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Group C

1: abduqadir sid ali mohamuud ( leader )


2:ali Mohamed addow
3: faadumo ali Mohamed
4: haliimo Mohamed afrah
5: abdisamad ahmed ga’al
6: maryan Hassan abdulahi
Appendicitis

INTRODUCTION The importance of the


vermiform appendix in surgery results
primarily from its propensity for
inflammation, which results in the clinical
syndrome known as acute appendicitis. Acute
appendicitis is the most common cause of an
‘acute abdomen’ in young adults and, as such,
the associated symptoms and signs have
become a paradigm for clinical teaching.
Appendicitis is sufficiently common
that appendicectomy (termed
appendectomy in North America) is
the most frequently performed urgent
abdominal operation and is often the
first major procedure performed by a
surgeon in training
ACUTE APPENDICITIS
While there are isolated reports of
perityphlitis (fatal inflammation of the
caecal region) from the late 1500s,
recognition of acute appendicitis as a
clinical entity is attributed to Reginald Fitz,
who presented a paper to the first meeting
of the Association of American Physicians
in 1886 entitled ‘Perforating inflammation
of the vermiform appendix’. Soon
afterwards
The incidence of appendicitis seems to
have risen greatly in the first half of this
century, particularly in Europe, America
and Australasia, with up to 16% of the
population undergoing appendicectomy.
In the past 30 years, the incidence has
fallen dramatically in these countries,
such that the individual lifetime risk of
appendicectomy is 8.6% and 6.7% among
males and females, respectively
Acute appendicitis is relatively rare in
infants and becomes increasingly common
in childhood and early adult life, reaching a
peak incidence in the teens and early 20s.
After middle age, the risk of developing
appendicitis is quite small. The incidence
of appendicitis is equal among males and
females before puberty. In teenagers and
young adults, the male–female ratio
increases to 3:2 at age 25; thereafter, the
greater incidence in males declines
Etiology
 There is no unifying hypothesis regarding the
aetiology of acute appendicitis. Decreased
dietary fibre and increased consumption of
refined carbohydrates may be important. As with
colonic diverticulitis, the incidence of
appendicitis is lowest in societies with a high
dietary fibre intake. In resource-poor countries
that are adopting a more refined western-type
diet, the incidence continues to rise. This is in
contrast to the dramatic decrease in the
incidence of appendicitis in western countries
observed in the past 30 year
Risk factors for perforation of the
appendix
● Extremes of age
● Immunosuppression
● Diabetes mellitus
● Faecolith obstruction
● Pelvic appendix
● Previous abdominal surgery
Clinical diagnosis
History

Symptoms of appendicitis
● Periumbilical colic
● Pain shifting to the right iliac fossa
● Anorexia
● Nausea
With progressive inflammation of the
appendix, the parietal peritoneum in the
right iliac fossa becomes irritated,
producing more intense, constant and
localised somatic pain that begins to
predominate. Patients often report this as
an abdominal pain that has shifted and
changed in character. Typically, coughing
or sudden movement exacerbates the
right iliac fossa pain.
Signs
The diagnosis of appendicitis rests more on
thorough clinical examination of the
abdomen than on any aspect of the history or
laboratory investigation. The cardinal
features are those of an unwell patient with
low-grade pyrexia, localised abdominal
tenderness, muscle guarding and rebound
Clinical signs in appendicitis
● Pyrexia
● Localised tenderness in the right
iliac fossa
● Muscle guarding
● Rebound tenderness
Signs to elicit in appendicitis
● Pointing sign
● Rovsing’s sign
● Psoas sign
● Obturator sign
Investigation

The diagnosis of acute appendicitis is


essentially clinical; however, a decision to
operate based on clinical suspicion alone
can lead to the removal of a normal
appendix in 15–30% of cases. The premise
that it is better to remove a normal
appendix than to delay diagnosis does not
Preoperative investigations in appendicitis

● Routine Full blood count Urinalysis

● Selective Pregnancy test

Urea and electrolytes

Supine abdominal radiograph

Ultrasound of the abdomen/pelvis

Contrast-enhanced abdomen and pelvic computed tomography scan

Consider low-dose protocol in young adults


 The Alvarado (MANTRELS) score.
Score Symptoms
Migratory RIF pain 1
Anorexia 1
Nausea and vomiting 1
Signs Tenderness (RIF) 2
Rebound tenderness 1
Elevated temperature 1
Laboratory Leucocytosis 2
Shift to left 1
Total 10
Differential diagnosis of acute appendicitis.
Gastroenteritis Regional Mittelschmerz Diverticulitis
enteritis

