“THE ROLE OF HYPERBILIRUBINEMIA AS A PREDICTOR OF GANGRENOUS OR PERFORATED APPENDICITIS
Partial fulfilment of the regulations requiredfor the award of
THE TAMILNADU Dr.
ROLE OF HYPERBILIRUBINEMIA AS A PREDICTOR OF GANGRENOUS OR PERFORATED APPENDICITIS
Dissertation Submitted in
Partial fulfilment of the regulations requiredfor the award of M.S. DEGREE
In
General Surgery Branch - I
THE TAMILNADU Dr. M.G.R. MEDICAL UNIVERSITY CHENNAI - 600 032
APRIL 2015
ROLE OF HYPERBILIRUBINEMIA AS A PREDICTOR OF GANGRENOUS OR PERFORATED APPENDICITIS"
Partial fulfilment of the regulations requiredfor the award of
M.G.R. MEDICAL UNIVERSITY
CERTIFICATE
This is to certify that the dissertation titled “The role of Hyperbilirubinemia as a predictor of gangrenous or perforated appendicitis” submitted to the Tamil Nadu Dr. M.G.R Medical University, Chennai in partial fulfilment of the requirement for the award of M.S Degree Branch- I (General Surgery) is a Bonafide work done by Dr. Thimmaiah K A, post graduate student in General Surgery under my direct supervision and guidance during the period of September 2013 to September 2014.
Prof. Dr. S.Natarajan, M.S. Prof. Dr. V. Elango, M.S.
Professor of Surgery Professor and Head of the Department Dept. of General Surgery Dept. of General Surgery
Coimbatore Medical College Hospital Coimbatore Medical College Hospital
Dr. S. Revwathy, M.D.
The Dean
Coimbatore Medical College Hospital
ACKNOWLEDGEMENT
I express my gratitude to Dr. S. Revwathy, M.D., D.G.O., D.N.B., Dean, Coimbatore Medical College Hospital for permitting me to use the clinical material for the study.
It gives me immense pleasure to express my deep sense of gratitude to my Unit Chief Prof. Dr. S. Natarajan, M.S., General Surgery, Department of General Surgery, Coimbatore Medical College Hospital, for his for his excellent guidance and valuable suggestions during the course of study and in preparation of this dissertation.
I am grateful to Prof. Dr. V. Elango, M.S., Professor and Head of the Department of General Surgery, Coimbatore Medical College Hospital, for his guidance throughout this study.
Ialso thank the former head of the department of surgery to Prof.
Dr. P.V.Vasantha Kumar, M.S.
I also express my heartfelt thanks to the unit chiefs, Dr. P.
Swaminathan, M.S., Dr. D. N. Ranganathan, M.S., Dr. Ravindran M.S., and Dr. S. Saradha, M.S. for their suggestions at the apt time that has helped me in the completion of this work.
I am deeply indebted to my Assistant Professors, Dr. R. Narayana Moorthy M.S., Dr. S. Meenaa, M.S., for their help and guidance throughout this study.
I express my thanks to my friends and all others who have helped me in the preparation of this dissertation.
Last but not the least; I heartily thank all the patients for their kind support without whom this study could never be done.
DECLARATION
I hereby declare that the dissertation entitled “the role of hyperbilirubinemia as a predictor of gangrenous or perforated appendicitis”was done by me at Coimbatore Medical College Hospital Coimbatore - 641018 during the period of my post graduate study for M.S. Degree Branch-1 (General Surgery) from 2013 to 2014
This dissertation is submitted to the Tamil Nadu Dr. M.G.R.
Medical University in partial fulfilment of the University regulations for award of M.S., Degree in General Surgery.
Dr. Thimmaiah K A Post Graduate Student M. S. General Surgery
Coimbatore Medical College Hospital
TABLE OF CONTENTS
Sl.No TITLE Page.No
1. Introduction 1
2. Aim & objectives 2
3. Review of literature 3
4. Methodology And Techniques 62
5. Observations and Results 67
6. Discussion 92
7. Summary 100
8. Conclusion 101
9. Bibliography 102
10. Annexures i) Proforma ii) Abbreviations
iii) Key to master Chart ii) Master Chart
iii)Consent Form
LIST OF TABLES
Sl. No. Title Page No.
1. Causative organisms of appendicitis 24
2. Alvarado score 44
3. Differential diagnosis according to age and sex in appendicitis 53 4. Reference Range of Serum Bilirubin and Liver Enzymes 65
5. Age distribution of patients 68
6. Sex wise distribution of patients 69
7. Sex distribution according to age group 70
8. Mean age distribution among sex 71
9. Liver function tests 72
10. Distribution of liver enzymes 73
11. Total bilirubin levels 75
12. Bilirubin levels in patients with uncomplicated acute appendicitis 76 13. Bilirubin levels in patients with complicated acute appendicitis 77
14. Total leucocyte count 78
15. Differential leucocyte count (DLC) 79
16. Pre-operative diagnosis 80
17. Ultra sonogram finding 81
18. Per operative diagnosis 82
19. Histopathological diagnosis 83
20. Comparison of mean serum bilirubin levels in patients with acute appendicitis and appendicular perforation/ gangrene
84 21. Correlation of acute appendicitis and appendicular perforation with
total serum bilirubin levels
86
22. Chi square test 88
23. Roc curve 89
LIST OF COLOUR PICTURES
Fig. No. Title Page No.
1. Anatomy of appendix 7
2. Various Positions of the Appendix 7
3. Stages in development of the cecum and appendix 9
4. Development of tip of Appendix 9
5. Congenital anomalies- Duplication of appendix 9
6. Arterial supply of appendix 13
7. Arterial supply of appendix 13
8. Caecal recess 16
9. Normal histology of appendix 16
10. Acute appendicitis histopathology 29
11. Ultra-sonography- inflamed appendix 39
12. Ultra-sonography- perforated appendix 39
13. CT scan showing dilated appendix 42
14. CT scan showing appendix surrounded by fat- stranding
42 15. Clinical algorithm for suspected cases of acute
appendicitis
43
16. Bilirubin metabolism and elimination 46
17. Per operative picture of inflamed appendix 60 18. Per operative picture of inflamed appendix 60 19. Per operative picture of perforated appendix 61 20. Per operative picture of gangrenous appendix 61
11
12
INTRODUCTION
Acute appendicitis is the commonest cause of “Acute Surgical abdomen”. Appendectomy is the most commonly performed emergency abdominal operation and is often the first major procedure performed by a surgeon in training.
