Ebook General surgery prepare for the MRCS key articles from the surgery journal Part 1

(BQ) Part 1 book General surgery prepare for the MRCS key articles from the surgery journal presentation of content: Anatomy of the anterior abdominal wall and groin, secretory functions of the gastrointestinal tract, physiology of malabsorption, abdominal access techniques,... and other contents.

Clinical Editor 

Michael G Wyatt MSc MD FRCS FRCSEd (ad hom) 

Consultant Surgeon, Freeman Hospital, Newcastle‐upon‐Tyne; Honorary Reader, Newcastle  University; Clinical Editor, SURGERY; Honorary Secretary, The Vascular Society of Great  Britain and Ireland; Member of the Court of Examiners for the Intercollegiate MRCS 

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Content Strategist:   Laurence Hunter 

Content Development Specialist:  Kim Benson 

Designer:  Miles Hitchen 

Preface 

Surgery has been at the forefront of providing quality articles especially designed for candidates 

sitting the Intercollegiate examinations for over 20 years. Now technology is making these quality  articles available not only in printed form but also on‐line. However the increasing demand for easy  access to quality information, has prompted the preparation of a series of ‘e‐books’ based on 

of ‘e‐books’ will significantly enhance the learning experience of all surgical trainees and also provide 

a useful update for all seeking to keep abreast with the latest advances in their particular branch of  surgery. 

science articles cover anatomy, physiology and pathology while the clinical sections cover all of the  skills across all of the topics required for and tested in the MRCS exams. The authors are all 

recognized specialists and Surgery is curated by a highly qualified team of Editors. 

This ebook brings together a comprehensive collection of all the articles on general surgery. Over  100articles in total create a comprehensive compendium of surgical knowledge that will be a perfect  resource for anyone preparing for the MRCS. Also included are MCQ and extended matching 

Consultant Surgeon, Honorary Senior Lecturer, Sheffield University; Member of Council and Past  Vice President of the Royal College of Surgeons of England, UK 

Peter Vowden MS FRCS 

Consultant Vascular Surgeon, Bradford Teaching Hospitals NHS Foundation Trust; Visiting Professor 

of Wound Healing Research, University of Bradford, Bradford, UK 

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Surgery is an authoritative, comprehensive collection of educational reviews that present the current knowledge and practice of surgery Surgery also indicates recent advances that improve the understanding of disease and the safe and effective treatment of patients It comprises concise and systematically updated contributions that are produced over a three-year cycle Surgery is an excellent didactic tool to help consultant surgeons train their junior staff to become safe and competent surgeons.

Series editor

W E G Thomas MS FRCS FSACS(Hon) Consultant Surgeon, Honorary Senior Lecturer, Sheffield University, Member of Council and

past Vice President of the Royal College of Surgeons of England

Clinical editor

Michael G Wyatt MSc MD FRCS FRCSEd (ad hom) Consultant Surgeon, Freeman Hospital, Newcastle upon Tyne; Honorary Reader, Newcastle

University; Clinical Editor, SURGERY; Honorary Secretary, The Vascular Society of Great Britain and Ireland, and Member of the Court

of Examiners for the Intercollegiate MRCS

Editorial adviser

Harold Ellis CBE DM FRCS FRCOG

Emeritus Professor of Surgery, London University

Clinical Anatomist, Guy’s, King’s and St Thomas’s

School of Biomedical Science, London, UK

Editorial Board

Andreas Adam FRCP FRCR FRCS

Professor of Interventional Radiology

King’s College London, UK

Jon Anderson FRCS(CTh)

Consultant Cardiothoracic Surgeon

Hammersmith Hospital NHS Trust, London, UK

Emily Jane Baird MBChB MRCS (Glasgow)

Trauma and Orthopaedic Specialty Registrar,

West of Scotland Rotation; and President of

the British Orthopaedic Trainees Association

Frank Carey FRCPath

Professor and Consultant Histopathologist

Ninewells Hospital, Dundee, UK

Christopher R Chapple MD FRCS(Urol) FEBU

Visiting Professor, Sheffield Hallam University

Consultant Urological Surgeon,

Royal Hallamshire Hospital, UK

Ben Cresswell MBChB FRCS(Gen Surg)

Consultant Hepatopancreatobiliary Surgeon

The Basingstoke Hepatobiliary Unit

North Hampshire Hospital, UK

Michael J Kelly MChir FRCS MRCP(UK)

Consultant Colorectal Surgeon, Leicester, UK and National

Advisor Colorectal Cancer, NHS Improvement Court of

Examiners RCSEng

Peter Lamb MBBS FRCS(Eng) MD FRCS(Gen)

Consultant Upper GI and General Surgeon

Royal Infirmary of Edinburgh, UK

Anthony Lander PhD DCH FRCS(Paed)

Senior Lecturer in Paediatric Surgery and Consultant

Paediatric Surgeon, Birmingham Children’s Hospital, UK

Consultant Senior Lecturer in SurgeryBristol Royal Infirmary, Bristol, UKHelen Sweetland MD FRCS(Ed)Reader in Surgery and Honorary Consultant SurgeonCardiff and Vale NHS Trust, UK

William Wallace MBChB(Hon) PhD FRCPE FRCPathConsultant Pathologist and Honorary Senior LecturerRoyal Infirmary of Edinburgh, UK

Robert Wilkins MA DPhil (Oxon)Lecturer in PhysiologyDepartment of Physiology, Anatomy & Genetics

St Edmund Hall, University of Oxford, UKMark Wilkinson PhD FRCS(Orth)

Senior Lecturer in OrthopaedicsUniversity of Sheffield, UKConsultant Orthopaedic SurgeonNorthern General Hospital, Sheffield, UK

Surgical and Clinical Anatomy for the MRCS exam

Investigation of the acute abdomen

Janette K Smith Dileep N Lobo

296

Investigation of abdominal masses

Quat Ullah Richard A Nakielny

306

Gynaecological causes of abdominal pain

Shehnaaz Jivraj Andrew Farkas

W E G Thomas ms frcs fsacs ( h on)

Consultant Surgeon, Honorary Senior Lecturer,

Sheffield University, Member of Council and Past Vice

President of the Royal College of Surgeons of England

www.surgeryjournal.co.uk

ONLINE, IN PRINT, IN PRACTICE

Anatomy of the anterior

abdominal wall and groin

Vishy Mahadevan

Abstract

This article describes, in a systematic manner, the anatomy of the anterior

abdominal wall, with emphasis being placed on clinical and surgical

aspects This knowledge should help the reader understand the

anatom-ical basis to various laparotomy incisions Also described in this article is

the anatomy of the inguinal canal and inguinal herniae and the

anatom-ical distinction between direct and indirect inguinal herniae.

Keywords anterolateral abdominal muscles; inguinal canal; inguinal

herniae; rectus sheath

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 ‘plane’ (which is architecturally

complex and composed of several laminae)

 transversalis fascia

 a properitoneal adipose layer

 parietal peritoneum

Skin: the skin covering the anterior abdominal wall is thin

compared with that of the back, and is relatively mobile over the

underlying layers except at the umbilical region, where it is fixed

Natural elastic traction lines of the skin (also known as skin

tension lines or 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

The superficial fascia: comprises two distinct layers

 An outer, adipose layer immediately subjacent to thedermis and similar to superficial fascia elsewhere in thebody This layer is also sometimes referred to as Camper’sfascia

 An inner fibroelastic layer termed Scarpa’s fascia (themembranous layer of superficial fascia) Scarpa’s fascia ismore prominent and better defined in the lower half of theanterior abdominal wall Also, it is more prominent inchildren (particularly infants) than in adults

Superiorly, Scarpa’s fascia crosses superficial to the costal marginand becomes continuous with the retromammary fascia Later-ally it fades out at the mid-axillary line Inferiorly, it crossessuperficial to the inguinal ligament and blends with the deepfascia of the thigh about 1 cm distal to the inguinal ligament.Below the level of the pubic symphysis, in the male, Scarpa’sfascia is prolonged quite distinctly into the scrotum and aroundthe penile shaft This prolongation of Scarpa’s fascia into theperineum is known as the superficial perineal fascia or Colles’fascia A similar, but less distinct and less readily demonstrableextension of Scarpa’s fascia occurs in the female perineum As inthe male this extension is known as superficial perineal fascia.Musculo-aponeurotic ‘plane’ (Figures 1 and 2):

The rectus abdominis e is a long, strap-like muscle one oneither side of the vertical midline Each muscle arises by twotendons; a lateral tendon from the pubic crest, and a medialtendon from the upper and anterior surfaces of the pubicsymphysis The two tendons unite a short distance above thepubis to give rise to a single muscle belly which runs upwards toattach to the anterior surfaces of the seventh, sixth and fifthcostal cartilages The upper part of the muscle usually showsthree transverse tendinous intersections; one at the level of theumbilicus, one at the level of the xiphoid tip and one halfwaybetween the two (Figures 1a and 2)

On either side of the rectus abdominis, the aponeurotic plane is made up of a three-ply (overlapping)arrangement of flat muscular sheets The outermost of these is theexternal oblique muscle, the innermost is the transversusabdominis muscle and the intermediate layer is the internal obli-que muscle Of these, only the external oblique has an attachmentabove the level of the costal margin Followed anteromedially,each of these muscles becomes aponeurotic These aponeuroses,between them, enclose the rectus abdominis muscle; the envelope

musculo-is termed the rectus sheath

The external oblique muscle e arises by fleshy digitationsfrom the outer aspect of each of the lower eight ribs near theircostochondral junctions (Figure 2) From this origin the musclefibres fan downwards and forwards The fibres that arise fromthe 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 offibres constitutes the free posterior border of the muscle Theremainder of the muscle ends in a broad aponeurosis The loweredge of this aponeurosis extends between the anterior superioriliac spine and the pubic tubercle It is rolled inwards to form

a narrow and shallow gutter, and constitutes the inguinal ment The fascia lata (deep fascia of the thigh) attaches to thedistal surface of the inguinal ligament The rest of the externaloblique aponeurosis runs in front of the rectus abdominis muscle

liga-Vishy Mahadevan FRCS(Ed) FRCS is the Barbers’ Company Professor of

Surgical Anatomy at the Royal College of Surgeons of England, London,

UK Conflicts of interest: none declared.

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

(Figure 1)

The internal oblique muscle e lies immediately deep to the

external oblique It arises, in continuity, from the lateral

two-thirds of the guttered inguinal ligament, from a central strip

along the anterior two-thirds of the iliac crest, and from the

lateral margin of the lumbar fascia along the lateral border of thequadratus lumborum muscle (a muscle of the posterior abdom-inal wall) The muscle fibres arising from the lumbar fasciarun upwards to attach along the length of the costal margin.The remainder of the muscle fibres run upwards and mediallyfrom their origin, becoming aponeurotic lateral to the outerborder of the rectus abdominis At the outer edge of the latter, theaponeurosis of the internal oblique splits into two laminae(anterior and posterior), which run medially, respectively, infront of, and behind the rectus abdominis muscle, to interdigitatewith their counterparts in the vertical midline, at the linea alba.The anterior lamina of the internal oblique is thus immediatelydeep to the external oblique aponeurosis The posterior laminarunning behind the rectus abdominis muscle is immediately infront of the transversus abdominis aponeurosis, down to thearcuate line (see below: rectus sheath)

Transversus abdominis e arises in continuity from the lateralhalf of the guttered surface of the inguinal ligament (immediatelydeep to the origin of the internal oblique), from the inner lip ofthe 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 runforwards and medially, closely applied to the inner surface of theinternal oblique The fibres become aponeurotic at the lateraledge of the rectus abdominis, and the aponeurosis continuesmedially behind the posterior lamina of the internal obliqueaponeurosis (and therefore behind the rectus abdominis) to meetits counterpart at the linea alba A few finger-breadths below thelevel of the umbilicus, however, the aponeuroses of all threemuscles run in front of rectus abdominis (see below: rectussheath) (Figures 1c and 2)

The linea alba (Figures 1 and 2) e is a longitudinallydisposed, midline interdigitation of the aponeuroses of the three-ply muscles (external oblique, internal oblique and transversusabdominis) of one side with those of the other side The lineaalba extends from the xiphoid process above, to the pubic

Figure 2 Anterior and anterolateral muscles of the abdominal wall (the

rectus and pyramidalis muscles have been removed on the right side to

reveal the posterior wall of rectus sheath and the epigastric vessels).

Rectus abdominis muscle and rectus sheath

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 abdominis Aponeurosis of external oblique

Aponeurosis of internal oblique

Aponeurosis

of transversus abdominis Peritoneum

PeritoneumExtraperitoneal fatTransversalis fascia

Skin

External obliqueInternal obliqueTransverse abdominis

Superficial fascia

Figure 1

symphysis below Lying between the medial edges of the recti,

the linea alba is a pale band of fibro-aponeurotic tissue,

consid-erably wider and thicker above the level of the umbilicus than

below In some individuals the linea alba may become weak

through abnormal attenuation and widening, thereby allowing

exaggerated lateral deviation of the two rectus sheaths whenever

intra-abdominal pressure is raised This condition is termed

divarication of recti

The rectus sheath (Figure 1b and c) e is the aponeurotic

envelope that ensheathes the rectus abdominis muscle Thus,

the rectus sheath may be said to possess an anterior wall

and a posterior wall The anterior wall of the rectus sheath is

composed of two adherent layers; a superficial layer made up of

the external oblique aponeurosis and a deep layer made up of

the anterior lamina of the internal oblique aponeurosis The

posterior wall of the rectus sheath is, likewise, composed of two

adherent layers The anterior layer of the posterior wall is the

posterior lamina of the internal oblique aponeurosis, while the

posterior layer is the transversus abdominis aponeurosis This

arrangement holds true only from the level of the costal margin

down to a level about 5e6 cm below the umbilicus Below this

level, all three aponeuroses run in front of the rectus abdominis

muscle, with the result that below this level, there is no

aponeurotic posterior wall to the rectus sheath This abrupt

change in the relationship of the aponeuroses to the rectus

abdominis, results in the posterior wall of the rectus sheath

having a sharp, free border, a short distance below the level of

the umbilicus (Figure 2) This border is called the arcuate line

Thus, below the arcuate line the posterior surface of the rectus

abdominis muscle is in direct relationship to the fascia

transversalis

Above the level of the costal margin, the rectus abdominis is

covered on its anterior surface only, by the external oblique

aponeurosis alone The transverse tendinous intersections in the

rectus abdominis muscle blend with the anterior wall of the

rectus sheath

Innervation and blood supply of the muscles of the anterior

abdominal wall (Figure 2)

The muscles of the anterior abdominal wall are supplied

segmentally by the seventh to 11th intercostal nerves and the

subcostal nerve These nerves (accompanied by their

corre-sponding posterior intercostal vessels) cross the costal margin

obliquely to run in the neurovascular plane of the anterior

abdominal wall, between the internal oblique and transversus

abdominis muscles The nerves supply these muscles and divide

into lateral and anterior branches The former penetrate the

overlying internal oblique to supply the external oblique muscle,

while the anterior branches run medially, before entering the

rectus abdominis through its posterior surface Having supplied

the muscles, these nerve branches eventually supply the

over-lying skin Cutaneous innervation of the anterior abdominal wall

by the seventh to 11th intercostal nerves and subcostal nerve is

represented by a series of oblique band-shaped dermatomes The

dermatome corresponding to the 10th intercostal nerve is at the

level of the umbilicus; that of the seventh 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 ligamentand pubic symphysis