Mesenteric adenitis Ureteric colic Pelvic Intestinal obstruction


inflammatory
disease
Meckel’s Perforated peptic Pyelonephritis Colonic carcinoma
diverticulitis ulcer

Intussusception Torsion of testis Ectopic pregnancy Torsion appendix epiploicae

Henoch–Schönlein Pancreatitis Torsion/rupture of Mesenteric infarction


purpura ovarian cyst

Lobar pneumonia Rectus sheath Endometriosis Leaking aortic aneurysm


haematoma
Treatment
 Non-operative management
While surgery remains the standard teaching, there
is an emerging body of literature to support a trial
of conservative mangement in patients with
uncomplicated (absence of appendicolith,
perforation or abscess) appendicitis. Treatment is
bowel rest and intravenous antibiotics, often
metronidazole and 3rd generation cephalosprin.
More recently, ertapenem has been used in this
setting and has the benefit of broad antimicrobial
cover administered as a single daily dose
Operative management
The traditional treatment for acute
appendicitis is appendicectomy.
While there should be no unnecessar.
patients, particularly those most at risk
of serious morbidity, benefit by a
short period of intensive preoperative
preparation
Intravenous fluids, sufficient to
establish adequate urine output
(catheterisation is needed only in the
very ill), and appropriate antibiotics
should be given. There is ample
evidence that in the absence of
purulent peritonitis, a single
perioperative dose of antibiotics
reduces the incidence of
postoperative wound infection
Appendicectomy

Claudius Amyand successfully removed an


acutely inflamed appendix from the
hernial sac of a boy in 1736. The first
surgeon to perform deliberate
appendicectomy for acute appendicitis
was Lawson Tait in May 1880. The
patient recovered; however, the case was
not reported until 1890. Meanwhile
Summary box 72.6
 Criteria for stopping conservative
treatment of an appendix mass
● A rising pulse rate
● Increasing or spreading abdominal
pain
● Increasing size of the mass
Postoperative complications
Wound infection
Intra-abdominal abscess
Respiratory
Venous thrombosis and embolism
Portal pyaemia (pylephlebitis)
Faecal fistula
Adhesive intestinal obstruction
RECURRENT ACUTE APPENDICITIS
 Rarely, inflammation of the appendix may present
as a chronic condition characterised by recurrent
episodes of lower abdominal pain. Recurrent
appendicitis is thought to arise as a consequence of
incomplete self-limiting obstruction of the
appendix lumen The attacks vary in intensity and
may occur every few months, and the majority of
cases ultimately culminate in severe acute
appendicitis. If a careful history is taken from
patients with acute appendicitis, many remember
having had milder but similar attacks of pain. The
appendix in these cases is thickened and shows
fibrosis indicative of previous inflammation
PERITONITIS
Peritonitis is simply defined as
inflammation of the peritoneum and may
be localised or generalised. Most cases of
peritonitis are caused by an invasion of the
peritoneal cavity by bacteria, so that, when
the term ‘peritonitis’ is used without
qualification, acute bacterial peritonitis is
often implied. In this instance, free fluid
spills into the peritoneal cavity and
circulates
Causes of peritoneal inflammation
● Bacterial, gastrointestinal and non-
gastrointestinal
● Chemical, e.g. bile, barium
● Allergic, e.g. starch peritonitis
● Traumatic, e.g. operative handling
● Ischaemia, e.g. strangulated bowel,
vascular occlusion
● Miscellaneous, e.g. familial
Mediterranean fever
Microorganisms in peritonitis
Gastrointestinal source
● Escherichia coli
● Streptococci
● Enterococci
● Bacteroides spp.
● Clostridium spp.
● Klebsiella pneumoniae
Other sources
● Chlamydia trachomatis
● Neisseria gonorrhoeae
● Haemolytic streptococci
● Staphylococci
● Streptococcus pneumoniae
● Mycobacterium tuberculosis and other
species
● Fungal infection
Clinical features of peritonitis
● Abdominal pain, worse on movement,
coughing and deep respiration
● Constitutional upset: anorexia, malaise,
fever, lassitude
● GI upset: nausea ± vomiting
● Pyrexia (may be absent)
● Raised pulse rate
● Tenderness ± guarding/rigidity/rebound
of abdominal wall
● Pain/tenderness on rectal/vaginal
examination (pelvic peritonitis)
● Absent or reduced bowel sounds
● ‘Septic shock’ (systemic inflammatory
response syndrome [SIRS] and multi-
organ dysfunction syndrome [MODS]) in
later stages
 Systemic complications of peritonitis
● Septic shock
● Systemic inflammatory response syndrome
● Multi-organ dysfunction syndrome
● Death
Abdominal complications of peritonitis
● Paralytic ileus
● Residual or recurrent abscess/inflammatory
mass
● Portal pyaemia/liver abscess
● Adhesional small bowel obstruction
 Management of peritonitis General care of
patient
● Correction of fluid and electrolyte imbalance
● Insertion of nasogastric drainage tube and
urinary catheter
● Broad-spectrum antibiotic therapy
● Analgesia
● Vital system support Surgical treatment of
cause when appropriate
● Remove or divert cause
● Peritoneal lavage ± drainage
INTRAPERITONEAL ABSCESS
. INTRAPERITONEAL ABSCESS
Following intraperitoneal sepsis (usually
manifest first as local or diffuse
peritonitis), the anatomy of the peritoneal
cavity is such that with the influence of
gravity (depending on patient position –
sitting or supine), abscess development
usually occupies one of a number of
specific abdominal or pelvic sites. In
general,
 Clinicalfeatures of an abdominal/pelvic
abscess Symptoms
● Malaise, lethargy – failure to recover from
surgery as expected
● Anorexia and weight loss
● Sweats ± rigors
● Abdominal/pelvic pain
● Symptoms from local irritation, e.g.
shoulder tip/hiccoughs (subphrenic), diarrhoea
and mucus (pelvic), nausea and vomiting (any
upper abdominal)
Signs