The diagnosis of Appendicitis still remains a dilemma in spite of advances in the radiological and laboratory investigations. Experienced clinicians accurately diagnose appendicitis based on a combination of history, physical examination and laboratory studies about 80% of the time. Although most patients with Acute Appendicitis can be easily diagnosed, in some cases the sign and symptoms are variable and a firm diagnosis can be difficult. This is particularly true where the appendix is retrocaecal or retroileal. The percentage of appendectomies performed where appendix subsequently found to be normal varies 15- 50% and postoperative complications can occur in up to 50% of these patients.
Delay in diagnosis of Acute Appendicitis leads to perforation and peritonitis and increased mortality.
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A safe alternative seems to do appendectomy as soon as the condition is suspected. This type of plan of management increases the number of unnecessary appendectomies. A timelier and more accurate diagnosis has been attempted by the employment of additional laboratory tests, scoring systems, ultrasound imaging, computed tomography (CT) scan, scintigraphy, MRI, and laparoscopy. None of these methods stands alone as they all come in support of, and are secondary to a primary clinical assessment.
Hyperbilirubinemia is a new diagnostic tool for perforation of appendix. Hyperbilirubinemia is the result of imbalance between synthesis and excretion of bilirubin by the liver. Portal blood carries nutrients and other substances absorbed from gut including bacteria and its product (toxins). It is commonly cleared by detoxification and immunological action of the reticuloendothelial system of the liver that acts as first-line defense in clearing toxic substances, bacteria and its products. But when bacterial load overwhelms the Kupffer cell function, it may cause dysfunction or damage to hepatocytes (liver parenchyma). It reflects a rise in serum bilirubin (SB) alone or in combination with liver enzymes depending upon the type, severity and site of the lesion
14
AIMS AND OBJECTIVE
AIM:
1. To establish the role of hyperbilirubinemia as a diagnostic tool to predict gangrenous/perforated appendicitis
OBJECTIVES:
1. To study the relationship between hyperbilirubinemia and acute appendicitis.
2. To evaluate whether elevated bilirubin levels have a predictive potential for the diagnosis of appendicular perforation.
3. To compare other variables such as age, duration of symptoms, clinical profile, white blood cell count, C-reactive protein and ultrasound in a similar role.
15
REVIEW OF LITERATURE
HISTORY OF APPENDICITIS [11, 12, 14 ]
Appendix was formally described only by 16th century, by Da Capri in 1524 and Vesalius by 1543. Probably the first case of appendicitis was described in a 7 year girl by Fernel in 1554. She was treated for diarrhoea with large quince after which she developed abdominal pain and succumbed to illness. Autopsy indicated that quince had cause obstruction of appendicular lumen and caused perforation and gangrene of appendix.
Initial surgery’s was done only primarily to drain right lower quadrant collection or pus due to appendicular perforation. First surgical procedure for appendicitis without abscess was carried out by Hancock in 1848. In which he opened the peritoneum and drained the right lower quadrant without appendectomy.
First appendectomy was done by Amyand on a boy in 1736. He found perforated appendix in sac of inguinal hernia which was resulting in enterocutaneaous fistula within inguinal hernia. Nearly after 150 years Lawson Tait did the first successful Trans abdominal appendectomy for
16
gangrenous appendix. During the year 1886, Reginald Fitz coined the name appendicitis. He also advised early surgical intervention for the disease. In 1889 Charles McBurney of New York presented series of successfully treated appendicitis by surgery. In which he described location of maximum tenderness which bears his name as McBurneys point now. 1n 1890’s Sir Frederick Treves of London introduced conservative line of management for acute appendicitis. Which was followed by appendectomy after reduction in infection. Regrettably he lost his youngest daughter due to above treatment in which she developed perforation of appendix.
In 1982 Kurt Semm a gynaecologist first performed laparoscopic appendectomy.
ANATOMY [7, 8, 9, 14, 16]
The appendix is a worm shaped muscular tube originating from caecum.it is narrow, opens into posteromedial wall of caecum about 2cm inferior to the ileocaecal valve. It is usually mobile except the base which is attached to caecum. Longitudinal muscle layer is formed by the taenia coli of colon which converge at the base of appendix. Length varies from 8 to 13 cms comparatively longer in children’s, shortens and atrophies after mid adult life. It is covered all around by the peritoneum. A
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triangular fold of peritoneum attaches to appendix extending whole length from base till the tip of appendix known as mesoppendix.
Mesoappendix contains appendicular vessel and the nerves. Appendix opens as a small orifice into the caecum situated below and little posterior to ileal opening. The above orifice may be guarded by a valve formed by semilunar mucosal fold. Lumen of appendix ranges from 1-3mm. It is patent during early period of life and partially or completely obliterated at later periods of life.
The tip of the appendix is highly inconstant in position. It can occupy one of the below positions.
• Retrocaecal – behind the caecum -74%
• Retrocolic –behind lower part of ascending colon
• Pelvic or descending – hanging or protruding down into the pelvis- 21%
• Paracaecal -2%
• Subcaecal – below the caecum-1.5%
• Preileal – front of terminal ileum -1%
• Postileal – behind the terminal ileum-0.5%
18
Fig 1 Anatomy of appendix
Fig. 2 Various Positions of the Appendix
19
EMBRYOGENESIS[11, 12, 19, 22, 23]
At around sixth week of gestation caecal bud is formed. It is a small conical shaped dilation present in caudal limb of mid gut loop.
Temporarily caecal bud situated below the right lobe of the liver in upper abdomen. From here it gradually descends to right iliac fossa along with simultaneous development of appendix.
Appendix is the terminal portion of the developing caecum.
Terminal part of the caecum fails to develop or enlarge as fast as the rest of the proximal caecum resulting in narrow worm shaped tube. It becomes visible at around 8 weeks of embryonic life. Initially base of appendix is at the apex of the caecum. As the caecum grows there is unequal elongation of the lateral wall compared to the medial wall. This causes the appendix to open into posteromedial wall of caecum.
20
Fig 3 -stages in development of the cecum and appendix a) 7 weeks, b) 8weeks, c) new born
Fig. 4 Development of tip of Appendix.
Fig 5 – congenital anomalies-Duplication of appendix
21
CONGENITAL ANOMALIES[8, 18, 22]
Due to its seemingly vestigial function one would expect congenital variations to be common in appendix, but it is not so. The below described congenital anomalies are extremely rare.
• Absence of appendix
Only 46 cases of absent appendix has been reported in literature till date
It can be absent appendix or absence of both appendix and caecum.
• Ectopic appendix
• Left sided appendix
Left sided appendix can occur in the below described conditions o Situs invertus of viscera
o Non rotation of the intestines
o Caecum with a long, mobile mesentery ‘ wandering caecum’
o Very long appendix crossing to the left side.
