularity, internal septations and associated solid components. Calcification in the mass may be detected in the latter as a high-echo focus with posterior acoustic shadowing. Doppler ultrasound gives further information about the vascularity of masses. The liver is a common site of metastasis. Secondary deposits are mostly blood borne, spreading to the liver via the portal venous system (e.g. gastrointestinal primary) or hepatic artery

Imaging methods
In most cases, ultrasound is the first-line investigation for a suspected abdominal mass. Depending on the initial ultrasound findings, further imaging (e.g. luminal contrast studies, multislice CT, MRI, PETCT, radioisotope studies) are requested. Plain radiograph of the abdomen Plain radiographs of the abdomen have a very limited role in diagnosis of an abdominal mass, most often it is requested in cases of acute abdomen to exclude intestinal obstruction and perforation. The UK Royal College of Radiologists state that the plain radiograph is not indicated in the investigation of palpable abdominal masses. The radiation dose of one film is equivalent to 50 chest radiographs or six months of background radiation.

Quat Ullah FRCR is a Specialist Registrar in Radiology at Sheffield Teaching Hospitals, Sheffield, UK. Conflicts of interest: none declared. Richard A Nakielny FRCR is a Consultant Radiologist at Royal Hallamshire Hospital, Sheffield, UK. Conflicts of interest: none declared.

Figure 1 ultrasound showing hepatocellular carcinoma (marked HCC) in the liver.

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(e.g. lung or breast primaries) or spread via lymphatic system. The ultrasound appearance of liver secondary tumours is quite variable. They can be high echo, low echo, isoechoic or of a mixed pattern. Some tumours spread along the peritoneal surfaces (e.g. ovarian, colon, pancreatic and gastric carcinomas). Omental deposits in these malignancies can be detected and biopsied using ultrasound. Associated findings such as ascites (as low as 100 ml) and lymphadenopathy (porta hepatis, mesenteric and para-aortic) can also be seen.

Intraluminal contrast studies


Barium examination: the entire gastrointestinal tract can be examined using barium or water-soluble iodinated contrast agents. Barium sulphate is the best contrast medium for gastrointestinal tract. It produces excellent opacification, good mucosal coating and is inert. It is contraindicated if bowel perforation is suspected because barium spillage into the peritoneal cavity can lead to peritonitis; water-soluble contrast agents are indicated in these cases. Water-soluble contrast aspiration would cause pulmonary oedema. Patients undergoing barium examination are prepared by having a low-residue diet for 48 hours, and fluid-only diet with laxatives 24 hours before the test. Disadvantages of barium enema are high radiation dosage (equivalent to 4.5 years of background radiation or 350 chest radiographs). Indications double-contrast barium enema is used to detect carcinoma of the colon. It is less invasive than colonoscopy and the entire colon can be examined in up to 95% of cases. The sensitivity of detecting colonic cancer is about 8590%. Polyps

of >1 cm diameter can be detected in 7590% of cases. Colonoscopy is the gold standard for detection of colonic cancer, but it is invasive, expensive, and occasionally the entire colon cannot be examined (Figure 2). If CT of the abdomen is required at the same time, CT should be done first because retained barium can lead to significant artefacts. Instant unprepared enema can be used for acute obstruction of the large bowel. Contraindications are toxic megacolon and pseudomembranous colitis because of the risk of perforation. Small bowel meals/enemas are sometimes used in the investigation of masses of the stomach or small bowel. Intravenous urography can be used to investigate the anatomy and function of the renal tract, but is of limited value in the diagnosis of non-renal tract masses. It can help to determine the effects of pelvic masses on ureters and the urinary bladder. Multislice/multidetector CT The multidetector CT scanner is the most important development in CT since the introduction of CT in 1972. A single-slice spiral CT scanner has a single-tube source that irradiates one row of detectors. In multidetector scanners, this is replaced by multiple rows of detectors that enable simultaneous acquisition of 464 slices during one gantry rotation. Patient preparation requires oral contrast (usually given in the Radiology Department one hour before the scan) and intravenous contrast (which highlights normal anatomy and abnormalities). Imaging is done in various phases of contrast enhancement i.e. arterial, portal venous and delayed phases, depending on the clinical indication (e.g. if clinical indication is characterization of focal liver lesion, scan should be done in arterial, portal venous and delayed phases).

Figure 2 barium enema in a 64-year-old woman, showing splenic flexure (long arrow) and caecal carcinomas (short arrow). Colonoscope failed to pass beyond the splenic flexure lesion. A: Appendix. source: dr A blakeborough, royal Hallamshire Hospital, sheffield, uK.

Figure 3 multislice CT (coronal view) showing a carcinoma of the transverse colon (marked mAss). Arrow denotes the portal vein. (s) stomach; (l) liver. source: dr J Hampton, northern general Hospital, sheffield, uK.