Because there is considerable overlap in the dermal territories

of adjacent cutaneous nerves, damage to one or two of thesenerves will usually not produce detectable anaesthesia

The posterior intercostal arteries (which accompany theintercostal nerves) supply the three-ply muscles in the lateralpart of the anterior abdominal wall, and in this function arereinforced by the lumbar arteries, which are branches of theabdominal aorta

The rectus abdominis has a different blood supply The upperhalf of the muscle is supplied by the superior epigastric artery(a branch of the internal thoracic artery) The artery enters therectus abdominis alongside the xiphisternal junction with itscompanion veins The lower half of the rectus abdominis issupplied by the inferior epigastric artery, a branch of the externaliliac artery

Myocutaneous rotation flaps may be fashioned using theupper or lower halves of the rectus abdominis muscle; the formerbeing based on the superior epigastric vascular pedicle and thelatter 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 theperitoneum It is thicker and less expansile in the lower part ofthe anterior abdominal wall The transversalis fascia is closelyapplied to the deep surface of the transversus abdominis musclebut is easily separable from the latter

Properitoneal adipose layer: the properitoneal adipose layer(also known as fascia propria) is interposed between the trans-versalis fascia and the parietal peritoneum This layer offers littleresistance to the spread of infection and, consequently, cellulitissecondary to surgical wound infections may spread rapidlywithin it

Inguinal regionThe groin or inguinal region denotes the area adjoining thejunctional crease between the front of the thigh and the lowerpart of the anterior abdominal wall, and includes the inguinaland femoral canals

The inguinal canal (Figure 3): is an obliquely placed slit-likespace within the lower part of the anterior abdominal wall Itmay be represented on the surface by a 1.5 cm-wide band, aboveand parallel to the medial half of the inguinal ligament Theinguinal canal starts laterally at the deep (internal) inguinal ring(a defect in the fascia transversalis), and runs downwards andmedially to open at the superficial (external) inguinal ring(a triangular defect in the external oblique aponeurosis) Inadults, the inguinal canal is about 5e6 cm long In males, theinguinal canal contains the spermatic cord and the ilioinguinalnerve; in females, it contains the round ligament of the uterusand the ilioinguinal nerve Another nerve which runs within theinguinal canal is the genital branch of the genitofemoral nerve.This slender nerve enters the inguinal canal through the deepinguinal ring In the male, it travels as a constituent of the

spermatic cord and innervates the cremaster muscle It also

provides sensory innervation to the coverings of the spermatic

cord In the female, the nerve runs alongside the round ligament

of the uterus and emerges at the superficial inguinal ring to

supply vulval skin The ilioinguinal and genitofemoral nerves are

branches of the lumbar plexus

The inguinal canal consists of a floor, a roof, an anterior walland a posterior wall The floor of the inguinal canal is the uppersurface of the in-rolled inguinal ligament; the floor beingcompleted 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 obliqueaponeurosis, reinforced on the lateral part of its inner surface bythose fibres of internal oblique which arise from the inguinalligament The roof of the canal is formed by those fibres ofinternal oblique and transversus abdominis which, originatingfrom the inguinal ligament, run superomedially arching abovethe spermatic cord (or round ligament), before fusing to form theconjoint tendon

The posterior wall of the inguinal canal is the fascia versalis, reinforced on its anterior surface medially by theconjoint tendon The deep inguinal ring is thus a natural defect inthe posterior wall of the canal, while the superficial ring is anatural defect in the anterior wall

trans-Running obliquely in a superomedial direction behind theposterior wall of the inguinal canal, medial to the deep inguinalring, are the inferior epigastric vessels

Inguinal hernia: is an abnormal protrusion of the peritonealcavity into the inguinal canal When this protrusion enters theinguinal canal through the deep inguinal ring, it is termed an

‘indirect inguinal hernia’ Such a hernia has the potential toenlarge and emerge through the superficial inguinal ring and, inmen, the hernia may enter the scrotum The neck of an indirectinguinal hernia sac lies in the deep inguinal ring and thus issituated lateral to the inferior epigastric artery When the peri-toneum protrudes into the inguinal canal, medial to the inferiorepigastric artery, through an attenuated and weakened posteriorwall, it is termed a ‘direct inguinal hernia’ The neck of a directhernial sac is therefore medial to the inferior epigastric artery.Occasionally, an inguinal hernia may possess two sacs, onedirect and the other indirect Such a hernia is termed a panta-

a With the external oblique aponeurosis intact

b With the aponeurosis removed

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

Inferior epigastric vesselsInternal oblique

Conjoint tendonIlioinguinal nerve

External ringllioinguinal nerveSpermatic cord

Figure 3

Secretory functions of the

gastrointestinal tract

Henrik Isackson

Christopher C Ashley

Abstract

The intestine is an organ of functional diversity The absorption of water,

nutrients, minerals, and vitamins is made possible through the coordinated

action of the intestine, stomach, exocrine pancreas and hepatobiliary system.

Keywords GI-tract; secretory mechanisms; luminal nutrient sensing;

gastric secretion; regulation

Introduction

As food stuff passes through the alimentary canal it is

manipu-lated through mechanisms controlled via endocrine, paracrine,

and neural elements The cephalic phase of digestion is mainly

under neural control mechanisms whereas hormonal

mecha-nisms dominate the gastric and intestinal The process whereby

the release of such hormones is controlled is termed luminal

nutrient sensing (LNS;Figure 1)

Luminal nutrient sensing

Amino acids have shown to stimulate glucagon-like peptide-1

(GLP-1) secretion from gut L-cells, although their potency is

lower than that of glucose and fat Fatty acids are potent stimuli

for both glucose-dependent insulinotropic polypeptide (GIP) and

GLP-1 secretion The digestion of triglycerides to fatty acids is

crucial as pancreatic lipase inhibition reduces the GIP and GLP-1

response seen from fat ingestion Suggested effects from bile

acids come from experiments with perfused explanted rat colon,

in which increasing the luminal presence of bile acids increases

the concentration of GLP-1 in the portal venous effluent The

G-protein coupled bile acid receptor-1 (GPBAR1), was found

highly expressed in mouse colonic L-cells High fat diet in

Gq-protein coupled free fatty acid receptors (GPR40)-null mice

fails to induce an increase in plasma GIP and GLP-1 levels.1,2

Gastric secretions

Most secretory cells in the stomach mucosa are situated in gastric

pits These comprise oxyntic (parietal) cells secreting parietal

juice of pH as low as 2.0, mucous secreting columnar and neckcells, and pepsinogen secreting chief cells Secretory cells in theepithelium also secrete HCO3
protecting the mucosa from theluminal HCl (Figure 2A)

The parietal cells secrete the intrinsic factor (IF) IF is a 55 kDaglycoprotein complexing with vitamin B12 facilitating ileal B12absorption Surgical resection of the fundus or gastritis can leavethe patient dependent on lifelong parenteral supply of B12 toavoid deficiency-related anaemia and neuropathy

Mucus is mainly secreted from columnar epithelium throughexocytosis or desquamation of epithelial surface cells duringchurning, but also from the mucous neck cells upon vagal stimu-lation Pyloric glands contain mucus-secreting cells identical to themucous neck cells The mucus layer of the stomach is 80e280 mmthick and made up from mucins, a tetramer glycoprotein familyprotected from pepsin digestion by long galactose and N-acetylglucosamine chains, but also small amounts of nucleic acid, lipids,and other proteins including immunoglobulin, all suspended in analkaline saline HCO3
is secreted from non-parietal epithelial cells.The small HCO3
confining volume enables the pH at the epithelialmembrane to be neutral whereas the stomach lumen pHw 2.0.4Pepsinogen is the 42.5 kDa precursor of pepsin It exists in twoisoforms: pepsinogen I and II Storage as inactive precursors preventsautodigestion of the stomach mucosa.4 Pepsinogen I is releasedthrough exocytosis from chief cells in the oxyntic glandular stomacharea and pepsinogen II from mucous and glandular cells in theoxyntic and pyloric mucosa.535 kDa pepsin I is formed through acid-dependent pepsinogen I hydrolysis Pepsin I degrades about 20% ofingested protein and is especially important due to its ability to digestcollagen in meat products Gastric acid establishes the optimumworking pH range for pepsin: 1.8e3.5 Pepsin denatures at pH > 5.Regulation of gastric secretion

Gastrin, acetylcholine (Ach), and histamine are major stimulants ofgastric secretion via independent G-coupled receptors on oxynticcells 80% of gastrin is secreted from G-cells in the pyloric antrummucosa and duodenum It exists in two main isoforms: G34 (34amino acids) and G17 90% of gastrin present in the antral mucosa

is G17 This indicates that G17’s main site of action is the stomachmucosa Gastrin is also produced in the pancreas and is a diverseplayer in GI-regulation; involved in parietal cell HCl secretion andmaturation, promoting pepsinogen secretion, stomach contrac-tions, and constriction of the lower oesophageal sphincter (LOS).Stomach lumen gastrin promotes histamine release fromenterochromaffin-like (ECL) cells via cholecystokinin-2 (CCK-2)receptor, but also acts directly on the parietal cell CCK-2 receptorscausing apical membrane Hþ/Kþ-ATPase translocation.5Gastrinand CCK share the same five C-terminal amino acid residues.Vagal action releases Ach and gastrin-releasing peptide (GRP)

to induce gastric acid secretion There is little evidence from

‘sham-feeding’ in man of cephalic phase-gastrin release However,gastric phase distension of the stomach wall induces gastrinrelease from wall neurons Ach acts directly on parietal cell M3

receptors causing acid secretion It also facilitates HCl secretion byinhibiting inhibitory somatostatin release from antral D-cells GRP

is released from vagal neurons stimulating G-cells to gastrinsecretion.5Histamine H2blockers, such as cimetidine, block theaction of histamine on the oxyntic cells, and acid release by Achand gastrin, illustrating histamine’s key role in these events The

Henrik Isackson MD received his clinical training from Lund University

and is currently doing doctoral work at the Department of

Cardiovas-cular Medicine, University of Oxford, Oxford, UK Conflicts of interest:

none declared.

Christopher C Ashley DSc (Oxon) Hon MRCP FMedSci is a Professor and

Medical Tutor Emeritus at Corpus Christi College, University of Oxford,

Oxford, UK Conflicts of interest: none declared.

Hþ/Kþ-ATPase inhibitor omeprazole is also highly effective at

controlling acid production by the parietal cell

Histamine is secreted from ECL cells deep in the gastric pits closely

associated with parietal cells It works in a paracrine fashion

stimu-lating HCl secretion via parietal cell H2receptors and induces

trans-location of Hþ/Kþ-ATPase to the apical membrane via increased

[cAMP]i Histamine secretion is mainly induced by gastrin.5

Pepsinogen secretion is induced by substances including Ach,

CCK, gastrin, and secretin Ach is regarded as the most potent

inducer through the association with M3receptors causing

acti-vation of phospholipase C (PLC) and increased [Ca2þ]i.6

Somatostatin is the main inhibitor of HCl secretion It is

released from d-cells throughout the gut mucosa as well as in the

endocrine pancreas, and from submucosal and myenteric

neurons Gastric release is mainly from antral and fundal cells in

close proximity to parietal, ECL, and G-cells The release is

stim-ulated by acid, free fatty acids (FFA), glucose and distension

Somatostatin acts directly on parietal cells and indirectly by

inhibiting histamine and gastrin release.7

Secretions from the intestinal wall

Brunner’s glands, found in the proximal duodenum, secrete

alkaline mucus to lubricate chyme and protect the duodenal wall

from digestion by gastric acid Mucus is also secreted from goblet

cells in the crypts of Lieberk€uhn along the whole intestine, the

stomach excluded

Luminal gastric acid stimulates HCO3
secretion from tory cells in the proximal duodenum neutralizing gastric acid(Figure 2B)

secre-Mucus formation is a process of mucin exocytosis from gobletcells throughout the intestinal epithelium In intracellular vesiclesthese are associated with Ca2þand Hþ Dissociation of these ions isimportant in the protein’s expansion and formation of luminalmucus The process is probably aided by the enterocyte secretion ofHCO3
This has been proposed as a mechanism underlying thehighly viscous mucus in cystic fibrosis (CF), the primary phenotype

of the disease of dysfunctional cystic fibrosis transductance lator (CFTR) where a local deficiency of HCO3
contributes toincreased mucus viscosity.8For nutrients to reach the absorptiveenterocyte villi, they have to move through the mucus In coeliacdisease, where a cross-reaction towards tissue protein is initiated by

regu-an immunological response towards gliadin in wheat, villus atrophyoccurs causing reduced stirring and transport of nutrients across themucosa to the epithelium brush border, adding to an alreadyreduced absorptive capacity The result is reduced absorption of fatscausing steatorrhoea, weight loss, reduced absorption of fat solublevitamins A, D, E, and K, and anaemia due to iron, folic acid and B12malabsorption Gluten-free diet restores absorptive capacity

Regulation of small intestine secretionNeurotransmitters Ach and vasoactive intestinal polypeptide(VIP) stimulate HCO3
secretion together with luminal

Proposed intracellular mechanisms of luminal nutrient sensing in K- and L-cells

Luminal nutrient sensing dependent incretin release

Mitochondrion

Endoplasmatic reticulum (ER)

exocytosis

G-coupled receptors FFA

Voltage-gated L-type

Ca 2+ channel

K + ATP

Figure 1 Secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) through exocytosis is dependent on a rise

in [Ca2þ] i Glucose is absorbed through sodium-coupled glucose transporters (SGLT-1) The rise in [glucose] i increases the ATP level which inhibits the activity of the ATP-sensitive Kþchannel (Kþ-ATP) Naþinflux as well as decreased Kþefflux depolarizes the cell membrane which increases the opening probability of the voltage sensitive L-type Ca2þchannels, causing an influx of Ca2þ Free fatty acids (FFA) and bile acids bind G-protein coupled receptors which activate intracellular pathways raising levels of cyclic adenosine monophosphate (cAMP) Their downstream activating pathways cause a rise in cAMP which results in increased opening probability of voltage gated Ca2þchannels, and also protein kinase C (PKC) and inositol(1,4,5)-trisphosphate (IP3) causing Ca2þ-release from intracellular stores to initiate exocytosis 1,2

prostaglandin E2(PGE2) Ach acts via an increase in [Ca2þ]i, and

PGE2 and VIP act via G-protein coupled receptor activation,

raising [cAMP]i Stimulatory factors include luminal acid,

glucose, and bile salts, but also wall distension Stretch reflexes

involve the parasympathetic as well as intrinsic enteric nervous

system The sympathetic neurotransmitters noradrenaline (NA)

and neuropeptide Y (NPY) inhibit secretion Somatostatin in the

duodenal wall works as a neurohormonal inhibitor released from

enteric nerve endings It acts directly on crypt cells by decreasing

[cAMP]ilevels via a G-protein coupled receptor (SSTR1).4Mucin

release is closely associated with that of HCO3
through the

CFTR, and is stimulated by PGE2 and serotonin.9 The choleratoxin enters secretory cells through receptor-mediated endocy-tosis causing permanent activation of G-protein receptorselevating [cAMP]i, activating the CFTR, and increasing Cl
andassociated Naþ secretion with watery diarrhoea as a result.Excessive loss of HCO3
generates metabolic acidosis

Pancreatic exocrine secretionPancreatic exocrine secretion contains digestive enzymes andalkaline saline Electrolytes are secreted from ductal and

