1

TUTORIALS FOR FOURTH YEAR STUDENTS OF SURGERY

DIVISION OF SURGERY FACULTY OF MEDICAL AND HEALTH SCIENCES UNIVERSITY OF AUCKLAND

Andrew G Hill Associate Professor of Surgery

PREFACE

The aim of Tutorials for fourth year Students of Surgery is to provide a core of material that needs to be known by our students by the end of their first general surgical attachment. These tutorials are simply an introduction to general surgery that are designed to make clinical work more meaningful and discussion with teachers more substantial. They are not an alternative to standard accounts in textbooks but are designed to give an overview and perspective which is complimentary to the more comprehensive descriptions contained in them. Indeed, it is anticipated that the student will read these tutorials alongside the prescribed text book fleshing out the material contained here and producing a more personal text for him or her self.

Throughout the text we point out where further knowledge is required by the end of fifth year. We indicate the pages in the book, edited by Tjandra, Clunie and Thomas, where this information may be found.

Andrew G Hill

CONTENTS
Tutorial 1 Preparing the Patient for Surgery Andrew Connolly

Page

Tutorial 2

Perioperative care Jonathan Koea

15

Tutorial 3

Metabolic Care of the Surgical Patient Stephen Streat

25

Tutorial 4

The Acute Abdomen Mike Hulme-Moir and Andrew G Hill

44

Tutorial 5

Obstructive Jaundice John Windsor

55

Tutorial 6

Upper Gastrointestinal Symptoms Iain Martin

65

Tutorial 7

Bleeding from the Anus, Rectum and Colon Bryan Parry and Andrew G Hill

79

Tutorial 8

Swellings of the Thyroid Gland (Goitre) and other Swellings of the Head and Neck Richard Harman

89

Tutorial 9

Carcinoma of the Breast and other Breast Disorders Wayne Jones

96

Tutorial 10

Hernias of the groin and abdominal wall Garth Poole and Andrew G Hill

112

Tutorial 11

Trauma Ian Civil

118

Tutorial 12

Peripheral Arterial Disease Andrew A Hill

125

Tutorial 13

Diseases of the Venous System Peter Vann

135

Tutorial 14

Common Skin Malignancies Pat Alley

143

Tutorial 15

Surgical Endoscopy David Theobald

148

Tutorial 16

Paediatric Surgery Erik Heineman and James Hamill

156

Tutorial 17

Transplantation John McCall

169

CONTRIBUTORS

Clinical Associate Professor Pat Alley, MBChB, FRACS Department of Surgery, North Shore Hospital Mr Ian Civil, MBChB, FRACS, FACS, MBE Department of Trauma Surgery, Auckland City Hospital Mr Andrew Connolly, MBChB, FRACS Clinical Director, Department of General Surgery, Middlemore Hospital Mr James Hamill, MBChB, FRACS Department of Paediatric Surgery, Starship Childrens Hospital Mr Richard Harman, MBChB, FRACS Department of Surgery, North Shore Hospital Professor Erik Heineman, MD, PhD, FRACS Professor of Paediatric Surgery, University of Maastricht, Holland Mr Andrew A Hill, MBChB, FRACS Department of Vascular Surgery, Auckland City Hospital Associate Professor Andrew G Hill, MD, FRACS Department of Surgery, Middlemore Hospital Mr Mike Hulme-Moir, MBChB, FRACS Department of Surgery, North Shore Hospital Mr Wayne Jones, MBChB, FRACS Clinical Director, Department of General Surgery, Auckland City Hospital Clinical Associate Professor Jonathan Koea, MD, FRACS Department of Surgery, Auckland City Hospital Clinical Associate Professor John McCall, MD, FRACS Professor of Surgery, Department of Surgery, Auckland City Hospital

7 Professor Iain Martin, M.Ed, MD, FRACS, FRCS Dean Faculty of Medicine and Health Sciences, University of Auckland Professor Bryan Parry, MD, FRCSEd, FRACS Professor of Surgery, Department of Surgery, Auckland City Hospital Mr Garth Poole, MBChB, FRACS Department of Surgery, Middlemore Hospital Dr Stephen Streat, MBChB, FRACP Department of Critical Care Medicine, Auckland City Hospital Mr David Theobald, MBBS, FRCS, FRACS Department of Surgery, North Shore Hospital Mr Peter Vanniasingham, MBBS, FRACS, FRCS Department of Surgery, Middlemore Hospital Professor John Windsor, MD, FRACS, FACS Head University Department of Surgery, Auckland City Hospital

Tutorial 1

Preparing the Patient for Surgery

Andrew Connolly and Andrew G Hill

There are few life events more important to a patient than a major operation. The surgeons first contact with the patient is crucial both to begin reaching a diagnosis and treatment plan and also to establishing trust and rapport with the patient. The surgeon will reassure the patient that help is available. The junior medical staff (including the student) will build upon this trust in their interactions with the patient. The patient must be involved in the care process and while the surgeon will guide and recommend certain courses of action to the patient, the patient ultimately must reach an informed decision regarding a management plan. Thus the first interaction with the patient lays the ground for establishing informed consent. There are data to suggest that a properly informed and counselled patient requires less postoperative pain relief and spends less time in hospital. In all of this, the surgeon-general practitioner interaction is of vital importance. Both before and after an operation, the lions share of the overall care of the patient rests with the GP. This is why communication between the GP and the surgeon is vital both before and after surgery. PRE-OPERATIVE EVALUATION Patients referred by their GP for a surgical consultation in the outpatient clinic will usually be placed on the Elective waiting list if they require surgery. The booking system is based on the concept of booking a patient for surgery at the time of specialist assessment, much as we book an airline ticket or make a hotel reservation. Clinical Priority Access Criteria (CPAC) are used to generate a score on which a given patient is prioritised. Those patients with an urgent or emergency surgical condition will be urgently referred as Acute surgical patients. The pre-operative evaluation will vary

9 between these two types of patients in some respects, however a thorough history and complete examination is common to both types of admission. The junior medical staff will often first meet the elective surgical patient at the preadmission clinic. The patient usually attends this one to two weeks prior to the date of surgery. The pre-admission clinic is designed to identify any specific issues that may need addressing to ensure a smooth and safe surgical admission. The patient will have a thorough history taken and a thorough examination performed along with appropriate blood tests, radiology and so forth. In this way, organic, physiological, biochemical, psychological, or social issues can be evaluated and potential difficulties identified and managed. The history not only covers the presenting surgical complaint, but also specifically seeks information on respiratory disease and smoking, cardiac and vascular disease including deep vein thrombosis and hypertension, and other conditions such as bleeding disorders and diabetes. All current medications and drug allergies must be noted along with previous surgical and anaesthetic experiences. The physical examination must be a complete one evaluating all systems. The value of this is both to detect abnormalities pre-operatively, and to record the physical state of the patient for future reference if a post-operative concern arises. Some patients can be immediately identified as being at increased risk of complications following a major operation and steps can be taken to minimise the impact of these adverse factors. Such patients include: Elderly patients: Patients over the age of 70 years have an increased risk, because of comorbidity, of major complications and death following surgery. Physiological adaptation is impaired in the elderly. They respond less well to blood loss, fluid shifts, drugs, sepsis, and anorexia. Obese patients: All operations tend to be more difficult if the patient is obese. Risks of wound, respiratory and thrombotic complications are increased. Malnourished & Hypoalbuminaemic patients: Those patients who have lost over 15% of body weight are at risk of increased post-operative complications but only if there is an associated impairment of physiological performance such as muscle function. These patients may benefit from a 5-7 day period of nutritional therapy pre-operatively. A pre-

10 operative serum albumin <30g/l is a marker of increased risk of post-operative complications. It is often caused by occult sepsis (not malnutrition) and must be brought to the surgeons attention. Surgeons often will try to identify and correct the underlying cause of the low albumin prior to any major surgery. Diabetic patients: These pose special problems especially with the risk of hypoglycaemia during surgery. Each hospital will have protocols for the management of diabetic

patients undergoing surgery. These will frequently involve the use of insulin and dextrose infusions. Particular care with blood glucose and electrolyte monitoring is necessary when a diabetic patient is nil by mouth. Diabetic patients are at increased risk of other complications. These include wound infection, poor wound healing, and pressure area development. Routine investigations include a full blood count and electrolytes, plus a blood grouping and antibody screen. Most hospitals will have specific guidelines as to when a crossmatch is required, but in broad terms, a blood grouping is sufficient if the antibody screen is negative. More detailed biochemical tests will be indicated for patients with specific illnesses or for patients undergoing specific procedures. For example, liver function tests (including coagulation tests) should be performed in all patients undergoing biliary or hepatic surgery. Patients with a history of smoking, cardiac, or respiratory disease or with physical signs of such disease require a chest x-ray. An electrocardiogram should be carried out in all patients over 50 years of age and in anyone with known or suspected cardiac or vascular disease. More specific tests will be indicated in certain circumstances. For example, pulmonary function tests and blood gas analysis may be required in cases of severe cardiorespiratory disease. The physical status of the patient is usually summed up according to the American society of Anaesthesiologists (ASA) classification in which the patients risk status is described on a 5 point scale. The patient may require advice regarding the medications they take. In most instances, cardiac, blood pressure, and respiratory medications are not stopped pre-operatively. Depending on the proposed operation, anti-coagulant drugs including aspirin will need to be either stopped or adjusted. However, it is vital to note that some patients must not stop

11 these types of drugs so attention to this issue must be made on a case-by-case basis. Specific problems such as English language difficulties must be noted. If an interpreter is needed, it is important to ensure one is booked to be with the patient at the hospital at the time of admission and surgery. Discharge planning begins at the pre-admission clinic. If physical or social issues are identified that will delay discharge post-operatively, these should begin to be addressed at the pre-admission clinic by involving the appropriate ancillary staff such as occupational therapists and social workers. The junior medical officers role does not stop with the completion of the history and examination and the writing of notes. If any areas of concern have been raised during the history and examination, further action is necessary. This may involve seeking advice from the surgeon, discussing the patient with an anaesthetist, or involving other specialist groups. For example, if a heart murmur is detected, the anaesthetist may well require an echocardiogram or cardiology review before surgery. Any blood, laboratory, or radiology tests that have been requested must be followed up prior to the admission of the patient in order to check for potential problems. It is important for all members of the surgical team to appreciate that failure to thoroughly complete the pre-admission process may result either in the cancellation or delay of the patients surgery, or in a complication to the patient. In broad terms, acute surgical patients require much the same assessment as elective patients, but the ability to obtain non-routine investigations may be lost due to the pressing nature of the surgical illness. Obviously the ability to correct co-existing problems may not exist to the same extent that it does in elective patients, but the need to be thorough and check all investigations remains. PRE-OPERATIVE PREPARATION FOLLOWING ADMISSION There are a number of important tasks to be undertaken in the 24 hours preceding an elective operating list. The surgeon will determine the order of patients on the operating

12 list. The junior medical staff must submit the operating list and contact the anaesthetic consultant assigned to the list. This is both a courtesy and a safe clinical practice as the anaesthetist may raise specific issues that have not been addressed before. Other tasks include: Drugs: The surgical staff must ensure the drug chart is accurate including those medications the patient is to take pre-operatively. Deep Venous Thrombosis (DVT) prophylaxis: Many surgical patients are at increased risk of DVT and therefore at increased risk of a pulmonary embolism (PE). Risk factors include increasing age, smoking, past history of DVT/PE, malignancy, obesity, malnutrition, immobility, varicose veins, cardiac disease, oral contraceptive medication, polycythemia, and the nature and extent of the operation. Identification of at-risk patients therefore allows for preventative measures to be instituted. It is important to note that DVT formation often occurs prior to the operation beginning. The commonest prophylactic measures used are compression stockings and lowmolecular weight heparin administration. The stockings should be worn throughout the hospital stay until the patient is fully mobile. The timing of heparin administration is controversial. If the anaesthetist is contemplating an epidural either for anaesthesia or post-operative analgesia, it is imperative that the anaesthetist is involved in any discussion regarding heparin administration prior to the drug being administered. This is because of concern regarding spinal haematoma formation in those who have received heparin products up to 12 hours prior to epidural insertion. Checking the Consent form: Both the patient and the doctor obtaining the consent must sign the consent form. Often the consent form is completed at the pre-admission clinic. It is important that the consent is informed. In other words, the doctor obtaining the consent must be able to discuss the procedure, the benefits, and the risks with the patient. Ideally, the operating surgeon obtains the consent, but this may be appropriately delegated depending on the experience of the junior staff, the type of procedure planned,

13 and the nature of the prior discussions between the surgeon and the patient. Marking of the surgical site: Each hospital will have a policy on marking of surgical patients, but in broad terms it must be obvious to all the theatre staff both what the operation is and where it is to be performed. An example is an arrow to the correct leg in a patient undergoing a hip replacement. It is important to note that the mark needs to be indelible and must not be across the line of an incision as this could potentially lead to the tattooing of the skin. Bowel preparation: Patients undergoing large bowel or rectal resection will often require gut lavage with an oral preparation. This is given the day prior to surgery. Older patients may experience some degree of dehydration depending on the type of lavage used. Patients may require encouragement to drink clear fluids along with the lavage and are given intravenous fluids when taking the preparation. An alternative form of mechanical bowel preparation that is often used is Fleet Phosphosoda solution. This may also result in fluid and electrolyte abnormalities. Prophylactic (Preventative) Antibiotics: Many procedures either carry a risk of infection, or are at an increased risk of subsequent infection. Therefore each surgical unit will have a policy on the use of antibiotics to prevent infection. Generally, these antibiotics are given intravenously at the time of surgery prior to the incision being made. Depending on the type of antibiotic used, the dose is either single or given repeatedly up to 24 hours following surgery. Only in rare exceptions are prophylactic antibiotics given for more than 24 hours post-operatively. Radiology: Many patients will have detailed x-rays and scans. These need to be in theatre. It is important to confirm that the appropriate films have been requested and will be available either in an XRay packet or on-line.

Preparation of the Skin: Hair over the surgical site is removed. This is either done on the ward or in theatre. The policy will vary from unit to unit. Some patients may be required to take a shower or bath in a cleansing solution prior to surgery, an example being cardiac

14 patients. Preparation for Anaesthesia: The anaesthetist will prescribe a pre-medication for many patients. This usually consists of a sedative to calm the patient prior to surgery. In some units preoperative carbohydrate loading is practiced. In this situation a clear solution of concentrated glucose can be taken orally up to two hours prior to surgery. FURTHER READING FOR FINALS Tjandra JJ, Clunie GJA, Thomas RJS (eds.). Textbook of Surgery. 2 Edition. Blackwell Science Ltd., Oxford, 2001; pp 2-5 and pp 241-243
nd

15

Tutorial 2

Peri-operative Care of the Surgical Patient

Jonathan Koea

Skilled care does not stop when the surgical patient leaves the operating theatre. In fact, for the Trainee Intern and House Surgeon, this is where their intimate involvement with the patient begins. Good peri-operative care is a combination of careful and regular observation, maintenance of normal physiology, anticipation and early treatment of complications. In order to accomplish this an understanding of the physiological and metabolic effects of surgery is important, as well as a knowledge of the common complications that may develop after surgery. PHYSIOLOGICAL AND METABOLIC EFFECTS OF SURGERY Surgical operations cause a number of physiological and metabolic effects. The nature of these changes is remarkably uniform regardless of the type of surgery performed although the magnitude of these changes is proportional to the magnitude of operation. Nearly every aspect of respiratory function is impaired by general anaesthesia. Ventilation, lung perfusion, gas exchange, ciliary activity and the cough reflex are all impaired by anaesthetic agents. Respiratory activity can be further impaired in patients in whom pain relief is inadequate. The activity of the cardiovascular system is increased with a rise in pulse rate and cardiac output in response to a number of humoral factors and fluid shifts. Extracellular fluid is sequestered around the dissection site (approximately 1 litre for every 2 hours of

16 operating time) and red cells and plasma are lost into the surgical field. In response to this loss of circulating volume there are increases in plasma levels of aldsterone and antidiuretic hormone (ADH) and consequently urinary output of both free water and sodium are decreased. Circulating levels of cortisol, adrenocortical hormone, and growth hormone are also elevated. The coagulation cascade is activated. There may be significant losses of body heat, activating mechanisms of heat conservation (raised basal metabolic rate due to increases in circulating Thyroid hormones, shivering, and peripheral vasoconstriction). The gastrointestinal tract develops a state of decreased motility (ileus) in response to both direct handling, opiates (given for pain relief) and increased circulating levels of adrenaline and noradrenaline, necessitating a period of obligatory starvation. In response to this there is an increase in glycogen and protein catabolism to provide substrate for cellular metabolism. It must be emphasized that these physiological responses to surgery are part of the patients normal physiological response to stress. Within the short term they are easily tolerated by most patients, however if the surgical convalescence becomes prolonged because of the development of complications then many elements of this normal response become consumptive and the avoidance of, and prompt treatment of, complications must be a priority of peri-operative surgical care. MONITORING Post-operative surgical patients must be monitored closely with thorough assessments performed at regular intervals appropriate to the magnitude of surgery and their stage in post-operative course. The best example of post-operative monitoring is in the intensive care unit (ICU) where continuous and dynamic measurement of most physiological parameters can be carried out. However, even on a surgical ward it is possible to closely follow a patients progress using a number of objective physiological parameters. Postoperative patients should be reviewed at least twice daily and objective assessment made of their progress. 1. Mental State. This can be subjectively assessed at the bedside. Care should be taken to look for signs of

17 confusion or disorientation which can often be the first clinical signs of shock or hypoxia, particularly in the elderly. In addition the patients morale should be carefully assessed. It is not unusual for patients to be depressed approximately 72 hours post-operation (the day 3 blues) and maintaining patient morale and motivation at this time is an important priority. 2. Vital Signs Temperature, pulse, blood pressure and respiratory rate are recorded regularly by Nursing Staff. In most post-operative patients this is carried out every 4 hours and provides a valuable record of the patients cardiovascular and respiratory systems. In addition, most surgical wards are able to measure oxygen saturation with portable pulse oximeters at the patients bedside. Central venous pressure can be recorded directly if the patient has a central venous catheter. This is particularly useful in determining intra-vascular volume status (with over or under hydration).

3. Fluid Balance Fluid balance is recorded in postoperative patients. This includes a regular measurement of urine output (generally performed hourly in patients in the first 24 hours postoperation and then every 4 to 12 hours depending on progress). An acceptable urine output in a post-operative patient is 0.5 ml/kg/hour or 35 mls per hour in a 70 kilogram patient. At the end of each 24 hour period the patients total fluid intake (including both intravenous and oral intake) and output (including urine, nasogastric tube, and surgical drain output) are added up and the overall fluid balance is calculated. Fluid balance can also be roughly estimated from daily weight and this is a very useful measure of overall hydration. 4. Respiratory Status In addition to measurement of respiratory rate and oxygen saturation, respiratory status can be assessed by determining whether the patient is mobilizing adequately and by the use of an incentive spirometer at the bedside. In addition the patient can be asked to cough and the quality of this monitored directly.

18 5. The Surgical Wound The surgical incision will be covered with a dressing in theatre and it is not usually necessary to disturb this for the first 24 hours. However after the first post-operative day the wound should be carefully inspected daily and careful assessment made of any erythema or discharge that may herald infection or disruption. 6. Drains Surgical drains may be placed at the time of operation to treat an existing or anticipated fluid collection. The volume and character of drainage should be assessed daily and this is usually recorded as part of the patients fluid balance. The exit site of the drain should be inspected for erythema and security. Generally drains are secured with a suture and if this is loosened then it must be replaced to avoid dislodgement. 7. Medications The patients medication chart should be reviewed daily. In particular intravenous preparations should be discontinued or changed to oral formulations when the patient resumes oral intake. The duration of peri-operative antibiotic therapy should be carefully documented. Depending on the type of antibiotic used, the dose is either single or given repeatedly up to 24 hours following surgery. Only in rare exceptions are prophylactic antibiotics given for more than 24 hours post-operatively.

8. Laboratory Tests Post-operative patients should have a daily determination of full blood count (FBC) and electrolytes (U & E) while they are receiving intravenous fluids. Many patients, particularly those with jaundice or biliary disease, will require daily determination of liver function tests (LFTs). Generally daily blood tests can be discontinued once the patients condition is stable and he/she has resumed an oral intake. ROUTINE POST-OPERATIVE ORDERS Fluids Maintenance: 0.18% saline with 4.2% dextrose at 30-40 ml/kg.day (ie 80-100 ml/hr in a

19 70 kg patient). Potassium may be withheld from most patients the first postoperative day and then, depending on urine output, be given as 20mmol/l (see Tutorial 3). Abnormal Losses: Allowance should be made for abnormal losses and these are replaced with 0.9% saline if they come from the stomach. All other losses are replaced litre for litre with a Balanced Salt Solution. (see Tutorial 3)

Blood Products Packed red cell transfusion should be considered if the post-operative hemoglobin is < 80 g/L. The decision to administer any blood product to patients should always be discussed with the Consultant Surgeon. Analgesia Epidural or PCA as ordered by the Pain Service. Medication Metoclopromide 10 mg IV PRN-q 6 hr. Cyclizine and Ondanestron are also used for nausea. Paracetamol 1 gm PO or PR PRN every 6 hours. Ranitidine 50mg IV every 8 hours for peptic ulcer prophylaxis

Antibiotics Uncomplicated surgery; usually requires one dose of antibiotics given at induction of anaesthesia. Some patients, in particular those who are having surgery for Crohns disease, have antibiotics for 5 days postoperatively. Pulmonary Incentive spirometry for all patients Physiotherapy: all patients to be seen post-operatively.

Daily blood Tests FBC, U & E, LFTs daily until oral intake commenced.

20 DVT Prophylaxis Subcut heparin (either fractionated or unfractionated) if indicated (see Table 1). TED stockings in most patients (see Table 1).

General Patients should ambulate upon their return to the ward. Daily weight. Chest x ray (CXR) if indicated. Electrocardiogram (ECG) if indicated.

COMMON SURGICAL COMPLICATIONS 1. Volume Requirement/ Bleeding/ Shock Most surgical patients will require intravenous fluids in the initial post-operative period. However if intravenous fluids are required to maintain pulse, blood pressure or urine output this indicates on going loss of extracellular fluid or blood. In extreme cases the patient may develop signs of hypovolemic shock (see Tutorial 3). In this situation on going fluid requirements must be provided and an investigation into the underlying problem begun. 2. Urinary Retention This commonly occurs in elderly men and is caused by a combination of bladder neck obstruction, immobilization and abdominal pain preventing the development of sufficient intra-abdominal pressure to initiate micturition. Some operations such as herniorraphy and haemorrhoidectomy are particularly associated with this complication. The diagnosis is made by palpation of a distended bladder and treatment is by insertion of a urinary catheter under sterile conditions. 3. Fever A post-operative fever of approximately 38 C in the first 48 hours after operation is part
0

21 of the normal inflammatory response to surgery. In general, patients are febrile but have no systemic signs of sepsis. However, in patients in whom fever is accompanied by other signs of infection (tachycardia, dyspnoea, hypotension, confusion) a search must be made for a cause of infection. This includes a thorough clinical examination and the taking of blood and urine cultures.

4. Pneumonia Post-operative pneumonia is a serious complication that has a number of causes. Many patients requiring surgery have chronic lung disease and all surgical patients are placed at risk of pulmonary infection because of the decreased cough reflex, impaired ciliary activity, and reduced tidal volumes that occur after abdominal surgery and general anaesthesia. Post-operative pneumonia presents as fever, tachypnoea, increased secretions and physical signs consistent with pulmonary consolidation. Treatment is with vigorous physiotherapy, adequate analgesia, oxygen supplementation and antibiotics. 5. Myocardial Infarction and Arrhythmia Cardiac complications including myocardial infarction and arrhythmia are uncommon following surgery but are life threatening. General anaesthesia depresses the myocardium and some agents predispose to the development of arrhythmias. The length and urgency of the operation and the presence of uncontrolled bleeding with hypotension have been individually shown to correlate positively with the development of cardiac problems. The incidence of myocardial infarction following general surgical procedures is 1% and the diagnosis should be suspected in any patient with persistent low blood pressure and low urine output or who complains of chest pain or dyspnoea. The diagnosis should be substantiated with an ECG and serum elevations of cardiac enzymes (Troponin). Up to 25% of post-operative myocardial infarctions are fatal. Cardiac arrhythmias are also seen in post-operative patients. Most commonly these are tachyarrhythmias (atrial fibrillation and flutter) and may be the initial signs of developing sepsis. In addition atrial fibrillation may occur in patients who have been overhydrated or in those with abnormalities in plasma potassium, sodium or magnesium concentrations.

22 6. Wound Infection. Post-operative wound infection results from bacterial contamination during or following a surgical procedure. Infection rates are approximately 1.5% in clean wounds with up too 30% of wounds becoming infected in patients operated acutely for intestinal perforation or bleeding. Wound infections usually appear between day 5 and 10 post-operation and usually present with fever and wound edge erythema. Treatment is by removing relevant skin sutures and, in some cases, systemic antibiotic therapy. Wounds may also develop seromas, which are defined as fluid collections in the wound other than pus or blood. Seromas usually develop after operations that involve the elevation of skin flaps and the interruption of local lymphatics. Seromas are usually treated with aspiration as they delay healing and provide a nidus for the development of wound infections. Wound hematomas are a collection of blood and clot in the wound. Hematomas are one of the most common wound complications and are caused by imperfect hemostasis. They produce elevation and discolouration of wound edges, discomfort and swelling. Treatment consists of evacuation of clot under sterile conditions, ligation of bleeding vessels and reclosure of the wound.

7. Wound Dehiscence Dishiscence is partial or total disruption of any or all layers of an operative wound. Rupture of all layers of the abdominal wall and extrusion of abdominal contents is called evisceration and occurs in about 1% of abdominal surgical procedures. This is a surgical emergency and is managed by prompt return to theatre and reclosure. 8. Intestinal Ileus/Obstruction Some degree of intestinal hypofunction is normal in the post-operative period after abdominal surgery and is the result of paralytic ileus. This is a normal response of the bowel to handling, circulating catecholamines and opiates given for analgesia. Intestinal function usually returns 3-5 days following abdominal operation and is accompanied by cramping abdominal pains, the return of bowel sounds and the passage of flatus. Mechanical obstruction can also develop in the post-operative period and can be difficult to differentiate from ileus initially. In most cases of obstruction, however, patients will

23 have resumed normal intestinal function for a short period before developing clinical and radiological signs of obstruction.

9. Deep Venous Thrombosis / Pulmonary Embolism Deep venous thrombosis (DVT) is a common problem in surgical patients and up to 40% of surgical patients will have evidence of small thromboses on investigation. Patients particularly at risk of developing DVT are those over 60 years of age with a diagnosis of cancer. A DVT should be suspected in any patient who complains of calf pain or swelling and anticoagulant treatment should be instituted promptly once the diagnosis is confirmed. Pulmonary embolus is a serious complication of DVT whereby part of the thrombus embolizes to the pulmonary circulation. This should be suspected in any postoperative patient who develops dyspnoea and/or chest pain or sudden shock in the postoperative period. Both DVT and pulmonary embolus are best managed with prevention and all patients undergoing surgery should be treated with TED stockings, low molecular weight heparin and early post-operative mobilization (see Table 1).

10. Psychiatric Syndromes Post-operative psychiatric syndromes develop in approximately 1% of patients following operation. Anxiety and fear are normal responses in patients undergoing surgery. Confusion and disorientation are common findings in post-operative patients, particularly the elderly. The most common cause of post-operative disorientation is decreased cerebral perfusion and oxygen delivery. Consequently the development of an altered mental status in the post-operative patient may be the initial indication of a developing infection or cardiopulmonary complication. The other common cause of post-operative confusion or disorientation is drug (usually benzodiazepine) or alcohol withdrawal. In all cases management is aimed at excluding a cause of cerebral hypoxia or hypoperfusion. Drug and alcohol withdrawal can be managed with sedation and provision of adequate vitamin B12 and folate supplementation.

24 Table 1. The protocol for deep venous thrombosis (DVT) prophylaxis in elective general surgical patients at Auckland City Hospital Patient Group Group 1 Risk Factors <30 minute operation regardless of age >30 minute operation and <40 years of age Patients with epidurals Oestrogen Therapy >30 minute operation and >40years of age Presence of Cancer Laparoscopic Surgery No epidural and any of: Previous DVT, PE Known Thrombophilia Pelvic Surgery >2 hours surgery expected Recommendation Nil

Group 2

TED Stockings 20 mg subcut Enoxaprin daily

Group 3

TED Stockings 40 mg subcut Enoxaprin daily

FURTHER READING FOR INTEREST Tjandra JJ, Clunie GJA, Thomas RJS(Eds) Textbook of Surgery 2 Science Ltd.Oxford 2001 pp 2-59 FURTHER READING FOR FINALS Nil
nd

Edition Blackwell

25

Tutorial 3

Metabolic care of the surgical patient

Stephen Streat

INTRODUCTION This tutorial covers fluid and electrolyte therapy including body composition, osmolality, the factors governing the distribution of infused fluids, common fluid and electrolyte abnormalities in surgery, specific intravenous fluid solutions and their appropriate use. It also includes sections on nutrition and on circulatory shock. FLUID AND ELECTROLYTE THERAPY Most surgical illnesses and operative intervention alter the distribution and composition of the body water spaces. A good understanding of these body water spaces and the way that they change is necessary if you are to look after surgical patients. In this section the composition of the body and especially the water spaces is presented first, followed by the changes in these spaces which occur in surgical illness and how fluid therapy should be used to promote clinical recovery and restoration of normal body composition. Body composition Body composition can be thought of as the basic chemical anatomy of the body. The components of body composition, or compartments, are chemically distinct but organs and tissues are made up of several compartments in varying proportions - for example bone is relatively free of water and high in minerals whereas blood is comprised almost completely of water and protein and adipose tissue contains around 85% fat the rest being mainly water and protein.

