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Appendicitis, perforated

bowel, anorectal disease

Appendicitis
The chance of a person developing
appendicitis over the course of his or her
lifetime is 7%.
Although generally considered a benign
disease, complication rates following
appendicitis are high (up to 30% in some
series).
Some patients, particularly the elderly or
those who present late, can be extremely
septic and require critical care support

Incidence
Male : female 1.4 : 1
Young age is risk factor. Nearly 70%
acute appendicitis are younger than
30 y.o
Highest incidence : male 10-14 y.o,
female 15-19 y.o
Patients at extreme age are more
likely to develop perforated
appendicitis
Maingot's, 2013

Etiology
Low in dietary fiber & high in refined
sugars and fat.

Pathophysiology
Low fiber diets lead to less bulky
bowel content, prolonged intestinal
transit time & increased intraluminal
pressure.

Clinical findings
Classically the pain is initially colicky or
aching in nature and located in the center
of the abdomen. As the disease
progresses it becomes sharper and
localized in the right iliac fossa.
However, due to the varying position of
the appendix, many patients present with
a different pattern of pain (preileal,
postileal, subcecal, promontoric, pelvic,
paracolic)

They may have their right hip flexed


and complain of pain on passive hip
extension (the psoas stretch sign
caused by irritation of psoas major
by a retrocaecal or retrocolic
appendix).

Andersson :
Temperature >37.7C
Localized (rather than diffuse) tenderness
Indirect tenderness (where the pain is
worst at the point of maximal tenderness
when the patient is palpated in the left
iliac fossa, also known as Rovsings sign)
Rebound or percussion tenderness
Guarding

Differential diagnosis
If the patient is female, a full
gynaecological history (especially the
date of the last menstrual period) should
be taken.
In older patients, it is important to
consider the possibility of malignancy.
Diabetic ketoacidosis, acute
pancreatitis and a perforated peptic
ulcer can all mimic acute appendicitis.

Despite advances in imaging technology,


the diagnosis of acute appendicitis
remains essentially a clinical one.
Certain laboratory investigations may
help make the diagnosis while others are
important in excluding other potential
differential diagnoses and preparing the
patient for possible surgery.

Laboratory findings
Anderssons systematic review
identified a raised white cell
count, C-reactive protein and a
neutrophilia as being most
predictive for appendicitis.

All women of childbearing age presenting


with abdominal pain are assumed to have
a ruptured ectopic pregnancy until
proven otherwise, so a urine sample
should always be tested for B-HCG as
soon as possible.
The presence of white cells and protein in the
urine may well be due to bladder irritation
caused by an inflamed retrocaecal or pelvic
appendix, so it should not be assumed that
they indicate a urinary tract infection.

Radio Imaging
Ultrasound has a sensitivity of 86% and a
specificity of 81% for diagnosing appendicitis.
It has several advantages it is non-invasive, carries
no radiation risk and is cheap and often easily
available.
However, it is operator-dependent and, as shown
above, can neither exclude nor confidently predict
acute appendicitis.
It is most useful in helping to exclude
gynaecological pathology in stable female patients
rather than in diagnosing appendicitis itself.

USG : thickening appendiceal wall,


loss of wall compressibility, increased
echogenicity of surrounding fat,
loculated pericecal fluid

The same review showed that


computed tomography (CT) scanning
has a sensitivity of 94% and
specificity of 95%.
Magnetic resonance imaging (MRI)
confers no added benefit over CT but
may be useful in patients in whom CT
is contraindicated (in particular
pregnant patients).

The hypothesis that analgesia may


mask the pain and result in an
incorrect diagnosis has no evidence
base, so all patients should be given
appropriate analgesia, prescribed
intravenous fluids and
thromboprophylaxis.

