62492558 abdominal surgery all in one

Volume 27:6 June 2009 Available online at www.surgeryjournal.co.uk

Abdo

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The continuously updated review of surgery

BASIC SCIENCE

Gastrointestinal physiology 225John McLaughlin

Digestion and absorption 231Anthony D Jackson

John McLaughlin

ABDOMINAL SURGERY

Abdominal access techniques (including 237 laparoscopic access)Ralph Smith

Sukhpal Singh

Abdominal wound dehiscence and 243 incisional herniaDavid C Bartlett

Andrew N Kingsnorth

Anatomy of the anterior abdominal wall 251 and groinVishy Mahadevan

Adult groin hernias: acute and elective 255Michael Nelson

Brian M Stephenson

Investigation of abdominal masses 262Quat Ullah

Richard A Nakielny

Blunt and penetrating abdominal trauma 266Adam Brooks

JAD Simpson

TEST YOURSELF

MCQs 272

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Basic science

sURGeRY 27:6 225 © 2009 Published by elsevier Ltd.

Gastrointestinal physiologyJohn McLaughlin

AbstractThis 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 conflict-ing 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 6–7. 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.

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+H2O→H2CO3→HCO3

−+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 secre-tion and is triggered by food in the mouth, although the sight, smell or thought of food can trigger this, as can any conditioned reflex (Pavlov’s dogs secreted acid in response to a mealtime bell when food was not given). It is a vagal mechanism and is virtu-ally 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, particu-larly 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 evi-dence suggests that the extracellular calcium receptor (originally cloned from parathyroid cells) acts as a polymodal nutrient sen-sor 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, predomi-nantly secreting gastrin-28 which has a longer circulating half-life than gastrin-14, the predominant antral G-cell product (see below). The intestinal phase is more complex because inhibi-tory 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 prepro-gastrin 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-secret-ing 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

Basic science


to the oxyntic mucosa indirectly via epidermal growth factors, which leads to the thickened folds found in Zollinger–Ellison syndrome. The enterochromaffin-like cell also operates under vagus nerve control, probably via pituitary adenylate cyclase-activating 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 concen-tration 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 mech-anisms, 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 inhibi-tors 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 sub-stantial proportion of acid secretion intact. Gastrin receptor antag-onists 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 hyper-gastrinaemic 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 sur-veillance 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 popula-tion in the crypt zone. There are four cell types resulting from differentiation pathways controlled by a complex array of tran-scription and differentiation factors. The key lineage commitment decision is whether to adopt the dominant pathway to an absorp-tive phenotype (enterocyte/colonocyte) or a secretory phenotype. This includes mucus-secreting goblet cells, hormone-secreting enteroendocrine cells (EECs) (Figure 1), and defence peptide-secreting Paneth cells. Progenitor cells originating from the stem cell population differentiate along an absorptive (enterocyte) or

Conceptual model: transepithelial signalling by EECs

EEC, enteroendocrine cell

Nutrients

Paracrine/endocrinefactors

Lumen

Apical

Basolateral

Neurones

Epithelia

Muscle

Immune cells

Figure 1

Basic science


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 crypt–villus axis, moving over a period of 3–5 days to be shed by apoptosis. Paneth cells move to the base of the crypts, and appear to have a longer lifespan. Increas-ing evidence implicates Paneth cells in the pathogenesis of inflammatory bowel disease, given their key role in epithelial recognition and defence against microorganisms. The Crohn’s gene, CARD15, encodes a Paneth cell protein. Abnormal epi-thelial 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 bac-teria 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. Increas-ing 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 pro-biotic bacteria to alter bacterial flora and enhance the barrier has

generated interest. Another approach is to give these with bacte-rial nutrients (prebiotics); the combination is termed a ‘synbi-otic’. 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 inflamma-tory 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 fermenta-tion). There is also evidence that psychological stress increases gut permeability via these or other structures. Increased perme-ability 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 cell- mediated mechanisms, and sampling antigenic content via spe-cialized 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 physi-ological roles, but their key function is to operate as transepithe-lial 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 intralumi-nally include nutrients, pH and osmolarity. Each EEC produces one or more regulatory peptide (or biogenic amines, principally histamine and 5-hydroxtryptamine) which are secreted predomi-nantly 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

SGLT-1, sodium-dependent glucose and galactose transporters; GLUT –2, glucose transporters; cAMP, cyclic AMP;

VIP, vasoactive intestinal peptide.

Glucose and galactose absorbed

from the lumen via SGLT-1

Glucose and galactose exported

through the basolateral

membrane via GLUT-2

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

Cl- transported via a Cl- channel

activated by cAMP and VIP

Lumen

Basolateral membrane

SGLT-1

Na+

Na+ Na+

Na+

2Cl–

K+

Glucose

Galactose

K+ K+

Enterocyte

Tight

junction

H2O

H2O

Na-K ATPase

Cholera toxin

cAMP

VIP

GLUT-2

Figure 2

Basic science


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 pepsinogen-secreting 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 gastropare-sis (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 secre-tions. 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 axono-plasm to peripheral terminals where they are activated by CCK. Recent work suggests that the vagal circuitry responds to sev-eral 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 pharmacologi-cal targets. The best characterized is GPR40, responsible for fatty acid-induced secretion of insulin by pancreatic β-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. Glucagon-like peptide-1 also mediates delayed gastric and intestinal transit,

whereas glucagon-like peptide-2 is implicated in epithelial tro-phism 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 glu-cose. 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 infec-tion, 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 irri-table 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 peri-stalsis, in which a bolus is propagated by a wave of contrac-tion. Peristalsis is an intrinsic property controlled by the neural plexus, and persists in extrinsically denervated gut (Figure 4).

Response to a fatty meal

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

Fatty acids

EEC

CCK

Mucosal

Basolateral

Pancreticexocrine secretion

GI motility Gallbladderemptying

Satiety

Figure 3

Basic science


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 support-ing 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 parasym-pathetic (vagal and sacral) pathways increase motility via post-ganglionic fibres utilizing acetylcholine, substance P and ATP. Sympathetic noradrenergic spinal fibres tend to inhibit motility; inhibitory α2-receptors are expressed on post-ganglionic vagal fibres and reduce cholinergic transmission. Hormones also affect motility. CCK inhibits gastric and small bowel motility, but stim-ulates the colon, and may be responsible for the gastrocolic reflex (in which eating can trigger an urge to defaecate). Thyroid hor-mones are stimulatory. Glucagon and opioids have strong anti-motility 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 pseudo-obstructive 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

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 contrac-tions’) 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 stagna-tion 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 hor-mone is mimicked by erythromycin, a prokinetic antibiotic.

Feeding interrupts this pattern. The proximal stomach under-goes 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, osmolal-ity 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

Peristalsis in the small intestine

ACh, acetylcholine;

VIP, vasoactive intestinal peptide;

NO, nitric oxide.

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

+ +

Excitatory motor fibre Inhibitory motor fibre

Contraction Relaxation

ACh

Substance P

VIP

NOMucosal

and wall

receptors

Myenteric

plexus

Figure 4

Basic science


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 expul-sive contractions to maintain relative sterility. Colonic transit may take 24–48 hours, and occurs by haustration and mass move-ment. 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: 559–78.

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: 315–24.

smout aJMP, akkermans LMa. normal and disturbed motility of the Gi

tract. stroud: Wrightson Biomedical, 1992.