• Duplication of appendix
Three types of duplication has been described by Waugh
22
o Double barrelled type- it is partial duplication of the appendix with a single base.
o Bird type of paired appendix- pair of appendix arise from single caecum from either side of ileocaecal valve.
o Taenia coli- type- normal appendix at the normal site with an additional little appendix arising from taenia.
• Congenital appendiceal diverticula
Even though appendix is subject to diverticular formation like any other intestine only few case has been reported.
23
VASCULAR SUPPLY[7, 8, 9, 11, 12, 14]
ARTERIAL SUPPLY
Appendix is usually supplied by a single appendicular artery. It is a branch of ileocolic artery. Ileocolic artery is a branch arising from right side of superior mesenteric trunk. It terminates into superior and inferior branches. Superior branch anastomoses with right colic artery supplying ascending colon. Inferior branch supplies ileocolic junction giving ride to branches anterior and posterior caecal arteries, an appendicular artery, ileal branch.
The appendicular artery enters mesoappendix by running behind terminal ileum. Anastomosis is formed at the base the appendix by a branch arising from anterior or posterior caecal artery and recurrent branch arising from appendicular artery. Appendicular artery runs in the mesoappendix initially in the free border, then close to the wall of appendix as it approaches the tip of appendix.
VENOUS DRAINAGE
Appendix is drained by single or multiple appendicular veins.
Appendicular veins joins posterior caecal veins which drains into ileocolic veins and hence into superior mescentic vein.
Fig 6
Fig 7-Arterial Supply
24
Arterial Supply
25
LYMPHATICS
Submucosa of the appendix contains numerous lymphoid tissue.
Appendix is drained by many lymphatic vessels. Along the length of appendix numerous lymphatic vessels ascend in the mesoappendix joins to form three to four larger vessels. These vessels drain into the chain of lymph nodes lying along appendicular, ileocolic and superior mesenteric arteries.
INNERVATIONS
The appendix along with the visceral peritoneum is innervated by sympathetic and parasympathetic nerves. Sympathetic innervation arises from celiac and superior mesenteric plexus. Parasympathetic innervation arises from vagus nerves. Afferent fibres arising from viscera transmits the sensation of distension and pressure. These carry the initial pain sensation felt in early stage of appendicitis. The parietal peritoneum overlying the appendix is supplied by the 8th, 9th and 10th thoracic spinal nerves. Pain arising from parietal peritoneum is of somatic type and is precisely localized.
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CAECAL RECESS[7, 8, 9]
Multiple folds of peritoneum are present between the caecum, ileum and appendix creating fossae or recess.
These include
• Superior Ileocaecal Fossa
It lies behind the vascular fold of the caecum containing anterior caecal artery. This fold lies anterior to terminal ileum, between the base of the mesentery and caecum. This fossa is bounded anteriorly by vascular fold of caecum, posteriorly by ileum and by ascending colon to the right. This fossa is also known as fossa of Luschka.
• Inferior Ileocaecal Fossa
A small peritoneal reflection called ileocaecal fold or bloodless fold of Treves extends between ileum to the mesoappendix. Space formed between the above fold and mesoappendix is called the inferior ileocaecal fossa.
• Retrocaecal or subcaecal fossa
This fossa is situated posterior to the caecum. Bounded anteriorly by posterior surface of caecum, laterally by right colic gutter, medially by mesentery and posteriorly by parietal peritoneum of iliac fossa.
Fig 8 Caecal recess
Fig 9 Normal histology of appendix
27
Caecal recess
Normal histology of appendix
28
MICRO STRUCTURE OF THE APPENDIX [18]
Mucosa:
The mucosa of appendix is lined by columnar epithelium.
Mucosa also contains lymphoid tissue. The epithelium that lie over the lymphoid tissue are lined by M cells. Glands (crypts) penetrate deep into the lymphoid tissue of the mucosal lamina propria. These crypts are few in number contains argentaffin cells (kulchitsky cells) from which carcinoid tumours can develop.
Sub- mucosa:
The sub mucosa usually consists of many large lymphoid aggregates. These lymphoid aggregates extends from mucosa and obscures the muscularis mucosa. Mucosa of the appendix bulges into the appendicular lumen due to these aggregates, hence the lumen narrows irregularly distally. These lymphoid aggregates are absent at birth and accumulates over years and becomes prominent feature by 10 years of age. It contains germinal centres within its follicles, it indicates b-cell activation. As the persons ages and attains adult these lymphoid follicles undergo atrophy and is replaced by collagenous tissue. In old aged individuals it may be filled with fibrous scar tissue.
29
Muscularis externa:
It is formed by longitudinal layer of smooth muscle. It has an inner and outer layers of longitudinal smooth muscle. The longitudinal muscular strands forms a continuous layer, with the exception of uniform outer layer over most of appendix. At the base of the appendix the longitudinal muscle fibres aggregates and thickens to form rudimentary taenia colie. These taenia is continuous with those of caecum and colon.
Serosa:
Whole of the appendix except the part where mesoappendix attaches is covered all around by serosa layer. Serosa comes in direct contact with the sub mucosa of appendix in few small areas which are deficient in longitudinal muscle covering.
FUNCTIONS OF APPENDIX[7]
The appendix is considered usually as a vestigial organ without any known functions in humans. Large amount of lymphoid collections are found in appendix similar to the ileum which contains peyers patches.
These collections of lymphoid cells contain both T and B cells within lamina propia of appendix. These lymphoid group of cells differentiate appendix from adjacent colon. Due to the abundant amount of lymphoid aggregates it has been hypothesized that appendix may have an immune function similar to the thymus or bursa of fabricius.
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It actively takes part in the production and secretion of immunoglobulins, predominantly immunoglobulin A.
EPIDEMIOLOGY OF APPENDICITIS[11, 12, 14, 16, 17]
Acute appendicitis is the most common cause of abdominal emergency in young adults. It accounts for nearly 1% of all the surgical procedures done. It occurs rarely in infants, increases in incidence throughout the childhood. Highest incidence is observed in patients in their second through fourth decade of their life. With peak incidence in teens and early 20’s. Appendicitis incidence is equal in both males and females before attaining puberty. In young adults the incidence in males increases attaining a male to female ratio of 3:2. This ratio gradually decreases until the sex ratio of incidence is equal by the mid 30’s age.
Incidence of appendicitis is highest in males of age group 10 to 14 year olds (27.6 cases per 10,000). Among females maximumoccurrence is seen in age group of 15 to19 years (20.5 cases per 10000).