Once a diagnosis of acute


appendicitis is made surgery should
be undertaked within 24 hours to
prevent an increase in morbidity and
mortality which results from
perforation.
Laparoscopy vs laparotomy

Appendectomy
Laparotomy

Laparoscopy

Shorter operating
room time
Lower costs
Fewer intra abdominal
abscess

Diagnosis of other
conditions
Decreased pain
Reduced length of
stay
Fewer wound infection
Quicker return to usual
activities

Perforated peptic ulcer


Peptic ulcer is used as a general term
for a gastric or duodenal ulcer
Etiology : smoking, NSAID, H.pylori.
Other risk factors include alcohol,
stress with burns leading to Curlings
ulcer, neurological insult (Cushings
ulcer) and major surgery.

The older age groups (>50 years)


commonly perforate in the prepyloric
and pyloric areas.
Anterior duodenal perforation leads
to free air in the peritoneum.
Posterior duodenal
erosion/perforation leads to bleeding
from the gastroduodenal artery and
possibly acute pancreatitis.

Signs & Radiologic findings


Signs include decreased bowel sounds, tympanic
percussive note over the liver and signs of peritonitis.
Diagnostic tests include an erect chest radiograph
showing air under the diaphragm or in the lesser sac.
If an erect chest X-ray is not possible then a left
lateral decubitus can be performed as air will be seen
over the liver and not confused with the gastric bubble.
Ten per cent of patients will have no radiological
evidence of free gas on erect chest X-ray.
Plain abdominal X-ray may reveal free gas by the
presence of gas on both sides of the bowel wall
(Riglers sign).

Differential diagnoses
acute pancreatitis, acute
cholecystitis, perforated acute
appendicitis, colonic diverticulitis,
myocardial infarction and any
perforated viscus.

Management
All gastric ulcers require biopsy.
Surgical management is usually by
excision and sutured closure.
All patients should be considered for
H. pylori eradication therapy.
Laparoscopy vs laparotomy

Prognosis
Mortality increases with three risk
factors: the presence of severe
comorbidity, perforation longer than
24 hours and the presence of
hypotension on admission (systolic
<100 mm Hg).

Hemorrhoid

Contrary to popular belief,


hemorrhoids are not related to the
superior hemorrhoidal artery and
vein, to the portal vein, or to portal
hypertension.4 In fact, hemorrhoids
are part of the normal anal anatomy.

ACS 2007

Anal cushion
cushions are aggregations of blood
vessels (arterioles, venules, and
arteriolar-venular communications),
smooth muscle, and elastic
connective tissue in the submucosa
that normally reside in the left
lateral, right posterolateral, and right
anterolateral anal canal

Internal hemorrhoidal disease is manifested by


two main symptoms: painless bleeding and
protrusion.4 Pain is rare because internal
hemorrhoids originate above the dentate line
in the insensate rectal mucosa.
External hemorrhoids are redundant folds of
perianal skin that generally derive from
previous anal swelling; they remain
asymptomatic unless they are thrombosed and
are treated entirely differently from internal
hemorrhoids.

Internal hemorrhoids are classified


into four grades on the basis of
clinical findings and symptoms.
Grade 1 represents bleeding without
prolapse; grade 2, prolapse that
spontaneously reduces; grade 3,
prolapse necessitating manual
reduction; and grade 4, irreducible
prolapse.

External hemorrhoids are asymptomatic except when


secondary thrombosis occurs. Thrombosis may result
from defecatory straining or extreme physical
activity, or it may be a random event. 1 Patients
present with constant anal pain of acute onset and
often report feeling the sensation of sitting on a
tender marble. Physical examination identifies the
external thrombosis as a purple mass at the anal
verge.
Treatment depends on the patient's symptoms [see
Figure 4].4 In the first 24 to 72 hours after the onset of
thrombosis, pain increases, and excision is warranted.

Treatment
Diet and life style modification
Non operative procedures : rubber
band ligation, infra red coagulation,
sclerotherapy
Operative procedures : open
hemorrhoidectomy, stapled
hemorrhoidopexy

Differential diagnose
Mucosal prolapse

Rectal prolapse

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