BASIC SCIENCE

SURGERY 27:6 231 © 2009 Published by Elsevier Ltd.

Digestion and absorptionAnthony D Jackson

John McLaughlin

AbstractThe 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 proc-

ess 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 diges-

tion and absorption (along with the regulatory inputs that converge to

coordinate these events) demonstrate how finely adapted the gastroin-

testinal tract is to its function.

Keywords absorption; basic science; carbohydrate; digestion; entero-

cytes; fat; minerals; nutrient transport; protein; vitamins

A typical meal comprises a complex mixture of nutritive sub-stances that the gastrointestinal system must separate and break down into its basic molecular subunits to permit systemic absorp-tion and assimilation.

This contribution begins with an overview of the entire pro-cess, then focuses upon specific classes of nutrients.

Overview of the progress of nutrients through the gut

Carbohydrate, protein and fat are the macronutrients that con-stitute 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.

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, signi-fying how finely and intricately adapted the gastrointestinal tract is for its function.

Digestive processThe digestive process begins during mastication (i.e. food is mechanically broken into smaller physical particles) which gen-erates a larger surface area for the digestive enzymes in sub-sequent 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 intes-tine. Gastric emptying is delayed by duodenal and ileal sensory ‘braking’ mechanisms in response to nutrient sensing and endo-crine 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 neutral-ized by bicarbonate (secreted by pancreatic ductal cells and duodenal Brunner’s 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 sub-mucosa (‘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 diges-tion 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 4–6 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.

BASIC SCIENCE


Digestion and absorption of lipids

Dietary fat is an important source of energy and daily consump-tion may be 90–100 g, contributing about 30% of energy intake. The hydrophobic nature of fat presents the gut with particu-lar 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 condi-tions, 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 ‘malabsorp-tion’ and presents clinically as steatorrhoea in more severe situations.

Triglycerides must be split into free fatty acids and monoglyc-erides (Figure 1) to be absorbed. Lingual lipases begin breaking down triglycerides during chewing, although very little diges-tion 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 enzy-matic 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 hor-mones 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 secre-tin 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 replace-ment therapy because alkaline pancreatic secretions are also lost in pancreatic insufficiency, and the endogenous or supple-mentary enzymes are poorly active in an acidic microenviron-ment.) Lipids in the lumen trigger release of cholecystokinin from enteroendocrine I-cells into the bloodstream. Cholecysto-kinin 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, liberat-ing 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.

a

b

Triglycerides (TG) in theduodenum are emulsified withbile salts (BS) released from thegallbladder. Lipase, in concertwith co-lipase, liberates free fattyacids and monoglycerides fromTG, which form mixed micelleswith BS.

Mixed micelles fuse with thejejunal epithelium and lipid digestionproducts access the cytosol. FATP4and CD36 are transporters for free fattyacids. TG are resynthesized in the cytosoland complexed with apolipoproteins(APO) to form chylomicrons, which enterthe lymphatics.

Breakdown of triglycerides

Lipid emulsion

Monoglyceride

Fatty acid

Lipase+

Co-lipase

TGBS

BS

BS

BS

Mixed micelle

FATP4/CD36

+

+

APO

Chylomicron

Lymphatics

Enterocyte

Figure 1

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Pancreatic lipase is the principal enzyme involved in triglyc-eride digestion, responsible for up to 70% of hydrolysis, though gastric and lingual lipases retain their activity in the small intes-tine, thereby acting synergistically. Bile salts act as detergents due to their amphipathic structure, breaking up large, hydro-phobic lipid droplets, giving increased exposure to the digestive lipases. The cofactor co-lipase is required for pancreatic lipase to be effective in attacking the lipid–bile salt mixture. This binds to the surface of emulsified droplets and stabilizes the interac-tions 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. Phos-pholipids 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 resynthe-sized 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 apo-lipoprotein component solubilizes chylomicrons, but their size prevents them from entering capillaries, hence they enter the sys-temic 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).

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.

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 α-amylase upon entry into the duodenum, yielding disaccharides and trisaccharides. Unlike lipids, sugars are freely soluble in water and emulsification is not required. Sugar absorp-tion 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 monosaccha-rides 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 trans-porter: 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. Mono-saccharides pass through intestinal enterocytes without further

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

Sugar absorption in the jejunum

GLUT5

Na+

K+

Na+

Blood

SGLT1

Na+/K+

ATPase

GLUT2Glucose

Galactose

Fructose

Figure 2

BASIC SCIENCE


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 (‘pep-sinogens’) are secreted in abundance by the stomach chief cells. They are converted to active pepsins by the low pH of the stom-ach, 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 power-ful 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 acti-vated 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 tryp-sin, 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 polypep-tide 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 gra-dients 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 lumi-nal 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 dipep-tides and tripeptides into amino acids. Basolateral exit into the mucosal capillaries is also via amino acid-specific transport proteins.

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 circulat-ing hormones, luminal factors and neural inputs. Predomi-nant 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

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 capil-laries 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, gas-tric, 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 para-cellular route. Several isoforms of specific water channels (aquaporins) are expressed along the length of the gastroin-testinal 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 1000–1500 ml per day, of which it manages to take up 80–90%.

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 absorp-tion, most dramatically in cholera and vasoactive intestinal polypeptide-secreting tumours via activation of guanyl cyclases. Increased cellular concentrations of cyclic guanosine monophos-phate 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 junc-tions). Upon entry into epithelial cells, calcium is bound to a cytosolic protein, calbindin, which delivers calcium to the baso-lateral membrane. Calcium is also transported through the cyto-sol 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 act-ing 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 epi-thelial cells (Figure 3). Fe3+ has a greater tendency than Fe2+ to form insoluble complexes with other ions in the lumen, hinder-ing its absorption. Ascorbate aids iron absorption by reducing

BASIC SCIENCE


it to the Fe2+ state. Iron reductases in the brush border of the duodenum also carry out this role. Fe2+ is taken up into epithe-lial cells by the divalent metal cation transporter DMT1, which cotransports H+ along with Fe2+(Fe3+ is not transported). Intra-cellularly, 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 com-plexes with available anions. Basolateral transport occurs by the transporter protein IREG1 and Fe3+ enters the circulation chap-eroned by its plasma carrier protein, transferrin.

In iron deficiency, the expression of iron transport mecha-nisms 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 down-regulates iron transport in the intestine, probably by inhibiting the function of the exit protein IREG1. This may be appropri-ate 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 intes-tine. 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 intes-tine. Fat-soluble vitamins (A, D, E, K) are absorbed along with the digestion products of lipids in the micellar process. Water-soluble vitamins (e.g. B-complex, ascorbic acid, folic acid), are easily absorbed by intestinal epithelia—uptake is via simple diffusion, following concentration gradients, although specific transporter proteins enhance uptake of most water-soluble vita-mins (e.g. thiamine, folic acid).

Absorption of vitamin-B12 is more complex (Figure 4). This water-soluble vitamin requires the chaperone protein, intrinsic

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

Entry of Fe2+ into duodenal epithelial cells is driven by an H+ gradient. Fe2+ is oxidized intracellularly to Fe3+ by theenzyme ferroxidase and iron-binding protein complexeswith available Fe3+. IREG1 is responsible for exporting Fe 3+

from the cell and into local capillaries, where it binds totransferrin to travel in the blood.