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PeTCT. Patient was known to have lung carcinoma, and PeTCT was done to assess the involvement of mediastinal nodes. nodal disease in the mediastinum was absent, but a second primary tumour was detected in the transverse colon. source: dr e lorenz, royal Hallamshire Hospital, sheffield, uK. Figure 4

Advantages include: faster speed of imaging (abdomen and pelvis scanned in single breathhold) which in turn reduces movement artefacts, allows for better use of contrast media, and less sedation isotropic imaging (identical resolution of a structure in all dimensions) results in excellent image resolution in axial, sagittal and coronal planes (Figure 3) unlike ultrasound, CT is not operator-dependent, and the image quality is not significantly affected by bowel gas or excess fat. Disadvantages include: higher dose of radiation; dose is even more than helical CT, which is four times more than barium enema or equivalent to 500 chest radiographs expense data overload (a large number of images are generated for each study)
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the need for iodinated contrast material, which is nephrotoxic and can lead to serious contrast reactions. Indications: CT is the most widely requested imaging method. Common indications include: detection and staging of abdominal cancers obstruction of the small and large bowel acute abdomen (e.g. bowel ischaemia, perforation secondary to duodenal ulcer/diverticulitis and abscess, and leaking abdominal aortic aneurysm) blunt and penetrating trauma to the abdomen CT colonography (patients who cannot tolerate barium enema or colonoscopy). PETCT PETCT combines two scannersPET (shows metabolism and the function of cells) and CT (shows detailed anatomy)into one. For example, PET can provide critical information about

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lesions can be characterized in up to 95% of cases) due to its superior contrast resolution. MRI is now routinely used in tumour staging of gynaecological, colorectal and genitourinary malignancies. The advantages over multislice CT are better contrast resolution (Figure 5), lack of ionizing radiation, safer intravenous contrast agent (gadolinium is less nephrotoxic and less allergenic). Disadvantages are that it is relatively expensive and time consuming (single examination of abdomen or pelvis can take up to 2030 minutes) and 10% of patients suffer from claustrophobia. Contraindications to MRI include cardiac pacemakers, ferromagnetic implants (aneurysmal clips, some heart valves and intraocular foreign bodies) and the first trimester of pregnancy (relative contraindication). Radioisotope imaging Radioisotope-labelled pharmaceuticals are used principally in the diagnosis of abdominal masses when other modalities produce equivocal results. Iodine-labelled metaiodobenzylguanidine is used in the diagnosis of pheochromocytoma and carcinoid tumours; these can be detected by CT, but isotope imaging is useful to detect ectopic, bilateral or multifocal lesions and to show metastases. Disadvantages are radiation exposure and patients must be scanned for two consecutive days. Octreotide scanning can detect small carcinoid tumours and also liver metastases. Exposure to radiation and scanning for three consecutive days are the disadvantages. Technetium-labelled methylene diphosphonate can detect bony metastases before they are visible on plain radiograph. It has low specificity because areas of raised uptake (hotspots) are also seen at sites of fractures, degenerative changes, inflammation and in Pagets disease of bone. 111Indium-labelled leukocytes can detect intra-abdominal/ pelvic abcesses.

Figure 5 mri of the liver. large mass in the left lobe (arrow). gb: gallbladder; rK: right kidney. source: dr J Hampton, northern general Hospital, sheffield, uK.

the metabolic function of cancer cells, and can detect very small tumours, but not the exact location. CT provides this anatomical information, so PETCT is a powerful new system for detecting and diagnosing cancer earlier and more accurately, increasing the chances of a good outcome. Advantages include: improved detection and localization of tumours precise staging of disease (PET covers the entire body; Figure 4) better monitoring of cancer recurrence excellent image quality and spatial resolution. Disadvantages include: availability; PETCT is very expensive and not widely available. ionizing radiation patient must fast for 46 hours to enhance tracer uptake monitoring of blood glucose is necessary in diabetic patients because glucose competes with the PET tracer (fluorodeoxyglucose). short half-life of the tracer (109 minutes) necessitates onsite cyclotron for production. some tumours (e.g. prostate) and low-grade malignancies cannot be detected. Indications include: detection and restaging of recurrent colorectal carcinoma when there is clinical and biological evidence, but not detectable by CT or MRI detection of distant metastatic disease before curative surgery follow-up of lymphoma. MRI MRI is a useful adjunct to other methods in complicated cases. Biopsy can be avoided in certain situations (e.g. focal liver

Summary
Plain radiographs of the abdomen have a limited role in the investigation of abdominal masses. Ultrasound is widely available and is usually the first-line investigation. CT is second-line investigation, but has a significant radiation dose. Other imaging methods (e.g. barium enema, PETCT, MRI, radioisotopes) are often useful; discuss with the radiologist when in doubt. Consider whether radiation can be avoided, and if the results affect management.

WEbSITES www.auntminnie.com www.radiologyeducation.com www.rcr.ac.uk www.rsna.com

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Blunt and penetrating abdominal trauma


Adam brooks JAd Simpson

Abstract
This article focuses on the management, assessment and examination of abdominal trauma.