Figure 2 A: ATP-dependent Hþ/Kþ-exchange, Cl
extrusion, and Kþrecycling, are central for HCl secretion Hþis derived from H 2 CO 3 which forms from H 2 O and CO 2 under the influence of carbonic anhydrase (CA) The Hþ/Kþ-ATPase is the major Hþ-extruder consuming approximately 1500 calories per litre of secreted gastric juice generating a 106times concentration gradient over the apical membrane It is effectively inhibited by omeprazole The Naþ/Hþexchange (NHE) transporter in the apical membrane transports Naþdown its concentration gradient in exchange for Hþ.3Together with the Cl
/HCO 3

exchange (CHE)-transporter the cystic fibrosis transductance regulator (CFTR) promotes the transport of Cl
against its electrochemical gradient into the stomach lumen The voltage gated Kþchannel (Kv) is required to sustain the action of the Hþ/Kþ-ATPase HCO 3
is secreted basolaterally down

a concentration gradient into the blood, in exchange for Cl
The NHE of the basolateral membrane also helps to regulate pH The NKCC conveys the electroneutral inward transport of one Naþ, one Kþ, and two Cl
Cl
also passes down its concentration gradient via exclusive Cl
-channels Naþ/Kþ- ATPase generates the electrochemical gradient of Naþand Kþ Tight junctions in the gastric epithelium are electrically tight, preventing paracellular ion diffusion B: In the duodenal epithelial cell apart from paracellular access of HCO 3
from the blood to the duodenal lumen over leaky tight junctions, there are facilitating transport mechanisms over the apical membrane together with Cl
Cl
-transport also occurs through the CFTR 4 An electroneutral NHE prevents intracellular pH decrease Processes supporting the apical export of HCO 3
include the NKCC, NHE, the Naþ/Kþpump, a Naþ/HCO 3
co- transporter (NBC), and an outward exclusive Kþchannel.

centroacinar cells whereas enzymes originate from acinar cells at

the terminal end of the secretory units HCO3
protects the

duodenal mucosa from acid and establishes an optimal pH for

digestive enzymes, and facilitates micelle formation, a process

described below The pancreatic juice, as it enters the

duodenum, holds a pH of 7.4e8.3 contributing to the settling of

duodenal chyme at approximately pH 7, inactivating pepsin

HCO3
is secreted to the pancreatic duct lumen in analogy with

the duodenal secretory process Protons from H2CO3dissociation

are transported across the basolateral membrane making the

postprandial pancreatic effluent slightly acidic reducing the effect

of the stomach alkaline tide The electrolyte fluid also contains

Naþ, and Kþwhich travels via the paracellular route down the

electric gradient increasing water flow through osmotic

mecha-nisms With increased flow the secretion entering the duodenum

becomes similar to the primary pancreatic composition due to

reduced ductal cell modification Cl
stands in reciprocal

rela-tionship with HCO3
due to antitransport in the CFTR channel of

the apical membrane Hence, with an increase in flow [HCO3
]

increases due to decreased reuptake, whereas [Cl
] is reduced as

less is secreted

Proteolytic enzymes are stored in intracellular zymogen

granules in the terminal acinar cells of the secretory lobules and

secreted as inactive precursors to avoid pancreatic tissue

auto-digestion Trypsin and chymotrypsin have a strict endopeptidase

cleavage pattern whereas carboxypolypeptidase releases single

amino acids from the carboxyterminal end of proteins reducing

polypeptides to single amino acids The trypsin precursor

tryp-sinogen is initially activated by enterokinase, situated on the

intestinal epithelium brush border Activating trypsinogen causes

an autoactivation cascade which if it occurs in the pancreas

causes tissue autodigestion To prevent premature activation

pancreatic juice contains pancreatic secretory trypsin inhibitor

(PSTI) Trypsin also activates other enzyme precursors in the

duodenal lumen Elastase is the only enzyme which is capable of

degrading connective tissue elastin

Postnatally intestinal cells can absorb protein by endocytosis,

a process designed to transfer passive immunity from the mother

Even adult intestines can absorb small amounts of protein and

polypeptide Although the majority of protein is absorbed

even-tually via specific amino acid co-transporter systems and defects

in these systems are responsible for Hartnup disease and

cystin-uria, the enterocyte can absorb di-, tri-, and tetra-peptides, these

being subsequently intracellularly hydrolysed The transporter for

this process is the oligopeptide transporter (PepT1) which is

effective at transporting multiple amino acids, rather than a single

amino acid, and is dependent upon Hþinward co-transport

Pancreatic a-amylase, the main carbohydrate-degrading

enzyme, hydrolyses sugars, starch, and glycogen to glucose and

disaccharides Pancreatic lipase is dependent on a coenzyme,

pancreatic colipase, in order to reach full activity as this

coun-teracts biliary acids’ inhibitory effects on pancreatic lipase

Pancreatic lipase hydrolyses triglycerides, forming FFA and

monoglycerides Cholesterol esterase hydrolyses ester linkages

between fatty acids and cholesterol, enabling micelle utilization

It forms proteolysis-resistant dimers when present in the

duodenal lumen Activated phospholipase hydrolyses

phospho-lipids to FFA and lysophosphophospho-lipids It is the only non-proteolytic

enzyme stored as an inactive precursor before secretion

Regulation of pancreatic exocrine secretionPancreatic exocrine secretion is mainly under autonomic nervouscontrol in the cephalic phase of ingestion and hormonal andenteropancreatic reflex control during the gastric and intestinal.10

In this phase, mainly enzymes are secreted but a vasodilatoryresponse is initiated through kallikrein secretion catalysing theproduction of vasodilatory bradykinin, increasing the pancreaticblood flow and consequently fluid secretion Ach from secondarynerve endings stimulates muscarinic receptors causing a release of

Ca2þfrom intracellular stores and zymogen granule exocytosis.Without increased electrolyte flow, large quantities of digestiveenzymes remain in the pancreatic ducts until the increased flow inthe intestinal phase moves them towards the Papilla Vateri Only25% of total pancreatic enzyme secretion is released during thecephalic phase During the gastric phase, hormonal stimulantsstimulate pancreatic enzyme secretion by another 5e10%,together with cholinergic neural stimulation CCK is responsible for

70e80% of the total pancreatic enzyme secretion during a meal It

is released from EEC of I-type in the duodenal and upper jejunalmucosa, when these are stimulated by fatty and amino acids duringthe intestinal phase HCl is less potent a stimulant CCK-I receptorstimulation induces increased [Ca2þ]i and zymogen exocytosis.Trypsin exerts negative feedback by inhibiting CCK release.10Secretin is a 27 amino acid inducer of electrolyte secretion Ithas been suggested to act by augmenting inward potassiumcurrents in acinar cells increasing Cl
and HCO3
-secretion Acidreleased in the duodenum stimulates S-cells in the intestinal wall

to release secretin stimulating alkaline fluid secretion from ductaland centroacinar cells The [HCO3
] can reach 150 mM Fattyacids, less potently, contribute to the release of secretin HClreacts with HCO3
and Naþto form H2CO3 and NaCl H2CO3

dissociates into H2O and CO2, the latter subsequently expiredthrough respiration CCK and Ach potentiates the secretion ofalkaline fluid induced by secretin.10

Somatostatin inhibits secretion through suppression of CCKand secretin release Its release, stimulated by the samehormones and gastrin, illustrates another negative feedbackmechanism The identification of somatostatin receptors onacinar cells suggests an independent action.10,11

Hepatobiliary secretionsBile aid fat digestion through emulsification and micelle forma-tion, and carries metabolic waste products and toxins from theblood The efficacy of the former task is increased through the mealsynchronized-contraction of the gall bladder and entry of thisconcentrated bile into the duodenum The concentrating effect isachieved through the osmotic absorption of water through elec-trically ‘leaky’ tight junctions driven by active absorption ofsodium over the apical and basolateral membrane of the epithelialcell to the blood, and through aquaporin channels

Bile secretions are divided in two groups: hepatocyte secretionconsisting of bile salts as the major component, along withcholesterol, lecithin, bilirubin, fatty acids, excreted conjugatedmetabolites, albumin, immunoglobulin A (IgA), and plasmaelectrolytes, and cholangiocyte secretion containing alkalinesaline The liver parenchyma shows functional hexagone shapedmicroscopic units in which hepatocytes modify contents ofarterial and portal blood (Figure 3)

Bile acids are derived from cholesterol, and combine with

sodium or other monovalent cations The main bile acids are

cholic and chenodeoxycholic acids which combine with taurine

or glycine before sodium Bile salts emulsify fat, increasing the

fat water-interface and enzymatic fat digestion

Bile salts are taken up from the enterohepatic circulation via

hepatocyte basolateral sodium co-transporters A concentration

gradient is created by Naþ/Kþ-ATPase Naþ-extrusion Apical

secretion into the canaliculi occurs through an active transport

As they enter the canaliculi they are stored in micelles

Lecithin is the major phospholipid secreted with bile It is

mainly derived from the hepatocyte cell membrane Cholesterol

is to a major extent derived from a circulating pool, but a liver de

novo synthesis provides a fraction

Bilirubin is derived from erythrocyte haemoglobin and muscle

myoglobin in the reticuloendothelial system (RES) The

inter-mediate metabolite biliverdin, which is reduced to bilirubin, is

also present in hepatic secretion Gall bladder stored bilirubin

tends to reoxidize generating the bile’s characteristic green

colour To increase bilirubin’s water solubility, bilirubin

hepa-tocyte conjugation is mainly to glucoronic acid, whereas

a minority is conjugated to sulphate It is actively secreted into

the canaliculi Bilirubin is partly excreted with faeces Intestinal

bacteria convert unconjugated bilirubin to stercobilinogen which

is more readily absorbed to the blood stream and excreted via the

liver Exposure of stercobilinogen to air reoxidizes it to

sterco-bilin, giving faeces its dark colour Urinary secretion of bilirubin

occurs in the form of urobilinogen which is oxidized to urobilin

A minority of conjugated bilirubin will also be deconjugated bybacteria and pass back into the enterohepatic circulation.Along with hepatocyte bile secretion, cholangiocytes secrete

an alkaline saline into the ducts neutralizing the duodenal pH,optimizing conditions for pancreatic digestive enzymes as well asaiding micelle formation This adds as much as 100% to theinitial hepatocyte derived secretory volume With increased flow,the time of contact for the hepatobiliary secretion decreases andthe pH of the bile rises due to a reduced chloride/bicarbonateexchange In post-hepatic jaundice an obstruction of the bile ductprevents entry of gall into the duodenum As a result fat emul-sification and absorption will be impeded, along with a loss ofstercobilinogen causing steatorrhoea of pale colour In the classiccase the patient will also display darkened urine, and jaundicedue to increased systemic levels of conjugated bilirubin.Fat emulsification

For efficient digestion it is crucial to achieve fat emulsification.Lecithin is a major component in the micelle and also actsemulsifying in its free state Its hydrophobic acyl side-chainresides in the fat and its hydrophilic phosphorylcholine groupprojects towards the water face which reduces surface tension.The amphiphilic nature of conjugated bile salts also aids thisprocess Lipase hydrolyses triacylglycerol forming FFA andmonoacylglycerides, both used in micelle formation Micelleshave a diameter of 3e6 nm and contain 20e40 bile salt mole-cules Micelle bile salts have their hydrophilic side facing theperiphery and the hydrophobic sterol in the centre With lecithin

hepatocytelymphatic duct

cholangiocytebile ductule

Schematic representation of the liver hexagone

Figure 3 The liver parenchyma is organized in hexagones where hepatocytes modify contents of arterial and portal blood In each corner is a hepatic triad consisting of distal portal vein, hepatic artery, and proximal bile ductule The arrows indicate the direction of flow This counter-current system allows for hepatocytes to absorb substances for modification from the blood and excrete metabolites along with bile constituents into the bile ductule Excess fluid

in the space of Disse beneath endothelial cells drains into the lymphatic ducts.

incorporation the primary micelle expands into a secondary

micelle harbouring larger quantities of hydrophobic cholesterol

molecules in its core Their negative shells causes inter-micelle

repulsion, emulsifying the fat The micelle also aids fat

absorp-tion in the small intestine by effectively keeping the

concentra-tion of relatively water insoluble fatty acids, of more than C12, at

a saturation level in the aqueous phase

FFA are absorbed through diffusion Once in the enterocyte

triglycerides are re-synthesized from fatty acids and

mono-glycerides In the circulation, these lipids are transported as

chylomicrons to their site of storage or utilization Bile salts

are then reabsorbed into the enterohepatic circulation from

the terminal ileum by a secondary active transport system

Fatty acids of less than C12 in length are sufficiently

water soluble and do not necessarily need this system for

absorption

Regulation of hepatobiliary secretion

Gall bladder emptying requires the contraction of the bladder to be

synchronized with sphincter of Oddi relaxation Ach from vagal

secondary neurons acts on the biliary tree interprandially and

during the cephalic and gastric phases of digestion causing

contractile pulses in the gall bladder, a slight secretion of alkaline

fluid from cholangiocytes, and antegrade peristalsis of the sphincter

of Oddi, reducing the risk of gall stone formation During the gastric

phase, vagal action is supported by gastrin from ventricle G-cells

CCK, the most potent inducer of gall bladder contraction, is

released from EEC of the duodenum in response to luminal fatty

acids It acts on CCK-I receptors on gall bladder smooth muscle cells

but also facilitates release of Ach from gall bladder ganglia initiating

contraction through a rise in [Ca2þ]i The same hormone inhibits

the contractions of the sphincter Oddi which ensures release of bile

into the duodenum Sympathetic neurotransmitters such as

adrenaline and NA relaxes the gall bladder.12 Bile acids inhibit

further CCK release from the duodenum

Secretin is the major stimulant of cholangiocyte alkaline

secretion It is released from S-cells in the duodenum and induces

an increase in cholangiocyte [cAMP]i, activation of PKA and

opening of the CFTR and Cl
/HCO3
exchanger increasing

HCO3
secretion Ach potentiates the secretin effect by eliciting

cAMP activity Its sole effect appears limited Somatostatin has

an inhibitory effect on cholangiocyte secretion by interaction

with the somatostatin receptor 2 (SSTR2) preventing

secretin-induced increase in cyclic adenosine monophosphate (cAMP)

activity.13

Colonic secretion

Some acidic material is formed throughout the gut by bacterial

metabolism, and also by the activity of a colonic Hþ/Kþ-ATPase

Due to HCO3
secretions the mucus still has an alkaline pH The

HCO3
secreting epithelial cells of the colon occur sparsely

compared to the proximal gut, but also utilizes the CFTR and

HCO3
/Cl
exchanger As water is absorbed throughout the gut,

the chyme becomes progressively more viscous causing a higher

mechanical stress on the intestinal walls Goblet cells in the colon

secrete mucins to produce a lubricating viscoelastic gel The

mucus also serves the purpose of protecting the intestinal

epithelium from adhesion of harmful bacteria, and toxins

The colonic epithelium regulates bodily Kþ-levels, providing

an accessory excretion pathway to the kidney This occurs down

a concentration gradient through the passive conductancepotassium BK channel after its active absorption across thebasolateral membrane by the Naþ/Kþpump and Naþ/Kþ/2Cl
co-transporter In the distal colon Kþ is absorbed by Hþ/Kþ-ATPase, similar to that seen in the parietal cell A paracellular Kþtransport has also been suggested, driven by the electricgradient.14 Electrolyte balances is a consideration in colonicirrigation where external osmotically active volumes may initiatecolonic movements and increased potassium secretion This is ofparticular importance in patients where multiple pharmacologicagents, along with age, may already reduce kidney homeostaticcapacity, causing an increased dependence on the colon

Regulation of colonic secretionThe main stimulus for mucus secretion in the colon is tactilestimulation of goblet cells Reflexes also occur via the pelvicnerves involved in defecation, co-eliciting an increase in peri-stalsis Sympathetic nervous stimulation decreases colonicperistalsis and secretion

In kidney failure, an upregulation of colonic Kþ secretiondescribes the regulatory function of the organ to maintain

a stable serum [Kþ] Net colonic Kþsecretion is variable andresponds to increased dietary intake by increasing secretion viaincreased plasma aldosterone BK-KO mice fail to reduce plasmalevels of Kþon aldosterone administration, suggesting a regula-tory role of this channel Colonic Kþsecretion through the BKchannel increases on adrenalin and PGE2 stimulation viaincreased cAMP levels Aldosterone is also an inhibitor of the

Hþ/Kþ-ATPase, adding to the net Kþefflux effect Somatostatininhibits Kþsecretion through a decrease in [cAMP]i.14 A

REFERENCES

1 Parker HE, Reimann F, Gribble FM Molecular mechanisms underlying nutrient-stimulated incretin secretion Expert Rev Mol Med 2010; 12: e1.