DMT1: Divalent metal transporter-1;IREG1: Iron-regulated transporter-1.

Absorption of iron into duodenal epithelial cells

++

Fe2+

+++

Fe3+

++++++

+++

Transferrin–Fe3+ complex

+++

++++Ferroxidase

H+

IREG1Iron-binding

protein

Blood

DMT1

Figure 3

Vitamin-B12 combines with intrinsic factor (IF) in the lumen whichin turn dimerizes. IF–B12 dimers bind to membrane receptors on terminal ileal enterocytes which internalizes, importing the IF–B12complex into the cytosol. It is thought that, after passage throughthe cytosol, extracellular transport is mediated by transport proteins and appears in the systemic blood flow bound to transcobalamin-II(TC).

Absorption of vitamin-B12

IF–B12

Blood

B12

IFTC–B12

?Internal-ization

Figure 4

BASIC SCIENCE


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 factor–B12 complex which is then internalized by endocytosis exclusively in the terminal ileum. B12 deficiency also follows terminal ileal

resection or disease (e.g. Crohn’s 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 chap-erone protein. ◆

ABDOMINAL SURGERY

Abdominal accesstechniques (includinglaparoscopic access)Ralph Smith

Sukhpal Singh

AbstractThis contribution discusses safe exposure of intra-abdominal organs

using laparoscopy and laparotomy; extraperitoneal access is not consid-

ered in detail. The techniques of Single Port Access (SPA) laparoscopy and

Natural Orifice 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.

Keywords laparoscopy; laparotomy; natural orifice transluminal endo-

scopic 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, influencing 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 flexed at the hips and

knees, with sufficient 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.

Ralph Smith MRCS is a Specialty Registrar in General Surgery, South

West Thames Rotation, London Deanery, UK. Conflicts of interest: none

declared.

Sukhpal Singh MS FRCS (Gen) is a Consultant General Surgeon at Frimley

Park Hospital, Frimley, UK. Conflicts of interest: none declared.

Surgery 27:6 237

Preoperative removal of hair

Hair should be removed preoperatively if necessary, ideally with

electric clippers. Premature (>6 hours before surgery), inappro-

priate or unskilled hair removal may traumatize the skin and

allow colonization with potentially pathogenic micro-organisms

at the surgical site.

Cleaning

The surgical site and surrounding area are cleaned with an

antiseptic agent, alcoholic or aqueous povidone-iodine or chlo-

rhexidine, 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 sufficient 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.

Drapes

The prepared area of skin and the drape fenestration should be

sufficiently 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 significantly fewer bacteria in the operative field

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 ¼ 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.

� 2009 Published by Elsevier Ltd.

ABDOMINAL SURGERY

Closed method

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 finger 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.

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 posi-

tion may be checked by instilling and aspirating normal saline:

� aspiration should not be possible if the needle is intra-

peritoneal

� saline may be aspirated if the needle is placed extra-

peritoneally

� 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 flow and intra-abdominal pressure gauges on

the insufflator should be carefully observed to ensure that the:

� gas flows freely

� initial intra-abdominal pressure is low and increases gradu-

ally with the volume of gas insufflated.

The first port is introduced blindly (Figure 3).

Most complications of laparoscopy (Table 1) are related to

blind insertion of the Veress needle or of the first port. A recent

review of 17 randomised controlled trails containing 3040

patients concluded there is no increase in major complications

Common abdominal incisions

Name of incision Incision used for

a Lanz Appendicectomy

b Rutherford–Morrison Right hemicolectomy

c Gridiron Appendicectomy

d Right upper quadrant transverse Cholecystectomy

e Right subcostal Cholecystectomy (left subcostal splenectomy)

f Upper midline laparotomy

g Lower midline laparotomy

h Midline laparotomy General access to peritoneum

i Medial paramedian

j Lateral paramedian

k Pfannensteil Urological and gynaecological procedures

l Palmer’s point Laparoscopy

bc

a g

k

fi j

l

hd

e

x

Figure 1

Surgery 27:6 238

compared with the open methods described below. Extra-

peritoneal or failed insufflation 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 first-choice method for many

surgeons.

Open methods
The first method is essentially a mini-laparotomy, whereby the
linea alba is identified, incised, the peritoneum identified,

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.

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 identified, grasped, and a 0.5 cm

incision made along its length (Figure 4). The abdominal cavity is

Figure 3 Insertion of the first trocar. The index finger prevents the trocar

from being fully inserted.


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

artery clip.

Complications of laparoscopy

Specific

Immediate: extra-peritoneal insufflation, 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 dia-

phragmatic splinting by excessive peritoneal insufflation or extreme

head-down position in an obese patient, pneumothorax, pneumo-

mediastinum, gas embolism

Early: deep vein thrombosis/pulmonary embolism, hypothermia,

nausea and vomiting

Table 1

ABDOMINAL SURGERY

probed using a clip (Figure 5) and the first 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 pneumo-

peritoneum may be created by placing the Veress needle in the

right or left upper quadrant (Palmer’s point, Figure 1) and the

first 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, disad-

vantages 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 fixity to the

abdominal wall and may dislodge more frequently than blunt

tipped trocars during laparoscopic procedures

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

through the vertical incision.

Surgery 27:6

� Extra-long trocars and ports for bariatric procedures

� Blunt tipped balloon ports reduce gas leak throughout the

insufflation 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).

239

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 extracor-

poreal anastomosis done

� reduce operation time

� allow more complex procedures to be performed

laparoscopically.

Gasless laparoscopy

In gasless laparoscopy, the operative field is created with

abdominal wall lift devices. However, poor exposure and tech-

nical difficulty have led to gasless laparoscopy being of historical

interest only.

Minimal access to the retroperitoneumorextraperitoneal space

Retroperitoneoscopy, with dissection of the retroperitoneal space

via a balloon catheter, balloon trocar or finger 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


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

Figure 6

ABDOMINAL SURGERY

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 trans-

umbilical port. A multi-instrument access port (e.g. SILS Port,

Tri-Port) is inserted to allow passage of commonly used laparo-

scopic 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 orifice 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 peri-

toneoscopy and flexible 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

Surgery 27:6 240

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 significant

morbidity. Operative access and the range of achievable

dissection is currently limited by the quality of suitable endo-

surgical instruments, the surgeons learning curve and patient

safety concerns.

Laparotomy

Exposure

There must be sufficient exposure to allow the procedure

to be done efficiently 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.

Classification of laparotomy incisions

Laparotomy wounds can be classified 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. Inci-

sions placed more transversely in Langer’s lines offer comparable


Single incision laparoscopic surgery (SILS) ports and TriPort in

use (reproduced with permission from Covidien Autosuture and

Olympus KeyMed).

Figure 7

ABDOMINAL SURGERY

Surgery 27:6 241

access to most intra-abdominal structures as vertical incisions,

with fewer complications (pain, pulmonary comorbidity, dehis-

cence) and an excellent cosmetic result, but are more difficult to

extend. More complex incisions offer access to specific 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 inci-

sions 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 require-

ment 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 peri-

toneal 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 significantly 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. Obtain-

ing adequate exposure must be balanced with minimizing

postoperative pain. The size and location of the incision is


Complications of laparotomy

Specific

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

ABDOMINAL SURGERY

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. Contin-

uous mass closure is recommended for closure of a midline lap-

arotomy wound, using number 1 absorbable (polydioxanone) or

non-absorbable (nylon) monofilament 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 first 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, signifies 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 superficial abdominal

wound dehiscence and laparostomy. An occlusive low negative

pressure continuous suction dressing is applied to the abdominal

wound to generate improved blood flow and formation of gran-

ulation tissue.1 Benefits include reduced frequency and pain

Surgery 27:6 242

during dressing changes and VAC may accelerate wound healing.