The incidence of appendicitis had raised sharply in early half of the 20th century in western world with up to 16 % of the population underwent appendicectomy. Over the past thirty years the incidence has sharply fallen in western world resulting in lesser number of appendicectomy. The life time risk of a person undergoing
31
appendicectomy is 8.6 percent in males and 6.7 percent in females respectively.
In spite the extensive application of ultrasonography scanning, CT scan and laparoscopy, the percent of misdiagnosed cases of appendicitis has remained high about 15.3%. Women are misdiagnosed as having appendicitis than men (22.2% in women, 9.3% in men). The negative appendicectomy rate among women in reproductive age group is 23.2%.
Women older than 80 years of age had the highest negative appendicectomy rate.
Appendicitis has been shown to be the disease of developed world.
Burkitt found out that appendicitis is common in western world compared to Africa, Asia, and other developing countries. He credited this to the western food which has low quantity of dietary fibres and high amount of refined fats and sugars. He theorised that the low fibre diet leads to less bulky intestinal content, increased transit time, and increased pressure within bowel lumen which causes bacterial translocation through bowel causing appendicitis.
In Asian and African countries there has been lower incidence of acute appendicitis compared to the western countries. This difference in the incidence has been attributed to the dietary habits of the inhabitants of
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these geographical areas. People having diet rich in dietary fibres are at a lower risk of developing appendicitis.
Over the last few decades, a decrease in frequency of appendicitis has been reported in western countries. This is most probably related to the changes in dietary fibres intake.
AETIOLOGY[5, 6, 8, 10, 11]
There is no satisfactory hypothesis explaining the aetiology of acute appendicitis. The factors causing appendicitis still remain unclear in spite of its common occurrence. It was universally rare prior to the adaptation of western standard of living. It is rare in rural population in developing and underdeveloped countries, its occurrence is rising with economic development, migration to urban area. No person having an appendix seem to be protected from developing appendicitis, but may have higher or lower risk depending on many factors described.
1. Age and Sex:
No age is protected from developing appendicitis, it has been reported even in a newly born and even in old age. Younger age is a risk factor, as 70% of the patients developing appendicitis are in the age group of less than 30 years. Patients at extremes of age are at increased risk of developing perforated appendix. The incidence of perforated appendix is
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19.2% of cases of acute appendicitis. The above incidence was much higher in in patients younger than five years and older than sixty five years. Even though acute appendicitis is not common in patients aged more than 65 years, they develop perforation more than 50% of patients.
Acute appendicitis is marginally common in males, with a male to female ratio of 1.4:1. In males incidence is highest in age group of 10 to 14 year old. In females incidence is highest in age group of 15 to 19 year old.
2. Familial susceptibility:
A family history of appendicitis have been reported to increase the likelihood of other members to be diagnosed with appendicitis.
3. Seasonal factors:
Seasonal variation in occurrence of acute appendicitis has been observed. There is increased cases of appendicitis occurring during the months of May and august than other time of the year.
4. Race and dietary factors:
Racial distribution of appendicitis may be related to the diet of the race, as those race said to escape appendicitis may develop when there is westernization of the race. Burkitt attributed the above variation to western diet which is low in dietary fibre and rich in refined carbohydrate and fats. This leads to less bulky bowel contents, delayed transit time and
34
increased intraluminal pressure causing bacterial translocation leading to appendicitis. Mc Carrison had stated that during his early stay in North West India he never came across a case of Appendicitis, which is not the case presently
5. Faecoliths:
Also known as appendicolith is made up of inspissated faecal material, calcium phosphates, bacteria and also epithelial debris. Major cause of acute appendicitis is believed to be obstruction of the lumen of appendix.
It will lead to closed loop obstruction leading to ulceration or perforation of appendix usually at or near faecolith.
6. Constipation and purgation:
Constant and frequent purgation for constipation can lead to excessive peristalsis, which may result in appendicitis with perforation.
7. Parasites:
Blackadder (1824) reported a case study in which a man had very severe episode of abdominal pain following which he died. Autopsy revealed a round worm impacted at the appendicular orifice. Other intestinal parasites like the pin worm also known as oxyuris vermicularis can multiply in the caecum, appendix and occlude the appendicular lumen.
35
8. The bacterial flora:
In a normal appendix is almost same of that of colon. The appendicular flora will remain constant all through the life expect Porphyromonas gingivalis. The principle organism cultured from normal, acute or perforated appendix are Escherichia coli and bacteriodes fragilis.
Appendicitis is a polymicrobial infection with upto fourteen different organisms cultured from patients with perforated appendix.
Table 1 – causative organisms of appendicitis
36
9. Bands and adhesions:
Various abnormal peritoneal attachments has been described. These are congenital in origin. It may cause kinking of appendix causing obstruction leading to appendicitis. Repeated appendicitis may form inflammatory adhesions that can cause final acute obstructive picture of appendicitis.
10. Trauma :
This is a very rare cause of appendicitis. If the patient develops acute appendicitis following a blunt injury of right iliac fossa the probable cause can be due to displacement of faecaliths by blunt injury causing sudden obstruction. Birrel (1928) has reported 4 cases, Black (1948) reported 2 cases and Bhaje kar (1953) 1 case.
11.Secondary to metastatic carcinoma:
Kenneth (1966) reviewed thirteen cases from literature, of the above seven cases have presented with acute appendicitis, five of them had appendicular perforation. In five cases breast was the site of primary tumour. Metastatic carcinoma of the appendix due to encroachment of the appendicular orifice by the growth leads to obstructive appendicitis causing perforation and other complication.
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PATHOGENESIS [11, 12, 14, 16, 17, 20 ]
The major cause of appendix is believed to be caused by obstruction of the lumen. Obstruction of the lumen causes closed loop obstruction which leads to bacterial over growth. Continuous secretion from the mucosa causes increased intraluminal pressure, distension and wall pressure. This intra luminal distension leads to visceral pain felt in the periumbilical region. Lymphatic drainage of appendix is obstructed due to increased luminal pressure leading to mucosal oedema, ulceration and translocation of bacteria into submucosa. With increased luminal distension venous obstruction occurs first followed by ischaemia. With ischaemia bacteria invades muscularis propia and submucosa producing acute appendicitis. Finally ischaemia of appendix leads to necrosis and gangrene of appendix leading to diffuse contamination of peritoneal cavity.
o Causes of appendicular lumen obstruction Facalith of appendicolith
Lymphoid hyperplasia Vegetable matter, seeds Intestinal Parasites
Inspissated barium from previous x-rays.
Neoplasm
38
During the course of acute appendicitis the greater omentum and loops of small bowel becomes adherent with the appendicular wall, preventing the spread of infection. This results in a phlegmonous mass or paracaecal abscess. Not commonly the acute features may resolve leaving a distended mucus filled organ called‘mucocoele of the appendix’.
