LO 1

 Anatomy, Histology, Physiology, Biochemistry

Anatomy
1. Cardiac Stomach 8. Ascending Colon
2. Fundic Stomach 9. Ileum
3. Stomach Body 10. Jejunum
4. Pyloric Stomach 11. Sigmoid Colon
5. Lesser Omentum 12. Spleen
6. Duodenum 13. Gastrospleenic Ligament
7. Pancreas (Ventral) 14. Bladder
1. Small Intestine 6. Transverse Colon
2. THE Mesentary 7. Descending Colon
3. Ileum 8. Sigmoid Colon
4. Cecum 9. Mesocolon
5. Ascending Colon 10. Greater Omentum
COLON
COLON
RECTUM
RECTUM - ANUS
Physiology
 Colon
• The movements of the colon :
– Segmentation contractions
– Peristaltic waves
– Mass action contraction
• Transit time in the small intestine and colon :
– The 1st part of a test meal reaches cecum in about 4 hours and
all of the undigested portions have entered the colon in 8-9
hours.
– On average, the 1st remnants of the meal reach the hepatic
flexure in 6 hours, the splenic flexure in 9 hours and the pelvic
colon in 12 hours
– From the pelvic colon to the anus, transport is much slower
 Colon
• Absorption in the colon :
– The absorptive capacity of the mucosa of the large intestine is
great
– The absorptive capacity of the colon makes rectal instillation a
practical route for drug administration, especially in children.
• Feces, stools contain :
– Inorganic material
– Undigested plant fibers
– Bacteria
– water
 Defecation
• Distention of the rectum with feces initiates reflex
contractions of its musculature and the desire to
defecate.
• In human, the sympathetic nerve supply to the internal
(involuntary) anal sphincter is excitatory, whereas the
parasympathetic supply is inhibitory.
• When rectal pressure increased to about 18 mmHg 
urge to defecate first occur.
• When rectal pressure reaches 55 mmHg  the external
as well as the internal expulsion of the contents of the
rectum.
 Feces
• Feces (also spelled faeces or fæces) are the waste products
from the digestive tract expelled through the anus during
defecation. In humans, defecation may occur (depending on
the individual and the circumstances)

• The distinctive odor of feces is due to bacterial action.

Bacteria produce compounds such as indole, skatole, and
mercaptans, which are rich in sulfur, as well as the inorganic
gas hydrogen sulfide. These are the same compounds that are
responsible for the odor of flatulence.
Histology
 Jejunum
Jejunum •This is very similar to the
duodenum except Brunner’s glands
are absent
•Extensive villi are present as are
the crypts of crypts of Lieberkuhn
•The pilcae cicularis are permanent
folds in the intestinal mucosa
•There are 2 layers of smooth
muscle: longitudinal and circular
•Mucosa consists of simple
columnar epithelium with goblet
cells.
Ileum
Ileum

•This is very similar to the duodenum except Brunner’s glands are absent
•The villi are present as are the crypts of Lieberkuhn
•The 2 layers of smooth muscle (TM) and the submocusa (SM)
•Contains lymphatic nodules called Peyer’s patches that are found in the
mucosa
Appendix
Appendix

•Epithelium lining, with goblet cells and underlying submucosa and

smooth muscle
•It also contains lymphatic nodules and other diffuse lymphatic tissue.
 Histology of colon
• No vili in tunica mucosal
• A lot of goblet cells among the epithel
• + Cryptus Liberkuhn
• Panneth cells and Argentaffin cells
• Solitaire lymphonodus spread among lamina
propria
Colon
Colon
 Histology of Rectum
2 parts of rectum :
1.Upper : colon like structure. Taller cryptus and
walled by goblet cells
2.Lower (anal canal) : Rectal collumn
longitudinal folds in mucosal end about 21/2
inchs from orrificium anal.
The junctional between anal and rectum called
linea pectinata
 Histology of Anus
1. Collumnaris zone
2. Intermedia zone
3. Cutanea zone
Anal gland