However there is the risk of promoting or delaying healing of

established entero-cutaneous fistulae.2

A number of prospective randomized clinical trials have

questioned whether there is a significant 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 assistant’s hand to:

� hand-held retractors (Deaver’s, Morris’, St Mark’s)

� self-retaining retractors (Goligher’s, Balfour)

� ring retractors (TurnereWarwick)

� fixed retractors (Thompson, Omnitract�).

Strategies to control unwanted viscera from entering the opera-

tive field include systematic packing with swabs, or using

a bowel bag, which also limits loss of heat and fluid from

externalized bowel. Ceiling-mounted overhead lighting, which is

moved and focused on the operative field, is an essential adjunct

for optimizing access. This may not be sufficient in certain

circumstances and headlights, or a light mounted on a retractor

(e.g. St Mark’s), may improve access.

Good access is fundamental to successful surgery, but opti-

mizing access requires careful planning. This is relatively

straightforward for elective surgery but, for emergencies, careful

preoperative examination, patient positioning and an appropri-

ately sited incision allows the operation to proceed smoothly and

successfully. A

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 dehis-

cence 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.


ABDOMINAL SURGERY

Abdominal wounddehiscence and incisionalherniaDavid C Bartlett

Andrew N Kingsnorth

AbstractAbdominal wounddehiscence and incisional hernias are commonproblems

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 emer-

gency 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 dehis-

cence. 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 briefly reviewed.

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 defined 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

defined 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. Conflicts of interest: none declared.

Andrew N Kingsnorth FRCS FACS is Professor of Surgery at Derriford

Hospital, Plymouth, UK. He qualified 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. Conflicts of interest: none declared.

SURGERY 27:6 243

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 first year post-

operatively and 90% of incisional hernias occur within three

years of surgery.5e7

Cause and prevention

The causes of acute and chronic wound failure are similar. Poor

surgical technique and wound infection can cause acute dehis-

cence; 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 sufficient 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 appo-

sition 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 monofilament suture.8e10 The

use of a slowly absorbable material, such as PDS, appears to

provide sufficient 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 rando-

mised 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, efficacy 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

monofilament 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.

� 2009 Elsevier Ltd. All rights reserved.

Figure 1 A large incisional hernia.

ABDOMINAL SURGERY

It is particularly important to identify the existence of a pre-

existing umbilical hernia when using an umbilical port, and to

ensure that the defect is properly defined 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 factorsC 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

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

SURGERY 27:6 244

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

Superficial wound dehiscence can often be managed conserva-

tively. 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 sufficiently to allow drainage should be removed. If

there is ongoing infection or surrounding cellulitis then antibi-

otics will be required. Large superficial 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 difficult cases. A fit patient with

a clean, non-infected wound may benefit 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 find the sudden ‘opening-up’

of their wound distressing.

A complete dehiscence, or ‘burst abdomen’, due to disrup-

tion 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’. Inter-

rupted 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.

Management of incisional hernias

Most patients with incisional hernias, at least initially, have few

symptoms. At presentation up to 25% of patients are asymp-

tomatic.17 If symptoms occur, they commonly consist of:

� Restriction of movement or of wearing certain clothes

� Embarrassment due to disfigurement

� 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).


Figure 2 A ‘burst abdomen’ resutured using retention sutures. Source: D J

Leaper, Cardiff University, Cardiff, UK.

ABDOMINAL SURGERY

Assessment

Clinical examination should be in the standing and supine

positions to allow easy identification 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 influence

surgical technique. The reducibility of the hernia should be

assessed.

Imaging

Figure 3

Radiological investigation may be required in obese patients with

small hernias that are difficult 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 identification 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 identification 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 identified, the

contents of the sac are more clearly defined 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 abdom-

inal 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

SURGERY 27:6 245

the contents into the remaining peritoneal cavity are likely to

result in abdominal compartment syndrome if significant 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 monofilament 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 Poly-

propylene (Prolene�, Marlex� etc) and polyethylene (e.g. Mer-

silene�) meshes are commonly used; they are flexible 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 inflammatory 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 flexible scar net, and a reduced inflammatory

response.27,28

The number of meshes available for intraperitoneal use has

increased significantly over recent years with the advent of

laparoscopic hernia repair. These fall into three categories:


ABDOMINAL SURGERY

expanded polytetrafluoroethylene (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 Exam-

ples of such materials include porcine dermal collagen (Perma-

col�) and human dermis (AlloDerm�, FlexHD�). Cost and a lack

of long term evidence currently limit the routine use of biological

meshes.

There is currently insufficient 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

Figure 4

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 defined 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 flaps. The fascial edges are

brought together using continuous non-absorbable mono-

filament 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 flat, 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 flaps to reduce seroma formation if

the skin flaps are particularly large. Suction drains should be

placed beneath the flaps. 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 fibrin

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 enter-

ocutaneous fistulas developing at the edges of the mesh where

SURGERY 27:6 246

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 obli-

que muscle layers.38

Laparoscopic repair

With the increasing popularity of laparoscopic surgery, the

laparoscopic repair of incisional hernias is becoming the tech-

nique of choice for many surgeons. This technique has the

potential to offer all the benefits 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


ABDOMINAL SURGERY

significant bleeding, which may be difficult 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 significantly 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 difficult 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

difficult 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 care-

ful mix of electrocautery or ultrasonic scalpel to prevent exces-

sive 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 posi-

tioning 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

monofilament 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

Figure 5

SURGERY 27:6

evidence that tacks alone are sufficient, and some surgeons

believe the use of transfascial sutures leads to increased post-

operative 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 laparo-

scopic 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 significant benefit over open repair in terms

of recurrence rates and there remain a number of patients in

whom laparoscopic repair is not possible. Relative contraindi-

cations 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.

247

Components separation

The Ramirez components separation technique allows enlarge-

ment 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 obli-

que aponeuroses. An additional procedure is the further mobi-

lisation 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 sufficient fascia must be preserved to maintain the overall

strength of the abdominal wall.

Preoperative measures to increase the volume of the abdom-

inal cavity have also been described.

Progressive pneumoperitoneum may be achieved by place-

ment of a catheter in the peritoneal cavity under local anaesthesia

followed by gradual insufflations of air or carbon dioxide.47,48 The


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.

Special cases of incisional hernia

C Parastomal hernias

C Lumbar hernias

C Iliac crest hernias after harvest of bone for grafting

C Subxiphoid hernias following median sternotomy

C Incisional hernias after nephrectomy

Table 2

ABDOMINAL SURGERY

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. compo-

nents 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

Contraindications to VAC therapy

C Malignancy in the wound

C Untreated osteomyelitis

C Non-enteric and unexplored fistulae

C Necrotic tissue with eschar (prior debridement required)

Table 3

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 modified repair tech-

niques (Table 2). The underlying principles of defining 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).