Acute appendicitis can lead to diffuse peritonitis due to free translocation of bacteria across the ischaemic appendicular wall, perforation of gangrenous appendix and delayed perforation of an abscess. There are multiple patient related factors leading to the above sequence
Extremes of age Immunosuppression Diabetes mellitus Faecolith obstruction Pelvic appendix position
Previous abdominal or pelvic surgeries.
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PATHOLOGY [20, 21 ]
Morphology:
Gross:
An appendix with an acute appendicitis will appear to be dull, granular, erythematous appearing. Serosa is covered by a coat which can be fibrinous or purulent in nature. Vessels over the appendix is usually engorged. In about one fourth to one third of the acute appendicitis lumen is obstructed by facalith or any other causes of obstruction mentioned earlier. In advanced stages the mucosa is lost, wall will undergo necrosis, and gangrene of appendix will occur.
Microscopy:
The mucosa shows ulceration with an increased hyperaemic background. It can range from a localised inflammatory changes to a total necrosis of the wall of appendix. In early stages neutrophils will be present at the base of the crypts. Once the inflammation reaches the submucosa rest of the appendix is affected in no time. As the disease progresses the mucosa undergoes extensive ulceration and is lost completely and wall of appendix undergoes necrosis creating acute gangrenous appendicitis which is usually goes in for rupture and diffuse peritonitis.
40
The diagnosis of acute appendicitis pathologically needs the presence of neutrophils infiltrating the muscularis propia. Even though presence of neutrophils in mucosa with focal areas of ulceration is seen in most, it is not the specific markers of acute appendicitis. Focal areas of abscess may form within the walls of appendix later leading to acute suppurative appendicitis.
Fig 10 – Acute appendicitis histopathology
Mucosal ulceration
Neutrophils infiltrating the muscularis propia
Neutrophils infiltrating the muscularis propia
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HISTORY [11, 12, 13, 14, 17, 23]
Acute appendicitis is perhaps the most common cause of abdominal pain which can be corrected surgically. But arriving at a diagnosis can be difficult many times as the signs and symptoms can be subtle for both the patient and the surgeon. Not all the signs and symptoms are present in the many instances. This may lead to delay in early diagnosis and treating which leads to the progression of inflammation leading to perforation.
This will lead to increased morbidity and mortality, subject to unnecessary surgical procedure.
Acute appendicitis classically presents as a crampy, on and off intermittent abdominal pain. The pain is thought to be due appendicular lumen obstruction and appendicial inflammation. Pain is initially located at the lower epigastrium or the umbilical area. After a duration about 12 hours, but usually 4 to 6 hours the pain is localized to right iliac fossa region. This classical pain migration from the periumbilical region to right lower quadrant occurs as the transmural inflammation of appendix inflames the overlying peritoneal covering of right lower quadrant. The above typical sequence of usually can occur but is not invariable.
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The pain episode is typically followed by nausea, vomiting may or may not occur. If pain is preceded by nausea and vomiting other causes of abdominal pain like acute gastroenteritis should be also considered. As the duration of pain increases it change from a dull and colicky type to a sharp and constant pain. This pain is aggravated on movements and Valsalva manoeuvre hence patients prefer to lie still. Anorexia is a useful and a constant history particular in children’s. Appendicitis is unlikely in patients with normal appetite.
In the initial six hours there is rarely any variation in temperature and pulse rate from baseline. As duration increases, slight pyrexia with a corresponding increase in heart rate occurs. Usually pyrexia will be low grade up to 1010 F. high temperature with shacking chills points to other diagnosis like non-gastrointestinal causes, perforative appendicitis.
The pain may also localize to area other than right lower quadrant in patient with altered appendicular anatomy as in pregnancy and malrotation of intestines. In retrocaecally placed appendix pain may never localize until it gets perforated presenting with symptoms of generalized peritonitis. Increased frequency of urination or bowel movements can occur due to inflammation of appendix irritating the adjacent bladder and the rectum.
43
Acute appendicitis can progress to perforated appendicitis. Pt commonly gives history of abdominal pain of 2 or more days, can be less in duration also. Pain can be localized to right iliac fossa if the perforation is walled off by the surrounding structures like the omentum, ileum. Or it can present with generalised peritonitis. They often have severe rigors and high pyrexia of 1020 F and above.
PHYSICAL EXAMINATION[11, 12, 13, 14, 17, 23]
Acute appendicitis depends greatly on a through clinical physical examination of abdomen. On inspection the lower abdomen movements for respiration may be restricted. Palpation is carried out gently starting from left iliac fossa. It is then proceeded in anticlockwise direction to the right iliac fossa.
Many signs can be detected in physical examination which will lead to diagnosis of acute appendicitis:
i. Mc Burney’s sign: Maximum tenderness felt by patient on palpation at Mc Burney’s point.
ii. The pointing sign: Patient is asked to point with one finger, where the pain started and to which part it moved.
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iii. Blumberg’s sign: A hand is kept over the right iliac fossa. It is progressively pressed down on each expiration. Suddenly the palpating finger is removed, the patient will cry with pain. If it is present it indicates inflammation of parietal peritoneum.
iv. Rovsing’s sign: On deep palpation over the left lower abdomen (left iliac fossa) produces pain in the right iliac fossa.
v. The psoas sign: Patient may lie in supine position with hip joint flexed for pain relief. An inflamed appendix lies on the psoas muscle causing the above sign.
vi. The Obturator (cope’s) sign: Appearance or aggravation of pain in hypogastrium on internal rotation of the flexed hip. It is due to contact of an inflamed appendix with obturator internus.
vii. Sherren’s sign: It is described by Sherren in the year 1925. He pointed out Sherren’s triangle, is bounded by line joining the umbilicus, right anterior superior iliac spine and symphysis of pubis. On gently striking the skin over this triangle hyperesthesia is elicited. If the sign is positive it indicates perforation of the appendix.
viii. Baldwin’s test for retrocaecal appendix: The point of maximum tenderness is identified over right iliac fossa, slight pressure is maintained over it and patient is asked to raise the ipsilateral lower
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limb without flexing at knee. This leads to increased tenderness in loin causing the patient to drop the limb. This points towards retrocaecal appendicitis.
ix. Shifting tenderness (alder’s): The site of maximum tenderness is marked in supine position, patient is made to change into left lateral position. Site of maximum tenderness is again marked. If the spot of tenderness shifts it probable is not a case of appendicitis. This sign is useful to differentiate appendicitis from mesenteric lymphadenitis and other pelvic conditions.