● Increased temperature and


pulse ± swinging pyrexia
● Localised abdominal
tenderness ± mass (including
on pelvic exam
ASCITES

Ascites is defined as an
accumulation of excess
serous fluid within the
peritoneal cavity
Causes of ascites
 Low plasma protein concentrations:

Malnutrition
Nephrotic syndrome
Protein-losing enteropathy
 High central venous pressure:
Congestive cardiac failure
 Portal hypertension

Portal vein thrombosis


Cirrhosis
Exudates (protein >25 g/L)
● Peritoneal malignancy
● Tuberculous peritonitis
● Budd–Chiari syndrome (hepatic
vein occlusion or thrombosis)
● Pancreatic ascites
● Chylous ascites
● Meigs’ syndrome
Clinical features
 swelling in abdomen
 Weight gain
 Sense of fullnes
 Bloating
 Sense of heaviness
 Nausea or indigestion
 Vomiting
 Sweling in the lower leg
 Shortness of breathing
 Hemmorhoids
Investigation
 In addition to relevant investigations to
determine the underlying cause, e.g. liver
function tests (LFTs), cardiac function,
ultrasonography and/or CT scanning (Figure
61.9) will determine much smaller
quantities of ascites than possible clinically.
These will often also diagnose aetiology,
e.g. carcinomatosis or liver disease. Ascitic
aspiration or tap (below) is now most
commonly performed under imaging
guidance to minimise the risk of visceral
injury.
Treatment
 Treatment of the specific cause is undertaken
whenever possible, e.g. if portal venous pressure
is raised, it may be possible to lower it by
treatment of the primary condition or by
transjugular intrahepatic portosystemic shunt or
transjugular intrahepatic portosystemic stent
shunting (commonly abbreviated as TIPS or TIPSS).
These procedures have become increasingly
popular since the 1980s and are performed by
interventional radiologists under fluoroscopic
guidance. Access to the liver is gained via the
internal jugular vein and
Group C
1: abduqadir sid ali mohamuud ( leader )
2:ali Mohamed addow
3: faadumo ali Mohamed
4: haliimo Mohamed afrah
5: abdisamad ahmed ga’al
6: maryan Hassan abdulahi

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