2 Reimann F Molecular mechanisms underlying nutrient detection by incretin-secreting cells Int Dairy J 2010 Apr; 20: 236 e42.

3 Kopic S, Murek M, Geibel JP Revisiting the parietal cell Am J Phys

10 Nathan JD, Liddle RA Neurohormonal control of pancreatic exocrine

secretion Curr Opin Gastroenterol 2002 Sep; 18: 536 e44.

11 Morisset J Negative control of human pancreatic secretion:

physiological mechanisms and factors Pancreas 2008 Jul; 37: 1 e12.

12 Portincasa P, Di Ciaula A, Wang HH, et al Coordinate regulation of

gallbladder motor function in the gut-liver axis Hepatology

(Baltimore, Md.) 2008 Jun; 47: 2112 e26.

13 Marzioni M, Fava G, Alvaro D, Alpini G, Benedetti A Control of

cholangiocyte adaptive responses by visceral hormones and

neuro-peptides Clin Rev Allergy Immunol 2009 Feb; 36: 13 e22.

14 Sorensen MV, Matos JE, Praetorius HA, Leipziger J Colonic potassium handling Pflugers Arch 2010 Apr; 459: 645 e56.

Acknowledgements

The authors are grateful to Dr Gabor Czibik, for critically reading the manuscript.

Malabsorption occurs when the function of the gastrointestinal tract is

suboptimal and nutrient absorption is reduced Malnutrition, weight loss,

diarrhoea, steatorrhoea, anaemia and other specific nutrient deficiencies

can be produced This article will review the principles of normal nutrient

absorption and the pathophysiology in disorders which result in

malab-sorption Normal absorption needs coordinated processes of motility,

hormone release, digestive secretion from the salivary glands, stomach,

pancreas, liver and intestine, and the expression of specific enzymes and

transporter molecules Gastric, pancreatic and intestinal disorders can all

produce malabsorption These can be complications of surgical procedures,

or be due to inflammatory and autoimmune disorders such as coeliac

disease, Crohn’s disease, small intestinal bacterial overgrowth, chronic

pancreatitis, or autoimmune gastritis Understanding the mechanisms

involved and how these are affected by surgical procedures and disease

will enable malabsorption to be recognized, investigated and treated

appropriately.

Keywords Absorption; bile; carbohydrates; coeliac disease; digestion;

lipids; micronutrients; minerals; proteins; short bowel syndrome

Introduction

The principal function of the gastrointestinal tract is the digestion

and absorption of nutrients consumed in the diet To achieve

adequate nutrition, specialized and coordinated functions have

evolved throughout the gastrointestinal tract and its associated

organs such as the pancreas and liver Malabsorption occurs

when these digestive and absorptive functions are suboptimal,

usually as a result of acquired disease or surgery

Malabsorption may be generalized, affecting many types of

nutrients, or may be limited to one specific nutrient It can be

suspected from the clinical history and examination: all patientsundergoing any procedure except the most trivial should havebeen screened for nutritional impairment, and this may be due tounsuspected malabsorption (although there are many othercauses) The malnutrition universal screening tool (MUST) is inwide-spread use for adults in the UK,1and requires only simplequestioning (weight loss, acute disease) and common measure-ments (height and weight) (Box 1)

Many patients with malabsorption will have diarrhoea orsteatorrhoea, but this is not always the case Careful questioningshould detect frequency of stools and/or the passage of lipidswhich have not been absorbed Use of the Bristol stool chart2helps to define the precise nature of a patient’s bowel habits.Other specific blood tests may detect deficiencies of other nutri-ents such as Fe or B12that have been malabsorbed

This article will review the principles of normal absorption,and the pathophysiology of some of the common disorders thatresult in malabsorption

Principles of normal absorptionNormal absorption relies on multiple processes, some starting assoon as food is seen, smelt and tasted Chewing starts thephysical transformation of food, and secretions from the salivaryglands, stomach, pancreas, liver and intestine dissolve compo-nents of the meal and lubricate its passage These secretionsinclude key digestive enzymes Coordinated muscle function isneeded to swallow the bolus, and gastric motility is critical formixing food in the stomach and emptying the semiliquid chymeinto the small intestine Intestinal peristalsis mixes and propelsthese nutrients which are further digested and mostly absorbed

Screening by MUST for malnutrition, which may bedue to malabsorption See The ‘MUST’ ExplanatoryBooklet for full explanations1

The 5 ‘MUST’ steps

Step 1 Measure height and weight to get a body mass index score using chart provided If unable to obtain height and weight, use the alternative procedures shown in this guide.

Step 2 Note percentage unplanned weight loss and score using tables provided.

Step 3 Establish acute disease effect and score.

Step 4 Add scores from steps 1, 2 and 3 together to obtain overall risk of malnutrition.

Step 5 Use management guidelines and/or local policy to develop care plan.

MUST, malnutrition universal screening tool.

Box 1

Jonathan D Nolan BSc MB BS MRCP is a Clinical Research Fellow,

Department of Gastroenterology, Imperial College NHS Trust,

Hammersmith Hospital, and Section of Hepatology & Gastroenterology,

Imperial College, London, UK Conflicts of interest: none declared.

Ian M Johnston MB ChB MRCP is a Clinical Research Fellow, Section of

Hepatology & Gastroenterology, Imperial College and Department of

Gastroenterology, Imperial College NHS Trust, Hammersmith Hospital,

London, UK Conflicts of interest: none declared.

Julian R F Walters MA MB BChir FRCP is Professor of Gastroenterology at

Section of Hepatology & Gastroenterology, Imperial College and

Department of Gastroenterology, Imperial College NHS Trust,

Hammersmith Hospital, London, UK Conflicts of interest: none

declared.

These processes are controlled by nerves and hormones

(Table 1) Reabsorption of secreted water, electrolytes and bile

acids occurs in the distal intestine Bacterial action releases some

further nutrients which can be absorbed in the colon.3

Digestion

The exocrine secretion of enzymes is essential for digestion

Digestive enzymes are also present on the brush-border apical

membrane of the intestinal enterocyte, and in the cytoplasm The

main enzymes involved in digestion of lipids, carbohydrates and

proteins are shown inTable 2 Proteolytic enzymes are secreted

as inactive precursors; intestinal brush-border enterokinase

activates trypsinogen to trypsin, which then activates the other

pancreatic proteases

The important non-enzymatic secretions are acid from thestomach and bicarbonate from the pancreas, intestine and bile.The enzymes in the stomach function best at acidic pH whereasthose in the intestine are more active at alkaline pH Bile acidsand phospholipids from the liver form micelles with ingestedlipids and by increasing the surface area at the lipid/waterinterface improve their digestion and absorption

AbsorptionThe digested components of a meal are absorbed by the small intes-tinal enterocyte, and cross the apical brush-border microvillusmembrane, the cytoplasm and the basolateral membrane of this cell.Specific carrier proteins, usually known as transporters, are involved

in many of these steps There are important differences in thehandling of various types of nutrient.4

Lipids: Triglycerides and phospholipids are not completelydigested but are absorbed as monoglycerides and lysophospho-lipids, along with free fatty acids Cholesterol esters are digested

to cholesterol and fatty acids Major functions of the enterocyteare to re-esterify these and to synthesis apolipoproteins, whichare then added to form chylomicrons and very low-densitylipoproteins (VLDL) These are secreted at the basolateralmembrane of the enterocyte and usually enter the lacteals in thevillus, and travel via the lymphatic system and the thoracic duct

Carbohydrates: these are relatively easily digested saccharides are absorbed rapidly in the upper small intestine(duodenum and proximal jejunum) Sucrose is split by sucrase toglucose and fructose which have their own brush-border membranetransporters Lactose, the main sugar in milk, is broken down bylactase to galactose and glucose, before being easily absorbed Theexpression of lactase is lost in most adults (see below) Starches takelonger to digest and absorb; poorly absorbed non-starch poly-saccharides form the basis for dietary fibre and prebiotics.Proteins: proteins are highly variable in structure, and there arenumerous enzymes and brush-border membrane transport

Mono-Neuroendocrine regulators of digestion

Type Component Actions

Neuronal Vagus Gastric acid secretion

Gastric emptying Motility Enteric nervous

system

Motility Peristalsis Secretion Endocrine Gastrin Gastric acid secretion

Histamine Gastric acid secretion

Cholecystokinin Bile secretion

Gallbladder contraction Pancreatic exocrine secretion Secretin Pancreatic exocrine secretion

Motilin Gastric emptying

Glucagon-like-peptide 1 (GLP1)

Gastric emptying Peptide YY (PYY) Gastric emptying

Table 1

Enzymatic digestion of different types of nutrient

Colipase Phospholipase Cholesterol esterase

Pancreatic amylase Trypsin

Chymotrypsin Elastase Carboxypeptidases

Lactase Maltase

Enterokinase (activates trypsin) Aminopeptidases Endopeptidases Oligopeptidases Dipeptidylpeptidase Table 2

systems which have evolved to cope with this diversity Short

peptides (dipeptides, tripeptides and oligopeptides) are absorbed

in addition to single aminoacids and these peptides then undergo

digestion in the cytoplasm of the enterocyte Monosaccharides,

aminoacids and most absorbed nutrients leave the intestine in the

portal venous system, passing to the liver for further metabolism

Electrolytes and water: water absorption is governed by

elec-trolyte absorption e principally that of sodium and chloride

Considerable secretion of these occurs in the upper

gastrointes-tinal tract and many litres have to be absorbed each day Sodium

is co-transported with many nutrients (glucose, amino acids,

etc.) and this forms the basis for rehydration solutions used in

diarrhoea There are also specific sodium and chloride absorptive

processes in the ileum and colon

Minerals, vitamins and other micronutrients: these nutrients

usually have specific absorptive transport mechanisms Iron and

calcium are more soluble in the acidic conditions produced by

the stomach and are absorbed in the proximal intestine Their

bioavailability can easily be reduced by binding to other

components Iron absorption is regulated by hepcidin and

calcium absorption is regulated by the active vitamin D

metabolite, 1a,25-dihydroxycholecalciferol Vitamin B12amin) is notable for the need to bind to intrinsic factor, produced

(cobal-by the stomach, and the limited region for B12absorption in theterminal ileum This region is also the site of reabsorption ofconjugated bile acids More than 90% of bile acids are absorbedinto the portal vein and are then taken back up by the liver andresecreted This is known as the enterohepatic circulation

Pathophysiology of malabsorption in diseaseThe mechanisms responsible for nutrient malabsorption vary inthe differing conditions that can cause this These are summa-rized inTable 3 We will describe various conditions affecting thestomach, pancreas and intestine conditions, and how they affectabsorption

Gastric causesGastric surgery: the storage function of the stomach is particularlyimportant during digestion, as it allows for controlled gastricemptying of an ingested meal into the duodenum and the rest of thesmall intestine Gastric emptying is under negative feedbackcontrol from gut hormone signals from the small bowel and colon.This feedback control ensures that the rate at which further

Mechanisms of malabsorption in various conditions

Stomach Gastric surgery

Coeliac disease

Crohn’s disease

SIBO Lactose intolerance Bile acid malabsorption Infections

Loss of absorptive area and intestinal digestive enzymes Rapid transit through intestine

Reduced area for absorption from villous atrophy Reduced enterocyte digestive enzymes

Impaired intestinal hormonal secretion Loss of functioning intestinal area (especially TI for B 12 /bile acids) Bypassed gut (fistulae) Small intestinal bacterial overgrowth (SIBO) Reduced brush border enzymes

Metabolic effects on enzymes, bile acids and nutrients Normal genetic non-persistence of lactase

Secondary forms from mucosal injury Secondary to impaired bile acids (BA) reabsorption Overproduction in primary BA diarrhoea

Villous atrophy, metabolic effects, lymphangiectasia and others Bariatric surgery Roux-en-Y gastric bypass Altered gastric storage and emptying

Loss of acid and pepsin Delayed mixing with pancreatico-biliary secretions Reduced intestinal length

Altered intestinal hormone secretion Table 3

nutrients leave the stomach does not exceed the digestive and

absorptive capacity of the small intestine Gastric surgery often

results in accelerated transit of nutrients through the small

intes-tine due to loss of these functions.5This leads to a shorter time for

the integration of digestive enzymes and bile salts with the ingested

macronutrients (carbohydrate, protein and fats) within the small

intestine There will also be less time for absorption, resulting in

some nutrients entering the colon unabsorbed

The mixing and grinding functions of the antrum and pylorus

will be lost if they have been resected (e.g Bilroth I or II

gastrectomy) This will result in food particles that are larger

than normal entering the small intestine The luminal digestive

enzymes and bile salts will therefore have a smaller surface area

with which to interact with macronutrients and fat droplets This

may be particularly relevant for the absorption of iron that is

bound in the solid phase of muscle myoglobin ingested meat.6

Gastrectomy can specifically interfere with iron absorption via

other mechanisms, including reduced gastric acid secretion

decreasing solubility Proximal gastrectomy will selectively

interfere with B12absorption through the loss of intrinsic factor

production from the fundal parietal cells

Autoimmune atrophic gastritis: pernicious anaemia is a

macro-cytic anaemia caused by B12deficiency, resulting from autoimmune

gastritis In this form of chronic gastritis, there is autoimmune

destruction of gastric parietal cells, responsible for the secretion of

hydrochloric acid, pepsin and intrinsic factor Malabsorption of B12

occurs due to the loss of secretion of intrinsic factor into the lumen

Impaired acid secretion (hypochlorhydria) also results from the

damage to the gastric parietal cells, and the increase in pH will

reduce the solubility and absorption of polyvalent cations such as

iron, calcium and magnesium Other vitamins such as vitamin C

can also malabsorbed due to reduced acid secretion Similar

consequences of hypochlorhydria are occasionally observed with

prolonged courses of gastric anti-secretory drugs such as proton

pump inhibitors (PPIs) or histamine antagonists

Pancreatic insufficiency

Maldigestion: maldigestion refers to defects in the digestive

processes throughout the gastrointestinal tract Pancreatic

digestive enzymes (amylase, lipases and proteases) are essential

for this process Any impairment in their secretion will therefore

lead to maldigestion and ultimately, malabsorption of nutrients

Impairment in the secretion of pancreatic enzymes is usually

referred to as exocrine pancreatic insufficiency (EPI) The most

clinically important causes of EPI result from loss of functioning

pancreatic tissue such as chronic pancreatitis or surgical

resec-tion Other causes include obstruction of the pancreatic duct

(strictures, neoplasm) and impaired stimulation of secretion

(vagotomy, gastrectomy) Causes are listed inTable 4 Loss of

pancreatic tissue usually also results in loss of islets and

endo-crine deficiency and diabetes

Chronic pancreatitis: chronic pancreatitis is characterized by

gradual irreversible damage to the pancreas The most common

cause in the western world is alcohol, contributing to as much as

70e90% of cases.7

Diseases affecting the pancreatic acinar cellsresult in EPI due to decreased volume or quality of secreted

pancreatic juices (as in cystic fibrosis) Fat maldigestion tends to

precede carbohydrate and protein maldigestion Several reasonsmay explain this: (i) the pancreas is the main source of lipase,with the stomach only contributing a small proportion (gastriclipase); (ii) lipase production is the first enzyme to becomedeficient as chronic pancreatitis progresses; and (iii) reducedbicarbonate secretions from the pancreas will lower the pH in theduodenum Pancreatic lipases are more sensitive to aciddestruction than the other pancreatic enzymes.8 It is notsurprising, therefore in clinical practice to find that steatorrhoea

is an early symptomatic manifestation of EPI Other importantbiochemical manifestations of EPI are deficiencies in fat-solublevitamins (A, D, E, K)