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

SURGERY 27:6 248

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

definitive 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, definitive closure

must be undertaken at a later stage once the patient is well and

other complications (e.g. sepsis, fistulas) 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 first 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


Figure 7 VAC dressing applied to a laparostomy.

ABDOMINAL SURGERY

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 tech-

nique. Basically, the dressing consists of a piece of foam which is

cut to the size of the wound and inserted into it to fill 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 fluid and decreased oedema, the alteration

of factors such as proinflammatory cytokines and matrix metal-

loproteinases, the promotion of blood flow 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 significantly more

patients, even several days following the initial laparotomy.55A

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surgery 27:6 251 © 2009 elsevier ltd. All rights reserved.

Anatomy of the anterior abdominal wall and groinVishy mahadevan

AbstractThis 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 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 com-pared 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 ten-sion lines or Kraissl’s 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.

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 Scarpa’s fascia (the mem-branous layer of superficial fascia). Scarpa’s fascia is more prominent and better defined in the lower half of the anterior ab-dominal wall. Also, it is more prominent in children (particularly infants) than in adults.

Superiorly, Scarpa’s 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 fas-cia of the thigh about 1 cm distal to the inguinal ligament. Below the level of the pubic symphysis, in the male, Scarpa’s fascia is prolonged quite distinctly into the scrotum and around the penile shaft. This prolongation of Scarpa’s fascia into the perineum is known as the superficial perineal fascia or Colles’ fascia. A simi-lar, but much less distinct, extension of Scarpa’s 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-aponeu-rotic plane is made up of a three-ply (overlapping) arrangement of flat muscular sheets. The outermost of these is the exter-nal oblique muscle, the innermost is the transversus abdomi-nis 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 enve-lope 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 costo-chondral junctions. From this origin the muscle fibres fan down-wards 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 remain-der 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 nar-row 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.

AbdominAl surgery


The internal oblique muscle lies immediately deep to the exter-nal oblique. It arises, in continuity, from the lateral two-thirds of the guttered inguinal ligament, from a central strip along the ante-rior 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 aponeu-rotic 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 medi-ally, respectively, in front of, and behind the rectus abdominis muscle, to interdigitate with their counterparts in the vertical mid-line, 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 (immedi-ately 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).

The linea alba is a longitudinally disposed, midline interdigi-tation 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 enve-lope 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 com-posed 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 umbili-cus. 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 trans-versalis.

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

Rectus abdominis muscle and rectus sheath

a

b

c

Linea semilunaris

Tendinous intersections

Linea alba

Rectus abdominis

Anterior superior iliac spine

Inguinal ligament

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.

Pubic tubercle

Rectus abdominisAponeurosis of external oblique

Aponeurosis of internal oblique

Aponeurosis of transversus abdominis Peritoneum

Peritoneum

Extraperitoneal fat

Transversalis fascia

Skin

External oblique

Internal oblique

Transverse

abdominis

Superficial

fascia

Figure 1

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rectus abdominis muscle blend with the anterior wall of the rec-tus sheath.

Innervation and blood supply of the muscles of the anterior abdominal wall

The muscles of the anterior abdominal wall are supplied seg-mentally by the 7th to 11th intercostal nerves and the subcostal nerve. These nerves (accompanied by their corresponding pos-terior 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 mus-cles. 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 ante-rior branches run medially, before entering the rectus abdomi-nis through its posterior surface. Having supplied the muscles, these nerve branches eventually supply the overlying skin. Cuta-neous 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 cor-responding 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 inter-costal 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 rec-tus abdominis alongside the xiphisternal junction with its com-panion 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.

Inguinal region

The groin or inguinal region denotes the area adjoining the junc-tional 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 5–6 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 com-pleted 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 ingui-nal ligament. The roof of the canal is formed by those fibres of internal oblique and transversus abdominis which, originating

Right inguinal canal

a

b

Inguinal ligament

Transversalis fascia

Internal ring

a With the external oblique aponeurosis intact b With the aponeurosis removed

Source: Ellis H. Clinical anatomy. 10th edition. Oxford: Blackwell Science, 2002.

ArteryVeinCanal

Femoral

External oblique aponeurosis

Inferior epigastric vessels

Internal oblique

Conjoint tendon

Ilioinguinal nerve

External ring

llioinguinal nerve

Spermatic cord

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 transver-salis, 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 cav-ity into the inguinal canal. When this protrusion enters the ingui-nal 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 her-nia may enter the scrotum. The neck of an indirect inguinal her-nial 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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Surgery 27:6 255 © 2009 Published by elsevier ltd.

Adult groin hernias: acute and electivemichael nelson

brian m Stephenson

AbstractThe 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 bassini’s 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 considera-

tions, 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 extra-

peritoneal approach; transabdominal preperitoneal repair; transinguinal

repair; wound problems

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 Bassini’s pioneering work in 1887. Their aim was to teach the principles of repair so that the average surgeon might attain acceptable recurrence rates.

Anatomical considerations

The groin is one of the weakest points of the anterior abdomi-nal wall and is the commonest site for hernias. Before the wide-spread 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 under-stood with the detail afforded by laparoscopy.

Michael Nelson MBBCh FRCS is a Consultant in General Surgery at

St Mary’s 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.

The anterior abdominal wall is formed by three flat muscles (external and internal obliques and the transversus abdomi-nis) 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 preperi-toneal (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 portal—the myopectineal orifice—in the lower anterior abdominal wall at its junction with the pelvis. The upper portion of the myopectineal orifice allows the pas-sage of the spermatic cord from the deep inguinal ring to the superficial inguinal ring along the inguinal canal. Inguinal her-nias 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 ante-riorly: 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 incom-plete along this line of descent: this can lead to a primary indirect inguinal hernia.

Why use prosthetic material in groin hernia repair?

Surgeons have sought to bridge the gap through which hernias occur since Bassini’s 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 tanta-lum 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 requi-site 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 fibroblas-

tic response (subsequent host incorporation forms a strong fibrous wall).

Anaesthesia for hernia repair

Groin hernias can be repaired under general anaesthesia, but must we subject all our patients to this approach? General anaes-thesia 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 rela-tively 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, sur-geons 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 30–35 ml. • Mark line of proposed incision with medial end over pubic tubercle. • Give intracutaneous and subcutaneous injections along this line. • Make deep vertical injections (1–2 ml) at right angles every 1–2 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 dis-comfort (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 20–30%.

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 sur-geons did not. Prosthetic mesh has gained in popularity in recent years and these repairs are described below.

Open repairLichtenstein 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 6–8 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

external oblique aponeurosis is cleared from the underlying inter-nal 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 cav-ity. 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 lat-eral 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 contin-ued 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 creat-ing 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 pre-vious 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). Dis-section 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. Fur-ther 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 pre-peritoneal 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 dis-section 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 2a–c), the sac is separated from the cord, and the thin, attenuated transversalis fascia circum-scribed 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™ com-prises 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 cir-cumscribed 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 prob-ably has a place in the management of large direct and recur-rent 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 repairsThe wound is closed in layers (continuous absorbable to EOA, interrupted to subcutaneous tissues); once the patient is comfort-able 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 recur-rence, but the use of mesh per se does not guarantee a perma-nently secure repair. How the individual operation is performed is much more important.

Lararoscopic repairsLaparoscopic techniques allow groin hernia repair to be under-taken without opening the anterior abdominal wall, but general

Figure 3 The bilayer Prolene Hernia System™.