Squamous to collumnar
In linea pectinata Thinning squamous epithel

Stratified keratinized squamous epithel

With hair follicle
Biochemistry
ACUTE ABDOMINAL PAIN
• Visceral pain comes from the abdominal viscera, which are
innervated by autonomic nerve fibers and respond mainly
to the sensations of distention and muscular contraction—
not to cutting, tearing, or local irritation. Visceral pain is
typically vague, dull, and nauseating. It is poorly localized
and tends to be referred to areas corresponding to the
embryonic origin of the affected structure.
– Foregut structures (stomach, duodenum, liver, and
pancreas) cause upper abdominal pain.
– Midgut structures (small bowel, proximal colon, and
appendix) cause periumbilical pain.
– Hindgut structures (distal colon and GU tract) cause lower
abdominal pain.
• Somatic pain comes from the parietal
peritoneum, which is innervated by somatic
nerves, which respond to irritation from
infectious, chemical, or other inflammatory
processes. Somatic pain is sharp and well
localized.
• Referred pain is pain perceived distant from
its source and results from convergence of
nerve fibers at the spinal cord. Common
examples of referred pain are scapular pain
due to biliary colic, groin pain due to renal
colic, and shoulder pain due to blood or
infection irritating the diaphragm.
 Projection Pain
• Cause by sensoric nerves stimualtion because
injured or nerves inflammation
• Ex: phantom pain after amputation, or
localized peripheral pain in herpes zoster
 Continue Pain
• Caused by peritoneum stimulation in the
parietal peritoneum and occur in continuous
time
• Peritonitis  localized pressure pain, defense
muscular to protect inflammation area and
avoid movement or localized pressure
 Cholic Pain
• Caused by smooth muscle spasm in hollow organs and usually
cause by passage obstruction in that organs (intestine
obstruction, kidney stone, bile stone, increase of intraluminer)
• Appear by hypoxia, feels come and go, nausea to emesis, and
very nervous
• Have specific TRIAS  reccurent abdominal pain followed by
nausea or emesis and force movement
 Ischemic Pain
• Very intensive, permanent, and not reduce.
This is sign of necrosis phase is inisiated.
Further more, general intoxification will
appear
 Approach to the patient
• History is THE MOST IMPORTANT part of the
diagnostic process
– Location, quality, severity, radiation, exacerbating or
alleviating factors, associated symptoms
• Visceral v. peritoneal
– A good through medical history
– A good through social history, including alcohol, drugs,
domestic abuse, stressors, etc.
– Family history is important (IBD, cancers, etc)
– MEDICATION INVENTORY
 Approach to the patient
• Physical exam
– Vitals, general appearance
– A good thorough medical exam
• Jaundice, signs of chronic liver disease
– Abdominal exam
• Look, listen, feel
• Know a few tricks
– DRE
– Pelvic exam
– MSK exam
 Approach to the patient
• Labs
– CBC, lytes, BUN, Cr, coags
– Amylase and lipase, LFTs
– UA
– bHCG
– Lactate
– Tox screen
– H. pylori serology
– FOBT
 Approach to the patient
• Imaging
– Plain films (KUB, UGI)
– CT
– Ultrasound
– MRI
– Angiography
• Endoscopy
– EGD
– Colonoscopy
– ERCP/EUS
 Surgical abdomen
• This is the first thing to be considered in acute
abdominal pain
– Early identification is a must as prognosis worsens
rapidly with delay in treatment
• Important to get surgeons involved early if this
is even mildly suspected
• This is a clinical diagnosis
 Surgical abdomen
• Presentation is usually bad
– Fevers, tachycardia, hypotension
– VERY tender abdomen, possibly rigid
• Presentation can vary with other demographic
and medical factors
– Advanced age
– Immunosuppression
 Surgical abdomen
• Peritonitis
– Often signals an intraabdominal catastrophe
• Perforation, big abscess, severe bleeding
– Patient usually appears ill
– Exam findings
• Rebound, rigidity, tender to percussion or light
palpation, pain with shaking bed
 Surgical abdomen
• Work-up
– Start with stat labs
– Surgical abdominal series (plain films)
– Consider stat CT if readily available
• Sometimes patients go straight to surgery as
initial step
• Again, get surgeons involved early for
guidance and early intervention
APPENDICITIS
 APPENDICITIS
• DEFINITION
Appendicitis is a painful swelling and infection
of the appendix.
 APPENDIX
• The appendix is a closed-ended, narrow tube up to
several inches in length that attaches to the cecum
(the first part of the colon) like a worm.
• The inner lining of the appendix produces a small
amount of mucus that flows through the open center
of the appendix and into the cecum.
• The wall of the appendix contains lymphatic tissue
that is part of the immune system for making
antibodies.
• Like the rest of the colon, the wall of the appendix
also contains a layer of muscle, but the muscle is
poorly developed.
 ETIOLOGY
• Obstruction caused by fecalith, which is accumulation and
inspissation of fecal matter around vegetable fiber
• Enlarged lymphoid follicles associated with viral infection
• Inspissated barium
• Tumor
• Appendiccal ulceration
• Infective
– Bacterial (Tuberculosis, Typhus, Actinomycosis, E. coli and
B. fragilis, Pseudomonas, Yersinia, Eikenella corrodens
infections)
– Viral (Adenovirus, Cytomegalovirus infections
– Fungal (Aspergillosis, Histoplasmosis)
– Parasitic (Enterobius vermicularis, Strongyloides stercoralis,
Entamoeba histolytica infections, Ascariasis,
Schistosomiasis, Cryptosporidiosis, Taeniasis)
 Pathophysiology
• Obstruction of the appendiceal lumen is the
primary cause of appendicitis
• An anatomic blind pouch, obstruction of
the appendiceal lumen leads to distension of the
appendix due to accumulated intraluminal fluid.
Ineffective lymphatic and venous drainage allows
bacterial invasion of the appendiceal wall and, in
advanced cases, perforation and spillage of pus
into the peritoneal cavity.
• SIGN and SYMPTOMS
– The abdominal pain usually
• occurs suddenly, often causing
a person to wake up at night
• occurs before other symptoms
• begins near the belly button
and then moves lower and to
the right
• is new and unlike any pain felt
before
• gets worse in a matter of
hours
• gets worse when moving
around, taking deep breaths,
coughing, or sneezing
– Other symptoms of
appendicitis may include
• loss of appetite
• nausea
• vomiting
• constipation or diarrhea
• inability to pass gas
• a low-grade fever that
follows other symptoms
• abdominal swelling
• the feeling that passing
stool will relieve
discomfort
Clinical Algorithm for the Evaluation of
Pain in the Right Lower Quadrant.
 Finding Association