Post-surgical pancreatic insufficiency: resective pancreaticsurgery is often performed in patients who have developedcomplications from chronic pancreatitis These indicationsinclude uncontrolled pancreatic pain, carcinoma or pseudocyststhat have failed non-invasive techniques EPI due to an alreadydiseased and damaged pancreas will be further compounded bysurgical resection of pancreatic tissue Maldigestion can alsooccur following operations that result in the asynchronous

Causes of exocrine pancreatic insufficiency

Chronic pancreatitis Alcoholic

Metabolic Hypercalcaemia Hyperlipidaemia Genetic

Cystic fibrosis (CFTR mutations) Hereditary pancreatitis (PRSS1 mutations) Autoimmune

Isolated autoimmune pancreatitis IgG4 autoimmune disease (often associated with other autoimmune disease)

Tropical Tropical calcific pancreatitis Idiopathic

Pancreatic duct obstruction Benign causes

Post-traumatic stricture Pancreas divisum Malignant causes Pancreatic head carcinoma Intraductal papillary mucinous tumour (IPMT) Impaired pancreatic stimulation

Truncal vagotomy Total gastrectomy Table 4

delivery of pancreatico-biliary secretions to the nutrients entering

the small intestine from the stomach Such operations are

char-acterized by disconnection of the stomach from the duodenum

The main operative examples are Kausch-Whipple’s operations,

Bilroth II gastrectomy and operations involving Roux-en-Y

reconstructions Meal-stimulated pancreatico-biliary secretions

must travel down an intestinal limb to ‘catch up’ with chyme

somewhere in the mid-jejunum This leaves less time for the

digestive actions of the pancreatico-biliary secretions and

a shorter length of small intestine for absorption

Cystic fibrosis (CF): CF is a recessive genetic disorder

charac-terized by mutations in the cystic fibrosis transmembrane

conductance regulator gene (CFTR) This gene codes for an ion

channel responsible for the transport of chloride ions into the

secretions of glandular exocrine tissue In CF there is a defect in

chloride ion transport leading to viscous exocrine secretions

Thick inspissated pancreatic secretions gradually obstruct the

small pancreatic ductules producing chronic pancreatitis EPI

ultimately occurs in 85e90% of CF patients

Intestinal causes

Short bowel syndrome: short bowel syndrome (SBS) occurs

when there is insufficient functioning bowel to meet an

indi-vidual’s needs for macronutrients, salt and water from an

ordi-nary diet, without artificial supplementation This usually occurs

when less than 200 cm of functioning bowel remains The most

common cause of SBS is Crohn’s disease Other causes include

vascular insufficiency, malignancy and radiation enteropathy.6

In health, more than 90% of absorption occurs in the jejunum

Following jejunal resection there is an immediate reduction in

absorption; however the ileum rapidly adapts and compensates

for the loss of jejunum There are, however, permanent changes

in enzyme secretion owing to the permanent loss of gut

hormones used for signalling This may also lead to rapid gastric

emptying

The ileum is normally responsible for reabsorbing the

majority of the 8e9 litres of secretions daily The most common

result of ileal resection is therefore diarrhoea, with loss of NaCl

and water Magnesium loss is also common Bile acid

malab-sorption may occur, leading to fat malabmalab-sorption and fat soluble

vitamin deficiency B12deficiency also results as this is absorbed

in the terminal ileum When the ileo-caecal valve is retained,

passage of ileal contents is slowed This also serves as a barrier to

reflux of colonic flora so preventing small intestinal bacterial

overgrowth, which may further worsen absorption.9

When the colon is in continuity, it is able to adapt to increase

water and electrolyte absorption Furthermore, it can absorb up

to 500 kcal per day by taking up short chain fatty acids resulting

from the bacterial fermentation of undigested carbohydrate

Following massive resection the small and large bowel start

to adapt almost immediately In the acute phase, there are

often life-threatening electrolyte and fluid balance

abnormali-ties owing to high stoma output.10Calorie absorption is limited

and parenteral or enteral nutritional support is required

Adaptation continues for up to 2 years, including enterocyte

hyperplasia, increased crypt depth, increased intestinal length

and diameter, all of which serve to increase surface area and

absorption

Coeliac disease: coeliac disease is a chronic autoimmunecondition, which, in genetically susceptible individuals, is trig-gered by dietary gluten found in wheat, barley and rye products.There is a wide spectrum of disease, from clinically silent tosevere malabsorption, which may occasionally be refractory totreatment There may be significant morbidity associated withthe disease, due to anaemia and osteoporosis Small intestinaladenocarcinoma and lymphomas are rare complications There isalso a significant association with other immune-mediateddiseases, including type 1 diabetes and thyroid disease Serumimmunoglobulin A (IgA)-class antibodies to tissue trans-glutaminase and endomysium are found in most patients and arehighly specific.11

There is a strong genetic contribution to the disease Almostall patients have HLA subtypes DQ2 or DQ8 Dietary glutenpeptides are deamidated by the enzyme tissue transglutaminaseand presented by HLA DQ2/DQ8 cells to pathogenic CD4þ Tcells These then release cytokines leading to a damaginginflammatory cascade and small bowel injury.12

These changes lead to distortion of the small bowel tecture, in particular villous atrophy, crypt proliferation, andincreased intraepithelial lymphocytes, which are the histolog-ical hallmarks of the disease Villous injury reduces the totalsmall bowel surface area for absorption, and impairedproduction of lactase and other enzymes further leads tomaldigestion

archi-Significant malabsorption of folic acid and iron are verycommon A large proportion of patients present with anaemia,and screening for coeliac disease with tissue transglutaminaseantibodies is essential in any patient with anaemia.13 Fatmalabsorption may occur leading to symptoms of steatorrhoeaand deficiencies in fat soluble vitamins

Crohn’s disease: Crohn’s disease is a chronic inflammatorybowel disease which may affect any part of the gastrointestinaltract Genetic susceptibility has an important role and theinteraction between gut microflora, mucosal permeability andhost immunity is thought to be central to the pathogenesis.Malnutrition is a significant problem in Crohn’s disease andthis is multifactorial, stemming from anorexia and increasedenergy expenditure, due to inflammation, in addition toreduced energy absorption due to maldigestion andmalabsorption.14

The pattern of malabsorption affecting Crohn’s patients willdepend largely on the site affected The small bowel is affected

in 70% of patients, leading to variable degrees of tion.15 In those with extensive small bowel involvement,

malabsorp-a picture similmalabsorp-ar to short bowel syndrome will ensue, withdeficiencies of both macro- and micronutrients, in addition towater and electrolyte abnormalities Bypass surgery or devel-opment of fistulae lead to malabsorption, depending on thesite affected Protein-energy malnutrition is a particularproblem with extensive small bowel disease, as carbohydrates,proteins and fats are absorbed mostly in the proximal 150 cm

of jejunum Specific micronutrients may be malabsorbed, inparticular B12and bile acids in terminal ileal disease Vitamin

D deficiency is common in Crohn’s disease leading to cant comorbidity in the form of bone disease and generalwellbeing

signifi-Those who have undergone surgery run into specific

prob-lems relating to the segment of bowel affected which in the most

severe case can lead to short bowel syndrome and intestinal

failure In patients with an ileostomy, the principal problems

relate to water and electrolyte balance, as the colon is not in

continuity Small intestinal bacterial overgrowth commonly

occurs in Crohn’s, in particular following ileo-caecal resection or

when there is enteroeentero, or entero-colonic fistulization

Small intestinal bacterial overgrowth (SIBO): SIBO is a common

but overlooked cause of chronic diarrhoea and malabsorption.16

The epithelial surfaces of the small bowel are not colonized in

health and there is usually less than 104organisms/ml in a small

bowel aspirate SIBO is generally diagnosed when there are more

than 105organisms/ml The prevention of colonization in health is

maintained through a combination of factors Low gastric pH,

small intestinal motility, an intact ileo-caecal valve,

immuno-globulins and defensins within small bowel secretions, and the

bacteriostatic properties of pancreatic secretions all play a role

When these natural defences are impaired, for instance in

achlorhydria (PPI use, atrophic gastritis) or in anatomical changes

(e.g post-surgical blind end loops), SIBO may arise.17

Malabsorption in SIBO is caused by a number of different

mechanisms Direct injury to brush border enterocytes impairs

disaccharidase production Small bowel bacteria can metabolize

vitamin B12, reducing availability for absorption Proteins may

also be broken down, reducing their availability, although

absor-bed metabolites may still provide calories Bacterial deconjugation

of bile acids leads to fat malabsorption and reduced fat soluble

vitamins Direct mucosal injury by bacteria and toxins can produce

inflammatory changes and villous atrophy

Specific nutrients: lactose is a disaccharide consisting of glucose

and galactose This is broken down at the brush border

membrane through the action of lactase Mucosal lactase

concentrations are highest at birth and are critical for the

absorption of energy from monosaccharides in milk Lactase

levels decrease following weaning during childhood in most

populations (lactase non-persistence) but do not change in 30%,

mostly of northern European ancestry (lactase persistence)

Lactase non-persistence and intolerance of dairy products is

consequently one of the commonest forms of malabsorption seen

in immigrant populations in the UK The undigested lactose

reaches the colon where it is metabolized by bacteria, producing

hydrogen, methane and short chain fatty acids These lead to

symptoms of bloating, cramping and diarrhoea.18

The congenital form of lactase deficiency affecting infants is

very rare Secondary lactase deficiency occurs in cases of

mucosal injury, for instance coeliac disease, giardiasis or

radia-tion enteropathy

Fructose is generally less well absorbed than glucose and

galactose Some people develop symptoms due to its

malab-sorption and diets low in fructose can then be beneficial.19

There are a number of rare congenital disorders of single

genes involved in digestion and absorption and these can cause

malabsorption in children

Bile acid malabsorption: bile acids (BA) circulate in the

enter-ohepatic circulation 4e6 times per day Secondary BA

malabsorption occurs when a resected or diseased segment ofterminal ileum reduces the proportion of reabsorbed BAs Thesethen pass into the colon where they produce water and electro-lyte secretion, leading to symptoms of cramping and diarrhoea.When the bile acid pool size is sufficiently depleted, emulsifica-tion of fat in the small bowel is reduced, leading to fat malab-sorption The SeHCAT test shows impaired BA retention.20

In primary BA malabsorption, recent research has suggested that

in the majority cases, diarrhoea is caused not by malabsorption but

by impaired negative feedback control of the synthesis of BAs,overwhelming the ability of the terminal ileum to reabsorb them.BAs then spill over into the colon, where they cause symptoms.21Infections: Giardia intestinalis is commonly associated withmalabsorption It can cause villous atrophy in the jejunum,leading to carbohydrate malabsorption, and ileal disease canimpair bile acid malabsorption, resulting in fat malabsorptionand steatorrhoea It may also predispose to SIBO Other protozoaassociated with malabsorption include Cryptosporidium parvum,Isospora belli, Cyclospora cayetanensis and Microsporidia species.Helminth infections such as Strongyloides stercoralis may lead

to malabsorption in the immunocompromised Steroid use andhuman T cell lymphotropic virus type 1 (HTLV1) are risk factors.Direct infiltration of jejunal and ileal mucosa is responsible forsymptoms.22

Tuberculosis commonly affects the gastrointestinal tract andsigns of malabsorption are apparent in most affected individuals.Patterns of malabsorption depend on the site involved Bile aciddeconjugation may lead to fat malabsorption and loss ofabsorptive surface of small bowel may lead to macro- andmicronutrient deficiencies Malabsorption may also result fromblocked lymphatics (lymphangiectasia)

Radiation enteropathy: gastrointestinal symptoms includingmalabsorption commonly occur following pelvic and abdominalradiotherapy Radiation damage can lead to a number of changes

in intestinal physiology which contribute to symptoms Motilitymay be affected, bile acid malabsorption results from terminal ilealenteritis, damage to brush border membrane enterocytes impairsdisaccharidase expression, and SIBO may occur Pancreaticinsufficiency from radiation injury will lead to maldigestion.23Drugs: a number of drugs impair aspects of absorption Forinstance, iron and tetracycline bind to each other and are thenpoorly absorbed Many laxatives increase stool volume and elec-trolyte loss Orlistat (Xenical) binds to the active site of lipase,impairing digestion and absorption of fat to assist weight loss Obesepatients treated with this who continue to consume large amounts

of fat develop intestinal symptoms including steatorrhoea.Bariatric surgery

Bariatric surgery sets out to induce some of the malabsorptivedefects described above, in order to induce weight loss inmorbidly obese patients Gastric bypass with Roux-en-Y anasto-mosis (Figure 1) is the most common bypass operation per-formed now.24There are two main components to this operation.The first is the creation of a small gastric pouch The second isthe disconnection of the small intestine, with the distal intestinallimb being brought up and anastomosed to the gastric pouch,

with the small intestine being reconnected in a Y configuration.

This surgery will lead to an asynchronous and delayed delivery

of pancreatico-biliary secretions to the intestinal chyme, resulting

in maldigestion and malabsorption Hormone secretion from the

distal intestine is also changed Patients who have undergone

bariatric surgery malabsorb significantly, and are at risk of

developing clinical significant deficiency of fat-soluble vitamins

and polyvalent cations, and experiencing steatorrhoea

Summary

There are many and diverse causes of malabsorption Treatment

depends on identifying the cause, and giving specific therapy

where possible Gluten-free diets for coeliac disease, pancreatic

enzyme supplements in EPI and antibiotics for SIBO are

exam-ples Detecting deficient nutrients and providing supplements

(B12, Fe, folate, fat-soluble vitamins etc.) is important

Preven-tion of the types of malabsorpPreven-tion complicating surgery is aided

by an understanding of the mechanisms involved A

REFERENCES

1 BAPEN Malnutrition universal screening tool (MUST) http://www.

bapen.org.uk/must_tool.html (accessed 31 January 2012).

2 Lewis SJ, Heaton KW Stool form scale as a useful guide to intestinal transit time Scand J Gastroenterol 1997; 32: 920 e4.

3 Johnson LR Gastrointestinal physiology 7th edn Mosby, 2006.

4 Barrett KE, Ghishan FK, Merchant JL, Said HM, Wood JD, Johnson LR Physiology of the gastrointestinal tract 4th edn San Diego: Academic Press, 2006.