Keywords abdominal trauma; laparotomy; management; wounds

Abdominal injury is a common result of trauma and, if undetected and evaluated inappropriately, can lead to significant morbidity and mortality. Abdominal injury frequently arises as part of blunt multisystem injury following motor vehicle crashes or pedestrian trauma and, much less frequently in the UK, penetrating injury. Accurate assessment, timely resuscitation and appropriate investigations are required to manage patients with abdominal trauma. The past decade has seen many changes in the way abdominal trauma is investigated and managed, and strong team leadership is required to triage injuries appropriately, prioritize investigations and manage the patient with multisystem injuries. When the abdomen is the major source of haemorrhage, the priority of the trauma team is to get the patient to the operating room for definitive surgical treatment as soon as possible.

not been reproduced by other authors. Of patients who survive major trauma and are transported to hospital, there are at least two major mortality peaks in those with abdominal trauma. The first peak occurs early in the emergency department or operating room, and is a result of significant damage to abdominal vascular structures or gross injury to vital organ systems. All unstable patients diagnosed with abdominal haemorrhage require emergency abdominal surgery to control bleeding. It may be necessary to consider damage control surgery (DCS) in these patients, as discussed later in this article. Patients who survive the initial phase of resuscitation and management remain susceptible to the development of a spectrum of critical illness. This group of patients forms the second mortality peak. These patients are at risk of developing systemic inflammatory response syndrome (SIRS). If SIRS is associated with infection then sepsis may develop and can progress to multi-organ dysfunction syndrome (MODS). Although MODS is by definition multifactorial, abdominal complications, including anastomotic leaks, peritoneal contamination and haemorrhage, are significant contributing factors.

Initial management
All trauma patients are assessed using the primary survey and the trauma team should be activated for those fulfilling trauma call criteria. The general surgery senior trainees are active members of the trauma team. Patients with abdominal injury suspected from either the mechanism of injury, physical signs or associated injuries should be triaged with a high priority, and be assessed and treated in the resuscitation room. The trauma team must maintain a high index of suspicion for abdominal injury in all trauma patients, and have a low threshold for transfer to a trauma centre for investigation and referral to general or trauma surgeons.

Epidemiology
Abdominal trauma can be considered in two main forms, blunt and penetrating. The USA, South Africa and some South American countries have a high incidence of penetrating injuries from both stab and gunshot wounds. The majority of hospital admissions in the UK, Australia, New Zealand and most European countries are for blunt trauma, although penetrating trauma has risen significantly over the past decade. Trunkey and colleagues described a trimodal distribution for trauma-related deaths after monitoring patients at a San Francisco Hospital for 2 years. This temporal distribution has impacted on the organization of pre-hospital and in-hospital trauma systems. However, this remains a contentious distribution and has

Abdominal assessment
Although a full abdominal assessment is not part of the primary survey, evaluation of the abdomen as a source of bleeding is an integral part of the circulation aspect of the primary survey. The purpose of the initial clinical assessment in the unstable patient is to confirm or exclude the abdomen as a source of concealed bleeding that requires immediate surgery, for example by using Focused Assessment with Sonography for Trauma (FAST). During the secondary survey, the abdominal assessment is systematic and should be repeated throughout all phases of care, preferably by the same clinician in order to provide the consistency necessary to evaluate changes. Complaint of abdominal pain from an alert patient is indicative of abdominal injury, although many patients have an altered level of consciousness, spinal or distracting injury and are unable to provide reliable information. The initial clinical examination of the abdomen can often be misleading for the unwary. Initially blood may cause little peritoneal irritation, and drugs, alcohol, head injury and other distracting injuries may act to mask abdominal signs.

Adam Brooks FRCS (Gen Surg) DMCC RAMC (V) is a Consultant in Hepatopancreatobiliary and Emergency Surgery and Lead in Emergency Surgery within the Nottingham University NHS Trust, Nottingham, UK. He is also a Senior Lecturer in Military Surgery and Trauma within the Academic Department of Military Surgery and Trauma, RCDM. Conflicts of interest: none declared. JAD Simpson FRCS is a Lecturer in Surgery at University Hospital, Nottingham, UK. Conflicts of interest: none declared.

Immediate resuscitation considerations


Several evidence-based algorithms guiding the clinician on penetrating and blunt abdominal trauma management have been
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developed over recent years (Table 1). In the unstable patient with identified abdominal haemorrhage, following the stabilization of airway and breathing, the priority of the trauma team is to expedite the patients movement to the operating room for surgery. An organized and coordinated team approach is vital to achieve this. Other patients with less catastrophic injuries may respond rapidly to the initial resuscitation, allowing time for more detailed investigation; however, subsequent cardiovascular deterioration in the light of suspected abdominal injuries requires rapid surgery.