Cullen's sign Bluish periumbilical Retroperitoneal hemorrhage

discoloration (hemorrhagic pancreatitis,
abdominal aortic aneurysm
rupture)

McBurney's sign Tenderness located Appendicitis

2/3 distance from
anterior iliac spine to
umbilicus on right side

Iliopsoas sign Hyperextension of right hip Appendicitis

causing abdominal pain

Obturator's sign Internal rotation of Appendicitis

flexed right hip causing
abdominal pain

Rovsing's sign Right lower quadrant Appendicitis

pain with palpation of
the left lower quadrant
 EXAM AND TEST
• White Blood Cell Count
• Urinalysis
• Abdominal X-Ray
• Ultrasound
• Barium Enema
• Computerized tomography (CT) Scan
• Laparoscopy
 Physical Examination
• Guarding.
– Guarding occurs when a person subconsciously tenses the
abdominal muscles during an examination. Voluntary guarding
occurs the moment the doctor’s hand touches the abdomen.
Involuntary guarding occurs before the doctor actually makes
contact.
• Rebound tenderness.
– A doctor tests for rebound tenderness by applying hand
pressure to a patient’s abdomen and then letting go. Pain felt
upon the release of the pressure indicates rebound
tenderness. A person may also experience rebound
tenderness as pain when the abdomen is jarred—for example,
when a person bumps into something or goes over a bump in
a car.
• Rovsing’s sign. A doctor tests for Rovsing’s sign by applying hand
pressure to the lower left side of the abdomen. Pain felt on the
lower right side of the abdomen upon the release of pressure on
the left side indicates the presence of Rovsing’s sign.
• Psoas sign. The right psoas muscle runs over the pelvis near the
appendix. Flexing this muscle will cause abdominal pain if the
appendix is inflamed. A doctor can check for the psoas sign by
applying resistance to the right knee as the patient tries to lift the
right thigh while lying down
• Obturator sign. The right obturator muscle also runs near the
appendix. A doctor tests for the obturator sign by asking the
patient to lie down with the right leg bent at the knee. Moving
the bent knee left and right requires flexing the obturator muscle
and will cause abdominal pain if the appendix is inflamed.
Appendicitis: Psoas Sign
Appendicitis: Psoas Sign
 Appendicitis: Obturator Sign