26 Fat and the fat-free mass Turning to the entire body mass - this is best thought of comprising the fat (the ether soluble fraction of the body) and the fat-free mass, sometimes referred to as the lean body mass. The fat-free mass is comprised of four compartments the total body water (TBW), protein, minerals and carbohydrate. Although the size of the body fat can vary considerably in health and tends to increase with age, the size and relative proportions of the components of the fat-free mass are remarkably constant in adult life. Fat is the dominant energy source during prolonged starvation including surgical patients who are not being fed. In a normal 70kg male the size of the total body fat is around 14 kg, leaving 56 kg of fatfree mass. This consists of around 40 kg (litres) of water, 12 kg of protein, 3.5 kg of minerals and 0.5 kg of carbohydrate. In a normal 60 kg woman the total body fat is also around 14 kg, leaving 44 kg of fat-free mass consisting of around 32 litres of water, 9 kg of protein, 2.5 kg of minerals and ~0.5 kg of carbohydrate. Protein Around 55% of the total body protein is inside cells where it is involved in the metabolic processes of life the engine of the body. The other 45 % (dominantly collagen and elastin) forms the supporting structures of the body and is not involved in metabolic processes.

Minerals Most of the mineral compartment is made up of calcium hydroxyapatite in the skeleton; the rest is largely the electrolytes in the body fluids. Changes in the size of the mineral compartment are very small in absolute terms over short time periods for example several months are required to loose 20% of total body calcium, even if there is no calcium intake. Carbohydrate This is a small and highly evanescent compartment, dominantly made up of glycogen in

27 muscle and liver and a very small amount of glucose in body fluids. It provides a small energy store (around one day) for short-term starvation.

Water and its subdivisions This is by far the largest component of the fat-free mass, comprising around 72% in health. The TBW can be measured as the distribution volume of tritiated or deuterated water (or indeed ethanol) and such tracers are evenly distributed in TBW very rapidly within 2-3 hours. TBW is comprised of two major compartments the intracellular water (ICW) and the extracellular water (ECW) sometimes called the extracellular fluid (ECF). The ICW makes up around 55% of TBW ~22 litres in 70 kg man, ~18 in 60 kg woman and the ECW around 45% or ~18 litres in 70kg man, ~14 litres in 60 kg woman. These two compartments are distinguished by their ionic composition the ICW is high in potassium (150 mmol/l) and low in sodium (10 mmol/l) and the ECW is high in sodium (140 mmol/l) and low in potassium (4 mmol/l).
th

The ECW can be further divided into two compartments the plasma volume (around 1/6

28 of the ECW) and the remainder of the ECW - termed the interstitial fluid (around 5/6 of the ECW). The plasma volume and interstitial fluid share the same ionic composition but differ with respect to their protein concentrations, which are much higher in the plasma. Around 10% of the ICW is inside a special cell population the red cells (which of course contain around 20% haemoglobin). The volume of the red cells (the Red Cell Volume, RCV) together with the plasma volume (PV) together make up the blood volume (BV) ~5 litres in 70 kg man, a little less in woman. Osmolality This is defined as the number of osmotically active particles (osmoles) per kg of body water. In health this ranges from 275 290 milliosmoles per kg (mosm/kg). Water diffuses freely throughout the TBW, including across cell membranes, and the osmolality of all body water compartments is thus identical. The rapid addition or removal of solutefree water from the body (which has a constant number of osmoles mostly electrolytes) will therefore alter the osmolality of body fluids (conveniently measured as the serum osmolality) in proportion to the size of the change in the TBW thus: Final [Osm] x final TBW = Initial [Osm] x initial TBW. For example - addition of a litre of solute-free (pure) water to a person with a total body water of 40 litres will reduce serum osmolality by ~2.5% or around 7 mosm/kg. It can be seen that in cases of dilutional hypo-osmolality where serum osmolality may be as low as 250 mosm/kg, that removal of several litres of solute-free water would be required to raise serum osmolality to normal.
ths

What governs the compartmental distribution of intravenously infused fluids? Intravenous fluids are of course infused into the circulating blood volume and may distribute variously into the various compartments of the TBW depending on their composition. Red cell size

29 Firstly, red cells will stay within the blood volume, as long as there is no source of ongoing bleeding, and will expand the size of the blood volume by exactly the same amount as their own volume. Note that red cells for transfusion are re-suspended in 0.9% saline and such units contain only around 60% red cells by volume. Water Secondly, fluids which are devoid of sodium (for example sterile water or 5% dextrose in water) will distribute their volume across the entire TBW and expand each of the compartments of the TBW equally in proportion to their existing size. As the plasma volume and red cell water volume are small (around 12% of the TBW) such fluids will have little effect on the size of the blood volume and are thus poor volume expanders when hypovolaemia is present. Note that such fluids will also reduce the serum osmolality if infused rapidly or in excess of the kidneys ability to excrete the water load. Inappropriately large volumes of such fluids can cause dangerous hypo-osmolar states when ADH secretion is increased (such as after injury or operation). The sodium ion Thirdly, fluids that contain sodium in concentrations approximating the concentrations found in the ECW (around 140 mmol/l) will expand only the ECW as the sodium ion is actively excluded from the ICW by membrane-bound pumps. These fluids may also contain physiological (low) concentrations of other cations (potassium, calcium, and magnesium). Most or all of the anion is as chloride (sometimes some lactate) and have a resultant osmolality of around 300 mosm/kg. They are therefore called iso-osmotic, often loosely referred to as isotonic. Such fluids with physiological sodium concentrations are called resuscitation fluids because they expand the circulating blood volume by expanding the plasma volume. Note that they also expand the interstitial fluid, which is several times the size of the plasma volume. The distribution of these fluids into the interstitial fluid is rapid, and usually complete in less than 2 hours. The relative size of the plasma and interstitial volumes determines the amount of such fluids that end up in each compartment. For example infusion of one litre into a normal 70 kg man with an ECW of 18 litres will expand the

30 plasma volume by only ~170 ml (1/6 of a litre) and the interstitial fluid by ~830 ml (5/6 of a litre). Fourthly, some such fluids share the same ionic composition but also contain oncotically active large molecules (for example plasma proteins or polymers of starch or gelatin). As these large molecules are oncotically active they tend to retain resuscitation fluids in the plasma volume preferentially but they also expand the interstitial fluid to some extent. Resuscitation fluids containing these molecules are called colloids and those without are called crystalloids. The distribution kinetics and final equilibrium distribution are different for different colloids but in general colloids expand the plasma volume to a greater degree than do similar volumes of crystalloids for example a litre of colloid may expand the plasma volume by 500 ml and the interstitial volume by the same amount. Colloids are generally much more expensive than crystalloids and may not be any more effective in most circumstances. Their use is therefore confined to special circumstances (such as where rapid resuscitation from hypovolaemic shock is needed). Finally, fluids, which contain sodium in concentrations less than those in the ECW, can be thought of conceptually as mixtures of solute-free water and ECW. For example 0.45% saline can be thought of as a 50:50 mixture of solute-free water and 0.9% saline and will have the predicted effects of this mixture on the size and osmolality of the body water compartments. COMMON FLUID AND ELECTROLYTE ABNORMALITIES IN SURGERY Hypovolaemia Hypovolaemia refers to an absolute or relative reduction in blood volume. This is the dominant abnormality found in the presence of shock in surgical patients. Signs of hypovolaemia include flat neck veins, tachycardia, impaired peripheral perfusion, narrow pulse pressure and oliguria. Severe hypovolaemia will lead to shock with the additional signs of hypotension, tachypnea, acidosis and blunting of consciousness. Hypovolaemia may result from loss of blood (haemorrhage), from loss of plasma from the plasma volume (e.g. in trauma and sepsis where plasma is lost into the interstitium) or
ths th

31 from loss of extracellular fluid of sufficient extent that the plasma volume is significantly reduced. This latter scenario (see below) is very common in surgical patients and can have a variety of causes including intestinal obstruction (where the fluid is lost into the gut lumen), vomiting or nasogastric fluid loss, enterocutaneous fistulas, diarrhoea, trauma - including surgical dissection, sepsis and burns. In the resuscitation of a patient with hypovolaemia the two principles are to replace the blood volume deficit and to simultaneously and rapidly control any ongoing loss (most commonly bleeding) by direct pressure, surgical or interventional radiologic procedures. Regardless of the nature of the fluid lost which has led to hypovolaemia, the initial fluid administered should be a crystalloid resuscitation fluid (0.9% saline or a balanced salt solution such as Plasmalyte-148). Boluses of 500 ml should be used initially and the patient should be carefully observed clinically for signs of response (improved peripheral perfusion, rise in urine output). Should hypovolaemia persist after 2-3 litres of such fluid then other fluids (colloids, red cells or clotting factors [plasma]) may well be required. It is not appropriate to try and resuscitate the actively bleeding patient without simultaneously and urgently controlling the source of bleeding.

ECW or ECF depletion This is sometimes erroneously and loosely called dehydration in clinical practice. It is erroneous because it is not water which has been lost but rather extracellular water -containing ~140 mmol/litre of sodium. Pure water deficit results in hyperosmolality not in ECF depletion. The signs of ECF depletion include signs of both interstitial fluid loss (e.g. loss of tissue turgor) and plasma volume loss (hypovolaemia, haemoconcentration). In addition the tongue will be dry and the patient may complain of thirst. Treatment of ECW depletion involves infusing balanced salt solution often involving several litres of fluid over a few hours. In addition, an ongoing source of ECF depletion should be sought and corrected if possible. Ongoing ECF depletion that cannot be immediately corrected (e.g. high-output ileostomy or nasogastric fluid loss) must be replaced until it stops with an

32 equivalent volume of balanced salt solution to prevent ECF depletion from developing again.

ECF over-expansion This iatrogenic syndrome occurs when large amounts of resuscitation fluids have been infused and have not yet been cleared by the kidneys. It can co-exist with hypovolaemia (for example in sepsis where the plasma volume is reduced by leak into the interstitium), normovolaemia or hypervolaemia (where the plasma volume is also overexpanded). The cardinal sign of ECF over-expansion is oedema which can affect both the peripheral tissues and also the lung. However the appropriate clinical response to ECF overexpansion is determined by the state of the plasma volume and blood volume at the time. For example, severely septic patients with hypovolaemia and oedema should receive cautious plasma volume expansion. These patients should usually be in an intensive care unit (ICU). Patients with ECF over-expansion who do not have signs of hypovolaemia and circulatory or respiratory compromise (tachycardia, hypoxia) should be treated with sodium restriction. In the absence of heart failure, kidney failure or excess mineralocorticoid activity they will excrete the oedema over a day or two. However, patients with ECF over-expansion and circulatory or respiratory compromise (tachycardia, hypoxia, frank pulmonary oedema) should be treated with oxygen, salt restriction and a judicious use of a loop diuretic (e.g. 20-40 mg of frusemide intravenously). Call for senior help for such patients.

Dilutional hypo-osmolality By definition this syndrome results from administration of solute-free water in excess of the patients ability to excrete the water load. This syndrome is often called dilutional hyponatraemia or even more loosely hyponatraemia but the reference to sodium must not lead to the erroneous conclusion that the problem is one of sodium deficiency. The problem is due to water excess. It can result from over-intake of water orally (pyschogenic polydipsia). However, in

33 surgical practice it is most common produced by excess administration of intravenous fluids of low osmolality to patients whose ability to excrete the water load is impaired because of the effects of antidiuretic hormone (ADH), which has been produced as part of the usual metabolic response to trauma (including surgery). Patients with small total body water (especially older women) and those with renal impairment are particularly at risk, but the syndrome can be produced in any patient and it is potentially lethal. It can be prevented by restricting water intake to that which is needed (~1ml/kg body weight/hour or around 1500 ml/day for a 60 kg woman and 2000 ml per day for an 80 kg man). Normal serum osmolality is around 275 mosm/kg and this corresponds to a serum sodium concentration of ~140 mmol/l. Serum osmolality of around 260 (corresponding to a serum sodium of ~130) should lead to a clinical response (water restriction and monitoring of serum biochemistry) and osmolality of less than this is dangerous and can cause seizures, brain oedema (ICW expansion) and death. Treatment is by severe reduction or even absolute restriction of water intake until normal serum osmolality is restored. Sodium-containing solutions e.g. 0.9% saline should not be administered to treat this syndrome. Often such patients have very high urinary sodium concentrations (e.g. 250 mmol/l) and very high urinary osmolality (e.g. 800-1000 mosm/kg) and they will excrete the administered sodium well, while at the same time conserving the water that came with it and thereby further lowering their serum osmolality. Hypokalaemic metabolic alkalosis Although hypokalaemia can occur without metabolic alkalosis, it is often associated with it in surgical patients. Most commonly this occurs as a result of loss of hydrochloric acid from the stomach (vomiting or large volume nasogastric fluid loss), which has not been adequately replaced (with 0.9% saline). The hormonal and renal compensatory response to ECF contraction involves the production of aldosterone, avid conservation of sodium and urinary loss of potassium and hydrogen ions. Patients who are given diuretics will also develop this syndrome as potassium, sodium and chloride are all lost in the urine. Treatment of the syndrome involves repletion of the ECF (and chloride) depletion, initially with 0.9% saline and later with additional potassium chloride as soon as an

34 adequate urine output has been achieved. Ongoing 0.9% saline replacement of such ongoing losses is essential to prevent this syndrome from recurring. Hypokalaemia without metabolic alkalosis Catecholamines, insulin or dextrose-containing fluids (which stimulate endogenous insulin production) may produce this. It can lead to dysrythmias (most commonly atrial fibrillation or ventricular ectopics) in susceptible patients. In the asymptomatic patient hypokalaemia should be treated slowly (e.g. 5-10 mmol/hour for 4-6 hours) but patients with circulatory compromise may need faster replacement rates and if these are needed the patients should be under ECG monitoring in a high-dependency or intensive care environment. Metabolic acidosis Metabolic acidosis (base deficit more than 5 mmol/l) in surgical patients is most commonly a late sign of shock with accumulation of lactic acid. Severe metabolic acidosis (e.g. base deficit of 10 mmol/l or arterial pH of <7.25) is a grave sign and should lead to an urgent clinical response. Treatment involves correction of the shock state, not infusion of alkali. Call for senior help early for such patients.

INTRAVENOUS FLUID SOLUTIONS There are many different intravenous fluid solutions but most surgical patients can be managed with very few. Blood products It is essential to know the volume and composition of these three blood products used in modern transfusion medicine red cells, fresh frozen plasma and platelets. However, most surgical patients will need none of these products outside of the operating room and the need for such products in a ward setting is an indication of a serious problem. Red cells

35 Red cells contain ~200 ml of cells which have been re-suspended in 0.9% saline to give a final volume of ~350 ml. One unit of red cells will thus raise the haemoglobin of a 70 kg patient by ~10 g/l.

Fresh frozen plasma Fresh frozen plasma contains coagulation factors and other plasma proteins in the same concentrations as are normally found in plasma. The coagulation factors retain >80% of their normal physiological activity. They come in plastic bags of ~250 ml (units) and contain an additional 20 mmol/l of sodium citrate but otherwise the same electrolyte concentrations as are normally found in plasma. Fresh frozen plasma must be thawed on request and this takes ~45 minutes. It is used to correct dilutional (washout) coagulopathy in large volume transfusion and 500-1000 ml (2-4 units) are commonly given at one time. Platelets Platelets come in plastic bags of ~300 ml containing the platelets from the whole-blood donation of four donors. Some platelets are lost during preparation Accordingly, such a four-pack contains around 250 x 10 platelets, which should raise the platelet count of a 70 kg patient by ~ 80 x 10 /l. In clinical practice, some platelets are often consumed (sepsis) or lost (bleeding) and the increment in platelet count is often smaller. Colloids It is prudent to know about the composition of two colloidal resuscitation fluids 3.5% polygelatin and 4% human serum albumin solutions. Polygelatin is presented in 500 ml plastic bottles containing a 3.5% solution of gelatin polymers of various molecular weights that are cross-linked by urea bridges. The solution also contains 0.9% saline (154 mmol/l of sodium and 154 mmol/l of chloride). There are a number of similar solutions sold by different companies but they are almost equivalent in effect. They are used for plasma volume expansion, after crystalloid solutions and before human blood products. Several litres may be given safely if needed.
9 9

36 A variety of human serum albumin solutions are available around the world. Currently in New Zealand 4% normal serum albumin is available. This is presented in 500 ml glass bottles, which must be kept refrigerated. The fluid contains 4% human albumin, obtained from blood donors, in a solution which otherwise has the same electrolyte concentrations as that found in normal plasma. This fluid thus acts as a potent blood volume expander but it is devoid of coagulation factors. It is expensive (~$100/500 ml) and is used rarely in seriously ill hypovolaemic patients who have not responded to crystalloids. Crystalloids

Replacement solutions (ECW expanders) There are two such fluids (0.9% saline and balanced salt solution) that are used in surgical practice and it is essential to thoroughly understand their similarities and differences and their differing clinical indications.

0.9% saline This fluid contains only sodium chloride with concentrations of 154 mmol/l of sodium and 154 mmol/l of chloride. It is thus (slightly) hyperosmolar (308 mosm/kg) with respect to normal body fluids (~280 mosm/kg) and is even higher than normal ECW in chloride (154 versus ~100) than it is in sodium (154 versus 140). It can be used for the initial resuscitation of hypovolaemia or ECW contraction but large volumes (>3 litres) for these indications may lead to hyperchloraemic metabolic acidosis. It is ideally suited to the situation of replacement of abnormal losses of gastric fluid where hydrochloric acid is being lost.

Balanced Salt Solutions There are a large number of such fluids which have very similar composition they have electrolyte concentrations close to those normally found in the ECW including sodium at ~130-150 mmol/l. potassium ~4 mmol/l and chloride ~100-120 mmol/l. The remaining anion may be bicarbonate, lactate or acetate, both of which latter are metabolised to bicarbonate in vivo. Examples of such fluids include Plasmalyte-148 and Ringers Lactate

37 (also known as Hartmans Solution). These fluids can be used for initial resuscitation of hypovolaemia and ECW contraction but will not correct the alkalosis associated with gastric loss or long-standing ECW contraction and renal compensatory hypokalaemic alkalosis. They are however ideal for replacement of gastrointestinal fluid losses from the Ampulla of Vater and below such as biliary, pancreatic, enterocutaneous fistula or ileostomy loss. Remember that these fluids are replacement fluids, they are not maintenance fluids. The inappropriate use of replacement fluids for maintenance will result in ECW overexpansion and possibly hyperosmolality. Maintenance solutions Before considering these fluids it is instructive to reflect on the changes in body composition, which occur consequent on successful resuscitation from surgical operation, trauma or sepsis. In all three scenarios there is an increase in TBW that is due entirely to an increase in ECW. After clean elective abdominal surgery the extent of this increase is smallperhaps 23 litres whereas after major emergency surgery (e.g. for perforated peptic ulcer) or major blunt trauma it may be 57 litres and after severe sepsis (e.g. perforated colon - intensive care patients) as much as 25 litres although 1015 litres is more typical. In the absence of renal or cardiac failure or ongoing sepsis this fluid will be mobilised from the interstitial fluid into the plasma volume and renally excreted beginning a day or two (non-septic surgery, trauma) or 35 days (sepsis) later. The speed of this homeostatic response is delayed in the elderly who may remain with significant ECW expansion for a week or more following resuscitation from sepsis for example. Although the size of this ECW expansion is not commonly problematic in ward patients, those patients who have required intensive care for trauma or sepsis may still have significant ECW expansion, manifest as oedema, at the time of their return to a surgical ward. Remember that the kidneys are very good at conserving sodium under conditions of sodium deprivation and can reduce urinary sodium excretion to less than 10 mmol/ day if necessary. In the absence of oedema it is reasonable to provide some sodium in maintenance fluids,

38 if for no other reason than to provide a small buffer against some ongoing pathological fluid loss, from wounds, drains and perhaps some gastric fluid loss. However, in the presence of significant ECW over-expansion (weigh the patient and examine for oedema, which unlike in congestive heart failure is not confined to the legs and sacrum) it is reasonable and appropriate to restrict sodium intake as long as circulatory and renal function is normal. This will allow some of the excess ECW to be lost as pathological loss and will not delay the renal excretion of the excess sodium and water accumulated during the resuscitation phase of fluid therapy - in the Emergency Department, Operating Room and Intensive Care Unit. Two maintenance solutions will meet these requirements 5% dextrose in water and 0.18% saline with 4.2% dextrose. 5% Dextrose This is devoid of sodium and provides only water (and a small amount of glucose, sufficient to make the resulting fluid iso-osmolar with body fluids so as not to induce haemolysis of red cells). It is appropriate to use this fluid (1 ml/kg/hr or 1500 2000 ml/day) for the patient with significant persisting oedema after resuscitation from acute surgical illness. When oedema has been mobilised it may be more appropriate to provide some sodium intake and this is conveniently done with 0.18% saline with 4.2% dextrose.

0.18% saline with 4.2% dextrose This fluid contains 30 mmol/l of sodium and 30 mmol/l of chloride together with sufficient dextrose to make the fluid iso-osmolar with body fluids. There are many different mixtures of saline and dextrose available avoid referring to dextrose-saline as if it were only one fluid, specify exactly which fluid you mean to use. It is appropriate to use this fluid (2000-2500 ml/day) in non-operative patients and in postoperative patients who still require IV fluids a few days after operation (when excess ECW has been mobilised).

Potassium

39 Potassium can be added to either of the two maintenance fluids indeed a solution of 0.18% saline and 4.2% dextrose is available with 20 mmol/l of potassium already mixed in. Potassium may be withheld from most patients the first postoperative day and then given as 20 mmol/l of whichever maintenance fluid is used. Remember to be very cautious with potassium administration to patients with known renal impairment and avoid potassium replacement completely in patients with oliguria or severe renal failure.

NUTRITION Common to all surgical illness are three metabolic processes. These are metabolism of fat for energy, catabolism of protein to provide glucose for the brain and aminoacids for tissue repair and expansion of the extracellular water. The patient with chronic surgical illness (e.g. gastrointestinal malignancy) will often present with deficits of both body fat and protein-i.e. with protein/calorie malnutrition. Sepsis in particular causes rapid and profound depletion of body protein. Loss of fat stores will have no consequences for most patients but loss of protein is accompanied by some loss of function. For example, severe protein loss impairs respiratory function, skeletal muscle function, immune function and wound healing. In order to prevent further loss of function resulting from the combined effects of surgery and starvation, patient with clinical evidence of impending or actual physiological impairment are given some form of nutritional support most commonly enterally, rarely parenterally. Most patients undergoing clean elective, uncomplicated surgery will have return of normal gastrointestinal function within a few days and will not require nutritional support. However, patients with severe malnutrition pre-operatively and those who develop sepsis or prolonged impairment of gastrointestinal function should be carefully observed for the development of protein depletion or functional impairment and considered early for nutritional support.

Nutritional requirements

40 Total energy requirements in surgical patients are not dissimilar to those in normal subjects. Although the component of energy requirement due to muscular activity may be reduced in ill patients this is counterbalanced by an increase in resting energy expenditure due to nature of the illness itself. Most non-septic patients will gain protein (and not lose fat) when 40 kcals/kg body weight/day and 1.52g of protein/kg body weight/day are administered, either enterally or parenterally. Septic patients will not gain protein until the sepsis has been eradicated but nutritional support may reduce the rate of protein loss in such patients. Enteral nutrition If the small bowel is functioning enteral nutrition is given as a continuous pumped infusion of a commercial liquid formula via a fine-bore (12F or smaller) nasogastric, nasojejunal or surgical jejunostomy tube. Conveniently, formulae with around 1 kcal/ ml and 40 gm of protein/litre are available which also contain electrolytes, trace elements and vitamins so that ~15002500 ml will provide all fluid, electrolyte and nutritional needs. Enteral nutrition requires supervision to ensure that it is tolerated and to avoid the development of complications but is considerably safer and cheaper than parenteral nutrition. Parenteral nutrition When nutritional support is required and the gastrointestinal tract is blocked, proximally fistulated, too short or simply cannot cope then nutritional support is given parenterally. Solutions containing amino acids, glucose, fat, electrolytes, trace elements and vitamins are prepared under laminar flow sterile conditions by a pharmacy or commercial manufacturer and supplied in large (23l) plastic bags containing enough supply for 24 hours. These are infused at a continuous rate with a volumetric pump into the superior vena cava, most commonly via a single lumen subclavian vein catheter. Parenteral nutrition is a complex and expensive treatment, which requires skilled supervision by a multidisciplinary team using strict protocols in order to be safe. Complications can be life threatening and include catheter-related complications (arterial puncture, pneumothorax, misplacement of the catheter outside the vein, catheter-related sepsis) and a legion of

41 other complications (including serious metabolic derangement and fluid overload).

CIRCULATORY SHOCK Definition and recognition Circulatory shock is the state when tissue perfusion is inadequate to meet metabolic demands. Cardiac output may be low, normal or high. The haemodynamic abnormalities may include blood volume disturbances, alterations in heart rate and rhythm, cardiac contractility and changes in systemic and pulmonary vascular resistances. Shock is often multifactorial and regardless of aetiology successful therapy may involve attention to all of these haemodynamic abnormalities. Circulatory shock is a medical emergency and delay or inadequate treatment will lead to worsening of the shock state, multiple organ failure and death. Early recognition of the signs of shock coupled with a high index of suspicion (a suspension of disbelief) and early aggressive therapy are the keys to a successful outcome. Call for experienced help early in the management of a patient with shock. The earliest signs of shock are seen in the peripheral perfusion. Examine the warmth, colour and rapidity of capillary refill in the most distal tissues the nail beds and tips of the hands and feet. Dusky nail beds and cool fingers with slow capillary refill (>1 sec) should alert you to look for other signs, including oliguria, tachypnea, hypoxia (check pulse oximetry), tachycardia, narrow pulse pressure, confusion and finallyfrank hypotension. Failure of a pulse oximeter to provide reliable measured oxygen saturation is a further useful sign of inadequate peripheral perfusion and restoration of this ability can be used as a guide to successful therapy. Remember that co-morbidities and various common therapies (e.g. epidural analgesia, previous beta-blockade) may mask or exacerbate some of these signs. Laboratory abnormalities including hypoxia, metabolic acidosis, renal dysfunction and coagulation abnormalities are commonly associated with shock.

42 Diagnosis and therapy Diagnosis and therapy of shock should proceed simultaneously and focus on two aspects aetiology and physiological derangement. Examination of the specific physiological derangements present will usually rapidly lead to an etiologic diagnosis, which might then allow some specific therapy.

Emergency care Think ABC (see Tutorial 11) Lie the patient flat, take a rapid history from the case-notes and the nursing staff and examine the patient carefully, especially the respiratory and cardiovascular system, focusing on the nature and extent of the physiological disturbance to these systems. Give the patient supplemental oxygen (4060%) by mask as some degree of hypoxia is always present in shock. Flat neck veins

Hypovolamia Flat or low neck veins in the presence of shock suggest that hypovolaemia (absolute or relative) is present and should lead to an infusion of resuscitation fluids as above and a search for fluid loss (bleeding, gastrointestinal or other pathological fluid loss, excessive use of diuretics). Bleeding should be controlled by direct pressure if possible followed as soon as possible by surgical or interventional radiological control. Most patients with simple hypovolaemia can be resuscitated quickly and easily in a ward setting. Failure to resuscitate such patients quickly implies that the underlying problem (e.g. bleeding) has not been addressed or that there are additional abnormalities (e.g. impaired cardiac contractility, sepsis, and vasodilatation) not previously appreciated. Call for help if correction of hypovolaemia does not lead to rapid resolution of the shock state. Sepsis Hypovolaemia is always present in sepsis and the presence of local or systemic signs of inflammation (fever, pain and tenderness of local inflammation, leukocytosis) should lead to a working diagnosis of septic shock and a search for a septic focus (abscess,

43 perforation, infarcted tissue) which is amenable to operative source control. Remember to take blood cultures, cultures of other potentially infected fluids and then start appropriate antibiotics. Septic shock carries a high mortality (~40%) even with modern care. In addition to hypovolaemia patients with sepsis have impaired cardiac function (reduced ejection fraction) and can therefore only maintain stroke volume by increasing ventricular enddiastolic volume. This requires expansion of the blood volume above normal. Finally, sepsis (and certain other stimuli which stimulate the inflammatory cytokine cascade) leads to a reduction in systemic vascular resistance by stimulation of nitric oxide production by inducible nitric oxide synthase. Most patients with severe sepsis will therefore require some inotropic or pressor support to maintain adequate perfusion pressure to vital organs, in particular the heart, brain and kidneys. Call for help from the intensive care unit early for septic shock. Elevated neck veins Elevated neck veins in the presence of shock suggest either impairment to right heart filling (pneumothorax, superior vena caval obstruction, cardiac tamponade) or impaired cardiac function (myocardial infarction, haemodynamically important dysrhythmia, pulmonary embolism). These patients require special investigations (e.g. chest x-ray, ECG, ECHO, spiral CT) for definitive diagnosis and may also need ventilatory and inotropic support or specific therapies (e.g. intercostal drain, pericardial drainage, cardioversion, thrombolysis, angioplasty) Call for experienced help early in these patients.