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

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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 dissec-tion 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 chal-lenging than transabdominal preperitoneal repairs (particularly when dealing with large indirect hernias), but major complica-tions 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.

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 perito-neal 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 hernia-tion includes a lymph node and saphena varix, but femoral her-nias 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

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 Cooper’s 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

Plane of dissection for totally extraperitoneal(TEP) repairs

Figure 4

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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 fem-oral hernias, but the exposure obtained makes the situation dif-ficult to deal with if ischaemic bowel is encountered (e.g. Richter’s hernia).

Transinguinal approach: the floor of the inguinal canal (trans-versalis fascia) can be opened to allow reduction of the sac of the femoral hernia. When the margins are clearly defined, Cooper’s 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 preperito-neal 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

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 simi-lar 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 accompany-ing postoperative mortality, particularly in the elderly. The Con-fidential 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 fur-ther 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 her-niation. 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 strangula-tion, 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.

Complications of groin hernia repair

Wound problems: postoperative problems (e.g. bruising, hae-matoma) 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 1–2% of patients and, although there is no firm evidence for routine antibiotic prophylaxis, the authors give adults a single dose of amoxicillin.

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

Figure 5

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The inplantation of mesh in hernia repairs leads to an inflam-matory process and the development of a seroma which can be detected by ultrasound within a few days of surgery. This is usu-ally 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 uncom-mon and certainly more common after repair of large or bilat-eral hernias. Ischaemic orchitis and testicular atrophy occurs in 0.5–3% of men, and is possibly due to venous congestion (from surgical trauma) rather than from primary arterial dam-age. 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 cuta-neous areas supplied by the iliohypogastric (L1) and ilioingui-nal (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 con-trast to persistent postoperative pain that is an increasingly rec-ognized 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 laparo-scopic hernioplasty, but some are unique and specific to this approach. Apart from the complications from general anaesthe-sia, vascular, bowel and bladder injury may occur during the creation of the pneumoperitoneum, as required in transabdomi-nal preperitoneal repairs. Small bowel obstruction, due to entrap-ment in peritoneal defects (after transabdominal preperitoneal

repairs) and trocar site herniation is seen in 1–2% of repairs. Neural injuries are observed after open repair, but damage to the lateral femoral cutaneous nerve (L2, L3) is unique to laparo-scopic repairs. Wound seromas can occur in up to 7% of preperi-toneal (totally extraperitoneal) repairs, but most resolve within 6–8 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

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

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 Hesselbach’s 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

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more years after initial surgery, and 20% may not be apparent for 15–25 years! Recurrence in the first few years is probably due to technical failure (technique, tension, missed hernia, infec-tion). 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’ recur-rence rate of a repair.

It appears that ‘general’ surgeons may have recurrence rates of 5–10%, while more dedicated surgeons have rates of 1–2%, 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 <1–2% and the surgeon must choose the repair he/she is most com-fortable 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.’

Open tension-free or laparoscopic groin hernia repair?

Laparoscopic cholecystectomy has many advantages for the patient, hospital and employer when compared to the open pro-cedure. 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

has been estimated that a laparoscopic repair has an additional UK NHS cost of about £300 per procedure. Given the higher intra-operative 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, <5–10% of repairs in the UK are done this way.

The UK NHS National Institute for Health and Clinical Excel-lence 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 laparo-

scopically (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. ◆

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: 1124–8.

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: 185–90.

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: 293–7.

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surgery 27:6 262 © 2009 Published by elsevier ltd.

Investigation of abdominal massesQuat ullah

richard A nakielny

Abstractdue 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 (usu-ally image-guided) is required if doubt exists about the tissue diagnosis.

Imaging methods

In most cases, ultrasound is the first-line investigation for a sus-pected abdominal mass. Depending on the initial ultrasound find-ings, further imaging (e.g. luminal contrast studies, multislice CT, MRI, PET–CT, radioisotope studies) are requested.

Plain radiograph of the abdomenPlain radiographs of the abdomen have a very limited role in diagno-sis 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.

UltrasoundIn diagnostic ultrasound examinations, very-high-frequency sound waves (typically 3–5 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 electri-cal 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 inexpen-sive. Ultrasound machines are portable and can be used in ITU, HDU and ward settings if the patient cannot visit the Ultrasound Depart-ment. 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, exces-sive 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 dif-ferentiate a simple from a complicated cyst by showing wall irregularity, internal septations and associated solid compo-nents. 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 depos-its are mostly blood borne, spreading to the liver via the portal venous system (e.g. gastrointestinal primary) or hepatic artery

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. ovar-ian, colon, pancreatic and gastric carcinomas). Omental depos-its 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 peri-tonitis; 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 85–90%. Polyps

of >1 cm diameter can be detected in 75–90% of cases. Colonos-copy 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 inves-tigation of masses of the stomach or small bowel.

Intravenous urography can be used to investigate the anat-omy 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 CTThe 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 4–64 slices during one gantry rotation.

Patient preparation requires oral contrast (usually given in the Radiology Department one hour before the scan) and intrave-nous contrast (which highlights normal anatomy and abnormali-ties). 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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Advantages include: • faster speed of imaging (abdomen and pelvis scanned in sin-

gle 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)

• 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 ab-dominal aortic aneurysm)

• blunt and penetrating trauma to the abdomen • CT colonography (patients who cannot tolerate barium enema

or colonoscopy).

PET–CTPET–CT combines two scanners—PET (shows metabolism and the function of cells) and CT (shows detailed anatomy)—into one. For example, PET can provide critical information about

PeT–CT. Patient was known to have lung carcinoma, and PeT–CT 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

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the metabolic function of cancer cells, and can detect very small tumours, but not the exact location. CT provides this anatomical information, so PET–CT 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; PET–CT is very expensive and not widely

available. • ionizing radiation • patient must fast for 4–6 hours to enhance tracer uptake • monitoring of blood glucose is necessary in diabetic patients

because glucose competes with the PET tracer (fluorodeoxy-glucose).

• 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 detect-able by CT or MRI

• detection of distant metastatic disease before curative surgery

• follow-up of lymphoma.

MRIMRI is a useful adjunct to other methods in complicated cases. Biopsy can be avoided in certain situations (e.g. focal liver

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 resolu-tion (Figure 5), lack of ionizing radiation, safer intravenous con-trast agent (gadolinium is less nephrotoxic and less allergenic).

Disadvantages are that it is relatively expensive and time con-suming (single examination of abdomen or pelvis can take up to 20–30 minutes) and 10% of patients suffer from claustrophobia.

Contraindications to MRI include cardiac pacemakers, ferro-magnetic implants (aneurysmal clips, some heart valves and intraocular foreign bodies) and the first trimester of pregnancy (relative contraindication).

Radioisotope imagingRadioisotope-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 metasta-ses. 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, inflamma-tion and in Paget’s disease of bone.

111Indium-labelled leukocytes can detect intra-abdominal/pelvic abcesses.

Summary

Plain radiographs of the abdomen have a limited role in the investigation of abdominal masses. Ultrasound is widely avail-able 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, PET–CT, MRI, radioisotopes) are often useful; discuss with the radiologist when in doubt. Con-sider 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

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.

http://www.auntminnie.com

http://www.radiologyeducation.com

http://www.rcr.ac.uk

http://www.rsna.com

AbdominAl Surgery

Surgery 27:6 266 Crown Copyright © 2009 Published by elsevier ltd. All rights reserved.