Passively flex
right hip and knee
then internally
rotate the hip
 How is appendicitis treated?
Surgery
• Typically, appendicitis is treated by removing the appendix. If
appendicitis is suspected, a doctor will often suggest surgery
without conducting extensive diagnostic testing. Prompt
surgery decreases the likelihood the appendix will burst.
• Surgery to remove the appendix is called appendectomy and
can be done two ways.
• The older method, called laparotomy, removes the appendix
through a single incision in the lower right area of the
abdomen.
• The newer method, called laparoscopic surgery, uses several
smaller incisions and special surgical tools fed through the
incisions to remove the appendix. Laparoscopic surgery leads
to fewer complications, such as hospital-related infections,
and has a shorter recovery time.
• Sometimes an abscess forms around a burst
appendix—called an appendiceal abscess. An abscess is
a pus-filled mass that results from the body’s attempt
to keep an infection from spreading.
• An abscess may be addressed during surgery or, more
commonly, drained before surgery. To drain an abscess,
a tube is placed in the abscess through the abdominal
wall.
• CT is used to help find the abscess. The drainage tube
is left in place for about 2 weeks while antibiotics are
given to treat infection.
• Six to 8 weeks later, when infection and inflammation
are under control, surgery is performed to remove
what remains of the burst appendix.
 COMPLICATION
• Abses periappendicitis
• Septikemia
• Mucocele
• Peritonitis
 DIFFERENTIAL DIAGNOSIS
• Limphadenitis Mesentericum
• Colic appendix
• GIT bleeding
• Salphingitis
• Crohn Disease
• Diverticel Meckel Inflamation
INTESTINAL OBSTRUCTION
 DEFINITION
• Intestinal obstruction is significant mechanical
impairment or complete arrest of the passage
of contents through the intestine
 Classification
Mechanical obstructions
• The bowel is physically
blocked and its contents can
not pass the point of the
obstruction.
• This happens when the
bowel twists on itself
(volvulus) or as the result of
hernias, impacted feces,
abnormal tissue growth, or
the presence of foreign
bodies in the intestines.
Non-mechanical obstruction
• Called ileus or paralytic ileus,
occurs because peristalsis
stops.
• Peristalsis is the rhythmic
contraction that moves
material through the bowel.
• Ileus is most often associated
with an infection of the
peritoneum (the membrane
lining the abdomen). It is one
of the major causes of bowel
obstruction in infants and
children.
• Mechanical obstruction is divided into:
– obstruction of the small bowel (including the
duodenum)
– obstruction of the large bowel
• Obstruction may be partial or complete.
 Causes of Intestinal Obstruction
Location Causes
Colon Tumors (usually in left colon), diverticulitis
(usually in sigmoid), volvulus of sigmoid or
cecum, fecal impaction, Hirschsprung's disease
Duodenum Cancer of the duodenum or head of pancreas,
(Adults) ulcer disease
Duodenum Atresia, volvulus, bands, annular pancreas
(Neonates)
Jejunum and ileum Hernias, adhesions (common), tumors, foreign
(Adults) body, Meckel's diverticulum, Crohn's disease
(uncommon), Ascaris infestation, midgut
volvulus, intussusception by tumor (rare)
Jejunum and Ileum Meconium ileus, volvulus of a malrotated gut,
(Neonates) atresia, intussusception
 Examples of Causes of Intestinal
Obstruction

Obstruction due to Obstruction due to Obstruction due

adhesions mesenteric occlusion to hernia

Obstruction due to Obstruction due to Obstruction due to

intussusception tumor volvulus
 Ileus
Adynamic ileus
Mechanical ileus
 ILEUS
• DEFINITION
is a term for a difficulty of intestine passage.
– Ileus is divided into two:
• Ileus obstructive
• Ileus paralytic.
– Ileus obstructive is caused by an obstruction.
– Ileus is paralytic is caused by nerve problems.
 Adynamic ileus
Paralysis of intestinal motility