RECTAL EXAMINATION:
Examination of an acute abdomen is incomplete without a digital rectal examination. Tenderness can be usually elicited in the right side. In pelvic placed appendix examination will reveal tenderness in rectovesical pouch or pouch of Douglas more in the right side.
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INVESTIGATIONS[11, 12, 13, 14, 17, 23]
The diagnosis of acute appendicitis is mainly clinical. However appendectomy done based on only clinical suspicion can lead to normal appendix removal in 15-30% of the cases. A number of blood investigations and imaging studies are available to help in the diagnosis.
Laboratory tests:
These tests can help in the identification of appendicitis, but now test is diagnostic on its own.
White Blood Count (WBC):
The white blood count is probable the most valuable laboratory investigations. These counts are elevated in most patients with appendicitis with 75% made up of neutrophils. In approximately 10% of patients with appendicitis these counts can be normal, both total and differential counts.
Leucocytosis between 10,000 to 18,000 cells/mm3 with moderate polymorphonuclear predominance is mainly present in acute appendicitis without any complications. WBC counts of more than 18,000/mm3 is rarely seen in uncomplicated appendicitis and these high counts is suggestive of perforated appendix with or without abscess.
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C- Reactive Proteins:
C-reactive proteins (CRP) are acute phase reactants that appears in response to infection or inflammation. This is synthesized in the liver within the first 12 hours in response to acute inflammation. CRP has been reported to aid in the diagnosis of acute appendicitis but it lacks specificity for appendicitis. CRP levels in acute appendicitis is elevated commonly more than 1 mg/dl. High level of CRP in patients with acute appendicitis is highly suggestive of gangrenous appendicitis.
CRP trends to attain base value 12 hours of onset of symptoms.
Several studies have been done in adults with symptoms for more than 24 hours, a normal CRP value has negative predictive value of 97-100% for acute appendicitis.
Urinalysis:
Urinalysis is mainly done to exclude urinary tract infections which are the potential causes of pain abdomen. Significant haematuria with colicky abdomen points towards ureteric calculi. Presence of urinary tract infection does not rule out acute appendicitis, but it should be treated. Even though pyuria is indicative of urinary tract infection, it is common in appendicitis patients to have few WBC due to inflammation of ureter due to adjacent inflamed appendix.
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In women of reproductive age group, the urine chorionic gonadotropin should be tested for ruling out ectopic or concurrent pregnancy. Ectopic pregnancy is another cause of right lower abdomen pain requiring emergency diagnosis and management.
IMAGING STUDIES[11, 12, 13, 14, 17, 23]
There are many useful imaging modalities are available for the diagnosis of acute appendicitis. These include plain and contrast radiographs, ultrasound and computer tomography.
Plain and Contrast Radiographs:
Before the availability of advanced imaging modalities, radiographs were extensively used for acute abdominal pain. Plain radiographs has valuable use in ruling out other pathology of acute abdomen. In acute appendicitis plain radiographs reveal abnormal bowel gas pattern, it is a non-specific findings. A calcified Faecolith can be present in plain films in 10% to 15% of the patients with appendicitis.
Studies conducted by Teicher and colleagues regarding appendicolith in radiograph and appendicitis concluded that appendicolith in plain films are not pathognomic for presence of appendicitis. As some patients with pain abdomen and appendicolith in plain films had a normal appendix.
Hence plain radiographs has a limited value, is not cost effective in diagnosing acute appendicitis.
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Additional contrast radiographic series can be done like barium enema.
On barium enema if the appendix shows filling with contrast, appendicitis is excluded. If not filled with contrast the test is inconclusive.
Ultrasonography [11, 12, 13, 16, 14, 17, 23]
Patient with abdomen pain when subjected to ultrasonography has a sensitivity of about 85% and specificity of about 90% for diagnosing appendicitis. Graded compression ultrasonography is been suggested as a precise way to diagnose appendicitis. Sonographically appendix is visible as a blind ending, narrow bowel loop without peristalsis arising from caecum. The diameter of the appendix is measured in anterior posterior dimension on maximal compression.
Sonographic findings suggestive of acute appendicitis is given below:
• Anteroposterior diameter of appendix 7 millimetre or greater.
• Wall thickened Non compressible, luminal structure visualised in cross-section, called as target lesion.
• Presence of Faecolith in appendix.
• Presence of periappindiceal fluid or mass formation in more severe cases.
Ultrasonography has advantage of being not invasive, no ionising radiation exposure, easily available. Disadvantage is it depends on the
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skill and expertness of the operator, difficulty in analysing the images other than the operator. Pelvic sonography is useful in identifying pelvic pathology like ovarian torsion, tubal mass, which may imitate appendicitis.
Fig 11 – inflamed appendix with diameter > 7 mm, surrounded by hyper echoic inflamed fat.
Fig 12- perforated appendix as seen in ultra-sonography.
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Computer Tomography [11, 12, 13, 14, 17, 23]
Computer tomography is another very useful imaging modality for patients suspected with appendicitis, especially in elderly. Several techniques like focussed and non-focussed, enhanced and not enhanced have been used. This has the advantage of having high diagnostic accuracy in presence of appendicitis.
The radiographic features in appendicitis in CT scan:
• Inflamed appendix is visualised as dilated to more than 5 centimetres.
• Wall of appendix is thickened, inflammation is identified by presence of dirty fat, thick mesoappendix and presence of phlegmon.
• Wall thickened appendix that showed filling defect with contrast agent or bowel gas, with fat stranding around suggests inflammation.
• Fecaliths if present is easily seen, but if present is not necessary definite sign of appendicitis.
• Arrowhead sign can be visualised which is important and suggestive of appendicitis. It is formed by thickened caecum, which will funnel contrast solution towards the appendicular opening of inflamed appendix.
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Computer tomography demonstrated a sensitivity of 94% and specificity of 95%. Thus due to its high negative predictive value it is mainly useful in ruling out appendicitis in doubtful cases.
CT scan done early in course of the disease may not show the characteristic findings. In doubtful cases it is advisable to repeat the scan after 24hours.
Many recent studies have compared the accurateness of CT and ultrasonography in appendicitis. Balthazar and associates did CT and ultrasonography on 100 patients with suspected appendicitis Horton and colleagues randomized patients with suspected appendicitis to either CT or ultrasound. Sensitivity of CT was better than ultrasonography, specificity was similar in both and found to be high. CT is better than ultrasonography in visualising other cause of pain abdomen in absence of appendicitis.
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Fig 13 –CT scan showing dilated appendix.
Fig 14 – CT scan showing appendix surrounded by fat-stranding
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Diagnostic Laparoscopy:
Most patients suspected of having appendicitis will be diagnosed by history, physical examination, laboratory investigations and when required imaging modalities. A small number of patients will remain undiagnosed. For the above undiagnosed patients diagnostic laparoscopy can be done.