FURTHER READING FOR INTEREST Moore FD, Olesen KH, McMurrey JD, Parker HV, Ball MR, Boyden CM. The body cell mass and its supporting environment. Body composition in health and disease. WB Saunders Co, Philadelphia 1963 Streat SJ, Plank LD, Hill GL. An overview of modern management of patients with

44 critical injury and severe sepsis. World J Surg 2000 Jun;24:655-663. Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R; SAFE Study Investigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. 2004 May 27;350:2247-56 FURTHER READING FOR FINALS Nil

45

Tutorial 4

The Acute Abdomen

Mike Hulme-Moir and Andrew G Hill

Many patients who have had severe abdominal pain for greater than 6 hours will have a condition of surgical importance. If the condition is severe enough to warrant admission to hospital then the patient is said to have an acute abdomen. INVESTIGATION OF THE PATIENT WITH THE ACUTE ABDOMEN Diagnostic research has shown that more than seventy percent of patients who present with the acute abdomen can have an accurate diagnosis made if a good clinical history is taken and a proper physical examination is performed. The following schema is recommended: History of Pain Obtain a clear history of the patients pain by asking the patient these key questions: 1. 2. 3. 4. What were you doing when the pain came on? Where was the pain when it started? Has the pain shifted? (Remember visceral vs. parietal-peritoneal pain) Have you had this pain before?

Obtain a full description of the pain (Ryles 10 questions) 1. 2. 3. Character Severity Situation

46 4. 5. 6. 7. 8. 9. 10. Localisation Radiation Duration Frequency Times of occurrence Aggravating factors Relieving factors

Ask about vomiting Ask about bowel habit and the passage of flatus (in complete bowel obstruction the patient does not pass flatus or bowel motions-obstipation). Ask about urinary or menstrual symptoms. Remember Colic - Colic occurs when there is an abnormal distention of a hollow organ and the pain has the following four characteristics: 1. very severe 2. makes patient restless 3. makes the patient vomit 4. may make the patient sweaty or clammy

It should be noted, however, that each colic has its own cry. e.g. the pain of biliary colic is usually continuous and that of ureteric colic is continuous with knife-like stabs, whereas with small and large bowel colic it usually comes on in spasms. Having ascertained these features one should be able to lucidly describe the characteristics of the patients abdominal pain. Physical Examination Examine the patient thoroughly. The following points are very important:

47 Inspection Watch the patient as he lies in bed, is he/she febrile, or hypermetabolic? Is he /she lying still or is he/she restless? Look at the abdomen to see if it moves with respiration (in peritonitis the abdomen looks rigid). If the abdomen is distended look to see if this is localised (e.g. gallbladder or appendix mass), or generalized as in small bowel obstruction (central) or large bowel obstruction (in the flanks). Palpation With a warm hand, very lightly at first, feel for areas of tenderness. The sine qua non of peritonitis is rebound tenderness. However, it is much less stressful for the patient to elicit this by gentle percussion of the abdominal wall. Deep tenderness is then felt for exquisite deep tenderness over McBurneys point is usually due to appendicitis.

Percussion For free air over the liver (as in perforation) or intralumenal air as in intestinal obstruction. The percussion note may be dull over solid masses.

Auscultation The character of the bowel sounds is noted: high-pitched bowel sounds indicate mechanical obstruction of the intestine; absent bowel sounds indicate peritonitis. SOME IMPORTANT CAUSES OF THE ACUTE ABDOMEN Acute Appendicitis History The patient is usually a young adult, but may be of any age. Usually there is a history of central abdominal pain which has moved to the right iliac fossa over a period of hours. The patient is usually nauseated and off their food and may find it difficult to walk properly because of abdominal tenderness. Examination The patient may have a modest fever and usually the tongue is coated. Inspection of the

48 abdomen may show some rigidity over the right side. The patient almost always is exquisitely tender over McBurneys point or on rectal examination (Pelvic Appendicitis). Diagnosis This is essentially clinical. Ultra Sound Scan (USS) can be helpful in young women with low abdominal pain to help exclude gynaecological pathology. Laparoscopy is increasingly being used as both a diagnostic tool and a means of treatment in young women especially. Where doubt exists it is reasonable to re-examine the patient in 4 hours to look for change. Treatment In order to understand the treatment of appendicitis it is helpful to recall the pathophysiology of the condition. For the first 24 hours the appendix is inflamed, distended and tense. After this time, over the next 2-3 days, the inflamed appendix becomes surrounded by omentum. This is known as an appendix mass. Next, the appendix ruptures and forms an abscess within the surrounding omentum (appendix abscess). In the very old and the very young, omentum may not surround the appendix and generalised peritonitis is a possibility. Appendicectomy must be performed in the early phases. If an appendix mass is discovered it is treated with antibiotics and intravenous fluids followed by removal of the appendix some months later. An appendix abscess, when shown to be present by

ultrasound, is treated by percutaneous drainage under USS or CT guidance. Some months later the appendix may be removed. Acute Cholecystitis History The patient is often a middle-aged woman who has had previous attacks of biliary colic, or right upper quadrant pain, which have resolved spontaneously. On this occasion, however, the pain has remained fixed in the right upper quadrant and extreme tenderness has developed. She has become generally unwell with fever.

49 Examination The patient is toxic and prefers to lie still. The right upper abdomen does not move with respiration. There is rebound and tenderness and possibly a mass in the right upper quadrant. Murphys sign can usually be elicited. Diagnosis Ultrasound shows stones in a distended thick walled gallbladder often with pericholecystic fluid. Treatment The treatment is antibiotics, nil by mouth and surgery on the next available list (within 2 to 3 days preferably). Occasionally the gallbladder perforates causing biliary peritonitis which requires urgent surgery. Perforated Duodenal Ulcer Perforated duodenal ulcers are much more common than perforated gastric ulcers. History About two thirds of patients have a history suggestive of a chronic duodenal ulcer. The patient presents with a sudden, catastrophic upper abdominal pain. Examination The patient is unable to move and has a rigid abdomen. Occasionally it will be possible to detect absence of the normal area of liver dullness due to the presence of free air in the peritoneal cavity. Pelvic tenderness may be elicited on rectal examination. N.B. - Beware the period of illusion, which occurs 3-6 hours after the perforation. Rigidity and rebound tenderness may lessen because the outpouring of peritoneal fluid in response to the inflammation diminishes the degree of peritoneal irritation. Diagnosis The diagnosis is confirmed by the presence of free air under the diaphragm seen on an erect chest film or lateral decubitus film and, in difficult cases, by the use of a

50 gastrografin Treatment Treatment is by the passage of a nasogastric tube, intravenous antibiotics, fluid resuscitation with normal saline and urgent surgery. Surgery consists of peritoneal toilet, and closure of the defect with a patch of omentum. All patients should undergo Helicobacter eradication therapy postoperatively Acute Pancreatitis Acute Pancreatitis is usually caused by one of two conditions - gallstones or alcohol. Other causes are rare. History The patient presents with severe epigastric pain passing through to the back, often associated with profuse vomiting. Examination The patient is very unwell and has epigastric tenderness. In severe cases, the patient may be hypovolaemic and in respiratory distress. Diagnosis Serum amylase levels are raised 5-10 times (levels are also raised in acute gangrenous cholecystitis, bowel obstruction, perforated ulcer and infarcted bowel, but it is unusual for the levels to be so high). Patients with acute pancreatitis can become very sick very quickly. It is important to adequately assess their fluid balance and also obtain a set of biochemical criteria such as Ransons criteria or the modified Glasgow criteria. These criteria or scores assess the systemic response to the inflammed pancreas. An USS should be performed to look for gall stones. CT scans are the best objective way of looking at the pancreas to assess the degree of inflammation and/or necrosis. swallow.

Treatment Pancreatitis ranges from a mild oedematous swelling of the pancreas through to

51 widespread necrosis with release of cytokines, vasoactive peptides and multiorgan failure. Someone who initially looks stable may deteriorate rapidly. Treatment consists of supportive treatment with nasogastric suction, indwelling catheter, intravenous fluid replacement (see Tutorial 3), oxygen and careful observation. Where a person has severe pancreatitis as defined by their biochemical criteria they should placed on a high dependency unit with a central line and on-line monitoring. Broad spectrum antibiotics have been shown to help in these severe cases. Early ERCP (within 48 hours) is indicated for severe gallstone pancreatitis, especially those people with raised bilirubin or dilated bile ducts on USS. Occasionally surgical debridement is required for pancreatic necrosis.

Complications of Acute Pancreatitis Pseudocyst or abscess Occasionally acute pancreatitis will result in the formation of a pseudocyst in the lesser sac. Necrotic pancreas may develop into an abscess. Treatment options include percutaneous drainage, endoscopic drainage and open surgical drainage. Small Bowel Obstruction Small bowel obstruction is most often caused by adhesions, which have developed after a previous operation. Obstruction of a loop of small bowel in the neck of a hernial sac is another common cause. All other causes are uncommon. History The patient presents with periumbilical small bowel (green apple) colic. He/she rolls around the bed when a spasm comes on but lies still and relaxes when the spasm subsides and disappears. Examination The patient is vomiting, not passing flatus and has central abdominal distension. Bowel sounds are active and high pitched and the abdomen is resonant to percussion. Rebound tenderness and a rising pulse rate suggest that the small bowel is strangulated. It is important to search for abdominal scars, hernias and abdominal masses. Small bowel obstruction in the absence of abdominal scars usually requires surgery.

52

Diagnosis The surgeon asks three questions: 1. Is there an obstruction? An erect or lateral decubitus plain x-ray film is taken of the abdomen to answer this question. These films will show fluid levels when the bowel is distended (the only other conditions in which fluid levels are seen are in patients with gastroenteritis and in patients who have had a recent enema) 2. If so, where is the obstruction? A supine abdominal film may show the level of the obstruction by the air outline of the distended intestine. Remember the ileum is featureless. 3. Is the small bowel strangulated? If there is tenderness on abdominal palpation or rebound tenderness, strangulation is suspected. Remember that a rising pulse may indicate Treatment Initial management is placement of a nasogastric tube to decompress the stomach, fluid and electrolyte replacement and pain relief. Gastrograffin (a radiological contrast agent) is then given by nasograstric tube. If strangulation of the small bowel cannot be excluded (and very often it cannot) or if Gastrografin does not reach the caecum within 24 hours (on an Xray) then an operation to find the cause and relieve the obstruction is required. strangulation.

Large Bowel Obstruction There are three usual causes of large bowel obstruction. By far the most common is obstruction of the left colon by an adenocarcinoma. Strictures secondary to chronic diverticular inflammation or volvulus are rarer causes of large bowel obstruction. History The patient presents with colic and obstipation.

53

Examination The abdomen is distended. The bowel sounds are active and high pitched. Diagnosis As with small bowel obstruction diagnosis is aided by plain abdominal Xray film. A rectal exam and sigmoidoscopy are performed to look for a distal carcinoma. Usually an urgent single contrast enema will make the diagnosis. Treatment Treatment is directed at relieving the distention and removing the obstructing lesion. For pathology in the right colon and around to the splenic flexure this involves a right hemicolectomy or extended right hemi-colectomy and restoring continuity by doing a primary anastomosis. In left sided colonic cancer the bowel containing the cancer is removed. Depending on the stability of the patient the surgeon will resect the obstructing lesion and bring out a proximal colostomy or choose to rejoin the colon. If a colostomy is chosen some weeks later colonic continuity is restored. This operation was first devised by Professor Henri Hartmann (1860-1952) of Paris. In modern surgical practice any operation on the rectosigmoid in which a lesion is removed, the rectal stump oversewn and a proximal left iliac fossa colostomy is constructed is called a Hartmanns Procedure. Volvulus may be untwisted and decompressed with a colonoscope. A modern approach to the treatment of large bowel obstruction is to resect the obstructing lesion and after the proximal large bowel has been emptied of faeces.

Acute Diverticulitis Diverticular disease is common in the sigmoid colon and is usually asymtomatic. It may, however, become complicated and present as an acute abdomen:

54

Diverticulitis In this condition the diverticulae have become inflammed. This produces symptoms and signs similar to acute appendicitis but in the left lower quadrant of the abdomen. The treatment is supportive with intravenous fluids and broad spectrum antibiotics. Failure to improve on this regime is an indication for further investigation (usually CT scan) and possibly surgical resection of the affected area with primary anastomosis. Pericolic Abscess The diverticulum may perforate locally and become surrounded by omentum resulting in a pericolic abscess. This is best diagnosed by CT scan with oral contrast. Where possible this should be drained percutaneously under radiological guidance. Free Perforation Perforation into the peritoneal cavity will cause purulent or fecal peritonitis. The later is a condition with a very high mortality. Treatment of both is surgical and consists of peritoneal toilet and resection of the affected area of bowel (Hartmanns procedure with a left sided colostomy.)

Other Causes of the Acute Abdomen Renal Colic This is caused by a stone passing through the ureter. The patient is seized with excruciating loin pain, often radiating into the scrotum. The pain is constant with knife like exacerbations and he/she is unable to lie still and writhes in bed. In ninety percent of cases a stone can be seen on plain x-ray lying along the line of the ureter. Most ureteric stones pass spontaneously. Ruptured Abdominal Aortic Aneurysm (AAA) In a patient with a pulsatile epigastric or umbilical mass and abdominal pain the diagnosis is ruptured or bleeding AAA until proven otherwise. The pain is severe, constant, in the

55 centre of the abdomen and radiates through to the back. On examination a tender expansive pulsation can be felt. The patient has the general signs of massive blood losspallor, sweating, tachypnoea, tachycardia and hypotension. Treatment is immediate laparotomy and replacement of the diseased aorta with a graft. Acute Ischaemia Mesenteric ischaemia produces severe abdominal pain, out of all proportion to the physical findings. It is often associated with a history of atrial fibrillation or vascular disease. It can be very difficult to diagnose and therefore should be considered in all patients with severe abdominal pain. An acidosis on a blood gas can aid in diagnosis. This condition has a bad prognosis. Ectopic Pregnancy This must be suspected in every woman of childbearing age with abdominal pain. The diagnosis is suggested by a period of amenorrhoea, colicky abdominal pain and vaginal bleeding. Bimanual examination may reveal a uterus smaller than would be expected for date and a tender mass in one or the other fornix. Referred shoulder tip pain results from irritation of the diaphragm by intraperitoneal blood. A ruptured ectopic pregnancy can be a catastrophic event with the patient presenting in shock. It is a surgical emergency and immediate transfusion and operation are imperative. FURTHER READING FOR INTEREST Silen, W. Copes Early Diagnosis of Acute Abdomen. 15th Edition. Oxford University Press, 1979 FURTHER READING FOR FINALS Tjandra JJ, Clunie GJA, Thomas RJS(Eds) Textbook of Surgery 2
nd

Edition Blackwell

Science Ltd.Oxford 2001 pp128-129; pp154-170; 199-206; 236-240; 269-276; 295-301.

56

Tutorial

Obstructive Jaundice
John Windsor

Jaundice is the yellow appearance of a patient due to hyperbilirubinaemia and deposition of bile pigments in the sclera, skin, and mucous membranes. It is relatively common on surgical wards. In this tutorial we discuss the surgical aspects of jaundice, but not the wide range of medical causes of jaundice

CLASSIFICATION OF JAUNDICE It is helpful to divide jaundice into post-hepatic (obstructive), pre-hepatic and hepatic jaundice. Obstructive (post-hepatic) Jaundice Obstructive (post-hepatic) jaundice is usually due to an obstruction of the biliary tree, preventing bilirubin from easily entering the duodenum and causing the stools to become pale. The urine is dark or tea coloured because it contains bilirubin in the water soluble conjugated form. Bile salts in the skin can cause severe itch - one of the hallmarks of obstructive jaundice. Hepatic Jaundice The cause of the hyperbilirubinaemia is hepatocellular damage due to infectious hepatitis, alcoholic liver disease, primary biliary cirrhosis, sepsis, or metabolic abnormalities.

57 Pre-hepatic Jaundice The hyperbilirubinaemia usually comes from haemolysis or breakdown of large haematomas. The bilirubin, not yet conjugated in the liver, is insoluble and does not appear in the urine.

COMMON CAUSES OF OBSTRUCTIVE JAUNDICE The two most common causes of obstruction of the biliary tree are stones and strictures. Long term obstruction can cause secondary biliary cirrhosis. Stones Stones in the common bile duct (choledocholithiasis) are the most common cause of obstructive jaundice. Strictures These can be benign or malignant strictures. Benign strictures are not as common and are either due to inadvertent injury to the common bile duct at the time of surgery (e.g. cholecystectomy), narrowing of a biliary anastomosis or due to scarring from chronic pancreatitis. Rarely a stricture may be due to sclerosing cholangitis - a progressive autoimmune disease that can cause multiple strictures throughout the biliary tract. In 75% of cases this disease is associated with ulcerative colitis. Malignant strictures are more common and may be due to primary or secondary (e.g. nodal metastases) tumours in the region of the common bile duct. The most common primary tumour is adenocarcinoma of the head of the pancreas and it is often incurable. Other tumours may have a better outlook and arise from the bile duct (cholangiocarcinoma), ampulla or duodenum.

58 PATHOGENESIS OF GALLSTONES Cholesterol Stones These account for about 75% of gallstones. Cholesterol, lecithin and bile salts exist in a super-saturated solution in the gallbladder even in many normal subjects. If there is a relative deficiency in bile salts, cholesterol or lecithin, crystals may precipitate, aggregate and form stones. This is, of course, a vast over simplification and a number of other factors are now beginning to emerge as important in the development of cholesterol stones. These include a reduction in phospholipid vesicles, the presence of aggregating and anti-aggregating factors, cholesterolosis and poor gallbladder emptying which may allow the formation of biliary sludge. Ultrasound shows sludge in the gallbladder during starvation and pregnancy.

Pigment Stones In New Zealand, pigment stones account for about 25% of gallstones and they are predisposed to by biliary infection, haemolysis, bile stasis and cirrhosis. Approximately half are radio-opaque due to their calcium content. They are composed of a dense mixture of bacteria, their breakdown products, large amounts of bilirubin and bile acids. CLINICAL PRESENTATIONS Gallstones Jaundice presenting with pain is usually caused by gallstones in the common bile duct (choledocholithiasis). Because of the pattern of innervation it is not possible to distinguish between the pain due to a stone in the common bile duct or in the gallbladder. Gallstones are common, and more so in females and in older patients. The majority of gallstones remain clinically silent and do not need treatment. Only about 10% of patients with gallstones in the gallbladder have stones in the common bile duct, and these stones are usually secondary stones (having migrated from the gallbladder). Primary choledocholithiasis is less common; the stones are softer and usually indicate impaired bile flow.

59

Biliary Colic and Cholecystitis When a gallstone becomes impacted in the neck of the gallbladder or in the cystic duct, distention of the gallbladder occurs and the patient is seized with a severe unremitting pain (biliary colic). This pain comes on over a few minutes, often within 30 minutes of a meal containing fat, is sited in the upper abdomen (usually under the right ribs), may last for several hours and is often associated with nausea and vomiting. The pain may radiate to the tip of the right shoulder blade. If the obstruction is not relieved, the gallbladder becomes inflamed by the chemical action of bile salts. Later, infection supervenes (often E.Coli) the gallbladder wall becomes reddened, thickened and oedematous, and the patient is said to have acute cholecystitis. Examination reveals that the patient is tender in the right upper quadrant, particularly when asked to breathe in. This sign of inspiratory arrest was first described by Dr. John B. Murphy (1857-1916), a famous Chicago Professor of Surgery who was trained in Vienna under Billroth. Murphys sign is the result of the tense and inflamed gallbladder impinging on the fingers when the liver is pushed down on inspiration. Patients with acute cholecystitis are toxic with a fever, tachycardia and leucocytosis. In severe cases there may be a slight rise in bilirubin. Ultrasound shows stones in the gallbladder associated with a thickened and oedematous wall, and often some free fluid around the gallbladder. Although acute cholecystitis usually settles with conservative treatment, a quarter of the patients do not and there is the risk of gallbladder perforation and biliary peritonitis. It is now recommended practice to arrange for the removal of the gallbladder (cholecystectomy) on the next available elective operating list, rather than treat with a prolonged course of antibiotics. Other Clinical Manifestations of Gallstones Stones originating in the gall bladder may also pass into the common bile duct. Very small stones may pass on into the duodenum, but in most cases the stones will not be able to traverse the sphincter of Oddi. A stone or stones in the common bile duct will usually give rise to pain, jaundice and often become associated with infection of the bile

60 (cholangitis). The three cardinal signs of acute ascending cholangitis are pain, jaundice, and rigors with fever (Charcots Triad). These signs were first described by Dr. Jean Charcot (1825-1893), of Paris who created a great neurological clinic. Immense audiences attended his lectures on neuropathic joints and the cardinal signs of cholangitis associated with a gallstone impacted in the common bile duct. He also pointed out the serious implications of untreated cholangitis, which may cause septicaemia and death. Cholangitis can also complicate a benign biliary stricture. Chronic obstruction of the common bile duct can result in cirrhosis of the liver (secondary biliary cirrhosis). Another important condition associated with choledocholithiasis is acute pancreatitis. This is because the common bile duct and pancreatic duct exit into the duoduenum through a common channel in the ampulla. The migration of a stone can initiate acute pancreatitis. Although the mechanism is not well established, it probably involves reflux of the bile into the pancreatic duct and activation of pancreatic enzymes in the gland. A gallstone can erode from an inflamed gallbladder through the underlying duodenal wall to then pass on to the mid small bowel and cause an obstruction (gallstone ileus) or it can erode directly into the common bile duct to cause jaundice. In both cases a fistula is formed.

Strictures Patients with strictures usually present with painless obstructive jaundice. This is an intense cholestatic jaundice with pale stools, dark urine and intense itch. The itch may precede the jaundice. A malignant stricture may be associated with anorexia and weight loss, and a sinister sign is the presence of mid-back discomfort. An important sign, which helps to differentiate a tumour from stones, was described by Dr. Ludwig Courvoisier (1843-1918), a famous Basle surgeon who founded the specialty of Hepato-biliary surgery. He observed that a jaundiced patient with a readily palpable gallbladder usually harbors a malignancy. If the jaundice is due to stones, the gallbladder (from which the stones came) is usually chronically inflamed (chronic cholecystitis) and unable to distend. Although dignified by the term Courvoisiers Law, it can be wrong, as when the

61 gallbladder is chronically obstructed due to a stone (mucocoele of the gallbladder) and there is also a stone in the common bile duct.

INVESTIGATIONS Liver Function Tests There are a number of biochemical tests when interpreted together and in the clinical context give an indication of liver function. With obstructive jaundice the key features are the elevation of serum conjugated bilirubin, serum alkaline phosphatase and the INR (International Normalised Ratio, a measure of coagulation). Alkaline Phosphatase Produced by the cells lining the small bile ducts in the liver, in response to biliary obstruction. Serum Transaminases Are used as markers of hepatocellular damage, and are not usually significantly elevated in obstructive jaundice. Aspartate amino transferase (AST) and alanine amino transferase (ALT) are the ones most commonly measured. Gamma glutamyl transferase (GGT) is also a sensitive and non-specific indicator of liver disease. ALT is found primarily in the liver but AST is present in many tissues as well including the heart, kidney, skeletal muscle and brain. Striking elevations of these transaminases are seen in hepatitis and hepatocellular failure (where the impaired synthetic function of the liver is also reflected in low serum albumin). INR This is a marker of coagulation function. When there is biliary obstruction, bile salts fail to enter the small intestine, critical micellar concentrations are not reached and dietary fat is not absorbed. As a result, fat soluble vitamin K, essential for normal coagulation, is not absorbed and coagulation becomes deranged. The prolongation of the prothrombin time is measured as the international normalised ratio (INR). Patients with obstructive

62 jaundice are given vitamin K intra-muscularly to restore coagulation to normal. This is important before invasive procedures (surgery, endoscopic and/or radiologic).

Imaging the Biliary Tree

Ultrasound This is the first specific investigation of a patient with obstructive jaundice. It is non invasive and readily available. The key things to look for are the presence of stones in the gallbladder, the gallbladder wall thickness, tenderness of the gallbladder when indented by the ultrasound probe (ultrasonic Murphys sign), and the diameter of the common bile duct. Dilatation of the common bile duct (> 5 mm) is expected in patients with obstructive jaundice. Ultrasound is not particularly good at imaging tumours or stones in the lower end of the common bile duct. ERCP This stands for endoscopic retrograde cholangio-pancreatography. It is fundamental to the management of patients with obstructive jaundice. It involves using a side-viewing endoscope to visualize the ampulla of Vater in the duodenum. Cannulation of the

ampulla allows x-rays to be taken of the bile and pancreatic ducts and the insertion of a stent through a stricture to overcome the obstruction. If there is a stone(s) in the bile duct it can be extracted by dividing the sphincter of Oddi (sphincterotomy) and pulling the stones through into the duodenum by using a basket or balloon. CT scan When a tumour is suspected as the cause for the obstructive jaundice, a CT scan is the best way to image it. It may also give important staging information (e.g. hepatic and nodal metastases). MR scan This is an alternative to a CT in some situations. It has the added advantage of being able to reconstruct the bile (cholangiogram) and pancreatic (pancreatogram) ducts (MRCP).

63 This non-invasive approach to duct imaging is being used increasingly. Percutaneous Transhepatic Cholangiography (PTC) If ERCP fails it is possible to access the biliary tree by injecting contrast through a fine needle introduced percutaneously into a bile duct in the liver. The radiologist can also introduce a stent over a guidewire to overcome an obstruction and can also extract stones by this route.

Operative cholangiography (OC) It is also possible to perform a cholangiogram at the time of cholecystectomy by introducing a fine catheter into the cystic duct. If a stone is detected the surgeon has a number of options available to remove them. The common bile duct can be opened and explored using a fine flexible endoscope (choledochoscopy). After removal of the stone(s) the duct is closed over a T-shaped rubber tube. This helps prevent bile leakage and allows subsequent cholangiography to confirm stone clearance (T-tube cholangiogram). Another option is to remove stones during a postoperative ERCP. Plain X rays These are not very helpful as only 10% of gallstones are radio opaque. Pneumobilia is the situation when there is gas in the biliary tree. This can be seen on a plain abdominal Xray or CT scan when there is infection due to gas forming organisms, division of the sphincter of Oddi (sphincterotomy) or when there is a biliary-enteric anastomosis or a fistula. TREATMENT Stones For stones in the gallbladder which are causing symptoms (i.e. biliary colic) the best management is to remove the gallbladder (cholecystectomy). In patients with acute cholecystitis cholecystectomy is best done within a few days of onset. The majority are now done laparoscopically.

64 Patients with gallstones are more likely to have stones in the common bile duct when there is a history of acute pancreatitis, there is evidence of cholestasis on the liver function tests, and there is dilatation of the duct on ultrasonography. If the patient needs a cholecystectomy and has a low chance of common bile duct stones then there is no need to undertake an ERCP before surgery. An OC can be done to confirm that the duct contains no stones. An MRCP is a non-invasive option that is useful when there is the possibility of common bile duct stones. If this is positive the stones can be removed preoperatively with an ERCP. If the patient needs a cholecystectomy but has a high chance of common bile duct stones (i.e. acute ascending cholangitis or severe acute pancreatitis) it is best to undertake a preoperative ERCP to remove the likely stones from the common bile duct. The cholecystectomy can be undertaken later when the patient is not as sick. In some circumstances it is best to perform a cholecystectomy, operative cholangiogram and exploration of the bile duct to remove stones (if found) as one procedure (one stop shopping). Although this can be done laparoscopically, most surgeons still prefer the endoscopist to deal with common bile duct stones. Strictures The minority of patients with malignant strictures can be offered a resection of their tumour, which is the only hope of cure. The CT scan has an important role in excluding patients with evidence of metastatic spread or extensive local invasion. Staging laparoscopy will pick up some additional patients with peritoneal metastases not seen on CT scan. Biopsies are not performed before attempted resection. Resection involves a very major operation to remove the head of the pancreas along with the lower common bile duct, antrum and the entire duodenum. This operation has been named after the New York surgeon, Dr. Allan Whipple, who first described it in 1935. His research showed that it was possible to reverse the bleeding tendency in jaundiced patients by first performing the fairly minor procedure of cholecystogastrostomy. Because vitamin K could then be absorbed again, clotting returned to normal, enabling the major procedure of pancreaticoduodenectomy (Whipples Procedure) to be performed without fear of

65 torrential bleeding. Patients who cannot be resected because of advanced disease or because they are not fit enough for surgery are offered palliation. The obstruction of the bile duct is usually managed with a stent inserted at the time of ERCP. If an attempt at resecting the tumour has not been successful then the small bowel can be connected to the common bile duct (choledocho-jejunostomy) to achieve palliation of the jaundice. Approximately 20% of patients develop obstruction of the duodenum with tumours in this region. This obstruction can be bypassed by connecting the small bowel to the stomach (gastrojejunostomy) and this can often be achieved laparoscopically. Patients with benign strictures of the common bile duct who present with jaundice and/ or recurrent cholangitis can be managed by surgery (resection with reconstruction by performing a choledocho-jejunostomy) or by endoscopy (stent). The former is preferred in most cases.