Causes
A. Abdominal trauma
B. Abdominal surgery (i.e. laparatomy)
C. Serum electrolyte abnormality  Hypokalemia,
Hyponatremia, Hypomagnesemia, Hypermagensemia
D. Infectious, Inflammatory or irritation (bile, blood)
1. Intrathoracic  Pneumonia, Myocardial Infarction
2. Intrapelvic  Pelvic Inflammatory Disease
3. Intraabdominal  Appendicitis, Diverticulitis,
Cholecystitis, Pancreatitis, Perforated Duodenal Ulcer
E. Intestinal Ischemia  Mesenteric embolism, ischemia or
thrombosis
F. Skeletal injury  Rib fracture, Vertebral fracture
G. Medications  Narcotics, Phenothiazines, Diltiazem or
Verapamil, Clozapine, Anticholinergic
Symptoms
A. Abdominal distention
B. Nausea and Vomiting are variably present
C. Generalized abdominal discomfort
Colicky pain of Mechanical Ileus is usually absent
A. Flatus and Diarrhea may still be passed
Signs
A. Quiet bowel sounds
B. Abdominal distention
Differential Diagnosis
A. Mechanical Ileus
B. Bowel Pseudoobstruction
Radiology: Refractory ileus course
A. Indicated to evaluate for Mechanical Ileus
B. Upper GI series and small bowel follow through
1. May be diagnostic and therepeutic
2. Use gastrograffin instead of barium
3. Barium may further obstruct bowel lumen
4. Gastrograffin may stimulate bowel motility
C. Decompress stomach with Nasogastric Tube
D. Instill gastrograffin via Nasogastric Tube

Management
A. Initial
1. Limit or eliminate oral intake
2. Intravascular fluid replacement
3. Correct electrolyte abnormalities (e.g. Hypokalemia)
4. Consider Nasogastric Tube placement
B. Refractory Management
1. Consider Prokinatics
2. Consider lower bowel stimulation (e.g. Enema)
 Mechanical ileus
Types
A. Simple mechanical obstruction
1. Bowel lumen is obstructed
2. No vascular compromise
B. Closed loop obstruction
1. Both ends of a bowel loop are obstructed
2. Results in strangulated obstruction if untreated
3. Rapid rise in intraluminal pressure
C. Strangulated obstruction
1. Bowel lumen and vascular supply is
compromised
Causes
A. Most Common Causes
1. Postoperative Adhesions (accounts for 50%
of cases)
2. Hernia (25% of cases, especially younger
patients)
3. Neoplasms (10% of cases, esp. older
patients)
a. Colon Cancer (most common)
b. Ovarian Cancer
c. Pancreatic cancer
d. Gastric Cancer
Symptoms
• Frequent and recurrent Generalized Abdominal Pain
• Duration: Seconds to minutes
– Character: Spasms of crampy abdominal pain
– Frequency
a. Intermittent pain initially
b. Every few minutes in proximal obstruction
c. Constant pain suggests ischemia or perforation

Symptoms more severe in proximal obstruction

1. Proximal obstruction
a. Severe, colicky abdominal pain
b. Constant pain suggests ischemia or perforation
c. Develops over hours and occurs every few minutes
d. Bilious Emesis
e. Mild abdominal distention
2. Distal obstruction
a. Develops over days and becomes progressively worse
b. Emesis may occur and is brown and feculent
c. Significant abdominal distention
Signs
• Bowel sounds
– Initial: High pitched, hyperactive bowel
sounds
– Later: hypoactive or absent bowel sounds
• Tender abdominal mass  Closed loop Bowel
Obstruction may be palpable
• Abdominal distention and tympany on
percussion  Indicates distal obstruction
• Rectal examination for blood
Differential Diagnosis Mechanical ileus

A. Adynamic Ileus
B. Bowel Pseudoobstruction
C. Ischemic bowel (superior mesenteric syndrome)
D. Gastroenteritis
E. Cholelithiasis
F. Cholecystitis
G. Pancreatitis
H. Peptic Ulcer Disease
I. Appendicitis
J. Myocardial Infarction
K. Pregnancy
Management: Conservative Therapy
A. Fluid replacement
B. Bowel decompression
1. Nasogastric Tube
2. Long intestinal tube offers no advantage
C. Antibiotic
1. Indications
a. Surgery planned
b. Bowel ischemia or infarction
c. Bowel perforation
2. Cover Gram Negatives and Anaerobes
a. Second-generation Cephalosporin
Indications for surgery
1. Inadequate relief with Nasogastric tube
placement
2. Persistant symptoms >48 hours despite
treatment (strangulation)
3. Neoplasms