Diagnostic laparoscopy will offer a direct visualisation of the appendix and examination of organs of abdominal cavity for other causes for abdominal pain. This procedure is mainly useful in women in reproductive age group in whom pelvic sonography and CT did not provide conclusive diagnosis. Hence it will reduce the removal of normal appendix in middle aged females with lower abdominal pain.
Differentiating acute gynaecologic pathology from acute appendicitis can be effectively differentiated using laparoscope.
Fig 15- Clinical algorithm for suspected cases of acute appendicitis
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SCORING SYSTEMS [11]
Various soring systems are available for aiding in diagnosis of appendicitis. These are based on clinical and laboratory based scoring.
The most commonly used scoring system among is Alvarado score also abbreviated as “MANTRELS” score. The score of 7 and above is highly predictive of acute appendicitis.
Table 2: Alvarado score
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Liver function tests:
Bilirubin:
Bilirubin is the end product produced from breakdown of heme.
During the early phase of the breakdown 20% of the bilirubin is formed hemoproteins. Rest of the 80% of bilirubin is formed from the breakdown of senescent red blood cells. Heme is firstly broken down into green coloured biliverdin by complex enzyme system heme oxygenase. The biliverdin is broken down into orange yellow pigment called bilirubin by the enzyme biliverdin reductase [24].
Bilirubin formed in the peripheral organs is transferred to liver by plasma albumin. The terminal end metabolism of bilirubin takes place in liver. The process takes place in three main steps
1. Bilirubin uptake by hepatic parenchymal cells 2. Bilirubin conjugation
3. Secretion of conjugated bilirubin into bile.
Free bilirubin in circulation is binded with albumin to protect organs from toxic effects of bilirubin. The bilirubin albumin complex is taken into sinosoids of liver and enters space of Disse through fenestrations present in sinosoids. Bilirubin is freed from albumin in this space, free bilirubin is taken by hepatocytes and conjugated with glucuronic acid.
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This conjugated compound is secreted in energy dependent process into canalicular bile against gradient. Bilirubin is secreted into gastrointestinal tract with bile.
Fig 16- Bilirubin metabolism and elimination
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Serum bilirubin is present in two forms. It is detected and quantifiable by laboratory tests
1. Unconjugated or indirect bilirubin 2. Conjugated or direct bilirubin.
Modern analytical methods states that normally plasma does virtually contain no bilirubin conjugate. The 10 to 20% of the bilirubin in normal plasma that gives rise to prompt (Diazo) reaction is an artefact of kinetic of the Van Den Berg reaction which along with various modifications is the method most commonly used to quantitate bilirubin in clinical laboratories. Thus when the amount directly reacting is less than 15% of total bilirubin concentration, sample will contain essentially unconjugated bilirubin.
Conjugated bilirubin is transported into bile canaliculus across the plasma membrane. The transport process is ATP dependant process mediated by canalicular membrane protein known as multi drug resistant associated protein 2. This transport system is very sensitive to injury.
Hence in hepatocellular disorder, cholestasis or mechanical obstruction to bile ducts, bilirubin undergoes conjugation within hepatocytes. These conjugated bilirubin are not transported into bile canaliculus and down the bile duct, refluxed into the blood stream resulting in a conjugated hyperbilirubinemia.
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Hyperbilirubinemia occurs due to various causes. It can be due to haemolytic, hepatocellular or cholestatic diseases. Cholestatic and hepatocellular disease is associated with Hyperbilirubinemia along with rise in liver enzymes. These cases will have bilirubin predominantly conjugated type. An elevated serum bilirubin level (without enzyme elevation) may be seen familial liver disease or due to haemolysis [25]. Cholestasis is the failure of bile to reach the gastrointestinal tract particularly duodenum. It may be due to pathology from hepatocytes and ampulla of vater. Intrahepatic cholestasis are the condition of cholestasis where no demonstrable obstruction is detected. It can be cause by hormones, drugs primary biliary cirrhosis and sepsis [19]. Sepsis from the gastrointestinal tracts reach the liver by various routes. The commonest route is through portal vein from the gastrointestinal tract. Any inflammation or infection will cause transmigration or translocation of bacteria, toxins, inflammatory mediators causing suppression of normal hepatocellular function and cholestasis causing reduced excretion of bile from bile canaliculi[12].
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HYPERBILIRUBINEMIA AND APPENDICITIS:
Hyperbilirubinemia, is defined as increased content of bilirubin in blood. It can be either due to increased bilirubin production or defect in bilirubin metabolism and clearance. It is not well recognized as a laboratory marker for perforated or gangrenous appendix. Both the above mentioned mechanisms increase creation and decrease bilirubin clearance, leading to the accumulation of bilirubin as observed in perforated and gangrenous appendicitis.
Numerous type of bacterial infection has been proved to accompany hepatic dysfunction in bile acid formation and its flow. This in the end will produce hyperbilirubinemia, a well-known side effects in severe bacterial infection mainly in septic patients [25]. Septic patient having extra hepatic bacterial infection, such as gangrenous appendix, perforated appendix will synthesize proinflammatory cytokine and nitric oxide. These inflammatory mediators will cause cholestasis by impairing hepatocellular and bile duct function.
The most common microorganism cultured from appendicular wall of patients with appendicitis have been E. coli and Bacteroids Fragilis, both of these organisms has been proved to interfere with
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hepatocytes microcirculation , with sinusoidal damage as seen in rat liver model [26, 27]. Lipopolysaccharides of E.coli has been shown to have effect on hepatocyte uptake and bile acids clearance [28]. E.coli endotoxin will cause dose dependent impairment of choleresis (production of bile by hepatic tissue), which has been demonstrated in rat model[29]. E.coli has also shown to cause haemolysis of erythrocytes causing increased bilirubin load in already compromised liver causing hyperbilirubinemia.
Patho-physiology of elevation of serum bilirubin in perforated or gangrenous appendicitis [4, 5]
Perforated or gangrenous appendicitis
Translocation / transmigration of bacteria/toxins/cytokines
Causes endotoxemia/ bacteraemia
Invasion of bacteria into hepatic parenchyma and interferes with bile excretion
Hyperbilirubinemia
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Hence the mechanism of hepatic injury in sepsis may be due to bacteria, its toxins, inflammatory mediators produced. In the early phase sepsis along with hyper dynamic circulation, bacteria and its toxins are involved. In late phase of sepsis ischaemia due to decreased blood flow to liver is the mechanism of injury. Due to above mechanism both will lead to hepatic injury with dysfunction of hepatocytes and bile duct leading to mixed type of hyperbilirubinemia.