History
The mechanism of injury is very important as it provides information on the likely forces involved and potential injuries. In addition, patient signs and symptoms, and response to treatment must be obtained from pre-hospital personnel. Unconscious patients, or those with obvious injuries above and below the abdomen are assumed to have abdominal injury until proven otherwise. Blunt or penetrating lower chest trauma can result in abdominal injury, which should therefore be suspected even when there are no external abdominal signs. Splenic or liver injury should be suspected if the patient has lower rib fractures. Seatbelt bruising is associated with concomitant fractures of T12/L1, lumbar spine fractures and has a high association with bowel perforation. The probability of abdominal injury increases significantly at velocities exceeding 20 km/hour, with age over 75 years, or the presence of head, leg or chest injuries even at low velocities. Genitourinary trauma is divided into upper urinary tract, lower urinary tract and genital injuries, and should be considered in patients with severe lower abdominal blunt trauma and pelvic fracture. Urinary tract injury should also be suspected for all patients with penetrating injuries to the abdomen, chest or flank until proven otherwise.

injury. Patients with SBS and abdominal tenderness are more likely to have an intra-abdominal injury than patients without SBS. Distension may be noted but is not a reliable sign (2 litres of intraperitoneal fluid increases abdominal girth by only 1.9 cm) and there is no role for repeated abdominal girth measurement. Auscultation and percussion of the abdomen is unlikely to provide useful information; it is usually impossible to hear percussion sounds in the middle of trauma resuscitation. The value of abdominal palpation comes from repetition, particularly if the same clinician performs each examination. The abdomen is palpated carefully for pain, rigidity, tenderness and guarding, examining all four quadrants. Tenderness is the most frequent and reliable sign of abdominal injury. Guarding and rebound tenderness is associated with peritoneal irritation, either from blood or bowel gastric contents. However, even large amounts of blood can cause remarkably little peritoneal irritation and only very subtle signs on examination. The patient may experience referred pain, most commonly Kehrs sign, which is pain in the left shoulder secondary to diaphragmatic irritation by blood after splenic rupture, although alterations in Glasgow Coma Score, distracting injury and drugs can mask these subtle signs. Rectal examination includes testing for gross blood and anterior tenderness, which can indicate bleeding or peritoneal irritation. A small group of patients will have an obviously distended or rigid abdomen; however, if the abdominal assessment is equivocal, special investigations must be used early and appropriately.

Investigations
The abdomen is a major source of missed injury and inadequate recognition of intra-abdominal bleeding. Studies have highlighted the importance of rapid accurate abdominal investigation. The introduction of technology such as FAST and further sophistication of CT in the assessment of the abdomen should allow rapid and accurate diagnosis of injury. Their merits are summarized in Table 2. However, these tools are generally not available in the rural setting, and the choice of investigation should be based on

Clinical examination
The abdomen, flank, back and perineum should be inspected for bruising, abrasions, lacerations and bleeding. This involves removal of all patient clothing and, as with all trauma patients, conducting a log roll, keeping in mind the importance of recovering the patient, preventing heat loss and maintaining patient dignity. Bruising that mirrors the location of the seat belt, seat belt signs (SBS), may be evident on admission to the emergency department, but usually does not occur for several hours after

Comparison of abdominal CT and ultrasound for investigation of abdominal trauma


CT organ specificity movement to CT scanner negative CT valuable 98% specificity for organ injury reviewable images Can guide non-operative therapy Value in trajectory in penetrating trauma FAST evaluation for free fluid bedside investigation limited value of negative FAST 90% specificity for blood limited by operator and patient morphology A rule-in not rule-out investigation minimal role in penetrating trauma

Indications for trauma laparotomy


intra-abdominal bleeding gunshot wound Haemodynamically unstable from stab wounds and blunt abdominal trauma Hollow viscus injury on CT or signs of peritonism Penetrating truncal injuries with potential peritoneal injury Table 1

FAST, focused assessment with sonography for trauma.

Table 2

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technical merit and individual patient circumstances. There is a limited role for plain radiographic film in the diagnosis of abdominal trauma except to identify the location of foreign bodies. It is important to obtain a chest film as thoracic injury is frequently associated with abdominal injury. Trauma patients requiring further abdominal assessment and potential surgery should be transferred to a trauma centre as soon as possible. Focused Assessment with Sonar for Trauma FAST is a focused ultrasound examination to assess for free intraabdominal or pericardial fluid, consisting of examination of four areas (Figure 1). FAST is a rapid, reproducible, portable and non-invasive bedside test that may be performed simultaneously with ongoing resuscitation. These characteristics, and research demonstrating that trained emergency department doctors and surgeons can perform FAST accurately, has enabled this examination to become accepted as the bedside investigation of choice in abdominal trauma. It has also been shown to reduce CT and diagnostic peritoneal lavage rates in major trauma centres. Modifications in the use of FAST, including assessment of the chest and extremities, depend on the experience of the operator and have not yet been well evaluated in the literature. While there is no doubt about the accuracy of FAST in detecting free fluid in the abdominal or pericardial space, limitations to its use have been recognized. It is integral to the technique that it does not assess specific organ integrity or function, it is operator dependent, may miss hollow viscus injury and has a low sensitivity (2935%) for organ injury without haemoperitoneum. An unstable patient with a positive FAST should have a laparotomy; however, a negative FAST must either be repeated or an alternative investigation performed as FAST is unreliable in ruling out injury, especially in penetrating trauma where the sensitivity is only 50%. CT CT is the investigation of choice in stable trauma patients. It provides accurate evaluation of the abdomen and retroperitoneum, and is increasingly used in both blunt trauma patients and in penetrating ballistic trauma for evaluation of the trajectory and subsequent appropriate surgical approach if required. Many institutions have developed CT protocols that encompass scans of the head, cervical spine, chest, abdomen and pelvis in patients with blunt multisystem injury. Such an approach also allows