5 McKelvey ST Gastric incontinence and post-vagotomy diarrhoea.

11 Green PH, Cellier C Celiac disease N Engl J Med 2007; 357: 1731 e43.

12 Troncone R, Jabri B Coeliac disease and gluten sensitivity J Intern Med 2011; 269: 582 e90.

13 Richey R, Howdle P, Shaw E, Stokes T Recognition and assessment of coeliac disease in children and adults: summary of NICE guidance.

16 Fan X, Sellin JH Review article: small intestinal bacterial overgrowth, bile acid malabsorption and gluten intolerance as possible causes of chronic watery diarrhoea Aliment Pharmacol Ther 2009; 29: 1069 e77.

17 Bures J, Cyrany J, Kohoutova D, et al Small intestinal bacterial overgrowth syndrome World J Gastroenterol 2010; 16:

2978 e90.

18 Lomer MC, Parkes GC, Sanderson JD Review article: lactose ance in clinical practice emyths and realities Aliment Pharmacol Ther 2008; 27: 93 e103.

intoler-19 Gibson PR, Newnham E, Barrett JS, Shepherd SJ, Muir JG Review article: fructose malabsorption and the bigger picture Aliment Pharmacol Ther 2007; 25: 349 e63.

20 Walters JR Defining primary bile acid diarrhea: making the diagnosis and recognizing the disorder Expert Rev Gastroenterol Hepatol 2010; 4: 561 e7.

21 Walters JRF, Tasleem AM, Omer OS, Brydon WG, Dew T, Le Roux CW.

A new mechanism for bile acid diarrhea: defective feedback inhibition of bile acid biosynthesis Clin Gastroenterol Hepatol 2009; 7: 1189 e94.

22 Ramakrishna BS, Venkataraman S, Mukhopadhya A Tropical sorption Postgrad Med J 2006; 82: 779 e87.

malab-23 Andreyev HJ, Davidson SE, Gillespie C, Allum WH, Swarbrick E Practice guidance on the management of acute and chronic gastro- intestinal problems arising as a result of treatment for cancer Gut 2012; 61: 179 e92.

24 Buchwald H, Cowan GSM, Pories WJ Surgical management of obesity Saunders Elsevier, 2007.

Liver

Small gastric pouchanastomosed tosmall intestine Disconnectedstomach

Post-prandrialnutrients passing through smallintestine

Bariatric gastric Roux-en-Y bypass

Figure 1 Luminal nutrients (blue arrow) passing down the small intestine

after a meal Meal-stimulated release of pancreatico-biliary secretions

(green arrow) has to pass down the long intestinal limb (usually 40 e60

cm) before it ‘catches up’ with the ingested nutrients at the junction of the

Roux-en-Y anastomosis This leads to a degree of maldigestion and

subsequent malabsorption and abnormal hormone secretion from the

distal gut.

This article discusses the safe exposure of intra-abdominal organs using

laparoscopy and laparotomy Newer methods of minimal access surgery

including single incision laparoscopic surgery (SILS), and natural orifice

transluminal endoscopic surgery (NOTES) are also discussed Common

abdominal incisions are illustrated.

Keywords Laparoscopy; laparotomy; natural orifice transluminal

endoscopic surgery; single incision laparoscopic surgery

Introduction

The word laparotomy has Greek roots, ‘lapara’ referring to ‘the

soft parts of the body between the costal margin and hips’ and

‘tome’ meaning ‘cutting’ The first successful elective laparotomy

is attributed to Ephraim McDowell, in 1809 in Kentucky, USA

Through a nine-inch left lower abdominal incision he removed

a large ovarian cyst in a 46-year-old lady on his kitchen tablee

without anaesthetic! The lady recovered and lived to the ripe age

of 78 years The first laparoscopy in a human was credited to

Hans Christian Jacobaeus of Sweden in 1910 In 1981, a German

gynaecologist Kurt Semm published on the first laparoscopic

appendicectomy and Phillipe Mouret is credited as performing

the first laparoscopic cholecystectomy in France in 1987

Mini-mally invasive laparoscopic methods are now routinely used in

many branches of surgery

Considerations of surgical method

Preparation in the operating theatre

The abdomen of the anaesthetized patient should be examined as

further information regarding intra-abdominal pathology may be

elicited when the musculature of the abdominal wall is relaxed,influencing the surgical approach Common abdominal incisionsare shown inFigure 1

PositioningThe patient is positioned to allow optimal access to the area ofinterest This is most often supine, however for surgery involvingthe pelvis or perineum, the Lloyd-Davies or lithotomy (‘legs up’)positions provide better access In the latter, so named from theGreek to ‘cut for the stone’, the patient is supine with thebuttocks placed at the lower break in the table and the legs flexed

at the hips and knees, with sufficient abduction to allow access tothe perineum The lower legs are placed in attachable pneumaticsupports or hanging stirrups In the Lloyd-Davies position, oftenused in colorectal surgery, the legs are abducted with slightflexion of the knees and hips Supports are now usually a cush-ioned boot design to reduce pressure, especially on the popliteal

Name of Incision Commonly used for

A Palmer’s point Insertion of Veress needle

B Kocher’s Open cholecystectomy

C Rooftop Liver surgery

D ‘Mercedes Benz’ Liver transplantation

E Midline Can be upper, lower – many abdominal operations

F Paramedian Now less commonly used for laparotomy

G Transverse Closure of stomas

H Gridiron Open appendicectomy

I Lanz Open appendicectomy

J Rutherford Morrison Renal transplant

(either on left or right side of abdomen)

K Pfannenstiel Gynaecological, laparoscopic colectomy

D

K

B C

Cara Baker MRCS PhD is a Surgical Registrar in the Southwest Thames

Deanery, UK Conflicts of interest: none declared.

Ralph Smith MRCS is a Research Registrar at the Royal Surrey County

Hospital, Guildford, UK Conflicts of interest: none declared.

Sukhpal Singh MS FRCS (Gen) is a Consultant Oesophagogastric Surgeon

at Frimley Park Hospital and the Regional Oesophagogastric Unit, Royal

Surrey County Hospital, Guildford, UK Conflicts of interest: none

declared.

fossa and common peroneal nerve Prolonged placement in this

position increases the risk of deep venous thrombosis or

compartment syndrome and intermittent pneumatic compression

can be applied to reduce the former

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

Preoperative removal of hair

Hair should be removed preoperatively if necessary, ideally with

electric clippers Premature (before theatre), inappropriate or

unskilled hair removal may traumatize the skin and allow

colo-nization with potentially pathogenic microorganisms at the

surgical site

Cleaning

Surgical-site infection has been estimated to occur in up to 5e

15% of clean and 30% of contaminated surgery Skin is cleaned

with an antiseptic agent, usually povidone-iodine or

chlorhex-idine in either aqueous or alcoholic solution, progressing from

the incision site to the periphery A randomized control trial has

shown a significantly lower rate of surgical-site infection (41%

reduced risk) with chlorhexidine (2% in alcohol) compared to

aqueous povidone-iodine (10%).1

Areas of high microbiological 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 or open wounds 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 the skin and 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

imperme-able (disposimperme-able or non-disposimperme-able) Impermeimperme-able 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 drapes, with or without

iodine impregnation, through which the surgeon makes the

inci-sion are sometimes used, however a systematic review has shown

no evidence of reduced surgical-site infection and some evidence

of increased infection rates (relative risk 1.23, p ¼ 0.03).2

Laparoscopy

Laparoscopy provides a less traumatic access to all parts of the

abdominal cavity, superb views of anatomy, excellent cosmetic

result and an attenuated stress response to surgery

The pneumoperitoneum may be achieved via open (Hasson) or

closed (Veress needle, see below) methods The initial incision is

most commonly infra- or supra-umbilical, longitudinal or verse, depending on surgeon preference; the intended procedureand risk of conversion; surface anatomy; previous scars.Important adjuncts to optimizing access at laparoscopy arecatheterizing the bladder to allow better views of the pelvis, anddecompressing the stomach with a naso/orogastric tube.Closed method

trans-The closed method uses a spring-loaded Veress needle to flate the peritoneal cavity with carbon dioxide followed by blindintroduction of the first port The anterior abdominal wall is oftenelevated to provide countertraction, traditionally manually, moreusually with skin clips, or following dissection down to theumbilical cicatrix-linea alba junction and elevation with clips orsutures (Figure 2) The needle angulation should vary from 90

insuf-in overweight or obese to 45 in thin patients As the needletraverses the abdominal wall two clicks/points of resistanceshould be noted, the first passing through the linea alba and thesecond entering the peritoneal cavity Confirmation of the correctposition can be by several methods as well as the ‘double click’,these include:

Manometer test: the insufflator is connected with low flow Ifthe needle is in the correct place, the gas flows freely, initialintra-abdominal pressure is low and increases gradually with thevolume of gas insufflated If not correctly sited, the pressure ishigh and the flow should be halted and the needle replaced oranother entry method performed

Hanging drop test: a drop of saline is placed on the open end ofthe Veress needle and is sucked into the peritoneal cavity bynegative intra-abdominal pressure when the anterior abdominalwall is manually elevated

Aspiration test: a syringe with saline is attached to the Veressand instilled and aspirated: aspiration should not possible if theneedle is intraperitoneal, but saline may be aspirated if theneedle is placed extraperitoneally Bowel content or blood may

be aspirated if the needle is within an intra-abdominal viscus orvessel If blood or bowel contents are present, the needle should

be left in place and preparation made for a rapid laparotomy tocontrol and repair the injury

The first port is then introduced blindly (Figure 3) Mostcomplications of laparoscopy (Box 1) are related to blind inser-tion of the Veress needle or first port A recent review of 17randomized controlled trials containing 3040 patients concludedthere is no increase in major complications compared with theopen methods described below Extraperitoneal or failed insuf-flation was reportedly higher when using the Veress needle.Safety shields, retracting or optical trocars do not prevent injury,however the potential complications associated with blindinsertion of the Veress needle and primary port make the opentechnique the first-choice method for many surgeons

It is important to be aware of the proximity of the abdominalwall and the retroperitoneum, and in thin people this can be aslittle as 1e2cm The distal aorta and the origin of the rightcommon iliac artery can lie directly below the umbilicus and areparticularly vulnerable Fatalities can occur related to massivegas embolism or bleeding

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 (Figure 4) 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

balloon-tip port

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 an

incision made along its length The abdominal cavity is probedusing a clip (Figure 5) A gas leak is less likely with this method.The procedure may not be appropriate if a patient has hadmultiple previous operations because the abdomen is not enteredunder direct vision Under such circumstances, the pneumo-peritoneum may be created by placing the Veress needle in theright or left upper quadrant (Palmer’s point,Figure 1) and thefirst port introduced under direct vision using an optical trocar(e.g VisiportÔ, OptiviewÔ) (see below)

When inserting secondary trocars, this should be performedunder direct vision to avoid visceral injury In the pelvis, careshould be taken to avoid the bladder (reduced risk if cathe-terized) The most common minor vascular injury is to theinferior epigastric vessels, especially in hernia repairs, and theseshould be visualized if possible and avoided

Ports and trocars

A wide range of port and trocar designs have been developed(Figure 6) Each has their own specialist indications, advantages,

Figure 2 Veress needle insertion (a) Following incision just below the

umbilicus, the umbilicus is elevated with a towel clip and the stalk is

dissected and the junction with the linea alba defined (b) Insertion of the

Veress needle The needle is held halfway down the shaft with the tap

open The ring and little finger stabilize the needle as it is advanced

through the abdominal wall at the base of the umbilicus with abdominal

wall elevation as countertraction.

Figure 3 Insertion of the first trocar following induction of toneum with Veress needle ( Figure 2 ) The index finger prevents the trocar from being fully inserted.

pneumoperi-Complications of laparoscopy

Specific Immediate: extraperitoneal insufflation, injury to viscera or blood vessels, intra-abdominal, of the abdominal wall or retroperitoneum Early: pain in shoulder tip

Late: incisional (port site) hernia, metastases at port site General

Immediate: bradycardia, inadequate oxygenation secondary to diaphragmatic splinting by excessive peritoneal insufflation or extreme head-down position in an obese patient, reduced venous return, pneumothorax, pneumomediastinum, gas embolism

Early: deep vein thrombosis/pulmonary embolism, hypothermia, nausea and vomiting

Box 1

disadvantages and surgeon preference Trocars are usually

disposable, but reusable are available

Classification of trocars

Cutting: trocars with cutting blades e either a flat blade or

pyramidal-tipped to cut the tissue in either a single plane or three

planes, and generally are fitted with retractable shields

Non-cutting: basic designs include pointed conical trocars that

penetrate by separating tissue fibres along the paths of least

resistance and blunt conical trocars that dilate an expandable

sheath inserted over a Veress needle

Optical trocars, either with or without a blade, are composed of

a transparent distal shaft into which the 0 laparoscope is

inserted to visualize the tissue planes as the trocar goes through

the abdominal wall They are especially useful in obese patients

with a deep abdominal wall

Hand-assisted laparoscopic surgery

Hand-assisted laparoscopic surgery (HALS) is so-called because

the surgeon inserts a hand into the abdomen through a hand-port

device to assist with surgery while the pneumoperitoneum is

maintained This has been applied to many surgical procedures,

from colorectal resections to nephrectomy and aneurysm

surgery Hand-assistance has the advantage of allowing tactilefeedback, safe retraction, facilitates dissection, tumour assess-ment and anastomosis

Minimal access to the retroperitoneum or extraperitonealspace

Retroperitoneoscopy, with dissection of the retroperitoneal spacevia a balloon catheter, balloon trocar or finger dissection with

a hand-port, allows excellent access to the kidneys (e.g in donornephrectomy for renal transplantation), adrenal glands, bloodvessels, lymph nodes and the lumbar spine

Access to the extraperitoneal space for mesh repair of bilateral

or recurrent inguinal hernia is achieved via a subumbilicaltransverse incision, starting in the midline and extended 2 cmlaterally The anterior rectus sheath is dissected out, incised inthe line of the incision, and the rectus muscle retracted laterally

to reveal the posterior rectus sheath The extraperitoneal space isthen developed manually with the laparoscope or with a balloondissector

Single incision laparoscopic surgery (SILS)The introduction of multi-instrument access ports has enabledlaparoscopic surgery through a single incision, that is, SILS, alsoknown by a myriad of other acronyms including SPA (single portaccess), SAES (single access endoscopic surgery), OPUS (oneport umbilical surgery) and LESS (laparo-endoscopic single-sitesurgery) (Figure 7) Many procedures have now been per-formed by SILS and include appendicectomy, cholecystectomy,inguinal hernia repair, gastric banding and sleeve gastrectomy,colectomy and hysterectomy Potential benefits include reducedpostoperative pain, improved cosmesis and postoperativerecovery Difficulties associated with this technique includeloss of triangulation and clashing of instrumentation andconsiderable experience with standard laparoscopic surgery isrequired Curvilinear and angulated laparoscopic instruments arenow available that allow more intracorporeal triangulation andimprove surgical ergonomics

In development is magnetic anchoring and guidance system(MAGS) technology, whereby deployable intra-abdominalinstruments can be manoeuvred, for example to facilitateretraction or provide imaging, by an external handheld magnet.Natural orifice transluminal endoscopic surgery (NOTES)

NOTES is a term coined in 2005 to describe ‘scarless surgery’.Access to the peritoneal cavity is gained by a viscerotomythrough either stomach, oesophagus, vagina, rectum or bladder

An operating endoscope is inserted for peritoneoscopy and ible instruments used to perform the surgical procedure Diffi-culties relate to achieving adequate triangulation, retraction andthe quality of suitable endosurgical instrumentation There isalso still a major concern about the consequences of causing

flex-a perforflex-ation in flex-an otherwise normflex-al orgflex-an for flex-access flex-andsubsequently achieving a secure closure

A recent review of published NOTES in humans has described

432 operations, 90% of which were performed in a hybridfashion with laparoscopic assistance.3Cholecystectomy was themost common procedure with transvaginal access and closurethe most feasible technique for entry into the peritoneal cavity(inevitably precluding half the population) Other procedures

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

through the vertical incision.