FURTHER READING FOR INTEREST Chopra, S, Griffin, P.H. (1988): Laboratory Tests and Diagnostic Procedures in Evaluation of Liver Disease. Am J Med 79, 221 Norrby,S. et al. (1983): Early or Delayed Cholecystectomy in Acute Cholecystitis? A Clinical Trial. Br J Surg 70, 163. Perissat, J et al. (1994): Management of bile duct stones in the era of laparoscopic cholecystectomy. British Journal of Surgery 81, 799. Warshaw AL, et al. Medicine 326, 455. FURTHER READING FOR FINALS Tjandra JJ, Clunie GJA, Thomas RJS (eds.). Textbook of Surgery. 2 Edition. Blackwell
nd

(1992): Pancreatic adenocarcinoma. New England Journal of

66 Science Ltd., Oxford, 2001; 270-306

67

Tutorial 6

Upper Gastrointestinal symptoms

Iain Martin
DEFINITIONS Dyspepsia (indigestion): This is a collective term for the non-specific symptoms, which are thought to originate from diseases of the upper gastrointestinal tract. It encompasses many different symptoms and disorders. Generally the individual

symptoms themselves are insufficiently precise to make a specific clinical diagnosis. Dysphagia. Difficulty swallowing, from the Greek meaning disordered eating. Haematemesis: This is the vomiting of blood. Its source is usually proximal to the DJ flexure and most usually indicates a rapidly bleeding lesion. Vomiting of old blood which has been in the stomach for sometime resembles coffee grounds. Melaena: This is the passage of pitch-black stools. The colour and characteristic smell are due to bacterial degradation of blood which originates in the stomach, duodenum or small bowel.

This chapter deal with the common symptoms that patients may present with when suffering diseases of the oesophagus, stomach and duodenum. Whilst not intended to be comprehensive it covers the symptoms accounting for the majority of patients presenting with diseases of the stomach, oesophagus and duodenum.

DYSPEPSIA Most patients with significant pathology of the lower oesophagus, stomach and biliary tract do not present with a discreet, clinically definable, symptom complex but with a rather vague collection of symptoms including upper abdominal and lower chest pain,

68 regurgitation, heart burn and water brash, anorexia, nausea, vomiting, bloating, belching or flatulence. Collectively these symptoms are termed dyspepsia. Dyspepsia is

extremely common, affecting up to 80% of the population at sometime. Therefore investigation of every patient is not possible. Urgent assessment is required if the patient has any of the following alarm symptoms or signs: Chronic GI bleeding Progressive unintentional weight loss Progressive dysphagia Persistent vomiting Iron deficiency anaemia Epigastric mass

Patients aged 55 years or older with unexplained and persistent or recent onset dyspepsia should be referred urgently for endoscopy The investigation of choice for patients with alarm symptoms and those who have other reasons for investigation is upper gastrointestinal endoscopy. An abdominal ultrasound scan may also be ordered if the clinician suspects gallstones or if the upper gastrointestinal endoscopy is negative. Further treatment and investigation of the patient will be based upon the findings of the upper gastrointestinal endoscopy. For patients without alarm features and with previous investigations for dyspepsia, it is possible to treat on the basis that a similar pathology has recurred, (although further work up will be required if the symptoms do not respond to treatment or the diagnosis is in doubt)

Common upper gastrointestinal causes of dyspepsia would include peptic ulcer disease, gastroesophageal reflux disease, gastritis, gallstones and motility disorders of the oesophagus and stomach.

69 Table 2: Findings on upper GI endoscopy in patients presenting with dyspepsia

Diagnosis Reflux oesophagitis Duodenal or Gastric ulceration Gastroesophageal malignancy Essentially normal endoscopy

Proportion of Patients 10 25% 5 10% 1 2% 50 60%

REFLUX OESOPHAGITIS

Probably the commonest disorder of the upper gastro-intestinal tract is reflux oesophagitis. This is due to the failure of the normal mechanisms of the

gastroesophageal junction in preventing the reflux of gastric content into the lower oesophagus. Between 10-20% of the population will suffer from occasional acid reflux giving rise to typical symptoms such as heartburn, a burning retrosternal pain. They may also report an acid taste in the back of the mouth and symptoms of volume regurgitation upon bending or stooping.

The majority of patients with gastroesophageal reflux disease (GORD) can be treated with lifestyle modifications and simple antacids. A few will require longer term

treatment with an anti-secretory drug such as a proton pump inhibitor. A small minority of patients will go on to have surgical treatment of their gastroesophageal reflux disease. This would usual take the form of a fundoplication, either total or partial. This procedure is now usually performed laparoscopically. Chronic GORD can cause a number of complications noticeably lower oesophageal stricture and Barretts oesophagus. Barretts oesophagus is the metaplastic transformation of the normal stratified squamous epithelium of the oesophagus to a columnar intestinal type mucosa. This condition is important because it predisposes the patient to the development of lower third oesophageal adenocarcinoma.

70 Note on Hiatus Hernia There are two types of hemia that occur at the oesophageal hiatus. The majority is sliding hernias in which the gastro-oesophageal junction slides upwards into the mediastinum. This may lead to incompetence of the cardio-esophageal junction and GORD although the majority cause few symptoms and do not need surgical repair. Paraoesophageal hernias occur occasionally, usually in the elderly. Here the fundus of the stomach rotates in front of the oesophagus and hemiates through the hiatus into the mediastinum inside a large hernial sac. Most patients with para oesophageal hernias should have surgical reduction of the hemia and repair of the diaphragm because of the risk of stomach strangulation.

PEPTIC ULCER DISEASE

Peptic ulcer disease is the end result of acid/peptic digestion on a vulnerable gastric or duodenal epithelium. The most common causes for such vulnerability are infection with Helicobacter pylori or the use of non-steroidal anti-inflammatory drugs (NSAIDS). The most common sites for peptic ulceration are the first part of the duodenum and the lesser curve of the stomach.

Pain is the most common presentation for peptic ulceration and is usually epigastric, of a burning or aching nature. Some patients complain of a deep hunger sensation. Although many texts describe classical features of duodenal and gastric ulcer type pain, for the majority of patients the symptoms do not accurately differentiate between the two. Peptic ulceration may also present acutely with bleeding (haematemesis, melaena or anaemia) or perforation giving rise to an acute abdomen with peritonitis. A chronic ulcer of the antrum pylorus or duodenum may cause obstruction of the gastric outlet.

ETIOLOGY OF PEPTIC ULCERATION

Helicobacter pylori: This is an infection of the gastric mucosa and is associated with more than 90% of duodenal ulcers and many gastric ulcers. Through a complex

71 mechanism, Helicobacter pylori renders the gastric or duodenal mucosa vulnerable to acid peptic digestion and may actually also increase gastric acid outputs.

Non steroidal anti-inflammatory drugs: The use of these agents represents the other major aetiological factor for patients with both duodenal and gastric ulceration.

Diagnosis
The diagnosis for most patients with peptic ulceration is confirmed by upper gastrointestinal endoscopy. It is important that biopsies are taken to ascertain the presence or absence of Helicobacter pylori both for gastric or duodenal ulceration and that any gastric ulcer is biopsied. Duodenal cancer is very rare indeed but gastric carcinoma is relatively common. A gastric ulcer found on the greater curve of the stomach is very likely to be an adenocarcinoma.

Treatment
A) Uncomplicated peptic ulcers. If Helicobacter pylori infection is found then this should be treated with 1-2 weeks of triple therapy. Triple therapy includes 2 antibiotics and high dose proton pump inhibitor therapy. For the majority of patients with duodenal ulceration such a regime is curative and follow-up endoscopy is not indicated in the absence of ongoing symptoms. However

patients with gastric ulceration should remain on proton pump inhibitor therapy and have at least one further endoscopy to fully assess healing and take a second set of biopsies for histological examination. If Helicobacter pylori infection is absent then the usual cause of the ulceration is the use of non-steroidal anti inflammatory drugs. These agents should then be avoided where possible and the patient treated with proton pump inhibitor therapy. B) Complicated peptic ulcer disease Peptic ulcers can cause three complications that can require urgent or emergency surgical intervention: perforation, bleeding and gastric outlet obstruction.

72

PERFORATION
Most ulcers which perforate do so from the anterior aspect of the duodenum and cause a sudden onset of severe upper abdominal pain secondary to a chemical peritonitis. The diagnosis is confirmed by a plain erect abdominal x-ray which reveals the presence of free air in 75 85% of patients. For the vast majority of patients the treatment is surgical and usually involves patching the duodenal perforation with omentum. A definitive anti ulcer operation is rarely performed for a perforated duodenal ulcer. Gastric ulcers may also perforate. Although there is a small chance that these are malignant the most commonly used operation for such ulcers now is ulcer excision and repair of the defect, with the excised ulcer being sent for histological examination. Gastric resection may be required for large, complex perforated gastric ulcers.

BLEEDING
The management of bleeding peptic ulceration is discussed elsewhere in this tutorial.

GASTRIC OUTLET OBSTRUCTION

The patient with gastric outlet obstruction presents with prolonged and continued vomiting. Often the patients will present with dehydration and a complex fluid and electrolyte disorder hypochloraemic hypokalaemic metabolic alkalosis. The initial treatment is medical with proton pump inhibitor therapy and intravenous fluid replacement. Estimated fluid losses are replaced with normal saline containing 20 mmol of potassium per litre of fluid (see tutorial 3). Ongoing losses from either vomiting or naso-gastric aspirates are also replaced with normal saline with added potassium. Most patients with gastric outlet obstruction will settle with medical treatment. A proportion will require surgical intervention which generally will take the form of a pyloroplasty possibly combined with a vagotomy.

73
GASTRIC AND OESOPHAGEAL MALIGNANCY

Between 1 and 2 % of patients having an endoscopy for dyspepsia will be found to have a gastric or oesophageal carcinoma.

The detailed management of these patients is beyond the scope of this tutorial, however there are a number of clear principles involved.

1)

Accurately stage the tumour Clinical history and examination Thoraco-abdominal CT Scan Ideally endoscopic ultrasound Laparoscopy in selected patients

2) 3)

Assess the patients overall fitness Manage the patient in consultation with gastroenterologists, oncologists and radiologists i.e. the specialist multidisciplinary team approach is the key to the best treatment outcome.

Surgery remains the main treatment for most patients but increasingly chemotherapy and radiotherapy has a role either alone or in conjunction with surgery.

DYSPHAGIA Dysphagia is a very important and significant symptom and should always should assessed and investigated fully. The initial part of the assessment is a full history and clinical examination. An awareness of the common causes of dysphagia will help guide the taking of a history and in suggesting examination findings to seek. The common causes of dysphagia to consider are:

74 Diseases of the wall of the oesophagus o Peptic oesophageal stricture. Caused from the effects of chronic and severe reflux oesophagitis. May be on the background of Barretts oesophagus o Oesophageal carcinoma. There are two common forms of oesophageal carcinoma. Adenocarcinoma (60%) which arises from Barretts

oesophagus and is again a long term complication of reflux oesophagitis. Squamous carcinoma (40%) which generally occurs in heavy smokers and drinkers although there is a cohort of elderly patients with squamous cancers who do not seem to have these risk factors o Caustic stricture. Caused by the ingestion of strong acids or alkalis. Less common than previously found due to the widespread use of child proof containers. More common in the developing world Diseases affecting the peristaltic ability of the oesophagus o Achalasia. This is a disorder where the lower oesophageal sphincter mechanism fails to relax when a peristaltic wave approaches. Often presents insidiously with intermittent symptoms and sometimes dysphagia for liquids rather than solids o Oesophageal spasm and other oesophageal motility problems o Neurological problems o Scleroderma Diseases causing dysphagia through external pressure on the oesophagus o Hilar lymphadenopathy

Investigations for dysphagia Barium swallow: This investigation is complementary with upper GI endoscopy and is often used as the initial test for dysphagia. It is particularly important in assessing the causes of dysphagia affecting the oro-pharynx and upper oesophagus, for example pharyangeal diverticulum

75 Upper GI endoscopy: Upper GI endoscopy will be carried out in the majority of patients with dysphagia. It allows accurate visulaization of the wall of the oesophagus but cannot assess well neuromuscular problems and has limitations in the upper oesophaus Oesophageal manometry: This investigation involves the passage of a pressure transducing catheter into the oesophagus to record the pressure waves of the peristaltic mechanism. It is always used as a second line test after barium swallow and / or endoscopy when neurological problems such as achalasia are suspected. Other tests: chest XR or thoracic CT scan may be required if hilar lymphadenopathy or other causes of extrinsic oesophageal compression are suspected. Management Detailed management will depend upon the cause of the dysphagia and is beyond the scope of this tutorial. The following paragraphs detail principles of treatment for the commonest or important causes of dysphagia Peptic oesophageal stricture The vast majority of patients with a peptic oesophageal stricture can be managed with endoscopic dilatation of the stricture and proton pump inhibitor therapy. It is important that prior to dilatation the stricture is biopsied because of the possibility of malignancy. Several dilatations may be required. The proton pump inhibitor should be continued long term. Only a very few patients will ever need surgical therapy. Achalasia Having established the diagnosis the treatment is either endoscopic balloon dilatation or laparoscopic myotomy of the lower oesophagus. The latter option is preferable provided appropriate surgical expertise is available. Oesophageal carcinoma is discussed earlier in the chapter

HAEMATEMESIS AND MELAENA

A patient presenting with either haematemesis or melaena must be taken seriously. Although for many patients it represents a short lived and easily treated clinical problem, the overall in-hospital mortality following admission with an episode of haematemesis or

76 melaena is between 10 and 14 percent. Table 1 lists the commoner causes of

haematemesis and melaena and the associated risk of mortality. Table 1-Diagnosis and mortality in upper GI bleeding
Disease Peptic ulcer disease Gastric erosion Mallory Weiss tear Oesophageal Varices Upper gastrointestinal cancer Multiple pathologies and other causes Proportion of all cases 40% 10% 5-10% 10-15% 5% 25% Mortality due to bleeding 5% 7% 2% 30% 15% 7%

When confronted with a patient presenting with haematemesis or melaena the first step in their treatment is a rapid overall clinical assessment. This should include a concise and focussed medical history including details of previous illnesses. As part of the clinical examination the blood pressure should be taken. The presence of shock (pulse>100 beats per minute, systolic blood pressure<100 mm of mercury) immediately places the patient in a high-risk category, which demands the full attention of the treating team.

Having taken a history and examined the patient the next phase of the treatment process is the initial resuscitation. It is important that basic principles are followed and to ensure that the patient is breathing well and is adequately oxygenated. The majority of patients with a significant upper gastrointestinal bleed require supplemental oxygen. Peripheral intravenous access should be obtained using two large intravenous cannulae. Blood should be taken for routine examination and sent for cross-match. Initial fluid resuscitation should be started with either crystalloid or colloid solutions (see Tutorial 3). The sick or shocked patient should have a urinary catheter inserted and consideration given to central venous pressure monitoring. Following resuscitation the next phase of the patients management is an urgent or emergency upper gastrointestinal endoscopy. The endoscopist will locate, if possible, the

77 source of blood loss and will identify two pathologies suitable for endoscopic treatment. These are oesophageal varices and gastric or duodenal peptic ulcers. Varices may be treated endoscopically by injection or, more commonly, banding. Peptic ulcers may be treated by injection, diathermy, heater probe, laser or endoscopic clips. In the presence of bleeding peptic ulcers the endoscopist will describe so-called stigmata, which are associated with increased risks of re-bleeding. Following completion of the upper GI endoscopy the patient can be placed in a group at higher risk of further problems and rebleeding or a low risk group. The high risk group includes patients over the age of 60, those who presented with shock, those who presented with a bleeding gastric ulcer and patients who are found to have endoscopic stigmata associated with their bleeding peptic ulcer. These high-risk patients demand special attention of the team under whose care they are. Patients with bleeding oesophageal varices form a particularly high-risk group and should be managed in a specialist unit with all relevant expertise available. If the patient is found to be bleeding from a peptic ulcer of the stomach or duodenum they should be placed on full dose proton pump inhibitor therapy (Losec) as there is now good evidence that this prevents re-bleeding in a number of patients. There is also good evidence that early eradication of Helicobacter pylori prevents re-bleeding in the convalescence phase and eradication therapy should be commenced as soon as is practical. The next question that arises is when to operate upon patients with upper gastrointestinal bleeding. This tutorial will confine itself to the decision making process for operating upon patients with bleeding peptic ulceration and will not deal with issues surrounding surgical treatment of other causes of upper GI bleeding. The first group of patients, which are in fact a very small minority of the total number of patients presenting with upper GI bleeding, who require operations are those who have exsanguinating haemorrhage that cannot be controlled endoscopically. The second group of patients are those who have had an initial sentinel bleed which either stops spontaneously or is controlled endoscopically and who subsequently have a further bleed.

78 For patients less then 60 years of age without any significant co-morbidities. These patients should be operated on after two re-bleeds or after they have required more than 6 units of blood in any 24 hour period or more than 12 units of blood in total. For patients older than 60 years or for those who have other significant co-

morbidities. An operation should be performed after one re-bleed or when more than 4 units of blood has been transfused in 24 hours or they have received more than 8 units of blood in total. Because of the greater risk of bleeding with gastric ulceration and the higher mortality associated with gastric ulcers there is some evidence that the threshold for operating upon a bleeding gastric ulcer should be lower then that for a bleeding duodenal ulcer. Having made the decision to operate upon a patient with bleeding peptic ulcer, the next question is which operation should be performed. The primary goal of the operation is to control the bleeding point. The secondary goal of the operation is to reduce the risk of re-bleeding.

Until recently it was felt inappropriate not to offer patients with a bleeding peptic ulcer a definitive anti ulcer operation at the time of their emergency laparotomy to control the bleeding. However, since the introduction of proton pump inhibitors many surgeons will now simply under run the bleeding point in the base of the ulcer and treat the patient with proton pump inhibitor therapy and, if appropriate, Helicobacter pylori eradication treatment. In the case of a bleeding gastric ulcer it may actually physically be necessary to excise the ulcer and bleeding point completely and close the defect made in the stomach. The excised ulcer is sent for pathological examination, because it has to be remembered that a number of gastric ulcers will in fact be a malignant tumour, which has ulcerated. Should a definitive anti ulcer procedure be deemed to be necessary then the choice is usually between truncal vagotomy and a drainage procedure (pyloroplasty or gastroenterostomy) or very occasionally a highly selective vagotomy. Gastric resection should be avoided in the majority of cases because of the risk of excessive mortality in this situation.

79

STOMACH OPERATIONS (GLOSSARY OF TERMS)

Vagotomy (two types of vagotomy) Highly selective vagotomy: Only the nerves to the parietal cell mass are cut and the stomach empties normally because the antrum is still innervated.

Truncal vagotomy: Both vagi are divided as they enter the abdomen. Not only is the parietal cell mass denervated but the antrum and pylorus are also and the stomach will not empty. A drainage procedure is therefore required (pyloroplasty or

gastrojejunostomy). Gastric Resection There are two broad groups of gastric resection. Partial gastrectomy: A proportion of the distal stomach is removed. This may just be the antrum or up to of the stomach in the case of a subtotal gastrectomy performed for carcinoma. Total gastrectomy: The whole stomach is removed. Intestinal continuity is restored using the Roux-en-Y link up. Gastric reconstruction
There are three ways of restoring gastrointestinal continuity after partial resection of the stomach:

a)

Billroth I reconstruction: When the proximal stomach is anastomosed to the first part of the duodenum.

b)

Billroth II reconstruction: Where the proximal stomach is anastomosed to a loop of proximal jejunum.

c)

Roux-en-Y reconstruction: The small bowel is divided just below the DJ flexure. The distal limb of the divided small bowel is anastomosed to the stomach or to the oesophagus in the case of a total gastrectomy. The proximal limb of divided small

80 bowel, carrying bile and pancreatic juice, is reanastomosed to the jejunum some 40 cm below the upper anastomosis. Such a reconstruction method reduces the problems with symptomatic bile reflux in the gastric remnant or oesophagus.

FURTHER READING FOR FINALS Tjandra JJ, Clunie GJA, Thomas RJS(Eds) Textbook of Surgery 2nd Edition Blackwell Science Ltd.Oxford 2001 pp 98-137

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Tutorial 7

Bleeding from the Anus, Rectum and Colon

Bryan Parry and Andrew G Hill

BLEEDING FROM THE ANUS Anatomy of the Anal Canal The anal canal is 4-5cms in length. It is surrounded by two concentric rings of muscle: an inner ring of involuntary muscle - the internal sphincter, and an outer ring of voluntary muscle - the external sphincter. The dentate line is seen as a wavy line in the mucous membrane of the anal canal exactly halfway up the internal sphincter. Above the dentate line there is columnar epithelium - thus no pain is felt in this region. Below the dentate line there is progressively thickening squamous epithelium - thus pain is felt in this area. The internal haemorrhoidal plexus of veins lies in the submucosal layer above the dentate line. This plexus comprises a circle of veins supported by connective tissue cushions. The external haemorrhoidal plexus of veins lies under the skin surrounding the anal verge. Physical Examination of the Anal Canal The external sphincter is under voluntary control, whilst the internal sphincter is under involuntary control. During digital rectal examination, one can feel the groove between the edge of the internal sphincter and overlapping external sphincter just inside the anal canal. After about 4 cms the finger reaches the capacious rectum. Posteriorly, a bar is felt in this region, this is the puborectalis sling. This sling pulls forward at the junction of the anus and rectum and provides a shutter mechanism which is the most important factor in

82 continence. If this muscle fails to relax on defaecation obstructed defaecation can occur. The anal canal is examined via a proctoscope (anoscope in America). This short tube is passed through the anal canal into the lower rectum. It is then slowly withdrawn as the patient strains down. When the opening of the proctoscope reaches the dentate line, the whole of the internal haemorrhoidal plexus can be visualized just above it. N.B. It should be remembered though that no examination of the anal canal is complete unless the rectum has been examined as well.

Haemorrhoids (Piles) A deficiency of the connective tissue cushions in which the internal haemorrhoidal plexus of veins is embedded predisposes to haemorrhoids which are simply varicosities (dilated abnormal veins) of the internal plexus. They are prone to occur particularly if there is associated constipation. If the patient is examined in the lithotomy position via a proctoscope, the varicosities can be seen to be present at the 3 oclock, 7 oclock and 11oclock positions. There are four degrees of severity: First degree Bleeding occurs from the anus after a bowel motion. In first degree haemorrhoids the hard stool coming down the anal canal crushes the veins and as a consequence bright red blood coats the stool or comes just after the stool is passed. These haemorrhoids are common. Almost everyone will have an episode of first degree haemorrhoids at some time in their lives particularly when constipated. Since the varicosities occur beneath the anal canal epithelium above the dentate line, there is no pain associated with internal haemorrhoids. Second degree The varicosed veins fall out after a bowel motion. Patients with second degree haemorrhoids have the feeling that a mass has come out of the anus after passing a bowel

83 movement. This mass reduces spontaneously but is associated with a dragging discomfort. These haemorrhoids do not usually bleed. Third degree The varicosed veins stay out of the anal canal after a bowel motion and may thrombose (fourth degree). Patients with third degree haemorrhoids have a mass which comes out of the anus and stays out. They are coated with mucus producing epithelium and perianal soiling occurs which is distressing for the patient. These haemorrhoids cause a dragging feeling, perianal tenderness and debilitating dull pain. Fourth degree Patients with fourth degree haemorrhoids have a large thrombosed mass protruding from the anus. The patient may suffer from excruciating pain.

Treatment First degree haemorrhoids are initially treated by increasing fibre in the diet. If this fails a sclerosant is injected just above the connective tissue cushions at the top of the anal canal, i.e. at the anorectal ring. This sclerosant (5% phenol in almond oil) excites fibrosis,and fixes the cushion to the anal canal wall. Alternatively rubber bands are put on the haemorrhoids, cutting the varicosities off totally (like the process used for removal of lambs tails on the farm). Second degree haemorrhoids are also treated by the injection of sclerosant or rubber band ligation. Some advanced second degree piles are treated surgically. Third and fourth degree haemorrhoids are usually treated surgically-the varicosed veins are dissected out, tied off and removed. Haemorrhoidectomy is one of the more painful operations of surgery. An alternative method using a circular stapling device has been developed which may reduce the pain.

External Haemorrhoids (Perianal Anal Haematoma)

84 This very painful condition occurs as a result of rupture of the veins of the external haemorrhoidal plexus. It may occur during vigorous activity. After a few days the haematoma undergoes fibrosis, but there remains a skin tag at the site. Sometimes the condition is so painful that the haematoma needs to be drained. Anal Fissures Anal fissures and haemorrhoids often occur together. A fissure is a tear in the anoderm below the dentate line. It usually arises after a hard faecal mass has been passed. Pain occurs during and after defaecation and as a consequence the patient is reluctant to pass a bowel motion and a chronic self perpetuating cycle can result. If the fissure becomes chronic, heaped up oedematous granulation tissues forms a characteristic sentinel pile. The internal sphincter goes into severe spasm and perpetuates the fissure. There is a history of severe anal pain occurring both during and for some time after passing a motion. Bright red blood coming after the stool has been passed is usually noticed. Diagnosis of fissure is made by inspection. The patient will be sitting on the edge of his chair. He will have an aching anus which is extremely difficult to examine (shy anus) and an anaesthetic may therefore be required to make a diagnosis. Fissures must be distinguished from anal fistulas. (These arise after a perianal or anal abscess has burst onto the skin surrounding the anus. If the skin opening connects with the anal canal then a fistula is said to be present.) Treatment of Anal Fissure Non surgical measures, including glycerol trinitrate ointment or botulinum toxin injection, to temporarily relax the internal sphincter along with pain relief and efforts to increase the bulk of the stool and regulate the bowel habit (Metamucil or Isogel) are used as initial therapy. A lateral subcutaneous sphincterotomy should be considered if the fissure remains refractory. A knife is passed between the external and internal sphincters and the lower portion of the internal sphincter is divided, thus breaking the spasm so that motions can be passed painlessly. The fissure usually heals promptly within three weeks

85 after this minor procedure.

BLEEDING FROM THE RECTUM Anatomy of the Rectum The rectum extends from the ano-rectal junction, about 4 cm from the anal verge, to the rectosigmoid junction at 13-15 cm from the anal verge. Physical Examination of the Rectum The lower two thirds of the rectum can be examined by the finger (P.R.examination). A sigmoidoscope (proctoscope in America) is a rigid metal tube about 30 cms long which contains a light source and a lens system and it is the instrument most commonly used to examine the rectum. Tumours of the Rectum Tumours of the rectum may bleed. The blood, usually bright red but sometimes clots, mixes with the stool or coats the stool as it is stored in the rectum. This bleeding may arise from: Benign Tumours of the Rectum (Polyps) Polyps are small masses of tissue that project into the lumen of the rectum. Most Polyps are asymptomatic but the larger the lesion the more likely it is to cause symptoms. Rectal bleeding is by far the commonest complaint - it is usually intermittent and blood flecks the stool. P.R. examination usually fails to detect any abnormality. The diagnosis is therefore made by sigmoidoscopy at which time the polyps are removed and sent for histology. There are 4 types of polyps: neoplastic, hamartomatous, inflammatory and metaplastic (see below under Benign Tumours of the Colon). Only the neoplastic polyps have malignant potential. Cancer is found in 45% of neoplastic polyps which are greater than 2 cm in diameter. Malignant Tumours of the Rectum

86 Adenocarcinoma is the only malignant tumour of the rectum of importance. There is a high incidence of this disease in New Zealand. Over two thirds of these tumours can be felt with the examining finger at which time a hard craggy mass or ulcer is palpated leaving little doubt as to the likely diagnosis. The clinical diagnosis is confirmed by sigmoidoscopy and biopsy. Because these tumours can so often be felt by the finger surgeons teach that in any case of rectal bleeding If you dont put your finger in it you will put your foot in it. Treatment is by anterior resection where the tumour containing rectum is removed and the colon is stapled to the remaining low rectum or anal canal. If the cancer invades the puborectalis muscle clinically or radiologically (MRI Scan), the whole rectum is removed together with the anal canal (abdomino - perineal resection of the rectum) usually after preoperative chemoradiotherapy. In this situation the patient is left with a permanent left iliac fossa colostomy. Prognosis depends on the pathological stage of the tumour. In 1958, London pathologist Dr. Cuthbert Dukes published his research on the spread of rectal cancer and its effect on prognosis based on the study of 2,500 operation specimens. The crude 5 year survival for all patients treated by surgical removal of the primary tumour was 50%. When he related the local spread of the tumour to ultimate survival he was able to describe 3 stages. Dukes A-the cancer is confined to the bowel wall - 90% 5 year survival Dukes B-through bowel wall, no nodal involvement - 60% 5 year survival Dukes C-through bowel wall with nodal involvement - 30% 5 year survival

Inflammation of the Rectum (Proctitis) This is associated with blood mixed in the stool. The stool is usually loose and frequently contains pus and mucus as well. Proctitis Diffuse inflammation of the rectal mucosa. When seen with a sigmoidoscope, the mucosa is inflamed, bleeds easily and may be coated with pus. Ulcers may also be seen. If this inflammation is confined to the rectum the condition is called proctitis. If it extends above the rectum it is known as proctocolitis or sometimes just colitis.