evaluation of the thoracic and lumbar spines, and reformatting of the images for coronal and sagittal views. CT can demonstrate specific organ injury, allowing a non-operative management protocol to be followed for low-grade injuries to the liver, spleen or kidney. CT does, however, have varying degrees of sensitivity for hollow viscus injury. Diagnostic sensitivity and accuracy may be related to the experience of the technician performing the scan and the clinician interpreting it. CT is not appropriate for unstable patients, who may rapidly deteriorate while in the scanner. Although modern machines can complete scans in seconds, time is required to transport, load and unload the patient. The use of oral contrast has not been demonstrated to increase the diagnostic accuracy of abdominal CT. In addition, its administration delays scanning and puts the supine, immobilized patient at risk of aspiration. Diagnostic laparoscopy Diagnostic laparoscopy is most commonly and effectively used to investigate for peritoneal breach in stable patents following an abdominal or thoracoabdominal stab wound, and aids in avoiding non-therapeutic laparotomy. If penetration is evident then further assessment at laparotomy is required as it is difficult to confidently exclude all intra-abdominal injuries laparoscopically. Serial clinical examination Serial clinical examination is an alternative approach to assess for the development of abdominal signs and is used in patients being admitted for observation for potential abdominal injury or conservative injury management. The clinician should assess the patient regularly for increasing pain levels, rigidity, increased heart rate and temperature which may be indicative of an acute abdomen, and ultimately a decreased blood pressure indicative of septic or hypovolaemic shock. Laboratory tests Standard blood tests are sent with each trauma patient including a full blood count, urea and electrolytes, coagulation studies and cross-matching. Although they may not always be of value in the initial resuscitation, they provide a baseline for ongoing assessment. Serial haemoglobin and haematocrit are used in conjunction with other clinical signs as an indication of ongoing blood loss. Elevated leucocyte or WBC counts are part of the bodys normal response to trauma, but ongoing elevation may indicate an inflammatory process in the peritoneal cavity secondary to hollow viscus injury, and wound infection or sepsis in later phases of patient care. Elevated amylase levels may indicate pancreatic or duodenal injury, or occasionally salivary gland injury, although some patients sustain injury to these organs without amylase elevation. The positive predictive value of elevated amylase in pancreatic trauma is only 10%. A serum lipase measurement should be obtained if the amylase level is elevated and pancreatic injury is suspected as it is an indicator of pancreatic function and interpreted in conjunction with other investigative tools

Ultrasound evaluation of blunt abdominal trauma


Fast

Positive Unstable Laparotomy Stable CT Unstable

Negative Stable Repeat/CT

Repeat/DPL

DPL, diagnostic peritoneal lavage; FAST, focused assessment with sonography for trauma

Wounds
All penetrating wounds of the abdomen need to be clearly documented in the patient record. Wounds, especially those from
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Figure 1

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ballistic injury and even those apparently distant from the abdomen, need to be evaluated thoroughly for possible communication with the abdomen. Radiologically opaque wound markers, such as a paper clip, should be used to identify entry and exit sites when plain radiographs are used to evaluate potential injuries. Protruding objects, such as a knife, should be left in situ and stabilized until operative removal as they may be adjacent to or penetrating vascular structures. The sudden release of tamponade may result in catastrophic haemorrhage. Wound exploration Wound probing in the emergency department is inaccurate. The negative predictive value (the ability to definitively rule out abdominal penetration) is poor. Surgical exploration in the operating room can be used as an alternative to laparoscopy to evaluate for penetration of the anterior fascia that would mandate a laparotomy.

The procedure begins with a midline laparotomy from below the xiphisternum to the pubis and around the umbilicus. All four quadrants of the abdomen are packed off to achieve temporary haemostasis. The packs are then removed, starting with the quadrant with the least amount of bleeding. Exploration of each quadrant includes achieving definitive haemostasis, identifying bowel injury and minimizing peritoneal contamination; definitive repair should be considered only if the patient is stable. Abdominal closure can be temporary or permanent. Temporary closure should be employed if packs remain in situ, if abdominal compartment syndrome (ACS) is likely, if a second-look laparotomy is required owing to extensive contamination or if there is a high risk of bowel ischaemia. Damage control surgery It is well recognized that a combination of hypothermia, coagulopathy and metabolic acidosis is associated with a high level of mortality in trauma patients, and the term the lethal triad has been coined. DCS is a concept designed to minimize the time a patient is exposed to this triad and expedite him/her to a higher-care setting where further organ support can be instituted (Table 3). Indications for considering DCS include multiple penetrating injuries to the torso, high-energy blunt trauma to the torso, multisystem trauma with competing operative priorities or profound haemorrhagic shock at presentation. Preparation is key, and the decision to perform DCS should be made in the emergency department or at the beginning of the operation. This allows a management strategy to be formulated, and communicated to the anaesthetist, operating room staff and critical care clinicians. In short, the operating surgeon will initially deal with haemorrhage and contamination only using a range of abbreviated techniques; the patient is then transferred to the ICU for correction of hypothermia, acidosis and coagulopathy. The aim is for the patient to return to the operating theatre for definitive surgery within 2448 hours. Premature return to theatre will convert what should be a definitive second operation into