Blunt and penetrating abdominal traumaAdam brooks

JAd Simpson

AbstractThis 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 inves-tigations 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 investiga-tions 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.

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 sig-nificantly 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 sys-tems. However, this remains a contentious distribution and has

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.

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 vascu-lar structures or gross injury to vital organ systems. All unstable patients diagnosed with abdominal haemorrhage require emer-gency abdominal surgery to control bleeding. It may be neces-sary 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 spec-trum 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 inju-ries should be triaged with a high priority, and be assessed and treated in the resuscitation room. The trauma team must main-tain 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.

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). Dur-ing 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 neces-sary 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 distract-ing 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 perito-neal irritation, and drugs, alcohol, head injury and other distract-ing injuries may act to mask abdominal signs.

Immediate resuscitation considerations

Several evidence-based algorithms guiding the clinician on pen-etrating and blunt abdominal trauma management have been

AbdominAl Surgery


developed over recent years (Table 1). In the unstable patient with identified abdominal haemorrhage, following the stabiliza-tion of airway and breathing, the priority of the trauma team is to expedite the patient’s 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 cardiovas-cular deterioration in the light of suspected abdominal injuries requires rapid surgery.

History

The mechanism of injury is very important as it provides infor-mation 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 abdomi-nal 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 bruis-ing is associated with concomitant fractures of T12/L1, lumbar spine fractures and has a high association with bowel perfora-tion. 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.

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 re- covering 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

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 per-cussion 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 irrita-tion and only very subtle signs on examination. The patient may experience referred pain, most commonly Kehr’s 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 equivo-cal, 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 sophistica-tion 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

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

Comparison of abdominal CT and ultrasound for investigation of abdominal trauma

CT FAST

organ specificity evaluation for free fluid

movement to CT scanner bedside investigation

negative CT valuable limited value of negative FAST

98% specificity for organ

injury

90% specificity for blood

reviewable images limited by operator and

patient morphology

Can guide non-operative

therapy

A rule-in not rule-out

investigation

Value in trajectory in

penetrating trauma

minimal role in penetrating

trauma

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 abdom-inal 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 TraumaFAST is a focused ultrasound examination to assess for free intra-abdominal 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 exami-nation 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. Modi-fications 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 detect-ing 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 sensi-tivity (29–35%) for organ injury without haemoperitoneum.

An unstable patient with a positive FAST should have a lapa-rotomy; 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 sen-sitivity is only 50%.

CTCT is the investigation of choice in stable trauma patients. It pro-vides 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 pro-tocol 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 laparoscopyDiagnostic 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 confi-dently exclude all intra-abdominal injuries laparoscopically.

Serial clinical examinationSerial 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 testsStandard blood tests are sent with each trauma patient includ-ing 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 ongo-ing blood loss. Elevated leucocyte or WBC counts are part of the body’s normal response to trauma, but ongoing elevation may indicate an inflammatory process in the peritoneal cav-ity 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 sali-vary 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

Wounds

All penetrating wounds of the abdomen need to be clearly doc-umented in the patient record. Wounds, especially those from

Ultrasound evaluation of blunt abdominal trauma

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

Fast

Unstable Stable

Laparotomy CT Repeat/DPL Repeat/CT

Positive Negative

Unstable Stable

Figure 1

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ballistic injury and even those apparently distant from the abdo-men, need to be evaluated thoroughly for possible communica-tion 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 inju-ries. 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 tampon-ade may result in catastrophic haemorrhage.

Wound explorationWound 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 oper-ating room can be used as an alternative to laparoscopy to evalu-ate for penetration of the anterior fascia that would mandate a laparotomy.

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 associ-ated with severe injury, and may impact on the survival of patients with abdominal trauma. Despite initial presentation, haemodynamically stable patients with penetrating abdomi-nal trauma may have significant ongoing haemorrhage and major intra-abdominal injuries. Peritonitis should be a trig-ger 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 laparotomyFollowing appropriate resuscitation it may be necessary to per-form 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 hypother-mia. 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 dia-phragm 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 surgeon’s 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.

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 tem-porary haemostasis. The packs are then removed, starting with the quadrant with the least amount of bleeding. Exploration of each quadrant includes achieving definitive haemostasis, iden-tifying 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 lapa-rotomy is required owing to extensive contamination or if there is a high risk of bowel ischaemia.

Damage control surgeryIt is well recognized that a combination of hypothermia, coagu-lopathy 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 insti-tuted (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 priori-ties or profound haemorrhagic shock at presentation. Prepara-tion is key, and the decision to perform DCS should be made in the emergency department or at the beginning of the opera-tion. This allows a management strategy to be formulated, and communicated to the anaesthetist, operating room staff and criti-cal 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 defini-tive surgery within 24–48 hours. Premature return to theatre will convert what should be a definitive second operation into

Stages of damage control surgery

Stage Description

dC 0 Assessment and resuscitation in trauma

resuscitation area

dC 1 intraoperative control of life-threatening

haemorrhage, gastrointestinal contamination,

pack solid organ and pelvic injuries, consider

interventional radiological procedures and

perform temporary abdominal closure

dC 2 in the iCu assess resuscitation, set end-points,

correct acidosis, coagulopathy, hypothermia.

monitor for abdominal compartment syndrome.

Consider adjunct procedures: radiography, CT

dC 3 on return to the operating room. identify and

definitively repair all injuries. Access abdomen

for fascial closure

dC 4 Perform definitive wound closure

Table 3

AbdominAl Surgery


a second damage control procedure and result in further physi-ological 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 hypoten-sive 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 coagulopa-thy or that which follows aggressive resuscitation. Thus, dam-age 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 restora-tion is accomplished using thawed plasma and packed RBCs as a primary resuscitation fluid.

Non-operative managementNon-operative management of solid abdominal organ injury was originally described in children, but has rapidly gained accep-tance in the management of adult trauma. A stable patient and accurate imaging by CT are prerequisites to this approach. Iso-lated 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 bleed-ing require an urgent laparotomy and haemorrhage control. Non-operative 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 trans-fer needed to injure the liver versus the spleen accounts for the greater rate of associated injuries. Failure of non-operative man-agement 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 radiologyInterventional radiology has a vital role in the management of abdominal trauma by providing alternative therapeutic proce-dures 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 clini-cally appropriate. In penetrating trauma it can be used to iden-tify pseudoaneurysms and arteriovenous fistulas. The technique involves percutaneous access to the vessels, usually in the groin, and a catheter is then introduced under radiological screen-ing. 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 out-put 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 pack-ing at surgery have a significant risk of ongoing bleeding; arteri-ography 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 con-trol 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 syndromeACS 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 com-parison to 22% of those treated with mesh or ‘open’ abdomi-nal 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 Respiratory Renal Splanchnic Intracranial

reduction in cardiac output High ventilatory pressure oliguria/anuria reduced mesenteric,

hepatic, portal venous flow

raised iCP

impaired venous return decreased compliance reduced renal blood flow early gut ischaemia

reduced cardiac contractility reduced total lung capacity Altered intrarenal blood flow

iCP, intracranial pressure.

Table 4

AbdominAl Surgery


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 cri-teria 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 re- opening and conversion to an ‘open abdomen’.