87 Proctitis may be due to a specific infection, be secondary to radiation therapy or due to inflammatory bowel disease (Ulcerative Colitis, or Crohns Disease). Bright blood is mixed in with the stool and the patient usually presents with bloody diarrhoea (up to twelve motions a day). Episodes of proctitis due to inflammatory bowel disease tend to be intermittent every few months, lasting about 3-6 weeks. The diagnosis is made by sigmoidoscopy and biopsy after exclusion of specific infections by stool culture. Ulcerative colitis and Crohns proctitis are treated by steroids administered locally via an enema. Radiation proctitis is treated by topical formalin or argon plasma coagulation.

BLEEDING FROM THE COLON Surgical Anatomy of the Colon Surgeons talk of the sigmoid colon, left colon, transverse colon and right colon because of their distinct blood supply. For surgical treatment of cancer the tumour bearing colon must be resected together with the draining lymph nodes. Since these lymph nodes follow the main colon arteries these resections are described as sigmoid colectomy, left hemicolectomy, transverse colectomy and right hemicolectomy. Physical Examination of the Colon This is done either by a double contrast Barium Enema, CT Colonography or by a video fibre-optic colonoscope. Tumours of the Colon Benign Tumours of the Colon Polyps can occur in any part of the colon. As in the rectum, neoplastic, hamartomatous, inflammatory and metaplastic polyps can occur. Neoplastic polyps (adenomas) are of three histological types which are variations of one histological process -tubular adenomas, tubulovillous adenomas, and villous adenomas. The potential for cancerous transformation increases with time and is related to the size of the adenomas and an increasing villous nature of the polyp. Most adenocarcinomas of the large bowel evolve from adenomas. For this reason, all polyps of the colon are removed. A snare, inserted

88 via a colonoscope, is passed around the base of the polyp which is then cauterized. Although it is not uncommon for patients to have several polyps there is a rare but important condition called Familial Adenomatous Polyposis (FAP) in which hundreds of polyps may be seen. Hereditary Colorectal Cancer Syndromes These include FAP and Hereditary Non-Polyposis Colorectal Cancer (HNPCC.) FAP is an autosomal dominant disorder although 25% of new cases are due to spontaneous new mutations of the APC gene. Cancer develops before the age of 40 in nearly all untreated patients. HNPCC is also inherited in an autosomal dominant pattern. It is characterized by early age of onset of a colon cancer, predominace of proximal lesions, tendancy for synchronous or metachronous tumours and often an excess of tumours at other sites. The genes linked to HNPCC are those involved with spellchecking DNA for replication errors. There are over 10 described in humans but the common ones affected are LMLH1 and LMSH2. Mutations of these can be easily indirectly inferred by immunostaining resected tumours for their respective gene products (LMLH1 and LMSH2 proteins), which will be absent. Malignant Tumours of the Colon Adenocarcinoma - New Zealand has one of the highest incidences of carcinoma of the colon in the world. As for the rectum, colon cancer is classified by Dukes classification, and the prognosis is the same as that for the rectum. Presentation Patients with right sided cancer of the colon usually present with occult bleeding and iron deficiency anaemia and a right iliac fossa mass may be palpable. Left sided cancer of the colon usually presents with intermittent diarrhoea and constipation, blood mixed in with the stool, or obstruction of the large bowel. Diagnosis This is made by barium enema or by colonoscopy.

89 Treatment For adenocarcinoma right hemicolectomy, transverse colectomy, left hemicolectomy or sigmoid colectomy with immediate anastomosis. For FAP total coloectomy and ileorectal anastomosis (many polyps) or proctocolectomy with ileo-anal J pouch anastomosis (hundreds or thousands of polyps). Diverticular Disease This is a disease of Western Society and usually involves the sigmoid colon. It may cause bright red rectal bleeding which is usually selflimiting. The diverticulae may also become inflamed (diverticulitis) and present as a left sided appendicitis or may perforate causing a local abscess (pericolic abscess) or faecal peritonitis.

Angiodysplasia Submucosal arterio-venous malformations may occur in elderly patients and present with bright red rectal bleeding. Diagnosis is usually made by colonoscopy. When noted these submucosal vascular abnormalities may be coagulated.

INFLAMMATORY BOWEL DISEASE The chronic passage of loose stools with blood, mucus and pus suggest the patient may be suffering from inflammatory bowel disease. Although there are a number of types of inflammatory bowel disease, the commonest are Ulcerative Colitis and Crohns Disease. Ulcerative Colitis Ulcerative colitis always starts in the rectum and progresses proximally. It is limited to the large intestine and is a disease which is histologically confined to the mucosa. It may predispose to cancer if it involves the whole colon over a period of 20 years or more. Treatment is at first medical (Pentasa to prevent attacks, steroids to limit attacks and cyclosporin when steroids fail) and if this is unsuccessful then surgery may have to be employed. Surgery involves removal of the rectum and colon with formation of a new

90 rectum from the ileum ( Ileo-anal- anastomosis with J Pouch). Crohns Colitis This disease may occur anywhere in the tubular gut and is patchy in its distribution. There are three broad patterns of Crohns Disease: jejuno-ileal disease, which has the worst prognosis, ileo-caecal disease which has the best prognosis and Crohns Colitis. Although the disease may be confined to and involve the whole colon, occurrence localised in the rectum or the ileo-caecal area is more common. Histologically, it is a transmural disease and when it involves the whole colon it may predispose to cancer but this is not as common as it is in ulcerative colitis. Treatment is at first medical but if the colitis becomes severe then panproctocolectomy and ileostomy is indicated. For disease proximal to the colon resection with end to end anastomosis or strictureplasty are the usual surgical procedures.

FURTHER READING FOR FINALS Tjandra JJ, Clunie GJA, Thomas RJS(eds.). Textbook of Surgery. 2 Edition. Blackwell Science Ltd., Oxford, 2001; 153-267
nd

91

Tutorial 8

Swellings of the Thyroid Gland (Goitre) and other Swellings of the Head and Neck
Richard Harman

ANATOMY Head and neck swellings usually occur within existing anatomical structures. The key to diagnosis is therefore an understanding of the principles of the regional anatomy. This includes: Anterior Triangle of the Neck The anterior triangle of the neck, where most swellings of the neck occur, is bounded laterally by the anterior margin of the sternomastoid muscle, superiorly by the inferior border of the mandible and medially by the midline. The anterior triangle contains the median visceral column comprising the pharynx, larynx and trachea and the thyroid and parathyroid glands. Cervical Lymph Nodes Lymph nodes occur in the suboccipital region, the posterior triangle, and the supra clavicular region. Much more important though are the deep cervical lymph nodes in association with the carotid sheath. Enlargements of these lymph nodes are the commonest cause of swellings in the neck.

92 THE THYROID GLAND This bilobed gland is not normally palpable and lies deep to the strap muscles in the neck. The recurrent laryngeal nerves supply the intrinsic muscles of the larynx and are closely applied to the posterior aspects of the thyroid lobes. During thyroidectomy the surgeon displays these nerves so that inadvertent damage is avoided.

THE PARATHYROID GLANDS There are usually 4 glands, each weighs about 30-40 mg. Their close approximation to the posterior aspect of the thyroid lobes also makes them vulnerable to damage during thyroidectomy. THE PAROTID GLAND The parotid gland lies in front of and below the lower half of the ear. Swellings in the gland may push the ear lobe upwards. The facial nerve passes through the stylo mastoid foramen into the parotid gland which divides it into a superficial and a deep lobe. Since the bulk of the gland is in the superficial lobe this is where most swellings occur. The operation of superficial parotidectomy removes the superficial lobe and preserves the facial nerve. Malignant tumours of the parotid may invade the facial nerve and cause facial paralysis.

SWELLING OF THE THYROID GLAND (GOITRE) The student should try to decide the thyroid status of the patient, whether thyrotoxic, hypothyroid or euthyroid. TSH (thyroid stimulating hormone levels) alone will confirm the status.

When examining the thyroid the student should ascertain if there is one lump (solitary thyroid nodule) or the whole thyroid is enlarged (Multinodular Goitre or Graves Disease).

93 THE EUTHYROID PATIENT (TSH NORMAL) Solitary Nodule Fine needle aspiration has become the cornerstone of assessment of solitary thyroid nodules. It will place the nodules into benign, suspicious or malignant groups. Suspicious and malignant lesions are treated with surgery. It will diagnose papillary, medullary, anaplastic but cannot differentiate between follicular adenoma or carcinoma. Therefore, most follicular lesions are removed. Most thyroid cancers are termed differentiated (papillary or follicular). Their behaviour is largely dependent on the patients age and the size of the tumour. A tumour in a young patient which is less than 2cm in diameter follows a benign course. Most thyroid cancers are treated with total thyroidectomy. This means the patients require thyroxine replacement lifelong. If the differentiated thyroid cancer is aggressive radioactive iodine is used to ablate remaining thyroid and metastatic disease.

Multiple Nodules and Diffuse Swelling Commonly caused by a multinodular goiter (MNG). The most common cause worldwide is iodine deficiency. In the western world the cause is probably multifactorial;

hereditary, dyshormogenesis, naturally occurring goitregens and circulating goitregens have all been proposed. Ultrasound examination is often useful in the assessment of MNG and any dominant nodules should be biopsied with FNA. Surgery is indicated for cosmesis, compressive symptoms and retrosternal goitres. THE HYPERTHYROID PATIENT (TSH SUPPRESSED) Solitary Nodules A single hot solitary nodule usually develops within a multinodular goitre, although it can result from localised hyperplasia (Plummers Disease). Nodules >3cm are generally removed surgically whilst those less than 3cm are treated with I .
131

94 Diffuse Swellings Most thyrotoxic diffuse swellings are caused by Graves Disease. 10% of patients will have associated infiltrative eye disease (proptosis and opthalmoplegia). Graves is commonly treated with antithyroid drugs (propylthiouracil and carbimazole) and then I ablation. Those with larger glands undergo surgery.
131

SWELLING OF THE SALIVARY GLANDS The salivary glands of surgical importance are the parotid gland and the submandibular gland. The swellings are of three types: Infective Acute viral (mumps) and bacterial illness can affect the parotid gland and less commonly, the submandibular gland. Acute suppuritive parotitis occurs in dehydrated ill patients and treatment is by rehydration, antibiotics and proper mouth hygiene. Obstructive The salivary glands may be blocked by calculi. These are composed of the same material as that which forms scale on the teeth. The submandibular gland is particularly prone to form quite large calculi which block its duct and cause pain on eating. Infection may also supervene. If the stone is located distally in the duct, it can be removed locally through the floor of the mouth, otherwise the whole gland must be removed. Fine calculi may occur in the parotid but these are uncommon.

Neoplastic Tumours of the salivary glands account for 5% of head and neck tumours. The incidence of malignancy in the glands is inversely proportional to the size. 70% of the tumours occur in the parotid, 80% of which are benign. 70% of the tumours in the parotid are pleomorphic adenoma (mixed parotid tumour). It is a slow growing adenoma with an incomplete capsule. Small protrusions of tumour through its capsule prevent its removal by enucleation. Hence, it is removed by the operation of superficial parotidectomy.

95 Pleomorphic adenomas are uncommon in the submandibular gland. Malignant The presence of a rapidly enlarging swelling, pain and large lymph nodes with facial nerve paralysis, suggests that the parotid swelling is malignant. 25% of parotid tumours are malignant and the figure is higher in the submandibular gland. The most common malignant tumour is a muco-epidermoid tumour. Adenocarcinoma and adenoid cystic carcinomas may also occur. Treatment is total parotidectomy with removal of involved lymph nodes.

OTHER SWELLINGS OF THE HEAD AND NECK Thyroglossal Cyst The thyroid gland develops from the lower portion of the thyroglossal duct which begins at the foramen caecum at the back of the tongue. If a portion of this duct remains patent it can form a cystthyroglossal cyst. These are commonly found in two sitesbetween the isthmus of the thyroid gland and the thyroid cartilage and just above the thyroid cartilage. Since they are attached to the base of the tongue, they move when the tongue is protruded. They should be removed for infection is common. Branchial Cyst These are thought to be remnants of the first or second branchial pouch. They present as painless swellings which protrude from behind the anterior edge of the upper third of the sternomastoid muscle. Since lymphoid tissue in the cyst wall may become infected, surgical removal is usually recommended. Cystic Hygroma (Lymph Cyst) These are congenital lymphangiomas which are usually found in the subcutaneous tissues at the base of the posterior triangle of the neck. They may reach a huge size and cause respiratory embarrassment.

96 Pharyngeal Diverticulum This is caused by herniation of pharyngeal mucosa through a weak area in the inferior pharyngeal constrictor muscle secondary to cricopharyngeal disco-ordination. The patient complains of dysphagia, regurgitation of food, chronic cough and recurrent aspiration pneumonia. Protein Energy Malnutrition may be severe. A swelling occasionally is noted in the neck and pressure on it causes gurgling sounds and regurgitation. A barium swallow confirms the diagnosis. Removal of the diverticulum and division of the cricopharyngeal muscle results in total resolution of the problem. SWELLINGS OF CERVICAL LYMPH NODES Acute Adenitis Infections of the head and neck may lead to acute lymphadenitis. These are firm tender nodes that decrease in size when infection is resolved. Chronic Adenitis These may be secondary to tuberculosis, sarcoidosis or glandular fever. Tuberculosis of the neck glands should not be forgotten. The patient complains of a lump in the neck that may or may not be painful. Examination reveals enlarged nodes matted together. The nodes may coalesce, liquify and turn into a cold abscess. This may burst through the deep cervical fascia and point on the skin (collar stud abscess). Diagnosis is by biopsy and treatment is by chemotherapy. Reticulosis Lymphoma usually (lymposarcoma and reticulosarcoma rarely) presents as painless lumps in the neck which grow slowly. Malaise, weight loss and pallor are common symptoms. Biopsy confirms the diagnosis. Metastases to Lymph Nodes Metastatic deposits of cancer cells in the cervical lymph nodes are the commonest cause of cervical lymphadenopathy in adults. The primary cancer is most often in the upper aero-digestive tract but every possible site must be examined. In 15% of cases the primary cancer is below the clavicles and in 5% the primary is occult. These swellings

97 grow slowly and new swellings may appear. Fine needle aspiration of the nodes is performed and the collected cells sent for cytological examination. This confirms the diagnosis of malignancy. The cancer can then be staged in order to classify the tumour, estimate the prognosis and plan treatment.

FURTHER READING FOR INTEREST Tjandra JJ, Clunie GJA, Thomas RJS(eds.). Textbook of Surgery. 2 Edition. Blackwell Science Ltd., Oxford, 2001; pp334-344
nd

FURTHER READING FOR FINALS

Nil

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Tutorial 9

Breast Disease
Wayne Jones

BREAST CLINIC One Stop Clinic The clinic relies on a multi-disciplinary team consisting of a Breast Surgeon, Radiologist, Cyto-pathologist and the Breast Care Nurse. There may also be input from Medical and Radiation Oncology, Plastic Surgery, Clinical Genetics and Health Psychology. The aim is to fully assess a newly referred patient in one visit. The diagnosis is then explained and treatment options given. For those women diagnosed with cancer ongoing support and education are provided. Indications for Referral Any woman with the following breast problems should be referred to a breast clinic for Specialist assessment: Discrete breast mass Persisting asymmetrical breast nodularity Nipple discharge, particularly if over 50 years Severe mastalgia Nipple changes

99 Strong family history of breast or ovarian cancer

Of those referred, only 5-10% prove to be malignant.

TRIPLE ASSESSMENT This involves: Clinical assessment medical history, risk factors and physical examination Imagingultrasound +/- mammography Fine needle aspiration cytology (FNA) Further tests such as core biopsy or open surgical biopsy are sometimes required. With triple assessment the accuracy of diagnosis is up to 99.6%. That is, if a lesion is assessed as being benign using all three modalities, the surgeon is wrong four times in a thousand. PRESENTING COMPLAINT Women tend to present with three types of symptoms, and each symptom needs further elucidation: Lump-duration, size, shape, tenderness and relationship to menses Pain-duration, unilateral or bilateral, cyclical or non-cyclical and severity Nipple dischargetiming of discharge, colour, unilateral or bilateral, single duct or multiple ducts and lactational state. RISK FACTORS The risk factors for breast cancer include: Female gender

100 Increasing age Previous breast cancer (Invasive or DCIS) Previous atypical ductal hyperplasia (ADH) on biopsy Family history particularly first degree relatives diagnosed with bilateral breast or ovarian cancer at a young age Factors that increase cyclical oestrogen exposure over the lifetime: -Early menarche (<11y) -First pregnancy after 35y of age -Breast feeding is protective -Delayed menopause (>53y) Prolonged use of the combined oral contraceptive pill (>10y) Prolonged use of hormone replacement therapy (>5y)

EXAMINATION Examination must be performed in a warm private environment with good light and a chaperone. The steps are: Inspection -Arms at side, raised, on hips -Look for colour change, dimpling, contours, and nipple changes Breast Palpation -Patient supine, use the flat of the hand

101 -Assess all four quadrants, the central area and the axillary tail -Fully assess the characteristics of any detected lumps -Examine the other side Nodal basins -Axillary & supraclavicular regions -40% false negative on examination -30% false positive on examination Chest Liver Axial skeleton

The clinician needs to address two questions: 1. 2. Is there a discrete palpable lump? If there is, full triple assessment is required. If this is a breast cancer, how advanced is the disease? This allows tumour staging

and the development of a treatment plan.

MAMMOGRAPHY Mammography is used for women over 30 years with symptomatic lesions. Both sides need to be imaged with two views of each side (MLO and CC). Magnification and compression views may also be needed. The Xray dose is low only 0.5mGy per view. The quality of the films depends on-good inclusion, contrast and adequate compression.

102 The characteristics of a malignant lesion include a circumscribed or stellate mass, architectural distortion and spiculate microcalcification. The advent of screening mammography has increased the diagnosis of premalignant changes such as ductal carcinoma in-situ (DCIS) and small non-palpable carcinomas. Regular screening mammography decreases breast cancer mortality in women over 40 years and most developed countries have instituted public screening programmes. In New Zealand breast screening is offered to women from 45 to 69 years of age on a 2 yearly basis.

Results of mammography: Sensitivity 86% Specificity 90% Misses up to 40% Ca <50y, 10% Ca >50y False positive 11%

ULTRASONOGRAPHY This is especially useful in young women but is often used in conjunction with mammography in those over 30 years. It is operator dependent and is not useful as a screening tool. Apart from differentiating solid from cystic masses, it can confirm the benign features of a fibroadenoma. Malignant lesions display characteristic features such as a towering profile, invading margin, irregular edge, heterogeneity, and dense shadowing

103 Results of breast ultrasound: Sensitivity 82% Specificity 85%

FNA CYTOLOGY Every palpable discrete lump or suspicious lesion on imaging should have a biopsy. The main advantage of FNA is that it can be reported immediately in the clinic. A common technique is to use a 21G needle and a 20ml syringe in a handle. The lesion is immobilised and multiple passes made while applying suction. The slides are air dried, stained & reported. Results of FNA: Sensitivity 95% Specificity 95% False positive 0.2%

The pathologist may use a shorthand reporting system such as the following: C1 = inadequate epithelial sampling C2 = benign C3 = atypical probably benign C4 = suspicious of malignancy C5 = malignant

104 CORE BIOPSY This provides tissue for histology rather than cytology. An automated gun is used to provide 3x 14G/16G cores under local anaesthetic. Advantages over FNA include: Differentiates DCIS from invasive Ca Oestrogen receptors can be performed Good for repeated C1, C3 & C4 FNA. May need to be done under image control (e.g. stereotactic biopsy or ultrasound guidance)

Results of core biopsy: Sensitivity 83% Specificity 100%

OPEN BIOPSY All lumps should have Triple Assessment before being excised. This is often performed if there is a suspicion of malignancy even if some or all of the modalities of triple assessment suggest a benign lesion. Excision may be requested by the patient, even if the lesion appears benign. Excision may be appropriate in women over 35 years with new lumps. Frozen section is now rarely used. It can be useful to confirm C4/C5 lesions or to assess excision margins.

105 MALIGNANT BREAST DISEASE Epidemiology This affects approximately 1 in 11 women. The overall mortality is 30 %. Breast cancer is the most common cause of death in women between 35 and 54 years.

The risk increases with age 1/5000 if 20-29 years of age. 1/8 if 80-89 years of age.

It may be familial in 5-10% of cases BRCA1 gene - up to 80% may develop breast cancer and 40% ovarian cancer BRCA2 gene Risk calculation can be made after construction of a pedigree.

Prognosis is related to: Primary tumour size Presence and number of involved lymph nodes Histological grade Nottingham prognostic index (NPI) a score that combines size, nodal status and grade.

106 Classification Carcinoma in situ Lobular carcinoma in situ (LCIS) a marker of increased risk of breast cancer Ductal carcinoma in situ (DCIS) premalignant condition, accounts for 30-40% of neoplasms diagnosed on screening mammograms Invasive carcinoma Lobular carcinoma- 20% of invasive cancers Ductal carcinoma 80% of invasive cancers Other

Staging This is the extent of the disease. It is assessed by examining the breasts, nodal basins, chest, abdomen and axial skeleton. Standard pre-operative tests include FBC, LFTs and a CXR. If there are involved lymph nodes a bone scan and liver ultrasound are required.

A common system used is the AJCC (American Joint Committee on Cancer) TNM staging, where: Tumour size: T1-4 Nodes: N0-3 Metastases: M0-1

107 TREATMENT Surgery is the mainstay of treatment: DCIS - Excision with 10mm margins, axillary dissection is not required Invasive carcinoma is treated with: i. ii. conservation treatment). iii. survival & similar local recurrence rates. iv. Axillary dissection is used to stage the disease for prognosis and to make decisions regarding adjuvant treatment. If breast conservation treatment is possible, i. and ii. have the same Total mastectomy & axillary clearance. Partial mastectomy, axillary clearance & radiotherapy (breast

Breast reconstruction is offered to women requiring a mastectomy, it can be immediate or delayed. The following techniques can be used: i. ii. iii. Expandable prosthesis Latissimus dorsi flap & prosthesis TRAM (transverse rectus abdominus myocutaneous) flap

Prophylactic mastectomy - This is sometimes performed at a womens request if she is at high risk of breast cancer

108 Sentinel node biopsy This technique is used to identify the first lymph node drained by a primary cancer. If this node is free of metastases, axillary dissection may be avoided. This is becoming the standard of treatment for small, clinically node negative cancers and will decrease the chance of causing morbidity by dissecting normal axillae. Adjuvant Treatment Radiotherapy - for all cases of breast conservation therapy and may be used for some cases of DCIS after excision to decrease the chance of local recurrence. Endocrine Therapy if a tumour is hormone receptor positive, altering the hormonal milieu may control systemic disease and decrease the risk of a contralateral breast cancer. Tamoxifen is the main agent used but newer aromatase inhibitor drugs have an improved side effect profile and may be more effective. Chemotherapy - for women at higher risk of systemic disease, for example large, high grade tumours with nodal involvement. This is more effective in the pre-menopausal state. Combination CMF chemotherapy is the most commonly used regimen, although there is increasing experience with anthracycline based protocols. Herceptin (a monoclonal antibody treatment) has shown excellent results as adjuvant treatment for those women who are Her-2 positive. Palliative treatment This is used in advanced disease, not to cure, but for symptom control. Hormonal treatment with the anti-oestrogen Tamoxifen is often used Psychological & emotional support After the diagnosis of breast cancer, women require information about the disease, their treatment options and ongoing support. The Breast Nurse is invaluable for this. Formal Psychologist referral may be needed. Follow-up & surveillance The aim of follow-up is to detect local, regional and systemic recurrence of breast cancer

109 and to detect contralateral disease. Annual mammography is an important part of surveillance. BENIGN BREAST DISEASE Congenital Abnormalities Amazia Absence of breast tissue. Polands syndrome - absence of breast, pectoralis major & arm abnormalities. Polymazia Accessory breast tissue. Can occur anywhere along the nipple line from the axilla to the groin.

Supernumerary nipples . . Occur in 1-5% of males and females Most occur below the normal breast

Inflammatory Conditions This includes: Acute mastistis Abscess lactating, nonlactating Mammary duct ectasia periductal mastitis Uncommonly - TB, actinomycosis and granulomatous mastitis

110

ANDI Definition = Aberrations of normal development & involution. This is a very common condition, not a disease process. It was formerly known as benign mammary dysplasia or fibrocystic disease. It can be associated with breast pain. Women may present with any one, or a mixture, of the following: Fibrosis Cysts Epithelial hyperplasia Adenosis The significance of ANDI is that it can be difficult to distinguish this lumpiness or nodularity from a discrete lump that may represent a breast carcinoma.

Fibroadenoma This is a common benign breast neoplasm often found between the ages of 17 and 35. In young women these form over 60% of breast lumps. Clinically they are firm to rubbery, round, smooth or bosselated and mobile lumps. They are easily diagnosed with triple assessment. They may enlarge with pregnancy and breastfeeding.

Excision is considered if a fibroadenoma is increasing in size, tender, or at the patients request.

Gynaecomastia This is the development of fibro-glandular breast tissue in males. It needs to be differentiated It is from to pseudo-gynaecomastia, rule out male breast which cancer consists with of triple fat only.

important

assessment.

111 Aetiology . . . . . . Physiological in teenage males, 80% resolve spontaneously Drugs alcohol, cannabis, digoxin and ACE inhibitors Cirrhosis Hypogonadism Testicular malignancy Idiopathic particularly in the elderly

Nipple Discharge This is a common condition, in that two thirds of women over 35 years can express some secretion. Discharge that is more concerning is that which is: Spontaneous Comes from a single duct on one side Bloodstained Persistent

It is assessed by examination, imaging and smear cytology. Ductography, which may be technically difficult, is sometimes helpful. Surgical excision of the duct is considered if the discharge is bloodstained or persistent. Aetiology No abnormality ~30% Duct ectasia ~30%

112 Duct papilloma ~10% Galactorrhoea ~5% Carcinoma ~5%

Breast Pain or Mastalgia This is also a common symptom, affecting 77% of screening populations. It is uncommon in breast cancer - 7% of breast cancers cause pain and 0.5% of women with breast pain have cancer. Mastalgia mostly occurs from 35 to 45 years of age. It is important to rule out acute infections such as mastitis or abscess. It can be classified as: Non breast pain: musculoskeletal, inflammatory and other causes Cyclical pain: mid-cycle on, hormonally related, mean age 34 years. Non-cyclical pain: random, continuous, mean age 43 years. A pain diary may help in elucidating the cause. Up to 80% of cases resolve spontaneously, particularly after reassurance.

Several treatments have been found to be useful: Reduction of dietary fat. Avoiding caffeine. Avoidance of stress and regular exercise. Simple analgesia and the application of heat Wearing a correctly fitting supportive bra

113 Hormonal treatment-oral contraceptive pill, Tamoxifen. Gamma linoleic acid-evening primrose oil, starflower oil Danazol-for severe intractable cases.

FURTHER READING FOR INTEREST Bland KI, Copeland EM. The breast: comprehensive management of benign and malignant diseases. Second edition. WB Saunders Co., 1998, 1631p. Dixon JM. ABC of breast diseases. BMJ, 2000, 96p. Dixon JM, Morrow M. Breast disease: a problem based approach. WB Saunders, 1999, 244p. Fentiman IS. Detection and treatment of breast cancer. 2 1998, 344p. FURTHER READING FOR FINALS Tjandra JJ, Clunie GJA, Thomas RJS (eds.). Textbook of Surgery. 2 Edition. Blackwell Science Ltd., Oxford, 2001; pp 308-332
nd nd

edition. Martin Dunitz Ltd

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Tutorial 10

Hernias of the groin and abdominal wall

Garth Poole and Andrew G Hill

INTRODUCTION The abdomen, including the pelvis, is a large cavity with a variable wall. This wall may be made of mainly bone (iliac crest), fascia only (midline), peritoneum only or one, two or three layers of muscle. Because of this complicated arrangement there are areas of the abdominal wall that are more vulnerable to develop a hernia. This vulnerability can express itself at birth or may take many years to manifest. Hernias may have other factors that add to the baseline vulnerability such as: . . . . . . the need for structures to leave the abdomen (such as femoral vessels or testicle) variations in body shape and size old age occupation previous surgical intervention smoking

DEFINITIONS Hernia: A hernia is a protrusion of a sac of peritoneum through a defect in the abdominal wall. A hernia may contain omentum or any part of the hollow alimentary tract, bladder

115 or even ovary. Reducible hernia: A hernia that can be fully reduced into the abdomen by surgeon or patient using palpation or positioning. Irreducible hernia: A hernia that cannot be reduced. This is also known as incarcerated (imprisoned). This may or may not be accompanied by compromise to the contained structures (strangulation). Strangulated hernia: compromised blood supply to fat or abdominal contents contained within a hernia. This may also lead to bowel obstruction

Groups of hernias: Groin hernias (complicated anatomy and great for exams) including Inguinal (direct and indirect) and femoral

Other common hernias (easy anatomy and great for exams) Umbilical and paraumbilical, epigastric, incisional

Rare hernias Spigelian, obturator, lumbar FUNCTIONAL ANATOMY OF GROIN HERNIAS: Groin hernias are common for two reasons: . . Structures exit the abdomen here (spermatic chord and femoral vessels). There is relatively little support in the form of the thin tranversalis fascia

and the peritoneum.