Ongoing management
Advances in resuscitation, assessment, new haemostatic agents and fundamental changes in the surgical management of the most severely injured patients have evolved from an improved understanding of the physiological derangements associated with severe injury, and may impact on the survival of patients with abdominal trauma. Despite initial presentation, haemodynamically stable patients with penetrating abdominal trauma may have significant ongoing haemorrhage and major intra-abdominal injuries. Peritonitis should be a trigger for emergency operation regardless of vital signs, because haemodynamic stability does not reliably exclude significant haemorrhage. Vascular injury, subsequent hypotension, blood transfusion, and complicated postoperative course are common in this population.

Management techniques
Trauma laparotomy Following appropriate resuscitation it may be necessary to perform a laparotomy. This requires adequate preparation. The patient should be placed supine in a crucifix position with arms out on armboards. It must be ensured that the anaesthetic team are happy with the intravenous lines and patient monitoring. Rapid infusion equipment and cell salvage should be set up. A warm air convection blanket should be used to avoid hypothermia. If not already anaesthetized, the patient should be prepared and draped before anaesthesia is induced on the operating table. Preparation should be from neck to knees (i.e. preparation for the worst case scenario, ensuring access to both sides of the diaphragm and the groins, with two large suckers and open large packs set up). A trauma laparotomy is not a place for the inexperienced and a consultant surgeon should always be present. It is always worth seeking senior advice sooner rather than later. The surgeons plans should be communicated to the theatre team. It should be borne in mind that the aims of surgery are to restore normal physiology before normal anatomy, to achieve haemostasis, to perform only essential bowel resections, and to close or divert all hollow viscus injuries.
269

Stages of damage control surgery


Stage dC 0 dC 1 Description Assessment and resuscitation in trauma resuscitation area intraoperative control of life-threatening haemorrhage, gastrointestinal contamination, pack solid organ and pelvic injuries, consider interventional radiological procedures and perform temporary abdominal closure in the iCu assess resuscitation, set end-points, correct acidosis, coagulopathy, hypothermia. monitor for abdominal compartment syndrome. Consider adjunct procedures: radiography, CT on return to the operating room. identify and definitively repair all injuries. Access abdomen for fascial closure Perform definitive wound closure

dC 2

dC 3

dC 4 Table 3

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a second damage control procedure and result in further physiological insult for the patient. This should be balanced against undue delays that may increase the risk of ACS, intra-abdominal sepsis and the progression of previously unrecognized injuries. Resuscitation has moved on from the didactic Advanced Trauma Life Support guidelines, with good evidence for hypotensive resuscitation and the use of blood and blood products. There is a specific traumatic coagulopathy in catastrophic injuries that is distinct from either disseminated intravascular coagulopathy or that which follows aggressive resuscitation. Thus, damage control resuscitation for the severely injured casualty has two parts: first, resuscitation is limited to keep blood pressure at approximately 90 mm Hg, preventing renewed bleeding from recently clotted vessels; second, intravascular volume restoration is accomplished using thawed plasma and packed RBCs as a primary resuscitation fluid. Non-operative management Non-operative management of solid abdominal organ injury was originally described in children, but has rapidly gained acceptance in the management of adult trauma. A stable patient and accurate imaging by CT are prerequisites to this approach. Isolated lower-grade injuries to the liver, spleen and kidneys are frequently self-limiting with minimal intra-abdominal blood loss. Patients with such injuries can be closely observed in a critical care area for any signs of deterioration or bleeding and the vast majority will avoid surgery and require less blood transfusion and have fewer complications than operated patients. Unstable patients and those who demonstrate evidence of ongoing bleeding require an urgent laparotomy and haemorrhage control. Nonoperative management of liver and spleen injury is associated with a small incidence of missed bowel and pancreatic injury; therefore, a high index of suspicion, especially with liver injury, should be maintained to avoid missing such injuries. It is thought that the greater amount and/or different vector of energy transfer needed to injure the liver versus the spleen accounts for the greater rate of associated injuries. Failure of non-operative management is uncommon in children, typically occurs within the first 12 hours after injury and is associated with injury severity and multiplicity, as well as isolated pancreatic injuries. Interventional radiology Interventional radiology has a vital role in the management of abdominal trauma by providing alternative therapeutic procedures to surgery, particularly in patients who are bleeding as a result of vascular injury. Interventional radiology can be used to