Complications
A. Intestinal Ischemia or infarction
B. Bowel necrosis, perforation and bacterial
peritonitis
C. Hypovolemia
 PERITONITIS
• Inflammation or infection of the peritoneum.
 RISK FACTOR
• Abdominal penetration or trauma
• Immune compromise
• Blood in the abdomen
• Ruptured appendix
• Peptic ulcer
• Colitis
• Diverticulitis
• Gangrene of the bowel
• Pancreatitis
• Pelvic inflammatory disease
• Inflamed gallbladder
• Recent surgery
• Tubes or shunts in the abdomen
• Cortisone drugs
 Symptoms
• Severe pain or tenderness in the abdomen
• Pain in the abdomen that is worse with motion
• Bloating of the abdomen
• Constipation
• Fever
• Nausea and vomiting
• Weakness or dizziness
• Shortness of breath
• Rapid pulse or breathing rate
• Dehydration—signs include dry skin and lips, decreased urine
production
Peritonitis Etiologic Organisms Antibiotic Therapy
(Type) Class Type of Organism
Primary Gram- E coli (40%) Third-generation
negative K pneumoniae (7%) cephalosporin
Pseudomonas species (5%)
Proteus species (5%)
Streptococcus species
(15%)
Staphylococcus species
(3%)
Anaerobic species ( <5%)
Secondary Gram- E coli Second-generation
negative Enterobacter species cephalosporin
Klebsiella species Third-generation
Proteus species cephalosporin
Gram-positive Streptococcus species Penicillins with
Enterococcus species anaerobic activity
Quinolones with
Anaerobic Bacteroides fragilis anaerobic activity
Other Bacteroides species Quinolone and
Eubacterium species metronidazole
Clostridium species Aminoglycoside and
Anaerobic Streptococcus metronidazole
species
 ETIOLOGY
• Disseminated infection from the infected
abdominal organ
• Hip Inflammation in women
• Infection from ovarium and uterus
• Heart and kidney failure
• After surgery
• Peritoneal dialysis
• irritation without infection
Tertiary Gram- Enterobacter species Second-generation
negative Pseudomonas species cephalosporin
Enterococcus species Third-generation
cephalosporin
Penicillins with anaerobic
Gram-positive Staphylococcus species activity
Quinolones with anaerobic
activity
Fungal Candida species Quinolone and
metronidazole
Aminoglycoside and
metronidazole
Carbapenems
Triazoles or amphotericin
(considered in fungal
etiology)
(Alter therapy based on
culture results.)
Patofisiologi
Peritonitis
 PATHOLOGY
• The peritoneum normally appears greyish and
glistening; it becomes dull 2–4 hours after the onset
of peritonitis, initially with scarce serous or slightly
turbid fluid.
• Later on, the exudate becomes creamy and evidently
suppurative.
• The quantity of accumulated exudate varies widely. It
may be spread to the omentum and viscera.
• Inflammation features infiltration by neutrophils with
fibrin-purulent exudation
 Laboratory findings and examination
• Fluid examination for identification of germ