The inguinal canal passes obliquely through the anterior abdominal wall just above the medial half of the inguinal ligament. It extends from the deep internal ring at the midpoint of the inguinal ligament to the superficial inguinal ring at the pubic crest. The spermatic cord, comprising of the remnants of the processus vaginalis, the vas deferens

116 and their nerves and vessels, enters the inguinal canal through the deep ring and leaves it to enter the scrotum through the superficial inguinal ring. Congenital and childhood hernias are almost always when the peritoneal sac that travels with the cord (processus vaginalis) remains open. Adult hernias are from a weakness of the inguinal region that may either allow a childhood hernia to manifest itself, or allow a new hernia to develop. An inguinal hernia may come medial to the inferior epigastric vessels directly through the posterior wall of the inguinal canal causing a direct hernia It may also come lateral to the inferior epigastric vessels indirectly into the canal causing an indirect hernia A femoral hernia comes below the medial end of the inguinal ligament and through a square with three hard sides and one soft side (the femoral canal)

DIAGNOSIS:

The diagnosis of a hernia is almost entirely based on history and inspection. History A lump in the right place that comes and goes in a predictable way is a hernia. Many paediatric surgeons operate on children purely on the strength of the history of a hernia from the parents. Accurate history taking will also give the diagnosis of a hernia in most adult cases Inspection Comment on general factors (patient comfort, scars, abdominal swelling)

Compare both sides.

117 Cough test

The biggest challenge with hernia examination is to know what normal is. Therefore comparison of the two sides is the key. Be aware that 10% of hernias are bilateral (synchronous or metachronous). Comparison needs to be performed with the patient lying supine, with the patient coughing and eventually with patient standing up. Thin patients have a very visible normal bulge on coughing The normal cough impulse must be compared with the slow rising and falling of a hernia..

Old scars can be very subtle in the groin so look carefully! Palpation Display the landmarks. Deduce the internal ring. Detect a hernia. Define the type of hernia. Warning: The crease in the groin has nothing to do with the inguinal anatomy. It is just there to confuse the student! Display : The key landmarks of a hernia are the symphysis pubis and the anterior superior iliac spine. Everything else is derived from this but cannot be comfortably palpated, so must be inferred. The pubic tubercle is about 3 cm lateral to the symphysis and inferior to the pubic crest. Deduce: The inguinal ligament runs from the pubic tubercle to the anterior superior iliac spine, with a slightly downward curve. The internal ring is at the midpoint of this ligament. Detect: Even very experienced surgeons can struggle with this. The student needs to use all the information gathered above to assist with the detection of a hernia. The obvious reducible bulge hardly needs palpation whereas the subtle hernia is often missed and the non existent can be over diagnosed.

Is the cough impulse fast or slow rising? Is there any palpable evidence of the squelch of bowel, omentum or fluid under your fingers? Define: Pressure over the internal ring will theoretically control an indirect but not a

118 direct hernia. There is a lot of historical emphasis on the differentiation between a direct and an indirect hernia. Although this distinction highlights the anatomy of the region it is

of little practical relevance for two reasons. Firstly, the clinical conclusion is often wrong. Secondly the operation to fix both hernias is the same! A femoral hernia is below and lateral to the pubic tubercle with two other features It is rare It tends to smooth out the groin crease whereas the inguinal hernia accentuates it

Other aspects of groin examination: Scrotum: Do not be afraid of scrotal examination. The testicle is one of the few organs in the body that can be completely palpated. Again inspection and comparison is the key. If the scrotum is swollen it must be decided whether the swelling is from above (hernia) or from within the scrotum itself (tumour/hydrocele/ epididymal cyst/infection). An epididymal cyst, unlike a hydrocoele which surrounds the testicle, may feel like a third testicle. In the fourteenth century the Pope granted petition to a man who wanted to marry two wives because he possessed three testicles Femoral triangle: Lymph nodes are common in this area and only rarely significant. A varicosity of the proximal saphenous vein (saphena-varix) may mimic a femoral hernia. A saphena-varix disappears when the patient lies down. INDICATIONS FOR SURGERY: With modern surgical techniques and anaesthesia almost all groin hernias can be fixed. As a general rule bigger hernias are more symptomatic and smaller hernias are more dangerous. It is important to note symptoms of prostatism or other conditions that may cause a rise in intra-abdominal pressure. Other types of hernias should be operated on if symptoms or risk of strangulation outweigh the morbidity of the procedure.

119

Surgical treatment: Most surgeons now agree that a tension-free polypropylene mesh is the treatment of choice for all types of inguinal hernias. Concern about prosthetic mesh infection has disappeared with technique and technology advances. The mesh can be placed through an open incision or through a laparoscope under local, regional or general anaesthetic. The choice of technique depends on: . . . . . . patient choice previous surgery comorbid conditions surgeon preference and experience unilateral or bilateral cost

Femoral hernias are usually fixed by suturing. Other abdominal wall hernias are fixed by suturing, mesh or a combination of both.

Outcomes of treatment: In the year 2006 a patient who has had a hernia repair should be mobile within 2 days and back to normal activity or work within 2 weeks. There are few, if any, restrictions placed on the patient from the day of surgery. The failure rate of the surgery should be less than 2% and the minor complication rate (infection, wound pain) should be less than 10%

FURTHER READING FOR FINALS Tjandra JJ, Clunie GJA, Thomas RJS(eds.). Textbook of Surgery. 2 Science Ltd., Oxford, 2001; pp 378-397
nd edn.

. Blackwell

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Tutorial 11

Trauma
Ian Civil

Trauma in New Zealand, as in other developed societies, has become the leading cause of death in the first four decades of life. It accounts for more than 1500 deaths and over 60,000 hospital admissions per year in this country. In 1996, 55,000 potential life years were lost as the result of injury. This represented 21% of years of life lost from all causes. You will commonly see patients on surgical wards who have sustained injuries of various types. CLASSIFICATION Trauma is generally categorised by both the mechanism of injury, and the body region affected. Mechanism of Injury Blunt trauma is the most common mechanism of injury and may occur as a result of road crashes, falls or assaults. Penetrating trauma is uncommon in New Zealand and describes gunshot, shotgun and stab wounds. Body Region For descriptive purposes the body is divided into six body regions.

121 Head Region, Face Region, Thorax Region, Abdomen Region, Extremities Region, ad External Region. Multiple trauma, such as often occurs in road crashes, results in injuries in more than one body region. CLINICAL PRESENTATION Unlike other conditions trauma does not lend itself to the taking of a detailed history, followed by clinical examination, investigations and subsequent treatment. Initial assessment of the patient must follow a sequence of priorities with life threatening injuries being treated as they are recognised. Primary Survey A - Airway Provision or maintenance of an airway has the highest priority as an inadequate airway can kill within minutes. Unconscious patients do not maintain an adequate airway. In patients suffering blunt trauma specific consideration should be given to the possibility of cervical spine injury and the patients neck should not be hyperflexed to establish or maintain an airway. B - Breathing Airway patency does not ensure adequate ventilation. Adequate air exchange, in addition to an open airway, is required. This can be established using the basic principles of look, feel and listen. Two traumatic conditions that most often compromise ventilation are tension pneumothorax, and large flail chest with pulmonary contusion. C - Circulation All traumatic conditions are associated with haemorrhage which is a prominent, treatable cause of early post-injury death. Rapid and accurate assessment of the injured patients hemodynamic status is therefore essential. Three elements of observation yield key information within seconds. These are state of consciousness, skin colour and pulse. When blood volume is reduced by half or more cerebral perfusion is critically impaired and unconsciousness results. The ashen grey skin of the face and the white skin of blood

122 drained extremities implies at least loss of 30% of blood volume. Significant haemorrhage usually occurs in one or more of the following areas. External haemorrhage results from external wounds and is easily identified and controlled by direct pressure. Internal haemorrhage results when bleeding occurs into one of the body cavities. Bleeding in the chest is called a haemothorax and up to 2 litres of blood (40% of blood volume) may accumulate in a single thoracic activity. Bleeding in the abdomen is called a haemoperitoneum and may result from any injury to an intraabdominal organ. Most commonly the solid organs (liver, spleen and kidneys) are injured in blunt trauma. Significant bleeding also occurs in association with fractures. A single fractured femur may result in loss of up to 1.5 litres of blood into the thigh muscle and a fractured pelvis may exsanguinate the patient. D- Disability A brief neurological examiniation should be performed at this stage comprising an assessment of the patients level of consciousness and pupillary size and reaction. Level of consciousness is assessed using the Glasgow Coma Scale:

Glasgow Coma Scale (GCS)

Assessment Area Eye Opening (E) Spontaneous To speech To pain None BEST Motor Response (M) Obeys commands Localizes pain 6 5 4 3 2 1 Score

123 Normal flexion (withdrawal) Abnormal flexion (decorticate) Extension (decerebrate) None (flaccid) Verbal Response(V) Oriented Confused conversation Inappropriate words Incomprehensible sounds None GCS Score = (E+M+V); Best possible score=15; Worst possible score=3 5 4 3 2 1 4 3 2 1

Patients who are initially awake and alert (GCS 14-15) and subsequently have a deterioration in their level of consciousness are particularly likely to have intracranial collections of blood (extradural and subdural haematomas) which are amenable to surgical evacuation. E-Exposure If not already completed the patient must be undressed at this stage so that a complete examiniation can be undertaken. Resuscitation Airway maintenance, cardiopulmonary resuscitation and other life-saving modalities must be initiated as the problems are identified. Resuscitation of the ABCs must continue with priority over other diagnostic and therapeutic considerations. Essential diagnostic Xrays (lateral cervical spine X-ray, chest X-ray, pelvic X-ray) should be undertaken and monitoring devices (Pulse Oximeter, ECG, nasogastric tube, urinary catheter) placed during this phase. Only when resuscitation has resulted in a stable or stabilising patient should further evaluation be undertaken.

124 Secondary Survey The secondary survey is a complete head-to-toe, front to back examination that aims to identify all injuries. Head The secondary survey begins with an examination of the head region. The entire scalp should be palpated for lacerations and fractures, the mastoid area inspected for evidence of a Battles sign and the ears examined for haemotympanum. Both these signs are evidence of a basal skull fracture. The eyes should be re-evaluated for pupillary size, and fundi for haemorrhages. The patients levels of consciousness should be reassessed using the Glasgow Coma Scale. The neck should be both visually inspected and palpated. The absence of neurological deficit, pain, or tenderness does not rule out injury to the cervical spine. Such an injury should be presumed to be present until ruled out by adequate radiological examination. Face The entire face should be palpated for evidence of fractures. Maxillo-facial trauma not associated with airway obstruction, however, should only be treated after the patient is completely stabilised. Thorax A complete examination of the chest requires visual examination, palpation of the entire chest cage, and auscultation. Contusions and haematomas of the chest wall are often signs of more serious occult injury. Pneumothorax and haemothorax are common in trauma to the chest region. Abdomen Any abdominal injury is potentially life threatening, but the specific diagnosis is not as important as establishing that an abdominal injury exists. Clinical examination (look, feel and listen) is unreliable in those who have suffered a head injury or who are intoxicated by drugs or alcohol. In these patients other forms of abdominal assessment are required such as diagnostic peritoneal lavage or abdominal CT scanning. Rectal examination,

125 however, is an important part of the abdominal evaluation as it will detect the presence of blood within the bowel, a high-riding prostate, the presence of pelvic fractures, the integrity of the rectal wall, and the quality of sphincter tone. Extremities The extremities must be examined visually for evidence of injury and then functionally. If the patient is awake a co-operative active range of motion should be sought in each limb. External Examination of the entire integument, including the back, should be undertaken. All trauma patients have external injuries which may be signs of more severe internal injuries. HISTORY A history of the mechanisms of injury is very helpful in identifying potential injuries suffered by the patient. In general, the severity of injury is proportional to the amount of energy transferred from an object to the human body. Direction of energy transfer is also important. With this information it is possible to predict injury patterns that may be suffered by that patient. An example would be the rapid frontal deceleration which occurs when a car collides head on with a bridge abutment. The pattern of injuries suffered by a restrained patient might include a closed head injury, flail chest, thoracic aortic rupture and fracture of the pelvis. In penetrating trauma the type of injury is determined by the region of the body sustaining injury and the transfer of energy from the projectile to the body. In gunshot wounds this transfer of energy is related to the mass and velocity of the bullet. Limited pertinent past medical history is usually available in these patients. Particularly relevant facts, if obtainable, may be remembered by the mnemonic AMPLE:

126 A - Allergies

M - Medications P - Past Illness L - Last Meal E -Events surrounding injury

RECORDS Trauma evaluation is a dynamic process with the patients status often changing rapidly. In addition, multiple specialties and doctors are often involved with the overall care of the patient changing from one team to another. For these, as well as medico-legal reasons, meticulous record keeping is essential. SUMMARY The injured patient must be evaluated rapidly with life threatening injuries being identified and treated at the same time. Once established, a thorough head-to-toe examination is required to identify all injuries. History of the mechanism of injury is crucial to the assessment as it may be the only clue to the likely injuries the patient has suffered. FURTHER READING FOR INTEREST Tjandra JJ, Clunie GJA, Thomas RJS (eds.). Textbook of Surgery. 2 Edition. Blackwell Science Ltd., Oxford, 2001; pp 434-473
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FURTHER READING FOR FINALS Nil

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Tutorial 12

Peripheral Arterial Disease

Andrew A Hill

Peripheral arterial disease affects all parts of the arterial tree. The two most common effects are occlusive disease or aneurysmal disease

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE (PAOD) Peripheral arterial occlusive disease (PAOD) is a degenerative process resulting from atherosclerosis affecting the arterial tree. It is so common that it could be regarded as universally present in the elderly but most patients are asymptomatic. Risk factors include smoking, diabetes mellitus, hypertension and hyperlipidemias. Atherosclerosis results from cholesterol plaque formation in the arterial wall, causing stenosis and occlusion. The resultant reduction in blood flow causes most symptoms. Sometimes thrombus associated with this reduction in blood flow (thrombosis), platelet aggregates or plaque itself can break off and cause further problems downstream (embolism). While any area of the peripheral arterial tree may be affected by atherosclerosis the three most common areas affected are the extracranial carotid system, the aorto-iliac system and the femoropopliteal system. Arterial branch points are particularly affected.

128 EXAMINATION Pulses can be graded: 0 = absent 1 = just palpable 2 = reduced 3 = normal 4 = enlarged/ectatic/aneurysmal

Examination of the peripheral vascular system should include as a minimum 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. Radial pulses Blood pressure Carotid bruits Aortic pulse Femoral pulses Popliteal pulse Dorsalis pedis pulse Posterior tibial pulse Examination of legs - scars, amputations, ulcers, colour Examination of feet - temperature, sensation

Radio-radial delay and radio-femoral delay are not particularly useful tests in adult

129 populations

INVESTIGATIONS Non-invasive investigations are those, which do not require any instrumentation of the patients body, but merely the placement of instruments on the outside to obtain readings of some type. The most common non-invasive investigations of the peripheral vascular system are duplex ultrasound (US), magnetic resonance imaging (MRI) and computerised tomography (CT). These can all be used with intravenous contrast agents to enhance images e.g. CT angiography (CTA) or MR angiography (MRA). Catheter angiography is the most common Invasive investigation, where a catheter is placed intra-arterially with contrast material injection. The main advantage of catheter angiography is the option for intervention. Angioplasty involves passing a guidewire and then a balloon tipped catheter across the stenosis or occlusion. When the balloon is inflated atheromatous plaque is split and squeezed outwards. A metal stent may be necessary to support the treated area, particularly if the angioplasty alone is inadequate treatment. Angiography carries risk of damage to the artery at the site of puncture site (usually the femoral artery in the groin) or treatment site, embolisation of atheroma or thrombus, and damage to the kidneys from the dye. EXTRACRANIAL CAROTID DISEASE This is predominantly stenotic disease with atherosclerotic plaque at the carotid bifurcation and proximal internal carotid artery. Aneurysms are rare. As is common with atherosclerosis, the precise site affected involves a bifurcation and in this region it is the point where the internal and external carotid arteries arise from the common carotid. Symptoms Occlusive vascular disease in the carotid system produces symptoms as a result of distal ischaemia. These may be: Stroke - a neurological deficit resulting from occlusion of a major intracerebral

130 artery (clinical symptoms >24hours) Transient Ischemic Attack (TIA) - a stroke that lasts usually a few minutes to

an hour and resolves without deficit. The cause is usually embolism of cholesterol debris or platelet aggregates. Amaurosis Fugax - a TIA affecting the blood supply to the eye. The sufferer

notes a loss of vision in one eye, usually coming down like a curtain over the upper half of the visual field and lasting for some minutes. This is related to an ipsi-lateral carotid stenosis. Can also result in retinal infarct.

Other causes of stroke include intra-cerebral hemorrhage, small-vessel cerebral disease, and embolism from the heart (e.g. mural thrombus after myocardial infarction and tachyarrythmias, especially atrial fibrillation) and ascending aorta. Migraine, cerebral space-occupying lesions, postural hypotension, and vertebro-basilar insufficiency can also cause symptoms. Carotid lesions typically cause ipsilateral middle cerebral artery territory symptoms. Cardiac emboli infrequently cause TIAs as they embolise larger fragments and the resultant cerebral damage affects larger areas resulting in stroke. Uncommonly, bilateral severe disease can result in symptoms of hypo-perfusion.

Investigations US is used to determine the haemodynamic significance of any obstruction to the extracranial carotid system. This is a good, safe investigation for determining stenosis and may pick up plaque irregularities and ulceration. Catheter angiography of the cerebral vessels carries a small risk of stroke or TIA (0.10.5%) and is often reserved for those patients with indeterminate lesions on ultrasound. MRA or CTA can give similar information and has the advantage of imaging the parenchyma of the brain at the same time.

131 Treatment Medical treatment of patients with extra-cranial cerebrovascular disease is important whether intervention is needed or not. All patients should have anti-platelet therapy (usually aspirin) in the absence of contra-indications. Consideration of other risk-factor intervention should also be made. The decision about how patients should be treated is a complex one and relates to the individual patients risk of stroke, their fitness for surgery, and the ability to perform a successful intervention. Most symptomatic patients can be considered for intervention if there is an internal carotid artery stenosis of > 70%. Asymptomatic lesions can also be considered for intervention, although the clinical advantage is less.

Intervention can be surgical or with endovascular techniques. Surgical endarterectomy involves removal of the lining of the carotid artery via a neck incision. This operation has a combined risk of stroke or death of 3-5% but if successful reduces the risk of subsequent stroke significantly. Endovascular treatment with angioplasty and stenting of the diseased artery is investigational. It is also used in high risk surgical candidates.

ANEURYSMS An aneurysm can be defined as enlargement of the artery to more than twice its normal size. An artery bigger than normal but not aneurysmal can be described as ectatic. True aneurysms involve all layers of the arterial wall whereas false aneurysms do not. The predominant etiology of true aneurysms is thought to be atherosclerotic degeneration but there is a genetic component in some (familial aneurysms and connective tissue disorders such as Marfans). Men outnumber women in a ratio of 9:1. Aneurysms affect the abdominal aorta (AAA), the iliac artery, the popliteal artery, the femoral artery and the thoracic aorta in descending order. Infrequently other arteries such as the mesenteric can

132 be affected. False aneurysms occur at points of intervention (surgical anastomoses or angiographic puncture sites) or infection (mycotic aneurysm). Symptoms Most aneurysms are asymptomatic and are diagnosed incidentally during physical examination or during investigation for some other condition (such as when a patient undergoes ultrasound examination for gallstones). With AAA, rupture causes severe back pain, abdominal pain or collapse. Thoracic aneurysms can present with chest pain. Aortoiliac aneurysms rarely embolise. Popliteal artery aneurysms more frequently present with acute occlusion or embolisation (ischemic symptoms). One aneurysm in a patient should lead to a search for other aneurysms. Investigations US examination is usually sufficient to diagnose the presence of an aneurysm and show its size. CT can show in more detail the extent of the aneurysm and if there are complications such as inflammation, rupture or associated arterial stenoses, e.g. in the renal or iliac arteries. Angiography is usually indicated in femoro-popliteal aneurysms to define downstream arterial anatomy. Treatment of Aorto-iliac aneurysms Once an aneurysm has enlarged to a size where risk of rupture exists (5-5.5 cm for AAA and 6-6.5 cm for thoracic aneurysms), consideration of repair is indicated. Usually this is a balance between the risk of rupture and the risk of repair. Rupture risk per annum 5-6cm AAA Rupture risk per annum >7cm AAA Overall ruptured AAA mortality Operative ruptured AAA mortality Elective AAA repair mortality 5% 20-30% 75% 30-50% 5%

133 In open repair, a laparotomy is needed and the weakened section of artery is replaced with a segment of a material sutured above and below to the normal artery. If the iliac arteries are also aneurysmal a bifurcated graft can replace the entire aorto-iliac segment. Some aneurysms can be repaired with a covered stent to seal off the aneurysm from aortic pressure. These are positioned in place with X-ray techniques from the groin. These endoluminal repairs rely on a relatively normal section of artery above and below the aneurysm. Treatment of Femoro-popliteal aneurysms The risks of occlusion and embolisation associated with popliteal aneurysms demands consideration of repair above 2 cm. In the common femoral region the most common approach is to replace the artery with a small segment of an artificial graft after excising the aneurysm. In the popliteal region the artery is less accessible and it is more common to bypass the artery from above the knee to below the knee and then exclude it from the arterial flow. OCCLUSIVE DISEASE LOWER EXTREMITY Occlusive disease of the lower extremities results in not enough blood flow reaching the lower legs. This may cause one or more of the following symptoms: Claudication This is a tight pain or cramp, not unlike that described in the chest region in angina. The site of symptoms depends on the level of disease. Most commonly the superficial femoral artery is affected and calf symptoms ensue. If the aorto-iliac segment is affected, buttock or thigh symptoms are felt, in addition to calf symptoms. It is predictable, in that it comes on after a set period of exercise and resolves after a short period of rest (usually 2-5 minutes). Claudication may be disabling if a patients employment or quality of life is affected. It usually remains stable for long periods of time and the rate of progression to leg threatening ischemia is low (especially in non-diabetics). Claudication does not damage muscles if a patient continues walking through the pain.

134 Rest pain In more severe ischaemia patients may suffer rest pain. This affects the toes and forefoot and is often severe requiring narcotic analgesia. It is worse with elevation and the lack of gravity assistance to flow results in critical ischaemia. Patients classically go to sleep at night and wake after 2-3 hours with pain in the foot which is relieved when they hang the foot out of bed. This symptom is indicative of leg threatening ischaemia. There is often a background of claudication.

Ulcers and Gangrene Severe ischemia results in tissue loss and indicates impending limb loss. Often this is associated with pain (rest pain or ulcer pain). Acute Ischemia More sudden occlusion may lead to symptomatic arterial insufficiency without preexisting trophic changes. Symptoms and signs may include Pallor Pulselessness Pain Parasthesiae Paralysis.

Acute ischemia can be caused by embolism from a distant site to the leg or thrombosis in the leg (usually on the background of existing chronic arterial disease). Risk factors for acute arterial embolism are Atrial fibrillation (particularly if not anti-coagulated) and recent myocardial infarction. Supportive evidence would be the presence of normal pulses on the other side, a lack of known arterial disease or pre-existing claudication.

135 Investigations Non-invasive investigation includes measurement of the Ankle-Brachial Index. A comparison is made between the ankle systolic pressure, as measured with a Doppler probe, and the brachial systolic pressure. A normal ratio is between 1.0 - 1.2. Claudication is unusual above 0.7. Rest pain and tissue loss usually represents a pressure below 0.3 - 0.5 Ankle Brachial Index = Ankle systolic/Brachial systolic pressure In patients with disabling claudication or limb threatening symptoms, angiography is indicated to delineate the nature of the occlusions and stenoses. Treatment Many patients with claudication only can be treated expectantly. Treatment of risk factors is important to prevent progression of disease. Walking is particularly useful and may stimulate collateral flow. If treatment is necessary and depending on the arteriographic findings, either surgery or angioplasty may be indicated. Angioplasty is more successful in larger arteries (especially the iliac) and with shorter areas of disease. In general angioplasty is indicated for stenoses and short occlusions (<10 cm) above the knee. In extensive occlusions surgical bypass is indicated. The more distal the occlusion (closer to the foot) the more difficult both therapies become. Bypass is preferably performed using the patients own saphenous vein, either in a reversed fashion (to prevent the valves stopping flow) or nonreversed after disruption of the valves. Vein can be obtained from either leg or the arm. If a suitable vein is not available bypass can be performed with an artificial graft, such as polytetrafluoroethylene (PTFE). Occasionally when neither of these approaches is possible nor has been successful it is possible to attempt to increase skin blood flow via lumbar sympathectomy. In this procedure the sympathetic chain responsible for autonomic inflow to the skin of the region is blocked. Phenol is injected around the sympathetic chain after passing a needle percutaneously.

136 Amputation is sometimes necessary. It is more likely if there is no possibility of arterial revascularisation or if the patient does not walk. The general medical state of the patient is taken into consideration, particularly the presence of Ischemic Heart Disease. FURTHER READING FOR INTEREST Tjandra JJ, Clunie GJA, Thomas RJS(eds.). Textbook of Surgery. 2 Edition. Blackwell Science Ltd., Oxford, 2001; pp 532-569 FURTHER READING FOR FINALS Nil
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Tutorial 13

Diseases of the Venous System

Peter Vann

VENOUS ULCERS Most leg ulcers are due to venous hypertension but remember that a significant minority are due to other causes. Venous ulcers occur in 1-2% of the elderly population. Recurrence rates are high with approximately 20% of venous ulcer patients having more than six episodes of ulceration. Pathology The essential element in chronic ulceration is ischaemia at the level of the microcirculation. Although the arterial supply of the limb as assessed by foot pulses may be adequate the ulcer refuses to heal because of ischaemia of the skin cells. In venous hypertension the cellular ischaemia is due to two factors, capillary stasis and oedema. The pathophysiology is best understood by considering the venous haemodynamics in the normal lower limb. The superficial veins of the limb are in the subcutaneous fat. They communicate with the deep veins via the perforating (communicating) veins. There are many valves in the superficial and deep veins, increasing in frequency from above downwards. In less than 20% of people there is a valve above the groin level. The valves in the superficial and deep veins only allow flow in a cephalad direction. The valves in the perforating veins only allow flow from superficial to deep. The deep veins of the limb are surrounded by muscle. In the calf the muscle is surrounded by a dense, virtually

138 unstretchable, membrane-the investing deep fascia. When the muscles relax blood is prevented from refluxing by the venous valves. This results in a relative vacuum in the deep compartment to be pumped up towards the heart and the pressure in the superficial veins is kept low. This is the mechanism of the calf muscle pump. If the valves in the superficial veins are defective, as they are in patients with varicose veins, blood will reflux from the deep to the superficial system, most commonly at the junction of the saphenous and femoral veins in the groin. This increases the pressure in the superficial veins. If the valves in the short saphenous or perforating veins are incompetent the same thing happens. If the valves in the deep veins are incompetent, blood will reflux in the deep veins between muscle contractions. The effects of an increase in venous pressure in either system are transmitted to the venous end of the capillary loop. This back pressure will result in reduction or abolition of flow in the capillary loop and results in oedema. Because the hydrostatic pressure at the venous end of the capillary loop exceeds the osmotic pressure within the loop, tissue fluid will not be reabsorbed so will remain as oedema. Because of the high pressure within the loop, whole blood extravasates, increasing the protein content of the tissue fluid and thus reducing further the osmotic pressure of the intravascular fluid on the extra vascular fluid. Blood pigments and fibrin will collect in the tissues resulting in hyperpigmentation and venous stasis changes. Because of the reduction in capillary flow there is relative ischaemia of the cells of the skin. This is compounded by the oedema. Oedema, whatever its cause, shifts cells further from their capillary supply thus reducing the gradient for diffusion of nutrients and metabolites. Clinical Picture/Symptoms Venous ulcers may or may not be painful. They are not as painful as arterial ulcers. The discomfort is often relieved by elevation and rest which is in contrast to the marked increase in pain which occurs on elevation of the leg in patients with arterial ulceration. Physical Signs

139 Venous ulcers occur most frequently on the medial side of the limb above or about the medial malleolus. They can, however, occur anywhere in the lower leg or on the foot. They are shallow and do not go deeper than the deep fascia. There may be surrounding cellulitis. The edges are relatively flat but this varies according to the amount of oedema present. There are 3 cardinal signs of venous ulceration -oedema, dry eczema and pigmentation. If these are not present the ulcer is not venous in origin. Sometimes there may be a wet eczema. This is due to an infection or an allergy to some preparation which has been put on the ulcer. Allergies are common in this group of patients for they have often had numerous chemicals applied to the area in attempts to produce healing. Differential Diagnosis It must be remembered that venous hypertension is common and that non venous ulcers may occur in patients who have signs of venous hypertension. Squamous cell carcinomas, basal cell carcinomas and melanomas are quite common in the lower leg and their appearance is often not typical. If an ulcer does not heal with proper treatment a biopsy of the ulcer edge should be taken. This can be done simply using local anaesthetic. Vasculitic ulcers which occur in patients with auto immune disease also commonly occur in this region, probably because the skin of the lower leg has a relatively poorer blood supply than skin elsewhere. Arterial ulcers are usually seen on the foot. They are painful and usually have a punched out appearance. Arterial insufficiency, however, may compound the problem of a venous ulcer and make healing more difficult. There are also other rarer causes of ulceration. Treatment Venous ulcers are usually a result of venous hypertension secondary to defective venous return due to either obstruction of the Deep Venous System (DVT), or a malfunctioning superficial venous system (refluxing long, short saphenous system and perforators); or a poor calf pump. (fixed ankle, knee or plastic cast, immobility). Patients with insufficiency of the Deep Venous System or a Poor Calf Pump cannot be treated surgically and require compression dressing or an elastic stocking with graduated

140 compression. The compression needs to be strong enough to sustain a pressure to overcome the hydrostatic pressure within the veins and aid in venous return. To be effective the support stocking needs to be worn from the time the patient rises in the morning until the moment of retiring to bed at night. Patients with superficial venous insufficiency can be treated by varicose vein surgery discussed later with good results for ulcer healing and preventing recurrence. Patients with an exacerbation of infection and cellulitis may require hospitalisation and parenteral antibiotics with leg elevation.