Cholestasis in severe bacterial infection commonly seen in children or postoperative, is most probably hepatocellular in nature. Can also be related to cholestatic effect of endotoxin on Na-K ATPase.
All the constituents of bile show an increased level in serum.
Conjugation of biliary substance is intact but excretion is defective.
Serum alkaline phosphatase is raised. The rise is due to increased synthesis or release of enzymes from liver or biliary plasma membrane.
The minimal hepatocellular damage may be suspected by noting minimal elevated transaminase value and sometimes serum bilirubin.
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DIFFERENTIAL DIAGNOSIS[5, 6, 8, 10, 17]
Even though acute appendicitis occurs commonly and it is most common surgical procedure done in emergency basis, the diagnosis is not easy at times. There are numerous common occurring conditions it can mimic. These differential diagnosis depend on four main factors described below.
• Location of tip of inflamed appendix.
• Stage of the disease( simple or perforated)
• Age of the patient
• Sex of the patient
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Table 3 – differential diagnosis according to age and sex in appendicitis.
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TREATMENT:
Except a few patient, all the patient with acute appendicitis are treated by surgical removal of appendix. A short period of preparation of patient for surgery with intravenous fluids is necessary for safe induction of anaesthesia. For simple appendix without any complications a single intravenous dose of antibiotics is sufficient to prevent wound infection and intraabdominal abscess formation postoperatively. In patients complicated with perforation or gangrenous appendix intravenous antibiotics is continued post operatively till the patient becomes afebrile.
Meta- analysis of large scale has showed the efficacy of preoperative infusion of antibiotics in reducing complications related to infection and abscess formation following appendectomy.
While emergency appendectomy remains standard teaching in acute appendicitis. There is emergence of various literature in favour of giving a trial of conservative treatment in cases thought to not have obstructive appendicitis hence less chance of complications. Conservative management includes bowel rest, intravenous antibiotics and analgesics.
With the available data interpretation 80-90% of patients are treated conservatively, rest undergo appendectomy. These patients showed 15%
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risk of developing appendicitis within a year. This regimen should be considered in patients with multiple comorbid factors.
APPENDECTOMY[11,12,13,14,15,16,17,23]
Claudius Amyland is the first person to removal of appendix. It was performed in a young boy in the year 1736 where inflamed appendix was found in the hernia sac. In 1880, Lawson Tait performed first deliberate appendicectomy.
Appendectomy is done under general anaesthesia. Patient should be positioned in supine position. When laparoscopic technique is considered bladder should be empty. Prior to preparing the surgical site with aseptic precautions patient’s right iliac fossa should be palpated for any mass. In the presence of mass, it is advised to adapt a conservative management for appendicular mass.
Open Appendectomy incisions:
1. Gridiron incisions:
This is the most commonly used incision. Grid iron literally means the frame of cross-beams that supports the ship when repairing. It was described by McArthur. This draw at right angle to the line joining the anterior superior iliac spine to the umbilicus, centred at Mc Burney’s
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point. If better exposure is needed it can be converted into Rutherford Morison’s incision any time.
2. Lanz incision (transverse skin crease):
It is made 2 cm below the umbilicus, centred over the line joining mid clavicular – midinguinal point. When needed of better exposure medial extension of the incision can be done. This is becoming popular because of better exposure and easy of extension when required.
3. Rutherford Morison’s incision:
It is basically a muscle cutting incision. It is made with its lower end at McBurneys point, extending obliquely laterally and upwards. In this incision all the layers are divided along the line of the incision.
4. Lower midline incision:
This is used when the preoperative diagnosis is in doubt, when intestinal obstruction is present.
5. Lower right paramedian incision:
Rarely used now as it is difficult to extend, less exposure to pelvis and peritoneum cavity, technically difficult in closing.
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Technique:
Caecum is recognised by the existence of taenia coli. It is delivered through the incision using finger or a swab. An inflamed, swollen, tense appendix can be felt by the finger at caecal base. When adhesions are present, it is separated gently using a finger, once freed appendix is hooked and delivered unto the wound. Appendix is held using Babcock forceps such that instrument completely encircles the appendix and still not damage it. The base of mesoappendix is divided between ligatures.
Once appendix is freed it is crushed at the base, forceps reapplied just distal to crushed portion. Absorbable 2-0 ligature is tied around crushed part of appendix. Amputation of appendix done between artery forceps and ligature. Stump may be buried or left alone.
Techniques in special situations:
• In extensive caecal wall oedema, burring of the stump using invagination technique should not be attempted.
• If appendicular base is excessively inflamed it should be ligated without crushing the base ,close to the caecal wall with tension just enough to close appendicular lumen
• Gangrene of base of appendix, it should neither be crushed nor tied.
Two stiches taken closely, through caecal wall and approximated with one another once flush amputation of appendix is done. Second seromuscular layer of interrupted sutures can be applied.
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• Retrograde appendicectomy:This technique is followed when appendix is retrocaecal and adhered to surrounding structures. Here appendix is divided first at its base between artery forceps, then vessels are ligated. Stump of appendix ligated next followed by gentle traction on appendix delivered the appendix out.
Laparoscopic appendectomy:
First laparoscopic appendectomy was first reported by Semm. It was not so popular before the success of laparoscopic cholecystectomy.
Laparoscopic appendectomy is usually done under general anaesthesia. Before creating pneumoperitonium stomach should be intubated by nasogastric tube and bladder by urinary catheter. Commonly three ports are required, additional forth port may be necessary in case to mobilize retrocaecal placed appendix. Operating surgeon is positioned to left of the patient. One assistant is required to operate camera.
10mm trocar is positioned at the umbilicus, second trocar of 10mm or 12mm is placed at suprapubic location. A 5mm third trocar is placed either in left iliac fossa, epigastric, right upper quadrant. The placement of trocar is dependent on position of appendix, preference of operating surgeon. Firstly the abdomen is thoroughly examined for any pathology.
Appendix is visualised with the help of anterior taenia to its base. A
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window is created at the base of the appendix between the mesentery and appendicular base by dissection. Appendicular base and mesentery are divided individually after securing it. Stump of appendix is not inverted or buried. Appendix is delivered out via a trocar site or through retrieval bag. The appendicular stump should be visualised for haemostasis.
Trocars are removed under vision.
Post-operative complications:
• Wound infection
• Intraabdominal abscess.
• Adynamic ileus.
• Respiratory complications
• Venous thrombosis and embolism.
• Portal pyaemia (pyelephlibitis).
• Faecal fistula.
• Adhesive intestinal obstruction.
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Fig 17 & 18 – per operative picture of inflamed appendix