gain an accurate diagnosis, as an adjunct to the non-operative management of solid organ injury in the abdomen, and to assess and control bleeding from pelvic and other vessels when clinically appropriate. In penetrating trauma it can be used to identify pseudoaneurysms and arteriovenous fistulas. The technique involves percutaneous access to the vessels, usually in the groin, and a catheter is then introduced under radiological screening. Contrast medium is injected while imaging continues, and extravasation of the contrast determines the site and degree of injury. Various techniques can be attempted to control or stop the bleeding. Embolization involves the deployment of multiple metallic coils through the catheter into the vessels supplying the injured organ. These act as scaffolding for clot formation, which then leads to occlusion of the damaged vessels. Alternatively, balloon catheters can be passed either side of a bleeding point in a vessel and inflated to occlude flow to provide temporary control until surgical access is gained. The intravenous contrast administered as part of interventional radiology or CT may cause allergic reaction, and can also impair renal function. Urine output and creatinine should therefore be monitored. Interventional radiology techniques may be employed in a number of situations. The presence of a contrast blush in the spleen on abdominal CT suggests ongoing bleeding; arteriography and coil embolization can be used to stop the bleeding and avoid surgery. Patients with significant liver injuries that require packing at surgery have a significant risk of ongoing bleeding; arteriography can be used to define ongoing bleeding and to embolize bleeding vessels before a planned return to the operating room. Interventional radiology is also valuable in the diagnosis and control of pelvic bleeding associated with pelvic fracture.

Postoperative management
After the operation it is important to monitor closely for further bleeding, to assess for wound infection and breakdown, and to attempt to optimize nutritional status. In addition, it is important to adhere to sepsis guidelines. Abdominal compartment syndrome ACS is increasingly being recognized as a cause of postoperative complications. Raised intra-abdominal pressure (IAP) has been reported to occur in more than 50% of patients who have direct fascial closure following penetrating abdominal trauma, in comparison to 22% of those treated with mesh or open abdominal closure techniques. The systemic effects of ACS are listed in Table 4. If undetected and left untreated, ACS progresses to

Effects of abdominal compartment syndrome


Cardiovascular reduction in cardiac output impaired venous return reduced cardiac contractility
iCP, intracranial pressure.

Respiratory High ventilatory pressure decreased compliance reduced total lung capacity

Renal oliguria/anuria reduced renal blood flow Altered intrarenal blood flow

Splanchnic reduced mesenteric, hepatic, portal venous flow early gut ischaemia

Intracranial raised iCP

Table 4

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anuria, hypoxia, hypercapnia and death. The clinician should maintain a high index of suspicion, examining for a distended and firm abdomen, monitoring respiratory function and vital signs, and carrying out routine IAP measurements every 8 hours using a bladder pressure technique for 24 hours. Absolute criteria for opening the abdomen when the IAP is raised remain controversial, but patients with pressures in excess of 20 mm Hg with evidence of end-organ sequelae are candidates for reopening and conversion to an open abdomen.

Summary
Abdominal trauma is a significant cause of morbidity and mortality. The patient can have life-threatening injuries with minimal evidence of injury or initially obvious clinical signs. This increases the importance of techniques such as FAST and CT in the thorough investigation of potential abdominal injury. Consideration of how the patient was injured can highlight potential injuries and enhance patient assessment.

Ongoing assessment is critical for the patient with abdominal trauma; the patients condition can change as he/she experiences continued blood loss or responds to bacterial contamination from a perforated intestine. Unstable patients who present with the lethal triad of hypothermia, coagulopathy and metabolic acidosis or show signs of deterioration may benefit from DCS. The operative management of these patients is often only the beginning of a long recovery phase, much of which is improved by attention to detail and continual reassessment of the patient. Success in returning abdominal trauma patients to the community requires early recognition of injury and transfer to definitive care, coordination of a multidisciplinary trauma team and early involvement of health professionals experienced in abdominal trauma.

FuRTHER READINg brooks A, mahoney P, Hodgetts T, eds. major traum: Churchill livingstone. elsevier, 2007.

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multiple choice questions

test yourself
the mcq and extended matching section in Surgery is designed to test your knowledge of selected topics in this issue of the journal. For questions 14, select which statements are true and which are false. the correct answers are given below. For questions 14, select the statements which are true and which are false. the correct answers are given below. E

mcq and extended matching

Michael G Wyatt MSc MD FRcS, Consultant Surgeon, Freeman Hospital, Newcastle upon Tyne, UK. Editorial Secretary for ASGBI, Member of SAC in General Surgery and Court of Examiners for the intercolle giate MRCS.

1 Gastrointestinal physiology
When considering gastrointestinal physiology: A

ydrochloric acid is secreted by parietal cells in the H gastric body (oxyntic mucosa), which express the H+K+ ATPase or proton pump. astrin is a regulatory peptide and is a major direct G regulator of acid secretion by parietal cells. astrin is also a direct growth factor for the G enterochromaffin-like cell, which explains the presence of enterochromaffin-like hyperplasia seen in some chronically hypochlorhydric and consequently hypergastrinaemic patients. n the small intestine, all the cell types ascend the I cryptvillus axis, moving over a period of 35 days to be shed by apoptosis. oods rich in lipids markedly slow gastric emptying F by exerting an inhibitory effect on the antral pump, stimulating pyloric contractions and maximally relaxing the proximal stomach.

hen the peritoneum protrudes into the inguinal W canal, medial to the origin of the inferior epigastric artery, through an attenuated and weakened posterior wall, it is termed an indirect inguinal hernia.