VARICOSE VEINS Definition A vein that is varicose is defined as one with a saccular dilatation and is tortuous. This excludes intradermal skin veins known as venous flares or thread veins. Varicose veins are very common affecting up to 25% of women and 15% of men worldwide. Pathology Varicose veins are either primary or secondary. Primary varicose veins, which are the vast majority, occur for no obvious reason. They tend to be familial and are much commoner in women than in men. They tend to appear first during times of hormonal change, i.e. at puberty (both sexes), during pregnancy and sometimes at menopause. The symptoms are often exacerbated by oestrogenic contraceptives and by menstruation. There is therefore clearly a strong hormonal influence. In young people usually the only demonstrable lesion is incompetence of the saphenous veins with resulting increased venous pressure. This pressure is transmitted to the tributaries of the long saphenous vein which being thinner walled and lying more superficially than the saphenous vein, bear the brunt of the venous pressure increase. They dilate and lengthen resulting in varicose veins. In 10-15% of patients the short saphenous

141 vein is incompetent, sometimes with the long saphenous and sometimes alone. In older patients there is a greater incidence of incompetent perforating veins and dilatation of the deep system. Since these occur more commonly in older patients it is reasonable to speculate that these changes are secondary to the superficial incompetence seen in younger patients. A possible mechanism for this is as follows: Blood pumped up the leg by the calf muscle pump refluxes down the long (or short) saphenous vein and is returned via the perforating veins to the deep system. This results in an increased volume of venous blood in the leg which will continue to increase as the superficial veins dilate. The flow through the perforators into the deep system will also increase. To accommodate this extra blood flow the perforating and deep veins will dilate thus eventually making their valves incompetent. Secondary varicose veins are the result of thrombosis of the deep veins causing an increase in pressure in the deep system and reversal of the normal flow. Blood flows from the deep to the superficial system rather than the other way. This damages the muscle pump and blood collects in the veins of the leg. The increase in pressure and blood volume produces dilatation and incompetence of the superficial system causing varicose veins. There is no benefit in operating on these varicose veins for the underlying problem remains. Sometimes, indeed, the superficial veins may be the main means of venous return from the limb and operating on these will make things much worse. Diagnosis Symptoms The commonest symptom (about 85%) is aching of the leg which gets worse as the day goes on. Throbbing in the veins occurs with the same frequency. Cramp at night is a common symptom (50%). Patients do not associate this with varicose veins so it must be asked about directly. Swelling of the ankles and feet occurs in about 30%. Less than 10% get an ache in the groin but this is an important symptom which may lead to a wrong diagnosis. Sometimes patients present with a swelling in the groin which aches and is referred to the surgeon as a femoral hernia but is in fact an aching saphena varix .

142 A family history is sought. If there is no family history in a male patient one is very suspicious that these are secondary varicose veins even though there may be no history suggestive of Deep Vein Thrombosis (D.V.T). A history of D.V.T. is carefully taken. Superficial thrombosis is common in varicose vein patients so any history of thrombosis must be carefully evaluated. If the patient has had a lower limb fracture or joint replacement, the chances that there was a D.V.T. is over 70%. A history of Vulval varicosities should be sought as these may be the main source of filling of varicose veins. A history of oral contraceptive use should also be asked for. Physical Signs Firstly the whole of the lower limb from groin to toes is examined with the patient standing. Venous dilatation in the groin (saphena varix) is felt for and a cough impulse elicited. In 20% of patients with sapheno femoral incompetence this will be absent for there will be a valve in the external iliac vein. The distribution of the veins is noted. The suprapubic and lower abdominal areas are examined for venous collaterals, indicating previous unilateral or bilateral ilio femoral thrombosis. The patient is turned around and the upper end of the short saphenous vein is palpated. To do this the patient is asked to stand on the contralateral limb and relax the muscles bounding the popliteal fossa by allowing the knee on the side to be examined to flex a little. If the short saphenous vein is of normal caliber or impalpable it is not incompetent. If it feels dilated its position is marked on the skin with a pen. It is important to look for vulval varicosities running from the vulva down the medial side of the upper thigh. The patient then lies on the couch with the leg raised and the blood is stroked out of the veins. A one cm rubber tube is then fixed tightly around the top of the thigh using an artery forceps to secure it. This tourniquet must be tight enough to move the skin inwards for a distance greater than the diameter of the saphenous vein which may be 2 cm or so wide. Fat will tend to move from under the tourniquet so allowance must be made for this. In a very fat thigh it may be impossible to get the tourniquet tight enough to occlude the saphenous vein.

143 The patient then stands up. If the veins remain empty for 15 seconds it implies that the veins fill from above the tourniquet and are therefore filling from the sapheno femoral junction or the vulva (or both). If there is evidence of vulval varicosities, while the high tourniquet is on, pressure should be put over the external inguinal ring with one thumb and over the femoral ring with the other. The tourniquet is released by an assistant and the problem is assessed by removing first one thumb and then the other. If a high tourniquet does not control the varicose veins, they must be filling from below the tourniquet. The tourniquet is applied just above the knee. If this controls the veins, a thigh perforating vein is incompetent. If control is still poor a tourniquet is put on the thigh and another just below the upper end of the short saphenous. The latter is firmly compressed with a thumb and the lower tourniquet released. If the thumb controls the varicosities and they fill again after removal of the thumb, short saphenous incompetence is present. If the tourniquet below the knee does not control the varicosities it means there are incompetent perforating veins in the calf. The exact position of these does not matter. They will be associated with venous blowouts which will be dealt with by operation or injection. Using the tourniquets may sound complicated but in fact it is only the thoughtful application of simple hydrodynamics and could be worked out easily. The important message here is that the tourniquet should be applied tightly enough. Failure to do this is very common. Investigation It is very important to ascertain if the patient has any evidence of arterial disease by examining the pulses in the leg and if not palpable checking the ABPI (ankle brachial pressure index as measured with a doppler probe). Beware of the diabetic patient. No patient with arterial compromise should be put in a compression stocking or offered varicose vein surgery without consultation with a vascular surgeon. The investigation of choice which is now compulsory for chronic venous insufficiency is a duplex examination using sound waves as a non invasive evaluation of the venous system. It can also be used to identify deep venous thrombosis in the large veins. Venography is now used very rarely and is no longer a standard investigation.

144 Treatment All female patients must stop oestrogen and contraceptive pills at least 4 weeks before surgery due to the increased risk of DVT. Long saphenous reflux can be treated by sapheno-femoral ligation and stripping of the long saphenous vein to the level of the knee.

Short saphenous reflux can be treated with simple ligation at the sapheno-popliteal junction. Perforator incompetence can be treated with simple ligation or the minimally invasive technique of sub-fascial endoscopic ligation using an endoscopic camera. Residual varicosities can be treated by the stab avulsion technique (phlebectomy) with good results. The superficial spider veins can be treated by injection sclerotherapy which can be tedious for both patient and surgeon due to the repeated sessions required. Sclerotherapy is also and adequate treatment for non saphenous local varicose veins, post-operative residual varicose veins, and recurrent varicosities. Endovenous Radiofrequency Heating or Laser Ablation This is a new procedure that uses a minimally invasive technique for the above knee long saphenous system. A specially adapted probe is introduced via the groin or the long saphenous vein above the knee and this heats the veins to 85oC circumferentially contracting the vein wall collagen and collapsing the vein thereby obliterating the lumen. Over time the vein becomes a mere cord. Long-term results are awaited.

Secondary varicose veins (deep venous incompetence) should be treated with support elastic stocks and not surgery. Primary varicose veins not medically fit for surgery can also be treated with elastic stockings to prevent the complication and symptoms of varicose veins. FURTHER READING FOR FINALS

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Tutorial 14

Common Skin Malignancies

Patrick Alley

INTRODUCTION In our country approximately 10,000 new patients with malignant skin tumours present each year, 800 of whom have primary malignant melanomas. At least 50% of all these tumours are basal cell carcinomas and two thirds of these arise on the head and neck. There has been a dramatic increase in the incidence of all cutaneous malignancy in recent years. Skin malignancy is rare in Maoris and Polynesians and melanoma is exceptional. There are three common skin tumours which can be distinguished clinically according to Table 1. BASAL CELL CARCINOMA Old name was Rodent Ulcer but few patients now present with large areas of skin and bone erosion from this infiltrative type of lesion. Multiple tumours are frequent but metastases are very rare. Treatment Because of the potential of these tumours to cause such destruction all should be treated. Surgical excision, usually on the basis of clinical appearance, with a margin of 0.5cm is

147 sufficient. Recurrences occur in 50% if histology shows tumour at the excision margins. If there has been complete excision, recurrence is only 5%

TABLE 1. Diagnostic Features of the Three Common Tumours Tumour

Basal Cell

History
Often>1 year

Symptoms
Often none

Appearance
Local pearly nodule with surface blood vessels or diffuse spreading

Squamous Cell Carcinoma

Many months

Sometimes pain from secondary infection

Raised edge, often symmetrical, with central keratin production

Malignant Melanoma

Few months or weeks

Irritation, Bleeding

Irregular border and surface contour: Irregular pigmentation; ulceration; rarely satellite nodules of tumour

SQUAMOUS CELL CARCINOMA The key to diagnosis is the presence of surface keratin. This, together with the features shown in the table, indicate the likelihood that the lesion is a squamous cell carcinoma. The lesions metastasize to lymph nodes and more widely if not treated. It is rare for a tumour less than 0.5 cm in diameter to metastasize. Treatment The tumour is excised with a 1 cm margin of normal skin. Surgical elimination of multiple low grade squamous cell carcinomas or premalignant keratoses of the face and

148 scalp is often impractical in the elderly patient. The daily application of the cytoxic 5% 5Fluoro-uracil cream over a 2 week period can be used instead. Note: A benign kerato acanthoma is a rapidly growing skin lesion which resolves spontaneously after a few months. Since these lesions are very similar in appearance to squamous cell carcinomas, most surgeons advise excision.

MALIGNANT MELANOMA Introduction The most potentially dangerous skin cancer is malignant melanoma. It arises from melanocytes in the basal layers of the epidermis. The incidence of melanoma worldwide is steadily increasing, the highest incidence being in Australasia. There are three common types of melanoma. Clinical and Histological Classification Lentigo Malignant.Melanoma This is the least common and the least malignant. It is a slow growing, flat brown lesion with blotchy pigmentation and the outline is very irregular. It is seen most often in older patients on the temple or malar region where it is called Hutchinsons freckle after Sir Jonathan Hutchinson (1828-1913), a famous London surgeon. Malignant change can be detected by the formation of darker areas and nodules or a general thickening. Superficial Spreading Melanoma This is the most common type and may occur on any part of the body. It is a slightly elevated and perhaps crusty brown lesion with an irregular but well defined edge. Nodular Melanoma This is not as common as superficial spreading melanoma but, being thicker, is more malignant. It is usually a uniform shade of grey, black or blue with a convex raised shape that can be felt. It may have a smooth surface and sharp edge and may be ulcerated.

149 In 1981 Dr A Breslow showed the relationship between thickness of the melanoma and recurrence or metastases (Table 2)

TABLE 2. Thickness of Melanoma and Prognosis Thickness (mm) < .76 0.76 1.5 1.51 2.25 2.26 3 >3 Percentage with recurrence or Metastases at 5 years 0% 33% 32% 69% 84%

It is now realised that the clinical descriptions of superficial spreading and nodular melanomas do not have prognostic value. With the advent of measurement of the thickness of malignant melanoma it has been shown that thickness for thickness there is no difference in prognosis. Differential Diagnosis The appearance of a new pigmented naevus should arouse suspicion of melanoma. Pigmented skin lesions include junctional naevi, dysplastic naevi, pigmented basal cell carcinomas, seborrhoeic keratosis and blue naevi. Treatment All agree that excision of the presenting lesion is the correct initial therapy for the histological proven melanoma. Other aspects of management are vigorously debated. Definitive treatment must be modified depending upon the type and location of the melanoma, the depth of invasion and the presence of lymph node involvement. The risk of local recurrence depends more on the thickness of the lesion than the width of the surgical margin. One to two cm margins for thin lesions and three cm margins for thick lesions (> l mm) are advocated by most authorities. If the regional lymph nodes are

150 involved and there are no signs of distant metastases a node dissection is performed. Some surgeons also perform prophylactic node dissections for thick lesions. About 30-40% of patients with malignant melanoma will eventually die from metastatic disease.

FURTHER READING FOR INTEREST Tjandra JJ, Clunie GJA, Thomas RJS(Eds) Textbook of Surgery 2 Science Ltd.Oxford 2001 pp 400-424
nd

Edition Blackwell

FURTHER READING FOR FINALS Nil

151

Tutorial 15

Surgical Endoscopy
David Theobald

PROCTOSCOPY & SIGMOIDOSCOPY The proctoscope (anoscope in the United States of America) and rigid sigmoidoscope are the simplest instruments to be used in the visualisation of the lower gastrointestinal tract. They are not flexible instruments but are hollow metal (or nowadays disposable plastic) tubes that are illuminated with simple light sources. They are bedside instruments and their use can be considered part of the clinical examination of a patient presenting with symptoms and signs relating to the anorectum. Proctoscopy The proctoscope is the best instrument for examination of the anal canal and distal few centimetres of the rectum. It is introduced after careful digital rectal examination and finds its most frequent use in the diagnosis of haemorrhoids , chronic anal fissures, anal neoplasms and proctitis. It enables the taking of biopsies and is used in the treatment of first and second-degree haemorrhoids by the methods of rubber band ligation and injection sclerotherapy. Sigmoidoscopy The rigid sigmoidoscope is 30cm long and would be better referred to as a rectoscope as it is principally used for visualising the rectum. With the advent of the flexible colonoscope it is no longer used to examine the distal sigmoid colon. Rectal tumours can

152 be biopsied and rectal polyps excised by diathermy snare. In inflammatory bowel disease (especially in the acute phase) a tissue diagnosis from an area of proctitis can be obtained when a full colonoscopy may be deemed hazardous for reasons of perforation in an inflamed oedematous bowel. A very large diameter operating sigmoidoscope has been developed to allow rectal microsurgery to be performed under general anaesthesia.

FIBREOPTIC TECHNOLOGY Direct visualisation of the mucosa of the gastrointestinal tract has been practiced for over a century. However the advent of the practical use of fibreoptic technology in the 1960s gave this a great boost. Technical advances in the instrumentation and new ways of looking at old problems over the last forty years has given rise to two major changes. 1) Surgical endoscopy has moved from being merely a diagnostic tool to having multiple therapeutic options, many of which are now alternatives to conventional surgical techniques. 2) Fibreoptic images have been replaced by electronic images, which opens vast possibilities of image storage, transmission and manipulation. It is expected that these advances will continue into the future. Modern endoscopes are sophisticated small diameter flexible optical/electronic instruments that are used increasingly in conjunction with other medical technologies in a seamless manner. It is important that a basic understanding of the scope and limitations of diagnostic and therapeutic endoscopy are grasped. Diagnostic Endoscopy and Contrast Radiology These two techniques are complementary and not mutually exclusive. Both provide extra information no more or less important than a careful history and examination in the process of reaching a diagnosis. Before choosing an investigation the advantages and disadvantages of each should be considered some patients will require both modalities. In general both techniques are minimally invasive but not totally without risk. All contrast radiology requires that the patient be exposed to radiation. Diagnostic gastroscopy should be attendant with morbidity and mortality approaching zero. At the other end of the scale diagnostic endoscopic retrograde cholangiopancreatography (ERCP) is attendant with an acute pancreatitis rate of about 3% - rarely this can prove

153 fatal. Contrast radiology can provide information about morphology beyond strictures of the gastrointestinal tract that the endoscope cannot traverse. Endoscopy allows the taking of biopsy and cytology samples for obtaining tissue diagnosis. A diagnostic endoscopic procedure can logically progress to therapy at the same sitting in appropriate circumstances. The diagnostic and therapeutic uses of gastroscopy, colonoscopy and ERCP will be outlined. Gastroscopy This is performed using topical local anaesthesia to the oropharynx, with or with out sedation employing a short acting benzodiazopine given intravenously. The oropharynx, oesophagus, stomach and duodenum to the third part can be examined, images recorded and biopsies taken. It is commonly used to aid in the diagnosis of patients presenting with pain of foregut origin, dysphagia and upper gastrointestinal bleeding. Other patients will undergo gastroscopy specifically for therapy with an already established diagnosis. The commonest therapeutic procedures undertaken at gastroscopy are the haemostasis of acutely bleeding lesions, relief of oesophageal stricturing and placement of feeding tubes. Haemostasis Commonly used in acute haemorrhage from peptic ulcers or oesophago-gastric varices secondary to portal hypertension. Bleeding vessels in peptic ulcers can be directly injected with a solution of 1 in 10000 adrenaline with a >90% rate of haemostasis in the short term. Patients who rebleed usually require surgery. Varices can be ablated using injection of sclerosant solutions or endoscopic rubber band ligation (similar to ligation of piles in the anal canal). It is essential that the portal hypertension and its cause be treated (if possible) at the same time. Oesophageal stricturing Benign obstruction is usually due to peptic stricturing secondary to chronic gastrooesophageal reflux. This is treated by dilating the stricture using wire-guided dilators

154 under fluoroscopic xray control. This may have to be repeated at intervals. The reflux needs to be concurrently treated with either proton pump inhibitors or surgical correction of the incompetent cardio-oesophageal junction. Malignant oesophageal obstruction is treated endoscopically in a palliative setting. The stricture is first dilated as outlined above to create a lumen and this lumen is then maintained by additional endoscopic therapy. This usually involves the placement of an expandable metal stent across the lesion but thermal tumour ablation using endoscopically delivered laser energy can be used. Feeding tube placement Percutaneous endoscopic gastrostomy (PEG) involves inserting a feeding tube into the stomach directly through the anterior abdominal wall under endoscopic vision. Its common uses are in the long term feeding of patients with swallowing difficulties after neurologic events (commonly bulbar strokes) and in the pre-operative nutrition of patients with large head and neck malignancies Colonoscopy This is performed using sedation and analgesia employing a combination of a short acting benzodiazeopine and a synthetic opiate given intravenously. The anal canal, rectum, colon and terminal ileum can be examined, images recorded and biopsies taken. It is commonly used to aid in the diagnosis of patients presenting with change in bowel habit, lower gastrointestinal haemorrhage and anaemia thought to be due to chronic occult blood loss from the gastrointestinal tract. It also has a well-established role in the follow up of inflammatory bowel disease, colorectal polyps and malignancies. Its role in screening for colorectal cancer is less well defined (with the exception of welldocumented familial cases). The diagnostic yield in patients with abdominal pain without lower gastrointestinal symptoms is poor. Polypectomy The commonest therapeutic measure carried out at colonoscopy is the resection of colorectal polyps. This is achieved by snare polypectomy using diathermy. Small polyps can be resected whole while larger lesions may require piecemeal excision. Resected

155 specimens are retrieved for histological examination. Polypectomy is attendant with a colonic perforation rate of approximately 0.1% and this usually requires emergency laparotomy. Endoscopic haemostasis in the colon is less commonly employed than in the upper gastrointestinal tract and usually is achieved with diathermy. The use of endoscopically delivered expandable metal stents to temporarily relieve acute left-sided malignant colonic obstruction has a place in surgically high-risk patients. Endoscopic Retrograde Cholangiopancreatography (ERCP) This is performed with a similar sedation/analgesia regime to that employed in colonoscopy. In addition an anticholinergic drug is given to reduce duodenal peristalsis. A side viewing endoscope is used to identify the Ampulla of Vater and then radio opaque dye is injected selectively into the pancreatic duct and the biliary tree to obtain a pancreatogram and a cholangiogram. Of all the gastrointestinal endoscopic procedures ERCP has the greatest potential for therapeutic benefit. The procedure related pancreatitis rate (approximately 3%) of even diagnostic ERCP is significant and if no therapy is contemplated the newer technique of Magnetic Resonance Cholangiopancreatography (MRCP) is now preferred. It has negligible morbidity and the quality of the images rival those obtained at ERCP. ERCP is commonly used to aid in the diagnosis of patients presenting with symptoms and signs of extra hepatic biliary obstruction (usually from biliary stone disease or pancreato-biliary malignancy), gallstone pancreatitis and its complications and post-cholecystectomy pain. The investigation of the latter group of patients involves the measurement of pressures within the Sphincter of Oddi and is yet to be universally regarded as a routine investigation. Therapeutic measures are most commonly directed at the biliary tree and can conveniently be divided into treatment of obstruction due to stone disease and that due to malignancy. Biliary stone disease Most stones in the biliary tree have their origin in the gallbladder. Thus when treating these patients it should not be forgotten that most will also require cholecystectomy at some juncture. If bile duct stones are found at ERCP, the papillary muscle can be cut with diathermy current (endoscopic sphincterotomy) and upto 85% of patients can have their

156 bile ducts cleared of stones with various extraction accessories (usually endoscopic balloons and baskets). Larger stones are more difficult to extract but can be broken into smaller fragments prior to removal. If the duct cannot be cleared endoscopically, drainage must be left either in the short term by a naso-biliary drain or the medium term by an indwelling stent to prevent post procedure cholangitis. It should be noted that neither procedure is a long-term solution (except perhaps in the very high-risk surgical candidate). Nasobiliary drainage or stent placement can be a life saving procedure in the emergency setting of acute cholangitis where the extra hepatic biliary tree has in effect been turned into an abscess - the basic principal of the treatment of pus is drainage applies. The stone disease can then be treated later in a more controlled setting once the acute phase of the illness has settled. Malignant biliary obstruction As with malignant dysphagia, endoscopic relief of malignant biliary obstruction is used in a palliative setting these patients best chance of long-term survival is a successful resection if feasible. Malignant obstructive jaundice can be caused by tumours of the duodenum, Ampulla of Vater, pancreatic head, extra-hepatic bile ducts or malignant portal lymphadenopathy. Although the natural history of these conditions is very different they are all treated endoscopically in basically the same way. Placing an indwelling stent across the tumour mass to drain bile directly from the liver to the duodenum relieves the obstruction. These stents are either small-bore plastic (cheap but prone to blockage giving rise to cholangitis and the need for replacement) or large bore expandable metal (expensive but much less prone to blockage). About 20% of patients with pancreatic head carcinoma will get symptoms of duodenal obstruction prior to death and this can be relieved by placement of an expandable metal duodenal stent. These endoscopic methods for relieving malignant jaundice are an alternative to surgical bypass.

Capsule Endoscopy The capsule endoscope, or Pilcam, is a very small self contained digital camera complete with LED light source and batteries that is the size of a large medicinal capsule. After being swallowed it takes pictures of the gut at a rate of 2 frames per second (newer

157 models are faster) and was initially developed to image the hidden area to conventional endoscopes, the small bowel. A faster, shorter battery life capsule with a camera chip at both ends of the capsule has recently been developed to screen for oesophageal disease. Images taken are transmitted by radio to a belt worn by the patient during the examination. These images are then downloaded onto a computer for viewing. This technology is the best way of viewing the small bowel mucosa and is used to look for obscure sources of GI bleeding and assess small bowel involvement of inflammatory bowel disease. At present the capsule has no therapeutic modalities.

Endoscopic Ultrasound (EUS) The resolution of ultrasound images is inversely proportional to the depth of penetration of the sound waves and directly proportional to the frequency of those waves. Higher frequency gives increased resolution but decreased penetration and vice versa. The ability to put ultrasound generators on the end of endoscopes has enabled the source to be placed very close to the target organs. This allows the use of very high frequency and very high resolution. The highest frequencies currently used can differentiate between the various layers of the bowel wall mucosa from submucosa from muscularis etc. This technology is now the best way of staging the T and N stage of upper and lower GI tract tumours and of tumours of the pancreas and extrahepatic bile ducts. It allows for the safe progression to endoscopic mucosal resection of suitable superficial cancers. Like other endoscopic technologies before it, EUS is now developing into therapeutic areas and it is being used to drain cystic collections of fluid (e.g. pancreatic pseudocysts following acute pancreatitis) and perform nerve blocks for intractable pain. These therapeutic indicatons will grow (probably very rapidly) with time.

The Future The possibilities are hampered less by technology, which is progressing at an alarming pace, but more by imagination and the safe implementation of the newer technologies. Magnifying endoscopy, giving images comparable to light microscopy, is already available in a research setting giving rise to the virtual biopsy a tissue sample without removing any tissue. The trend of endoscopy being initially a diagnostic tool and then

158 developing therapeutic modalities will continue, probably at an ever increasing pace.

CONCLUSION The preceding summary is not an exhaustive review of the subject but merely outlines the common indications and uses of diagnostic and therapeutic flexible gastrointestinal endoscopy. It should be remembered that as the complexity of the procedure increases (especially the therapeutic measures) the procedure related morbidity also increases and this must be carefully weighed against the planned benefit to the patient whether this be reaching a diagnosis or treating one already obtained.

FURTHER READING FOR INTEREST PB Cotton, CB Williams. Practical Gastrointestinal Endoscopy (4 Edition) Blackwell Science 1996 FURTHER READING FOR FINALS Nil
th

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Tutorial 16

Pediatric Surgery
Erik Heineman and James Hamill

Paediatric surgery is a relatively new surgical specialty. It came into being because of the recognition that many surgical conditions in children were peculiar to that young age group and their management required specific skills and knowledge. General practitioners, paediatricians and general surgeons alike should be familiar with the diagnosis and management principles and know when to refer paediatric surgical patients. This tutorial sets out to discuss the most common clinical presentations of surgical disease in infants, toddlers and children. VOMITING IN THE FIRST MONTHS OF LIFE In the first months of life, vomiting is most commonly due to non-surgical conditions or feeding difficulties (too fast, too much, too often). Important non-surgical conditions of non-bile-stained vomiting are septic causes (meningitis, urinary tract infection, other focal infections) and congenital adrenal hyperplasia. The vomiting is surgically significant when it is bile-stained, persistent, projectile, blood stained (coffee grounds) and/or accompanied by loss of weight or failure to gain weight. The mechanical causes, which have to be taken into account, are pyloric stenosis, gastrooesophageal reflux, strangulated inguinal hernia and malrotation with or without volvulus.

160

VOMITING

Bilious

Non-bilious

Mechanical

Medical

Mechanical

Medical

Volvulus Neonatal bowel obstruction Inguinal hernia (late) Intussusception (late)

Pyloric stenosis Gastroesophageal reflux Inguinal hernia Intussusception

Pyloric stenosis is the commonest surgical cause of vomiting in infancy. Boys are more affected than girls. Almost 20% of cases have a family history. Vomiting usually begins between 3 and 6 weeks of age, is initially non-bile-stained and occurs after all feeds, has a projectile character and the infant is otherwise well and keen to feed. Later the vomiting may contain coffee-ground material (secondary to gastritis and mucosal bleeding) and the infant may become weak, lethargic and listless with increasing dehydration, acid-base imbalance and electrolyte disturbance. There may be significant weight loss. The physical signs of pyloric stenosis are peristaltic waves of gastric contractions, indicating a gastric outlet obstruction, and the palpation of the thickened pylorus (olive). It is felt most easily when the infant is relaxed (flex hips, allow it to suck a dummy, wait until crying stops or the infant is asleep) and the doctor is patient. Feeling the olive is easier if you are on the babys left hand side and use your left hand for palpation. Test feeding can help the baby to relax the abdominal muscles use a glucose solution such as Pedialyte. If a definitive diagnosis cannot be reached an ultrasound examination by a paediatric radiologist will be helpful. The principle of the pre-operative management is to re-hydrate the patient and correct the

161 metabolic alkalosis. A nasogastric tube should be inserted. Once the electrolytes and hydration are normal the child is taken to theatre for surgical correction of the pyloric stenosis (pyloromyotomy, Ramstedt procedure). Normal oral feeds can generally be started shortly after the procedure. Problems which can arise are cardiac arrest on induction (inadequate re-hydration and correction of electrolyte disturbances), aspiration of vomit on induction, perforation of mucosa, bleeding, failure to resume spontaneous breathing after anaesthesia (due to uncorrected metabolic alkalosis) and wound infection and dehiscence. Pyloric stenosis Age peak: 5 weeks Age range: 1-11 weeks Male:female ratio: 4:1

Gastro-oesophageal reflux in the neonatal period is common and is caused by the immaturity of the sphincteric mechanisms at the oesophageal-gastric junction. It tends to become less of a problem when the infant grows older. Vomiting occurs at any time and is non-bilious. Sometimes the vomit may contain bright blood or coffee-ground material. In severe cases repeated episodes of aspiration and pneumonia or failure to thrive may be encountered. The diagnosis is initially made on clinical grounds. Only in severe cases, where the extent and severity of the oesophagitis have to be assessed, a barium swallow, oesophagoscopy and biopsy, pH monitoring and gastric outlet studies are indicated. The initial treatment is conservative, including putting the infant prone with the head of the cot elevated, thickening the feeds and the use of antacids. Surgery is only indicated when the conservative regime fails, or when there is a large sliding hernia or oesophageal stricture. Obstructed inguinal hernia is regularly a reason for both non-bilious and bilious vomiting and is most commonly diagnosed in infancy. This condition will be discussed in the clinical presentation (Intermittent) swelling of the inguinal region.