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

artery clip.

described include appendicectomy, percutaneous endoscopic

gastrostomy (PEG) rescue, cystgastrostomy and

trans-oesophageal myotomies in achalasia At present NOTES is

considered an interesting and developing new technology that

has some way to go before being used in routine clinical practice

Laparotomy

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

extend-ing the incision

previous surgical history, scars and body habitus

potential placement of stomas

Classification of laparotomy incisions

Laparotomy wounds can be classified as:

vertical (midline or paramedian)

transverse, for example Pfannenstiel (commonly

gynaeco-logical or pelvic surgery)

oblique, for example Kocher’s subcostal incision (open

cholecystectomy)

complex, for example Chevron (rooftop), Mercedes Benz

(an inverted Y, e.g liver transplant)

Midline vertical incisions allow rapid access, with minimal blood

loss, and are easily extended Non-midline incisions can be

muscle splitting or cutting Paramedian incisions provide access

to more lateral structures and, in theory, are more secure as the

rectus can support the re-approximated anterior and posterior

sheath incisions However, they take longer, are associated with

more blood loss, and risk denervating or devascularizing the

muscle medial to the incision

Incisions placed more transversely in Langer’s lines offercomparable access to focused intra-abdominal structures asvertical incisions and can have fewer complications (pain,respiratory complications, dehiscence) as well as an excellentcosmetic result, but are more difficult to extend

The incision: diathermy or knife?

Traditionally, a knife has been used for the skin incision, butrecent data suggest that the diathermy blade allows the incision

to be done more quickly, with less blood loss, less postoperativepain and no adverse effects on wound healing or cosmetic effect

The incision: pointers and pitfallsMuch has been written on whether to incise around orthrough the umbilicus when carrying out a midline lapa-rotomy Either method is acceptable if appropriate care istaken, although incising around the umbilicus provides lessrisk of inadvertent damage to the hernia contents if anumbilical hernia is present

The easiest place to enter the peritoneum with a midlinelaparotomy wound (having incised skin, subcutaneous fat, andthe linea alba) is the umbilicus The peritoneum is graspedbetween two clips, elevated and incised, and the peritonealcontents fall away as air enters the abdominal cavity The inneraspect of the incision line is palpated to ensure that there are noadherent structures, and the incision completed

The falciform ligament will be encountered in midline incisionsthat 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 theperitoneal cavity lateral to the falciform ligament The peritonealcavity should be entered on the left of the falciform for surgery inthe left upper quadrant, and conversely for surgery in the rightupper quadrant Injury to the bladder must be avoided for midline

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

incisions that extend towards the symphysis pubis The potential

requirement and site for a stoma should also be considered

One must avoid inadvertent enterotomy when entering the

distended abdomen, or where there have been multiple previous

laparotomies For this latter group, it is preferable to extend the

incision onto the unscarred abdominal wall and enter the

peri-toneal cavity there because there is less risk of damaging

adherent bowel The incidence of inadvertent enterotomy during

reopening of the abdomen can be as high as 20% Patients with

inadvertent enterotomy during adhesiolysis are more at risk of

postoperative complications, relaparotomies, intensive care unit

admissions, use of parenteral nutrition and hospital stay

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 (Turner-Warwick)

fixed retractors (Thompson, Omnitract)

Strategies to control unwanted viscera from entering the tive field include systematic packing with swabs, or using

opera-a bowel bopera-ag, which opera-also limits loss of heopera-at opera-and fluid fromexternalized bowel Ceiling-mounted overhead lighting, which ismoved and focused on the operative field, is an essential adjunctfor optimizing access This may not be sufficient in certaincircumstances and headlights, or a light mounted on a retractor(e.g St Mark’s), may improve visualization deep into theabdomen or pelvis

Postoperative pain and wound healingThe complications of laparotomy are shown inBox 2 Obtainingadequate exposure must be balanced with minimizing post-operative pain The size and location of the incision is para-mount, but the strategy for relief of postoperative pain must beconsidered preoperatively and should be multimodal

Pharmacological methods include:

local anaesthetic blockade at time of surgery or by infusioncatheter postoperatively

spinal injection or epidural catheter

patient-controlled analgesia devices to deliver intravenousboluses of opiod

regular or as-required use of analgesics (World HealthOrganization analgesic ladder) including paracetamol, non-steroidal anti-inflammatory drugs, opioids

Non-pharmacological methods are also important includingexplanation, reassurance, education, emphasized in the context

of enhanced recovery or fast-track surgical pathways

Careful closure of wounds avoids the complications of wounddehiscence (see below), infection or incisional herniae System-atic review and metaanalysis have concluded that a continuousclosure technique is superior to interrupted and a non-absorbable(nylon) or slowly absorbable suture material such as number 1(PDS) monofilament suture should be used Traditionally, massclosure involves 1-cm bites of tissue, 1 cm apart, at least 1 cmfrom the wound edge (through all layers of the incision apartfrom the skin) Studies have shown that the most importantfactor is using a suture length to wound length ratio of 4:1(Jenkins’ rule)

Figure 7 Single incision laparoscopic surgery (SILS) ports and TriPort in

use (reproduced with permission from Covidien Autosuture and Olympus

KeyMed).

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 (myocardial infarction/arrhythmias) tory (basal atelectasis, pneumonia, deep vein thrombosis/ pulmonary embolism), renal failure

respira-Box 2

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 can be initially

recognized by a serosanguinous ooze arising from the wound

and, on further inspection, intra-abdominal contents (usually

small bowel) can be evident If not recognized, intestinal

evis-ceration or a ‘burst abdomen’ can occur In the latter, the

mortality rate is dramatically increased The management of

wound dehiscence involves:

intravenous access, resuscitation and analgesia/reassurance

covering the wound and exposed bowel with sterile

dressings

urgent return to theatre and resuturing of the wound under

general anaesthesia

Occasionally, abdominal wound closure is not possible, for

example after dehiscence or loss of abdominal wall volume by

necrotizing infection, as part of damage-control surgery or

management of abdominal compartment syndrome Strategies

for management include temporary abdominal closure methods

with a sterile plastic sheet, that is, ‘Bogota bag’ or incorporation

of absorbable or non-absorbable mesh

Alternatively, vacuum-assisted closure devices (VAC) have

been used to accelerate wound healing following superficial

abdominal wound dehiscence and laparostomy.4 An occlusive

low negative pressure continuous suction dressing is applied to

the abdominal wound to generate improved blood flow and

formation of granulation tissue Benefits include reduced

frequency and pain of dressing changes and accelerated wound

healing However there is the risk of promoting or delaying

healing of established entero-cutaneous fistulae

Abdominal wall disruption can be complete or incomplete,

early as above or late, in the form of incisional hernia

Predis-posing factors to incisional herniae include:

poor surgical technique

rapidly absorbable sutures

wound infection

conditions associated with impaired healing of wounds(e.g diabetes mellitus, corticosteroid therapy, malnutrition,morbid obesity, smoking, pulmonary disease, malignancy,age)

Good access is fundamental to successful surgery, but mizing access requires careful planning This is relativelystraightforward for elective surgery but, for emergencies, care-ful preoperative examination, patient positioning and anappropriately sited incision allows the operation to proceedsmoothly and successfully Increasingly, enhanced recoveryprogrammes are being used with laparoscopic and open surgery

opti-to reduce surgical stress and optimize patient recovery after

2007 Oct Issue 4 Art No.: CD006353.

3 Auyang ED, Samtos BF, Enter DH, Hungness ES, Soper NJ Natural orifice translumenal endoscopic surgery (NOTES): a technical review Surg Endosc 2011; 25: 3135 e48.

4 Stevens P Vacuum-assisted closure of laparostomy wounds: a critical review of the literature Int Wound J 2009 Aug; 6: 259 e66 FURTHER READING

Ahmad NZ, Ahmed A Metaanalysis of the effectiveness of surgical scalpel

or diathermy in making abdominal skin incisions Ann Surg 2011; 253:

8 e13.

Ellis H Cambridge illustrated history of surgery, Greenwich Medical Media;

2000 Cambridge University Press Santos BF, Hungness ES Natural orifice translumenal endoscopic surgery: progress in humans since white paper World J Gastroenterol 2011; 17:

1655 e65.

Wound dehiscence and

The prevention and treatment of wound dehiscence and incisional hernia is

a constant challenge to surgeons and other specialists operating in the

abdomen This paper discusses the risk factors and proposed mechanisms

of pathophysiology of wound dehiscence and incisional hernia, followed by

a discussion of the evidence regarding the best surgical technique of

inci-sion and closure of the abdomen in open surgery with focus on prevention

of dehiscence and hernia Lastly, the principles of management when faced

with wound dehiscence and incisional hernia are addressed along with the

treatment algorithm used at our institution The focus of this paper is on

median incisions and ventral median incisional hernia repair, being most

common and extensively studied in the literature.

Keywords Biologic graft; component separation technique; incisional

hernia; mesh; wound dehiscence

Definition

Abdominal wound dehiscence is defined as separation of the

abdominal fascia after surgery, complete or partial, without

complete cutaneous healing and with or without protrusion of

bowel contents outside the abdominal cavity An incisional

hernia is defined as any abdominal wall opening in the area of

a postoperative scar, with or without a bulge, evident by clinical

examination or imaging

Incidence

Wound dehiscence occurs in 0.4e1.2% of patients after elective

laparotomy, while rates up to 12% are observed after emergency

procedures The consistency of its prevalence over the past

century despite improved surgical technique is attributed to the

counterweight of an increasingly morbid population that

undergoes surgery nowadays The associated mortality rate ishigh, lying somewhere between 15 and 35% Wound dehiscenceshows a mean presentation around postoperative day 9.Incisional hernia occurs in 10e20% of patients after lapa-rotomy Repair of incisional hernia results in recurrence rates of23.5% for first time repairs and 34.8% for recurring hernias after

5 years follow-up.1Even beyond 5 years incisional hernias tend

to occur at a steady rate well up to 10 years after operation.2

DiagnosisThe diagnosis of wound dehiscence is based on clinical signs and

is not easy to make as it generally coincides with superficialtissue disruption and infection Blood-tinged peritoneal exudatemay seep through the intact superficial tissue layer Exaggeratedabdominal pain and tenderness, and unexplained vomiting arealso indicative of wound dehiscence Radiographic imaging may

be aptly performed to confirm suspicion

In contrast to wound dehiscence, the majority of incisionalhernias are asymptomatic However, a hernia may grow largerand become debilitating Patients may also experience poor body-image Incarceration and strangulation are potential complicationsnecessitating emergency surgery to prevent ischemia, necrosis,and ultimately perforation of the afflicted bowel Diagnosis ofincisional hernia can usually be made at physical examinationwhile the patient is standing, in which position the hernia oftenbecomes evident However, clinical diagnosis remains a challenge

in small asymptomatic hernias and in obese patients, resulting inmany missed diagnoses Computed tomography (CT) is consid-ered the gold standard and is very accurate in defining the defect,and providing information on the musculofascial quality and onviscera outside the abdominal cavity

Mechanisms and risk factors of wound dehiscence and incisionalhernia

Stages of wound healingFundamentally, the wound proceeds through three stages ofhealing, namely, the inflammatory stage, the regenerative (orproliferative) stage, and the remodelling (or maturation) stage.The inflammatory stage commences directly after thedisruption of tissue (e.g after incision) and generally lasts forabout four days Vasodilatation and angiogenesis take place, andproteinglycanes from mast cells form a gel matrix for deposition

of collagen later on (in the regenerative stage) Macrophagesare recruited and clear the environment of bacteria and debris,but most importantly recruit fibroblasts for the later stages Thepresence of polymorphonuclear leukocytes is of relevance for thesurgeon They accomplish phagocytosis of debris partly byproteinases, which essentially weaken the tensile strength of thetissue The area in which these proteolytic enzymes are activenormally varies up to 5 mm on either side of the wound, but thiscan increase up to 1 cm in the presence of infection

The regenerative stage (or proliferative stage) is characterized

by movement of fibroblasts into the wound area, synthesis ofcollagen and contraction of the wound, and lasts for about

3 weeks At the end of this stage, almost all new collagen hasbeen formed in the wound Tensile strength, albeit increasedrelatively quickly due to the newly formed collagen matrix, is still

Nicholas J Slater BSc is a Medical Intern and PhD Student at the

Radboud University Nijmegen Medical Centre, the Netherlands.

Conflicts of interest: none.

Robert P Bleichrodt MD PhD is Professor of Surgery at the Radboud

University Nijmegen Medical Centre, the Netherlands Conflicts of

interest: none.

Harry van Goor MD PHD FRCS is an Associate Professor of Surgery and

Surgical Education at the Radboud University Nijmegen Medical Centre,

the Netherlands Conflicts of interest: none.

not sufficient due to the lack of cross-linking between collagen

molecules

During the final and remodelling stage which may last for

years, the new collagen matrix undergoes qualitative changes

brought on by mechanical environmental forces, resulting in

optimal alignment of fibres to withstand these pressures

Cross-linking, in which inter-molecular covalent bonds are formed

within the collagen matrix, is responsible for the continued

increase in tensile strength

Malnutrition

Besides adequate intake of carbohydrates, protein, and fat, it has

been shown that vitamins A, B complex and C, the

micro-nutrients copper, zinc and iron, and certain essential amino acids

are involved in one or more stages of the wound healing cascade,

and deficiencies hereof can cause poor and delayed healing

Interestingly, creating an adequate preoperative nutritional state

is more important to successful wound-healing (and susceptible

to intervention) than the overall nutritional status of the patient,

and proper preoperative assessment is essential

Risk factors and mechanisms of wound dehiscence and

incisional hernia

It is a widely held concept that dehiscence is primarily a result of

erroneous surgical technique Indeed, during the first stage of

wound healing the laparotomy wound has practically no

strength, relying completely on the sutures to hold it together

Documentation of the mechanisms of wound dehiscence after

major abdominal surgery indicates most cases are caused by

tearing of sutures through the fascia, followed by infection,

broken suture, fascial necrosis, and loose knots.3 Factors

asso-ciated with surgical technique are discussed in the How to

sections

Patient-related risk factors for wound dehiscence are: age,

male gender, chronic pulmonary disease, coughing, ascites,

jaundice, anaemia, emergency surgery, wound infection, obesity,

steroid use, hypoalbuminaemia, hypertension, perioperative

shock, and type of surgery.4Vascular procedures and surgery of

the large bowel and oesophagus are associated with increased

risk of wound dehiscence, whereas surgery of the small bowel

and gallbladder/bile duct result in less wound dehiscence.3

The mechanism of incisional hernia recurrence is most often

infection, or inadequate fixation or overlap of prosthesis

Although incisional hernia mainly occurs in the remodelling

stage or even after healing has taken place, hernia formation may

be attributable to improper healing in the inflammatory and

regenerative stages Indeed, risk factors involved in wound

dehiscence are also related to incisional hernia, and wound

dehiscence is itself a strong predictor of incisional hernia.5

Specifically, patient-related factors associated with incisional

hernia development are mainly obesity, chronic lung disease,

wound infection and age Interestingly, recurrent hernia is a risk

factor for future incisional hernias, implying that these patients

suffer a common underlying dysfunction in wound-healing that

predisposes to hernia formation.2

Collagen metabolism and incisional hernia

There are many types of collagen, of which type I and type III are

important in incisional hernia Type I collagen is responsible for

strong tensile properties, whereas type III collagen is thinner and

more flexible, and is considered an immature variant in tive tissue, as it is expressed early on in the healing process laterreplaced by type I A decreased collagen type I/type III ratio results

connec-in altered arrangement and smaller diameter of collagen fibrils,and a decreased amount of cross-linking, overall reducing themechanical stability of the connective tissue A decreased type I/type III ratio has been observed in patients with incisional hernia,6suggesting a causative role for abnormal collagen metabolism.Inordinate extracellular matrix degradation is probablyinvolved in the derangement of the collagen ratios Importantenzymes in this collagenolytic process are matrix metal-loproteinases (MMPs) A decreased expression of at least oneMMP subtype has been linked to incisional hernia development.However, it remains unclear whether responses set in motiondue to hernia development cause deviant MMP expression, or if

a genetic predisposition for abnormal MMP expression itselfinduces the hernia formation Interestingly, different meshmaterials appear to induce varying degrees of fibroblast MMPexpression in patients with recurrent incisional hernia, allowingfor new possibilities in prosthetics development.7