Summary

Abdominal trauma is a significant cause of morbidity and mortal-ity. 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 thor-ough 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 patient’s 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 opera-tive management of these patients is often only the beginning of a long recovery phase, much of which is improved by atten-tion to detail and continual reassessment of the patient. Suc-cess 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.

multiple choice questions

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 1–4, select which statements are true and which are false. the correct answers are given below.

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 intercollegiate MRCS.

test yourself mcq and extended matching

For questions 1–4, select the statements which are true and which are false. the correct answers are given below.

1 GastrointestinalphysiologyWhen considering gastrointestinal physiology:

A Hydrochloricacidissecretedbyparietalcellsinthegastricbody(oxynticmucosa),whichexpresstheH+–K+ATPaseorprotonpump.

B Gastrinisaregulatorypeptideandisamajordirectregulatorofacidsecretionbyparietalcells.

C Gastrinisalsoadirectgrowthfactorfortheenterochromaffin-likecell,whichexplainsthepresenceofenterochromaffin-likehyperplasiaseeninsomechronicallyhypochlorhydricandconsequentlyhypergastrinaemicpatients.

D Inthesmallintestine,allthecelltypesascendthecrypt–villusaxis,movingoveraperiodof3–5daystobeshedbyapoptosis.

E Foodsrichinlipidsmarkedlyslowgastricemptyingbyexertinganinhibitoryeffectontheantralpump,stimulatingpyloriccontractionsandmaximallyrelaxingtheproximalstomach.

2 Anatomyoftheanteriorabdominalwallandgroin

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

A Theinternalobliquemusclearisesbyfleshydigitationsfromtheouteraspectofeachofthelowereightribsneartheircostochondraljunctions.

B Abovethelevelofthecostalmargin,therectusabdominisiscoveredonitsanteriorsurfaceonlybytheexternalandinternalobliqueaponeuroses.

C Thegroinoringuinalregiondenotestheareaadjoiningthejunctionalcreasebetweenthefrontofthethighandthelowerpartoftheanteriorabdominalwall,andincludestheinguinal,butnotthefemoral,canal.

D Thebloodsupplytotherectusabdominismuscleisfromthesuperiorepigastricartery,abranchoftheinternalthoracicartery.

suRGeRY 27:6 27

E Whentheperitoneumprotrudesintotheinguinalcanal,medialtotheoriginoftheinferiorepigastricartery,throughanattenuatedandweakenedposteriorwall,itistermedanindirectinguinalhernia.

3 InvestigationofabdominalmassesWhen investigating patients with abdominal masses:

A Noimagingmethodiscompletelytissue-specificandbiopsy(usuallyimage-guided)isrequiredifdoubtexistsaboutthetissuediagnosis.

B TheUKRoyalCollegeofRadiologistsstatethattheplainradiographisnotindicatedintheinvestigationofpalpableabdominalmasses.

C Iodine-labelledmetaiodobenzylguanidinecanbeusedinthediagnosisofpheochromocytomaandcarcinoidtumours.

D ContraindicationstoMRIincludecardiacpacemakers,ferromagneticimplantsandthefirsttrimesterofpregnancy(relative).

E Technetium-labelledmethylenediphosphonatecandetectbonymetastasesbeforetheyarevisibleonplainradiograph.

4 BluntandpenetratingabdominaltraumaIn patients with blunt or penetrating abdominal trauma:

A Allareinitiallyassessedusingtheprimarysurveywhichincludesafullabdominalassessment.

B SeatbeltbruisingisassociatedwithChancefracturesofT12/L1,lumbarspinefracturesandhasahighassociationwithbowelperforation.

C FASTisafocusedultrasoundexaminationtoassessforfreeintra-abdominalorpericardialfluid.

D Isolatedlower-gradeinjuriestotheliver,spleenandkidneysarefrequentlyself-limitingwithminimalintra-abdominalbloodloss.

E Raisedintra-abdominalpressure(IAP)hasbeenreportedtooccurinmorethan50%ofpatientswhohavedirectfascialclosurefollowingpenetratingabdominaltrauma.

see next page

2 © 2009 published by elsevier ltd.

multiple choice questions

suRGeRY 27:6 273 © 2009 published by elsevier ltd.

questions cont.

5 DigestionandabsorptionTheme: The physiology of digestion and absorption

A Hasitsown,selectivecarrierprotein,GLUT5,whichisusedfortransportwithouttherequirementofthesodiumgradient.

B Aboutone-halfofitsdailyintakeisabsorbedatsitesinthesmallintestineandalthoughlittleisknownaboutthecellularmechanismsunderlyingepithelialtransport,DMT1mayplayarole.

C Predominantlyreabsorbedintheterminalileumandreturnedtotheliverviatheenterohepaticrecirculation.

D Absorptionisalongwiththedigestionproductsoflipidsinthemicellarprocess.

E Digestionisinitiatedbysalivaryamylasesecretedfromtheparotidandsubmandibularglands,whichbeginstobreakdownstarchesandglycogensintosimplerdisaccharidesandtrisaccharides.

F Absorptionpredominantlyoccursinthejejunumincotransportwithsugars(althoughactiveabsorptionoccursadditionallyintheileumandcolonwithouttheprerequisitesugars).

G Absorptionrequiresthechaperoneprotein,intrinsicfactor.

H Absorptionisinthejejunumandileumbypassivediffusionacrossaconcentrationgradient

Foreachofthecompoundslistedbelowselectthesinglemostlikelytruestatementfromthelistabove.Eachoptionmaybeusedonlyonce,morethanonceornotatall.

1 Bilesalts

2 Carbohydrates

3 Fructose

4 VitaminB12

5 Magnesium

6 VitaminK

7 Sodium

8 Potassium

Answers1 A,C,E

2 None

3 All

4 C,D,E

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

Answerstoincorrectstatements

Question 1

B Gastrinisaregulatorypeptidebutisnotamajordirectregulatorofacidsecretionbyparietalcells.

D Inthesmallintestine,thecelltypes,exceptPanethcells,ascendthecrypt–villusaxis,movingoveraperiodof3–5daystobeshedbyapoptosis.

Question 2

A Theexternalobliquemusclearisesbyfleshydigitationsfromtheouteraspectofeachofthelowereightribsneartheircostochondraljunctions.

B Abovethelevelofthecostalmargin,therectusabdominisiscoveredonitsanteriorsurfaceonlybytheexternalobliqueaponeurosisalone.

C Thegroinoringuinalregiondenotestheareaadjoiningthejunctionalcreasebetweenthefrontofthethighandthelowerpartoftheanteriorabdominalwall,andincludestheinguinalandfemoralcanals.

D Thebloodsupplytotherectusabdominismuscleisfromthesuperiorepigastricartery,abranchoftheinternalthoracicarteryandtheinferiorepigastricartery,abranchoftheexternaliliacartery.

E Whentheperitoneumprotrudesintotheinguinalcanal,medialtotheoriginoftheinferiorepigastricartery,throughanattenuatedandweakenedposteriorwall,itistermedadirectinguinalhernia.

Question 4

A Althoughafullabdominalassessmentisnotpartoftheprimarysurvey,evaluationoftheabdomenasasourceofbleedingisanintegralpartofthecirculationaspectoftheprimarysurvey.

B SeatbeltbruisingisassociatedwithChancefracturesofT12/L1,lumbarspinefracturesandhasalowassociationwithbowelperforation.

62492558 abdominal surgery all in one

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