162 Malrotation with volvulus is a life-threatening condition, which presents with bilestained vomiting with a soft non-distended abdomen. The diagnosis should be made at this early stage before ischaemic damage of the gut occurs. When strangulation occurs there are signs of abdominal distension, tenderness, rectal bleeding and shock. The most reliable investigation is a barium meal with fluoroscopy, which will show that the duodenojejunal flexure is located in a medial and more caudal position than normal (normal is left of the vertebral column and in the same horizontal plane as the pylorus). Furthermore a coil (mimicking the volvulus) might be seen. Malrotation with volvulus is a surgical emergency and should be dealt with urgently. If volvulus is not suspected then the potential dangers of the malrotation are still so significant that semi-urgent surgical correction is indicated. While any fluid balance disturbances are being corrected the patient is taken to theatre where the volvulus is untwisted and where Ladds operation is performed. The appendix is usually removed because, after a Ladds procedure, it would reside in the left upper quadrant leading to diagnostic difficulty should appendicitis subsequently occur.

VOMITING AND INTERMITTENT ABDOMINAL PAIN A patient presenting with intermittent abdominal pain and vomiting represents a diagnostic challenge. If the clinical picture includes severe episodic colicky abdominal pain with drawing up of the legs, vomiting, pallor, the passage of blood rectally and small volume diarrhea, and if the abdominal examination reveals a sausage shaped mass in the right and upper abdominal regions, intussusception is the likely diagnosis. However, the clinical presentation is only rarely that specific. The commonest clinical features in intussusception are rather non-specific and include vomiting, listlessness and lethargy, abdominal pain and pallor. The differential diagnosis includes a wide variety of conditions such as wind colic, gastroenteritis and meningitis. However, wind colic is uncommon after 3 months of age, rarely lasts more than an hour and is not accompanied by vomiting, gastroenteritis is generally accompanied by large volume diarrhea, and meningitis can be excluded by a lumbar puncture showing clear CSF.

163 Intussusception may occur at any age, the peak incidence is at 5 months of age. Most intussusception is idiopathic: the lead point of the intussusception is a hypertrophied Peyers patch. In neonates and in older children, intussusception is uncommon and more likely to be associated with a pathological lead point. If the diagnosis is delayed it is less likely that an intussusception mass can be palpated due to increasing abdominal distension and tenderness. A plain abdominal X-ray can show a proximal mass with a central depression protruding into the early transverse colon and signs of bowel obstruction. An ultrasound examination has a high sensitivity and specificity. Generally an air or barium enema will not only confirm the diagnosis, it will also be therapeutic. In most cases rehydration should be commenced prior to undertaking an enema. Enema reduction of the intussusception should be attempted, unless there is clinical evidence of peritonitis or septicemia. Other indications for surgery are a failure of enema reduction or the suspicion of a pathological lead point (rare, < 10%). Gas enema reduction is more effective and safer than the barium enema for reduction of intussusception. When a first attempt has resulted in a partial reduction and the patient is in a stable condition, a delayed repeat gas enema can be used. The problems encountered during attempted enema reduction are the inability to confirm full reduction, incomplete reduction and perforation. In 6-10% the intussusception recurs and a further enema should be performed.

Intussusception (idiopathic) Peak age: 5 months Age range: 3 months 2 years

ABDOMINAL PAIN AFTER ONE YEAR OF AGE Abdominal pain in children is very prevalent. Making the correct decisions when managing the acute abdomen in children is based on careful clinical assessment. An accurate history and a detailed examination will provide more information than a

164 multitude of investigations. The chronological order of appearance and the progression of each individual symptom must be obtained. Consideration of the dynamics of the signs and symptoms will often yield an accurate diagnosis. When taking a history in a child with acute abdominal pain, the following questions need to be asked and answered: Where did the pain first occur? What is the character of the pain? Is it constant, or cramping and intermittent? What was the order of onset of symptoms? Was the pain the first symptom, or did fever, diarrhea, or vomiting precede the pain? If vomiting, what was the color? Have any family members had similar symptoms? Has the patient had these same symptoms previously? Was there any diarrhea or blood in the stools? When subsequently performing a physical examination, the following points are important: heat up the hands and the room, optimize the environment; do not hurry, establish rapport with the child; observe; check the pulse (the barometer of the belly); be gentle and do not touch the sore area first; palpate with the flat, full hand (do not explore rebound tenderness: it is unreliable and very distressing for the child; assessment of percussion tenderness is much more useful); rectal examination has only very limited indications, learn to do it gently; communicate and document! For children in whom a diagnosis cannot be established during initial consultation, frequent reevaluation while under observation in the hospital often reveals the nature of the (abdominal) pathology within a relatively short time.

Appendicitis is the most common surgical cause of abdominal pain in children after the age of one year, and must be distinguished from other common causes of abdominal pain, such as mesenteric adenitis (non-specific viral infection), indigestion, wind pains, acute constipation, gastroenteritis, urinary tract infection, intraperitoneal bleeding at the time of ovulation (mittelschmertz bleeding) and rupture of a small luteal cyst. Proper examination should further exclude conditions like an inguinal hernia and acute scrotum.

165 In acute appendicitis in children pain is generally the first symptom. Pain may begin in the epigastrium or the umbilicus (visceral pain from the mid-gut) and later move to the right iliac fossa once local peritoneal irritation develops. Vomiting is quite common in children and occurs early after the onset of pain, but there is no progression as would be seen in a bowel obstruction. Low-grade fever (37.5 38 C) is often found. The results of the physical examination are dependant on the location of the appendix and the severity of the clinical presentation. When there is increased tone (guarding) of the right lower abdomen and local percussion tenderness the diagnosis is straightforward. However, when the appendix is situated in a retrocaecal, retro-ileal or pelvic position, or when an appendiceal mass has developed, the diagnosis is much more difficult to make. These children present with progressive abdominal pain, pain during micturition and increasing toxicity. Examination findings might not match the clinical severity. Where the diagnosis appendicitis is equivocal, the child should be re-examined at regular intervals. Furthermore, selective use of ultrasound and CT scan has proved to be very helpful. Preoperative preparation includes intravenous resuscitation and the start of antibiotic treatment. The aim of surgery is the removal of the appendix and intraperitoneal toilet. Peri-operative problems can arise when the appendix is located in a retrocecal position or when there is abnormal rotation and fixation of the mid-gut. Rarely the abdominal pain is caused by inflammation of a Meckels diverticulum, which cannot be distinguished clinically from acute appendicitis. The diagnosis appendicitis should always be confirmed by histological examination. In 0.5% of all removed appendices carcinoid tumors are found. Postoperative complications following appendicectomy include bleeding (rare), wound infection, intraperitoneal abscess formation, leakage from the appendix stump (rare), and urinary tract infection.
0 0

RECTAL BLEEDING

166 A number of common and rare conditions in children present with rectal bleeding. Only the most prevalent causes will be discussed. Generally the clinical setting will give direction as to the likely cause. In an otherwise healthy neonate anal fissure or swallowing of maternal blood (fissure of the nipple) are most likely the reason for rectal blood loss. In an ill child with an acute abdominal condition intussusception and gastroenteritis can cause rectal blood loss. Major hemorrhage can be caused by a Meckels diverticulum. An anal fissure or a rectal polyp can cause small amounts of bright red blood in a well child. Anal fissure occurs at any age including the neonatal age group and is usually due to constipation. The child passes large, hard stool that splits the anus, usually in the midline, either posteriorly or anteriorly. The child is uncomfortable during defecation and a small amount of bright red blood on the surface of the stool or immediately following it is seen. The fissure can be observed by gently parting the anus. Sometimes, a sentinel pile, which is a bit of edematous skin just external to the fissure, can be seen. Rectal examination should never be performed as this causes severe pain. The treatment of the anal fissure consists of dealing with the underlying constipation. Dietary advice with sufficient fibre and fluid and stool softeners is generally sufficient. Local application of anesthetic agents achieves little and surgery is virtually never required. Rectal polyp is relatively common in children. This condition should be suspected when in a healthy child intermittent rectal blood loss is the presenting symptom, when there is no history of constipation and pain during bowel motions and when an anal fissure has been excluded on physical examination. Generally these polyps concern juvenile polyps, which are located in the rectum. Occasionally the polyp prolapses through the anus. The diagnosis is confirmed on sigmoidoscopy. The polyp is removed, recurrence is unusual and malignancy is unknown. However, when more than three polyps are identified further investigations should be performed to exclude one of the multiple polyposis syndromes.

167 (INTERMITTENT) SWELLING OF THE INGUINAL REGION The testis descends into the scrotum during the seventh month of gestation through an extension of the peritoneum called the processus vaginalis. The processus vaginalis starts to obliterate shortly afterwards and is generally closed in the course of the first year of life. What remains is the tunica vaginalis surrounding the testis. Failure of obliteration of the processus vaginalis can result in the formation of a hydrocele, an encysted hydrocele of the cord, and most importantly an inguinal hernia. In girls, the canal of Nuck undergoes the same obliteration as the processus vaginalis in boys. The obliteration is more likely to be complete, with as a consequence a much lower incidence of inguinal pathology in girls than in boys. Premature born children (before 37 weeks of gestational age) are more prone to the development of inguinal hernias. An encysted hydrocele of the cord or a hydrocele presents as a painless swelling of the cord or in the scrotum. Generally it is possible to palpate above the swelling and to establish that there is no continuity with the abdominal cavity. The palpation is not painful and the swelling cannot be reduced. Transillumination demonstrates the nature of the swelling. Hydroceles and encysted hydroceles of the cord are repaired by herniotomy after the age of 2 years, if they are still present. An inguinal hernia presents as an (intermittent) swelling overlying the external inguinal ring in the groin or may extend into the scrotum as an inguinal-scrotal hernia. Crying and straining provoke its appearance. The swelling can be painless or can cause discomfort. When the swelling cannot be reduced it is called irreducible. All irreducible hernias are assumed to be strangulated, because clinical examination cannot determine the adequacy of the blood supply to the contents of the hernial sac, or compression of the testicular vessels. Strangulated hernias are seen more often in infants under 6 months of age. The differential diagnosis of a strangulated inguinal hernia includes an encysted hydrocele of the cord and torsion of a nondescended testis. Nearly all inguinal hernias in children are indirect, with an incidence of 1 in every 50 live male births.

168 A strangulated inguinal hernia is a surgical emergency and reduction should be attempted. Contraindications for manual reduction are signs of dead bowel, such as localized redness, edema and induration of the overlying skin, and signs of peritonitis and shock. If reduction is successful surgical correction of the hernia should be performed after 1 to 2 days. If reduction is not successful the groin should be explored urgently. All hernias should be repaired, preferably within 2 to 4 weeks after the diagnosis has been established. The following peri-operative risks and long term outcomes of herniotomy have to be discussed with the parents and/or the patient: bleeding, infection, transection of the cord structures, ectopic location after the operation and testis atropy.

UNDESCENDED TESTIS OR CRYPTORCHIDISM The testes develop as intra-abdominal structures, entering the inguinal canal during the seventh month of life. At or shortly after birth the testes are usually in the scrotum. Descent is unlikely to take place after 3 months of age. This condition, which is called congenital undescended testis or cryptorchidism, is found in 1% to 2% of boys. Normal testes in young boys are readily elevated to the upper scrotum by the cremasteric muscle. This commonly causes confusion at routine medical checks. Confirmation that the testes were both descended at the time of birth is helpful under those circumstances. A retractile testis is a testis, which may not be in the scrotum at the commencement of the examination, but which can be located and manipulated into the scrotum, where it remains, at least briefly, following its release. The boy is examined in a warm and relaxed environment, if possible he is asked to adopt a squatting position and the first action of the examiner is to block the escape route of the testis by digital compression of the inguinal canal at the site of the external inguinal ring. Retractility does not require surgical intervention and is most marked during mid-childhood. An undescended testis is a testis, which fails to reach the scrotum, and which can be classified into the following categories: congenital undescended testis and acquired undescended testis. The concept of the acquired undescended testis (the ascending testis)

169 is controversial. From a management point of view it does not really matter if the testis was ever in a scrotal position or not. The base line is that, if at the age of one year, the testis cannot be brought to the bottom of the scrotum, or it will not remain there following its release, the testis is considered to be undescended. It needs surgery to place it in its correct scrotal position. When the testis cannot be palpated (impalpable testis), it is either intraabdominal, intracanalicular, or absent. The presence or absence and the location of the testis have to be identified by surgery. The rationale for the surgical correction/exploration for an undescended or impalpable testis is that the extra-scrotal position of the testis causes failure of postnatal germ cell maturation and poor development of the seminiferous tubules. Furthermore a testis in the inguinal region is more liable to direct trauma and torsion. Finally, the risk of the development of a seminoma in later life is 5 to 10 times greater in an undescended testis than in a normal descended testis. Orchiopexy early in life (ideally at 6 months of age) is expected to prevent the development of infertility or tumors, however the real long term benefit as far as the prevention of tumor development is concerned has still to be proven. The consequences of this lack of evidence is, that boys who have been treated for undescended testis need life long follow up to minimize the change of missing the development of a testicular tumor. Orchiopexy is usually performed as a day-stay surgical procedure. A number of perioperative and post-operative problems can be encountered. Testicular atrophy can occur as a result of injury of the testicular vessels. The vas deferens can be transected or traumatized. The testis may not reach the scrotum or retract out of the scrotum. Haematoma or infection may occur. The parents should be made aware of both the perioperative and post-operative risks as well as the need for long-term follow up. ACUTE SCROTAL PAIN A boy who complains about a sudden onset of scrotal pain is a surgical emergency. There is a group of conditions that cause a red, swollen and often painful scrotum. These conditions are: torsion of one of the appendages of the testis (hydatid of Morgagni)

170 (60%), torsion of the testis (30%), epididymo-orchitis (<10%), and idiopathic scrotal oedema (<10%). Testicular torsion presents as a sudden onset of testis or ipsilateral iliac fossa pain, often accompanied by nausea and vomiting. On examination the scrotum is swollen and the testis and epididymis are very tender. The testis lies high in the scrotum. Urgent surgical exploration is required. The testis is untwisted and if it is viable it is anchored (pexed) to prevent re-torsion. If the testis is necrotic it should be removed. In all cases the contralateral testis should be pexed as well. Torsion of the appendix testis often has a similar clinical presentation as torsion of the testis. In the first few hours after the torsion has occurred however, a blue-black spot may be seen through the scrotal skin near the upper pole of the testis. Palpation of the spot rather than the whole testis is painful. The epididymis is non-tender and is not enlarged. The testis does not lie high in the scrotum. Once a secondary hydrocele has developed it may not be possible to distinguish torsion of the appendix testis from torsion of the testis. Urgent exploration is required either to exclude torsion of the testis and/or to provide relief of symptoms. Contralateral exploration is not required. Epididymo-orchitis is uncommon in childhood, except in the first year of life, where it can be secondary to urinary tract abnormalities or around puberty where it may occur secondary to reflux of secretions up a wide vas deferens. Mumps orchitis is very rare before puberty. Antibiotic treatment should be contemplated as well as further investigations. Idiopathic scrotal oedema is manifested in an otherwise well child by a marked swelling and redness of the scrotal skin and extensive redness of the adjacent perineal and inguinal region. No treatment is required.

FORESKIN PROBLEMS

171 The foreskin (prepuce) is naturally adherent to the glans penis in the first couple of years. It cannot and should not be attempted to be retracted until spontaneous separation of these preputial adhesions occur. Accumulation of smegma may produce a yellowish bulge in the preputial skin. This does not require intervention. Three abnormal conditions can arise in the prepuce. These are phimosis, paraphimosis and balanitis. Non-surgical (antibiotics, steroid cream, bath) and surgical treatment (circumcision) is recommended dependant on the severity of the problem.

HYPOSPADIAS Hypospadias refers to a urethral meatus on the ventral surface of the penis rather than near the tip of the glans. It is usually associated with a hooded foreskin (deficient ventrally) and may be associated with a curved penis (called chordee). The incidence is approximately 1:300 boys. Hypospadias associated with one or 2 undescended testes may indicate an intersex disorder. Surgical correction of hypospadias is ideally performed by a paediatric urologist at 6-18 months of age.

FURTHER READING FOR INTEREST Jones Clinical Paediatric Surgery. Diagnosis and Management. 5 edition 1999, Blackwell Science Asia.
st th

Essential Paediatric Surgery. Beasley SW, Hutson JM and Auldist AW. 1 edition 1996, Arnold. FURTHER READING FOR FINALS Nil

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Tutorial 17

Organ Transplantation
John McCall

In the last 50 years organ transplantation has progressed from a largely experimental science to become an established treatment for end-stage disease affecting vital organs including the heart, lung, liver, kidney, and pancreas. The steady improvement of graft and recipient survival rates for all transplants over recent years can be attributed to: advances in surgical technique and peri-operative care better understanding of the immunological mechanisms that cause rejection and the development of drugs to prevent it advances in the diagnosis, prevention, and treatment of infectious diseases in the immunocompromised patient

Organ donation
Transplantation would not exist without organ donation. Most solid organ transplants come from cadaveric donors. These are people who have suffered a catastrophic and irreversible structural brain injury resulting in brain death, usually from a cerebrovascular event or trauma. After consent is obtained from the family, the donor is maintained on a ventilator and supported with fluids and inotropes until the organ retrieval operation. At surgery the organs are perfused with a specially formulated preservation fluid (University of Wisconsin Solution) then stored on ice for transportation to the recipient hospital. Safe

173 storage times range from 4 to 36 hours, depending on the organ type (shortest for heart and longest for kidneys). Organs from a single cadaveric donor can result in transplants for up to 6 recipients. In addition, corneal and bone grafts may be obtained and used for sight and limb preserving surgery. Because there are more people needing transplants than there are cadaveric organs available, living donors are also sometimes used. About one third of kidney transplants are done using living donors. Some liver transplants are also from living donors. The paramount responsibility of all those involved in living donor transplantation is to ensure the safety of the donor and to be certain that coercion of any kind, including financial, is not a factor in the decision to donate.

Immune Response to Organ Transplants

A transplant from an individual of the same species is called an allograft (transplants between species are called xenografts and for a variety of reasons these have not yet made it into clinical practice). Although we all share common genes, each individual also possesses a unique set of genes (HLA or human leucocyte antigens) which code for proteins expressed on the surface of cells. These are important determinants of histocompatibility and are called MHC or major histocompatibility complex proteins. Class I MHC molecules are expressed on all cells whereas Class II MHC molecules are only expressed on antigen-presenting cells (eg macrophages). Peptides are coupled with Class II MHC molecules within donor antigen-presenting cells and presented on the cell surface membrane. This combination is recognised by unique receptors on the surface of recipient T cells, and sets off a cascade of intra-cellular events within the T cell that culminates in the production of IL-2 and other cytokines. These in turn stimulate cellular (T cell) and antibody (B cell) effector responses directed against the donor organ. Unmodified, this response results in immune mediated injury to the graft, or rejection. There are 3 main types of rejection. Hyperacute rejection. This is due to pre-formed antibodies that attach to vascular endothelium in the graft, activate complement and result in vascular injury and thrombosis. It occurs early, within hours, and usually results in graft loss. Kidney grafts are most at risk but the problem can nearly always be prevented by testing recipient

174 serum against donor leucocytes in vitro before the transplant, and by avoiding ABO incompatibility between donor and recipient. Acute rejection. This usually occurs between 1 and 2 weeks post-transplant and is caused by T cell mediated injury to the graft. It is common after all types of organ transplants and can usually be controlled by extra boluses of high dose corticosteroid. Chronic rejection. This occurs months to years post-transplant and is the major cause of late graft loss. The mechanisms are not well understood, and may be multifactorial (immunological, viral, drug side effects, non-compliance). The incidence and manifestations of chronic rejection vary widely in different organ grafts (table 1).

Table 1. Chronic Rejection in Solid Organ Grafts Organ Heart Lung Liver Prevalence Common Common Rare Main manifestations Coronary artery disease Bronchiolitis obliterans Vanishing bile duct syndrome, foam cell arteritis Kidney Common Interstitial fibrosis, endarteritis, glomerulosclerosis Pancreas Uncommon Chronic (allograft) pancreatitis (may not affect endocrine function)

Graft-versus-host disease (GVHD) is a special type of immune-mediated injury where donor leucocytes transplanted within the donor organ migrate to the periphery and engraft. These donor-derived leucocytes can then mount an immune response against

175 the host. GVHD can range in severity from a minor illness to a fatal systemic disease. It is most common after allogeneic bone marrow transplants. Fortunately GVHD is rare after solid organ transplants, with the exception of small bowel. Immunosuppression Immunosuppressive agents are required to prevent and control rejection. Too much immunosuppression results in infection and other unwanted side effects whereas too little immunosuppression results in rejection. The risk of rejection, infection, and other serious side effects varies with different organ transplants, as well as between different individuals. Fortunately there are a growing number of agents now available to enable regimens to be tailored to the needs of individuals. The main classes of drugs, their mechanism of action, uses and principal side effects are listed in table 2. In general, high levels of immunosuppression are required during the first few months following transplantation when the incidence of acute rejection is greatest. In the long term most patients can be maintained on a small dose of calcineurin antagonist, either alone or in combination with low dose steroids and/or an anti-proliferative agent.

Infectious Diseases The need for life long immunosuppression makes transplant recipients more susceptible to a range of infectious complications. In the early post-transplant period bacterial infections related to the surgical procedure prevail. The types of infection, pneumonia, wound infections, intra-abdominal sepsis, catheter related sepsis etc, are similar to those seen after other major operations, but because the patients are immunosuppressed prompt and aggressive treatment is essential. Latent viral infections, such as herpes simplex, may recur early post-transplant. Primary infection (transmitted with the transplant) or reactivation of cytomegalovirus (CMV) is common in the first 6 months post-transplant. CMV disease was a major cause of morbidity and mortality in transplant recipients prior to the availability of effective prophylaxis and treatment with gancyclovir. Pneumocystis pneumoniae also has a peak incidence in the first 6 months, and usually co-exists with CMV. Pneumocystis can

176 usually be prevented or effectively treated with co-trimoxozole. A wide range of other opportunistic infections occur less frequently, but some, such as invasive aspergillus infection, can be fatal. Any infective illness in a transplant recipient, no matter how trivial it may appear at first, must be taken seriously. Table 2. Major immunosuppressive agents
Class Calcineurin antagonists (Tacrolimus, Cyclosporin) Chronic Rejection (Tacrolimus) Hypertension Hyperglyacaemia Corticosteroids Anti-inflammatory Induction and acute rejection (high dose) Maintenance Peptic ulcer Chronic effects Hyperglycemis Neurotoxicity Mechanism Inhibit IL-2 production by T-cells Uses Maintenance Side effects Nephrotoxicity

Antibodies against T cells (OKT3 and ATG) Antibodies against IL-2 receptor (Dacluzimab, Basiliximab) Azathioprine

Deplete circulating lymphocytes

Induction

Cytokine release (OKT3)

Prevents IL-2 mediated activation

Induction

Minimal

Inhibits cell proliferation (non specific)

Maintenance

Myelosuppression Pancreatitis

Mycophenolate mofetil

Inhibits lymphocyte proliferation (specific)

Maintenance (Chronic rejection?)

GI intolerance Neutropenia

Rapamycin

Blocks cytokine induced T cell division cycle

Maintenance

Dyslipidaemia Thrombocytopaenia

177 Malignancy Skin cancers are very common in Caucasians, and sometimes more aggressive in immunocompromised patients. All Caucasian transplant recipients are advised to minimise ultra-violet light exposure and report new skin lesions if they occur. B cell lymphomas are 100 times more common in transplant recipients than the general population. The risk is highest in those who have acquired primary Epstein-Barr Virus (EBV) infection with the graft (usually children) and require high levels of immunosuppression early post transplant. EBV infects, transforms, and immortalises B cells which then proliferate unchecked in the absence of a normal T cell response. The treatment is reduction or cessation of immunosuppression, anti-B cell monoclonal antibodies and, if necessary, chemotherapy. Most tumours respond but there is a risk of graft loss as a consequence of reducing immunosuppression. The incidence of other cancers in transplant recipients is also higher than in the general population. This may relate to the underlying disease that initiated the transplant, or to the effects of long term immunosuppression on immune surveillance.

TRANSPLANTATION OF INDIVIDUAL ORGANS Heart transplantation is indicated for end-stage disease, mainly due to cardiomyopathy, and coronary artery, valvular or congenital heart disease not amenable to other forms of surgical correction. The procedure is undertaken through a median sternotomy. The transplant is sewn in to the normal (orthotopic) position after cardiectomy. The patients circulation is maintained by the heart-lung machine until the new heart is functioning well enough to take over. Approximately 75% of patients are alive 5 years after a heart transplant, with most enjoying a good quality of life. Lung transplantation is indicated for end-stage disease due to emphysema or other causes in whom active pulmonary infection can be adequately controlled. The procedure is usually single lung, in the orthotopic position, via a standard thoracotomy incision. The long term results are affected by a higher peri-operative risk (leakage from the

178 bronchial anastomosis), and significant rates of infection and chronic rejection. Approximately 50% of patients survive 5 years after a lung transplant. Liver transplantation is indicated for almost any cause of end-stage liver disease. In adults hepatitis B and C, cholestatic liver disease (PSC and PBC), and alcoholic liver disease are the commonest indications. In children biliary atresia is the most common indication. About 10-15% of liver transplants are done for acute liver failure, due mainly to viral hepatitis. The operation is performed through a bilateral subcostal incision and the liver is placed in the orthotopic position after total hepatectomy. The left lateral segment of an adult liver is used for children, and sometimes the remaining right lobe can also be used for an adult (split liver transplantation). Approximately 80% of patients are alive 5 years after a liver transplant, with a good quality of life. Kidney transplantation is an alternative to long term dialysis for patients with end-stage renal failure of any cause. The most common causes are glomerulonephritis, diabetic nephropathy, and polycystic kidney disease. The native kidneys are not usually removed and the transplant is placed extra-peritoneally in the pelvis (heterotopic) with the renal artery and vein anastomosed to the iliac artery and vein respectively, and the transplant ureter implanted into the bladder. Survival and quality of life are improved, and treatment costs reduced, with transplantation compared to dialysis. Over 90% of grafts are functioning at 1 year and 70% at 5 years post-transplant. The results are better for kidneys from living donors, and those with a good HLA match between donor and recipient. Pancreas transplantation is undertaken in selected patients with diabetic nephropathy and type I diabetes (type II diabetics are insulin resistant rather than insulin deficient and therefore may not benefit from pancreas transplant). Usually combined kidney and pancreas from the same donor are transplanted simultaneously. The pancreas is implanted heterotopically with the arterial and venous anastomoses to the iliac vessels on the opposite side to the kidney, and the pancreatic duct drained via a retained portion of duodenum into the bladder or small bowel. The surgery has a higher complication rate than kidney transplant alone and recipients must be fit enough to tolerate the additional risks. Eventually pancreatic islet cell transplantation may supercede the need for whole

179 pancreas grafts. At present 80-90% of patients are insulin free at 1 year and 70% at 5 years following pancreas transplantation. Small bowel transplantation is only considered when patients with intestinal failure have developed life threatening complications of parenteral nutrition, such as TPNinduced hepatic failure or recurrent life threatening catheter sepsis. The most common causes of intestinal failure are massive enterectomy due to volvulus, congenital abnormalities, or Crohns disease. The small bowel graft is placed orthotopically with an end stoma. Small bowel and liver grafts may be combined for TPN-induced hepatic failure. The small bowel is the largest lymphoid organ in the body and is highly immunogenic. Rejection causes bacterial translocation resulting in sepsis, which makes these patients very difficult to manage. However results have recently improved, with 50% 5 year survival rates being reported from specialized centres. FUTURE POSSIBILITIES Transplantation has come a long way but there are still many obstacles to overcome. Some of the aims of current research include: Developing ways of inducing tolerance so that tranplants can be maintained without long term immunosuppression Understanding the causes and ways of reducing graft loss from chronic rejection Overcoming the obstacles related to xenotransplantation to ease the shortage of organs available for transplantation Developing gene therapies for some inborn errors of metabolism to avoid the need for transplantation for those conditions Development of artificial support systems for the heart and liver FURTHER READING FOR INTEREST Nil FURTHER READING FOR FINALS

180 Nil