3 Investigation of abdominal masses


When investigating patients with abdominal masses: A

B C

o imaging method is completely tissue-specific N and biopsy (usually image-guided) is required if doubt exists about the tissue diagnosis. he UK Royal College of Radiologists state that T the plain radiograph is not indicated in the investigation of palpable abdominal masses. odine-labelled metaiodobenzylguanidine can be I used in the diagnosis of pheochromocytoma and carcinoid tumours. ontraindications to MRI include cardiac C pacemakers, ferromagnetic implants and the first trimester of pregnancy (relative). echnetium-labelled methylene diphosphonate can T detect bony metastases before they are visible on plain radiograph.

2 natomy of the anterior abdominal wall and A groin


When considering the anatomy of the anterior abdominal wall and groin: A

4 Blunt and penetrating abdominal trauma


In patients with blunt or penetrating abdominal trauma: A B

he internal oblique muscle arises by fleshy T digitations from the outer aspect of each of the lower eight ribs near their costochondral junctions. bove the level of the costal margin, the rectus A abdominis is covered on its anterior surface only by the external and internal oblique aponeuroses. he groin or inguinal region denotes the area T adjoining the junctional crease between the front of the thigh and the lower part of the anterior abdominal wall, and includes the inguinal, but not the femoral, canal. he blood supply to the rectus abdominis muscle is T from the superior epigastric artery, a branch of the internal thoracic artery.

ll are initially assessed using the primary survey A which includes a full abdominal assessment. eatbelt bruising is associated with Chance S fractures of T12/L1, lumbar spine fractures and has a high association with bowel perforation. AST is a focused ultrasound examination to F assess for free intra-abdominal or pericardial fluid. solated lower-grade injuries to the liver, spleen I and kidneys are frequently self-limiting with minimal intra-abdominal blood loss. aised intra-abdominal pressure (IAP) has R been reported to occur in more than 50% of patients who have direct fascial closure following penetrating abdominal trauma.
see next page

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multiple choice questions

questions cont.
5 Digestion and absorption
Theme: The physiology of digestion and absorption A

Answers
1 , C, E A 2 one N 3 ll A 4 , D, E C 5 -C, 2-E, 3-A, 4-G, 5-B, 6-D, 7-F, 8-H 1

as its own, selective carrier protein, GLUT5, H which is used for transport without the requirement of the sodium gradient. bout one-half of its daily intake is absorbed at A sites in the small intestine and although little is known about the cellular mechanisms underlying epithelial transport, DMT1 may play a role. redominantly reabsorbed in the terminal ileum P and returned to the liver via the enterohepatic recirculation. bsorption is along with the digestion products of A lipids in the micellar process. igestion is initiated by salivary amylase D secreted from the parotid and submandibular glands, which begins to break down starches and glycogens into simpler disaccharides and trisaccharides. bsorption predominantly occurs in the jejunum in A cotransport with sugars (although active absorption occurs additionally in the ileum and colon without the prerequisite sugars). bsorption requires the chaperone protein, intrinsic A factor. bsorption is in the jejunum and ileum by passive A diffusion across a concentration gradient

Answers to incorrect statements


Question 1 B astrin is a regulatory peptide but is not a major direct G

regulator of acid secretion by parietal cells.


D n the small intestine, the cell types, except Paneth I

D E

cells, ascend the cryptvillus axis, moving over a period of 35 days to be shed by apoptosis.
Question 2 A he external oblique muscle arises by fleshy digitations T

from the outer aspect of each of the lower eight ribs near their costochondral junctions.
B bove the level of the costal margin, the rectus A

abdominis is covered on its anterior surface only by the external oblique aponeurosis alone.
C he groin or inguinal region denotes the area adjoining T

G H

the junctional crease between the front of the thigh and the lower part of the anterior abdominal wall, and includes the inguinal and femoral canals.
D he blood supply to the rectus abdominis muscle is T

For each of the compounds listed below select the single most likely true statement from the list above. Each option may be used only once, more than once or not at all.
1 2 3 4 5 6 7 8

from the superior epigastric artery, a branch of the internal thoracic artery and the inferior epigastric artery, a branch of the external iliac artery.
E hen the peritoneum protrudes into the inguinal canal, W

ile salts B arbohydrates C ructose F itamin B12 V agnesium M itamin K V odium S otassium P

medial to the origin of the inferior epigastric artery, through an attenuated and weakened posterior wall, it is termed a direct inguinal hernia.
Question 4 A lthough a full abdominal assessment is not part of the A

primary survey, evaluation of the abdomen as a source of bleeding is an integral part of the circulation aspect of the primary survey.
B eatbelt bruising is associated with Chance fractures S

of T12/L1, lumbar spine fractures and has a low association with bowel perforation.

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2009 published by elsevier ltd.