Genetic disorders of connective tissue have also been linked toincisional or other types of hernia, including Ehlers-Danlos, Mar-fans syndrome, autosomal dominant polycystic kidney disease,osteogenesis imperfecta, and congenital dislocation of the hip.Similarly, increased incisional hernia rates in patients treated forabdominal aortic aneurysm are possibly related to an underlyingdisorder in collagen metabolism pathogenic for both ailments.These observations support an important biological role (genetic

or acquired) in the pathogenesis of incisional hernia

How to open the abdomenConsensus on the superior type of incision regarding early post-operative wound complications and development of incisionalhernia has remained elusive for a long time and subject ofdebate A recently updated Cochrane review of randomizedcontrolled trials comparing midline and transverse incisionsrevealed a trend of lower wound dehiscence and incisionalhernia rates associated with transverse incisions.4Even thoughpulmonary function was significantly less affected after a trans-verse incision, pulmonary complications did not differ betweenmidline and transverse incisions Analgesic requirements weresignificantly lower with transverse incisions, although thestudies involved displayed significant heterogeneity Data oncosmesis could not be pooled due to differences in assessmentcriteria, although the two studies that evaluated this aspect bothsuggested a significant preference for transverse incision Nodifferences were found with regard to recovery time (hospitalstay and time to return to work) and wound infection

Paramedian incisions were included in a systematic review byBurger et al.8Three randomized clinical trials compared lateralparamedian with midline incisions, with significantly increasedincisional hernia rates observed after the midline incisions Intwo other randomized trials the lateral paramedian was provensuperior to the medial paramedian technique concerning inci-sional hernia rates One randomized trial compared the medialparamedian with the transverse incision and found no statisticaldifference Also, no significant differences were found betweentechniques regarding wound dehiscence rates (Figure 1)

Intuitively, transverse incisions seem the most natural and

‘anatomic’, in which dissection through the aponeurotic fibres is

done in a parallel fashion, leaving the integrity of the contracting

apparatus relatively intact Still, midline incisions are preferred

while commencing emergency and exploratory procedures to

achieve quick and complete access to intra-abdominal organs

while allowing for easy extension of the incision Patients with

bowel disease that might necessitate repeated laparotomies are

preferably operated on using the midline incision

How to close the abdomen

Mass closure (all layers taken in each bite) of median laparotomies

has been advocated for a long time taking big bites However, new

developments suggest other techniques might be superior

Although not widely accepted, it has been argued that a suture

length (SL) to wound length (WL) ratio of at least 4 should be

used, as using a lower ratio increases incisional hernia formation

threefold In a comparative trial, using large stitches with a SL:WL

ratio of 4 or even well above yielded several risk factors for

infection, while the use of small bites with the same SL:WL ratios

revealed no such risk factors.9Experimental data show that small

bites (0.3e0.6 cm) and a small suture distance as opposed to big

bites (1.0 cm) with a big suture distance result in a stronger

wound strength.10 It is found that by stitching the aponeurosis

only, and avoiding sutures compression and cutting through

subcutaneous tissue, muscle, and peritoneum, there is less

sepa-ration of wound edges.11Layered closure (separate components

sutured separately) should be abandoned in any case, as it is

associated with longer operation time and an increased incidence

of wound dehiscence compared to mass closure

Regarding suture material, monofilament suture material ispreferred over multifilament suture in which bacteria can find

a niche between the braided material, adhere and grow Using

a continuous technique (vs interrupted) with slowly absorbable(vs rapid absorbable) suture material results in lower incisionalhernia rates

It is duly acknowledged that employing small bites throughthe aponeurosis seems to conflict with the knowledge that thevulnerable proteolytic area varies up to 0.5 cm from the woundedge under normal circumstances However, being able to applymore stitches this way, distributes the tension to a larger number

of stitches, thus reducing the tension on each stitch Also, the use

of thinner suture material (2-0) produces less inflammation andclosure of only the aponeurosis prevents tissue compression andthus minimises necrosis and proteolysis

Tissue adhesives have been introduced as an alternative tosutures for surgical wound closure, but generally take longer toapply and result in more wound dehiscence However, tissueadhesives may be safer and quicker in trocar port-site closureafter laparoscopy

There is current debate as to the safety and efficacy of placingprophylactic mesh at the initial operation to prevent future incisionalhernias in patients at risk (e.g the morbidly obese, open aorticaneurysm repair) This is currently being investigated in variousrandomized controlled trials The currently available evidencesuggests that prophylactic mesh prevents incisional hernias inpatients undergoing bariatric and open aortic aneurysm surgery.However, caution is needed concerning infectious complicationsthat may arise after mesh implantation necessitating subsequentmesh excision and risking the development of an incisional hernia

How to treat wound dehiscenceWound dehiscence needs an urgent patient-tailored managementplan If the wound dehisced secondarily to improper surgicaltechnique (e.g loose knots) the patient is brought straight back tothe operating theatre to resuture the wound In the majority ofcases, however, there are more severe underlying problems thatfirst need attention such as deep wound or intra-abdominalinfection and necrosis of the fascia If there is evisceration ofabdominal contents, they need to be checked for injury andreplaced in the abdomen Infection and necrosis of the fascialedges necessitate liberal debridement of afflicted tissue untilhealthy well-perfused fascia is encountered If possible, primaryclosure entails using the same technique as normal wound closureafter laparotomy Retention sutures are not recommended as theymainly result in inconvenience, pain and complications, and donot prevent incisional hernia Many surgeons prefer to leave theskin open in infectious circumstances to prevent wound abscessalthough evidence for this approach is lacking

Another cause of wound dehiscence is distended bowel withvisceral oedema, in which case ‘tension-free’ closure might not

be possible A delayed presentation of fascial dehiscence mayhave caused lateral retraction of the abdominal wall musclesfurther jeopardizing medial fascial advancement Before closureone has to check for an anastomotic leak as the cause ofabdominal infection and prolonged ileus If there is inability toclose the abdomen, the principles of incisional hernia repairshould be applied (see below)

Figure 1 Overview of common types of incision, represented by dashed

lines (a) Median incision (b) Paramedian incision (c) Lateral paramedian

incision (d) Transverse incision.

There are several techniques of temporary closure available

aiming at delayed closure or bridging the period to secondary

abdominal wall repair Negative pressure pumps or packs keep

pressure on the fascial edges and collect fluid which aid in

resolving oedema An artificial burr (Velcro patches), plastic silo,

prosthetic mesh (absorbable or non-absorbable) or a zipper can

be placed to maintain tension on the fascial edges and allow

for stepwise reapproximation Loose packing or skin

approxi-mation can also be applied but do not prevent retraction of

the fascia

How to treat incisional hernia

Except for very small defects (<3 cm, small trocar hernias),

direct suture repair of incisional hernias results in unacceptably

high recurrence rates There are two main categories of ventral

median incisional hernia repair; prosthetic mesh repair and

autologous tissue repair using the components separation

technique

Mesh repair: the use of synthetic mesh prostheses has become

the mainstay of treatment for incisional hernia repair showing

good short- and long-term results.2

There are various approaches depending on the anatomic

position of the prosthesis (Figure 2) Onlay placement requires

extensive undermining of subcutaneous tissue predisposing for

seroma and haematoma formation, while disrupted skin

perfora-tors may impair healing Also, given its anatomic position,

intra-abdominal forces may cause lateral distraction of the prosthesis

Conversely, underlay techniques should benefit from these forces

which may help keep the graft in place In contrast to onlay

positioning, prostheses positioned in an inlay or intraperitoneal

underlay fashion will more easily come in contact with viscera

potentially causing adhesions, erosion and fistulization

When using the prosthesis as a reinforcement of fascial

closure (onlay and underlay techniques), an overlap of at least 5

cm must be applied to provide sufficient anchorage while taking

mesh shrinkage into consideration Sutures are placed around

the periphery of the mesh 1e1.5 cm apart When this is not

possible for example in the case of a lumbar hernia, the

pros-thesis can inferiorly be fixated to bone-anchors placed on the

iliac crest

Unfortunately, there is no conclusive evidence pertaining to

the best anatomic position of the prosthesis However, when the

growing body of evidence of non-comparative studies is taken

into account, it seems that the underlay and sublay techniques

yield the most promising results, while inlay positioning of the

prosthesis has the highest recurrence rates.12

Most prostheses are made from either polypropylene,

expanded polytetrafluorethylene (e-PTFE), or polyester Main

differences are the material pore size, pliability, suppleness,

weight and thickness A large pore size allows for tissue in-growth

and adherence to surrounding structures, a property that is

desirable for the meshefascia interface, but disadvantageous

where mesh comes in contact with viscera For this reason

composite prostheses have been developed including a large pore

size (i.e polypropylene) on the side facing the fascia, with mesh of

smaller pore size on the visceral side (e-PTFE) It is suggested that

there are significant differences in the extent of mesh shrinkage

between the various prostheses, complications which may lead to

recurrence and pain However, experimental studies show greatinconsistencies with mesh shrinkage in the ranges 3.6e25.4% forpolypropylene, 4.0e51.0% for e-PTFE and 6.1e33.6% for poly-ester mesh,13and do not seem to translate very well to results inhumans Light-weight meshes in comparison to heavy-weightmeshes may reduce the ‘stiff abdomen feeling’ and chronic pain.Other developments are meshes coated with anti-adhesive barriers

at the visceral side preventing adhesion formation to the mesh,gentamicin-supplemented mesh aimed at improved tissue inte-gration and fibroblast growth-factor treatment aimed at strongerscar formation

Recently, biologic grafts have been developed consisting ofacellular collagen matrices processed from human or animaltissues They are supposedly degraded and replaced by nativefibro-collagenous tissue resembling the original tissue (fascia).Due to their bio-compatibility they hold potential for amelio-rating problems found with synthetic prostheses, notably infec-tion necessitating explantation This makes them a seemingly

Figure 2 Schematic drawings of the anatomic positions of mesh ment in incisional hernia repair Arrows indicate direction of dissection (a) Onlay mesh is placed subcutaneously and fixed onto the fascia of the anterior rectus sheath (b) Inlay mesh is placed within the defect as

place-a bridge between the two rectus muscles (c) Pre-peritoneplace-al underlplace-ay mesh is placed dorsal to the rectus muscle and anterior to the posterior rectus sheath (d) Intraperitoneal mesh is placed intra-abdominally onto the peritoneum.

attractive alternative to synthetic mesh when operating in

a contaminated or infectious wound environment Biologic grafts

are optionally cross-linked during processing, in which

addi-tional bonds are formed between the matrix polymers This

provides extra strength, preventing a too rapid graft degradation

that might weaken the repair, but potentially decreases their

bio-compatibility Biologic grafts are expensive, and proof of their

usefulness in incisional hernia repair remains unclear

Well-designed clinical trials are needed to properly delineate

the superior surgical technique and materials in different surgical

scenarios

Laparoscopic repair: laparoscopic repair of (uncomplicated)

incisional hernia is gaining popularity with potential benefits of

less pain, less infection and earlier recovery Potential

draw-back is the persistence of the hernia sac and the intraperitoneal

position of the mesh in contact with viscera Laparoscopic

technique employs an intraperitoneal mesh repair and is

a bridging technique by definition not approximating the rectus

muscles and not restoring abdominal wall contour Briefly, after

adhesiolysis and reduction of the hernia sac content, mesh is

placed and inspected of 5 cm overlap Tacks are placed 1e1.5

cm apart along the border of the prosthesis at 0.5 cm from the

edge Alternatively or in addition, sutures are placed in

a transfascial fashion for fixation Available evidence suggests

no superiority between the two fixation techniques concerning

recurrence rates, but infection rate increases with the use of

transfascial sutures A recent development is to glue the mesh

to the peritoneal layer avoiding pain associated with tacks and

sutures, but preliminary data on mesh fixation and recurrence

are equivocal

There is debate whether laparoscopic or open repair is the

superior method of repair Adequate comparison is hampered

by the differences in indication for open and laparoscopic

hernia repair with a predominance of relatively simple cases in

laparoscopic series A recent Cochrane review of randomized

trials revealed no significant difference in recurrence rate

between open and laparoscopic repair of incisional hernia.14

Duration of surgery, enterotomies, seroma and haematoma

formation, infection requiring mesh removal, patient

satisfac-tion, pain, and quality of life were also not significantly

different between groups However, the infection rate was

significantly lower after laparoscopic repairs Costs were

significantly higher with laparoscopic repairs Most trials

registered a significant advantage for laparoscopic repair

regarding length of stay The authors concluded that short-term

results of laparoscopic repair are promising, but that a longer

follow-up is needed.14 By minimizing peritoneal trauma and

postoperative inflammation, laparoscopic surgery may result in

less adhesion formation than with open abdominal surgery

As yet laparoscopic ventral hernia repair has not been linked to

a reduction of adhesive small bowel obstruction A major

concern with the use of laparoscopy is inadvertent enterotomy

This complication occurs in less than 2% of laparoscopic

repairs of incisional and ventral hernias, but when present it

increases mortality from 0.05% to 1.7%, and even to 7.7% if

unrecognized during surgery (18% of cases) Considering the

rareness of this complication, large trials are needed for valid

risk assessment of open and laparoscopic repair

Component separation technique

In the more complex incisional hernias, the use of prostheticmaterial is often contraindicated Complex hernias have not beenproperly defined, but include repairs combined with enter-ocutaneous fistula, multiple recurrent hernias, previous orcurrent wound infection, very large defects and defects followingtrauma or tumour resection resulting in significant loss ofdomain An alternative in these situations is the componentseparation technique (CST)

The CST was popularized by Ramirez et al in 1990 and is

a technique using transposition of autologous tissue in a way the

Figure 3 Schematic illustrations of the component separation technique Arrows and dashes represent direction of dissection (a) Dissection of subcutaneous fat from the anterior rectus sheath and the aponeurosis of the external oblique muscle (b) Longitudinal release of the aponeurosis

of the external oblique muscle just lateral to the rectus abdominis muscle, and separation of the internal and external oblique muscles up to the midaxillary line (c) Mobilization of the posterior rectus sheath for addi- tional medial advancement of the rectus abdominis muscle.