• Rontgen : supine and PA/AP

• Surgery
Terapi Antibiotik
 Taeniasis
• Of the 32 recognized species of Taenia, only Taenia
solium and Taenia saginata are medic
• Approximately 50 million people worldwide are infected
by T saginata or T solium. Approximately 50,000 people
die annually of cysticercosisally important
• The mortality rate for cysticercosis is low and is generally
caused by complications such as encephalitis, increased
intracranial pressure secondary to edema and/or
hydrocephalus, and stroke.
• T solium taeniasis has been reported in children older
than 2 years in certain rural communities of Mexico.
 History
Taeniasis cysticercosis
• Colicky abdominal pain •In cysticercosis, the cysticerci
(more common in children) are most often located in
• Nausea subcutaneous and
• Weakness intermuscular tissues, followed
• Loss of appetite by the eye and then the brain
• Increased appetite
• Headache
• Constipation
• Dizziness
• Diarrhea
• Pruritus ani
• Hyperexcitability
 Physical
cysticercosis
• In cysticercosis, the cysticerci are most often
located in subcutaneous and intermuscular
tissues, followed by the eye and then the
brain
 Causes
• Taeniasis is caused by ingesting inadequately
cooked beef or pork that contains the larvae
or cysticerci of T saginata or T solium
• Cysticercosis, which is caused by ingesting
eggs of T solium, occurs when larvae are
deposited in skeletal muscle, brain, eyes, and
other organs.
 Laboratory Studies
• CBC count detects eosinophilia in no more than 45% of
patients.
• Examine 3 consecutive stool samples (direct and concentrated
stool preparations) from patients and contacts.
– Determination of species on the basis of ova examination
is difficult because the eggs of T solium and T saginata are
identical.
– Examining the gravid proglottids helps identify the species;
count the main uterine branches after injection with India
ink (ie, 7-13 branches for T solium, 15-20 for T saginata).
– Examining the scolex helps differentiate the species
because a T solium scolex has 4 suckers and an armed
rostellum.
 Imaging Studies
• Plain films of the chest, neck, arms, and thighs can depict
calcified cysticerci, although calcification takes approximately
3 years, and sometimes longer, to occur.
• Although CT scanning is superior to MRI to detect
intracerebral calcification, calcification occurs less frequently
in children than in adults
• MRI
– MRI is superior to CT scanning in detecting intraventricular
and subarachnoid cysts.
– MRI may reveal a mural nodule within the cyst, which is
pathognomonic for NCC.
– MRI with parallel imaging may facilitate detection of cysts
 Anthelmintics
• Praziquantel (Biltricide)DOC for Taenia infection.
• Niclosamide (Niclocide)
• Albendazole (Albenza)Decreases ATP production
in worm
• Glucocorticoidscases of primary increased
intracranial pressure
• Dexamethasone (Decadron)Decreases
inflammation by suppressing migration of PMNs and
reducing capillary permeability.
 Complications
• Appendicitis
• Cholecystitis
• Pancreatitis
• Intestinal obstruction
• Tubo-ovarian abscess (rare)
• Systemic cysticercosis
Prognosis
• Treatment with praziquantel reportedly
provides cure rates of 99-100%.
Patient Education
• Educate patients and families about routes of
infection and preventive measures.
• Teach patients and families proper sanitary
and personal hygiene measures.
 Differentials
• Amebic Meningoencephalitis
• Appendicitis
• Cholecystitis
• Cysticercosis
• Gnathostomiasis
• Meningitis, Aseptic
• Meningitis, Bacterial
• Neurocysticercosis
• Small-Bowel Obstruction
• Tuberculosis
 Ascariasis
• Ascariasis is the most common helminthic
infection, with an estimated worldwide
prevalence of 25% (0.8-1.22 billion people)

Adult Ascaris lumbricoides.

• Adult A lumbricoides are white or yellow and
15-35 cm
• They live 10-24 months in the jejunum and
middle ileum of the intestine.
• Each day, female A lumbricoides produce
240,000 eggs
 Epidemiology
• The prevalence of ascariasis is highest in
children aged 2-10 years, with the highest
intensity of infection occurring in children
aged 5-15 years
 History
• during the initial lung migration, include coug
• Abdominal pain, distension, colic, nausea,
anorexia, and intermittent diarrhea partial
or complete intestinal obstruction by adult
worms. h, dyspnea, wheezing, and chest pain
• Jaundice, nausea, vomiting, fever, and severe
or radiating abdominal pain cholangitis,
pancreatitis, or appendicitis.
 Physical
• Rales, wheezes, and tachypnea may develop
during pulmonary migration
• Abdominal distension is nonspecific but is
common in children with ascariasis
• Abdominal tenderness, especially in the right
upper quadrant, hypogastrium, or right lower
quadrant, may suggest complications of
ascariasis.
Laboratory Studies
• Stool examination for ova and parasites
• Ascaris larvae may be observed in microscopic wet
preparations of sputum
• CBC counts
Imaging Studies
• Chest radiographs
• Abdominal radiographs
• ultrasonography and CT scanning.
Other Tests
• Endoscopic retrograde cholangiopancreatography
(ERCP)
 Medical Care
• Medical therapy is usually not indicated during active
pulmonary infection because dying larvae are considered a
higher risk for significant pneumonitis.
• Pulmonary symptoms may be ameliorated with inhaled
bronchodilator therapy or corticosteroids, if necessary.
• Albendazole 400 mg one dose orally is the drug of choice
• Albendazole is not recommended during pregnancy; pyrantel
pamoate is the drug of choice in these cases.
• Alternative therapy is mebendazole (100 mg bid for 3 d or 500
mg as a single dose)
• Paralyzing vermifuges (eg, pyrantel pamoate, piperazine,
ivermectin) should be avoided in patients with complete or
partial intestinal obstruction
• Recommended criteria for surgical exploration
include the following:
– Passage of blood per rectum
– Multiple air fluid levels on abdominal radiographs
– An ill child with abdominal distension and
rebound tenderness
– Unsatisfactory response to conservative therapy
– Appendicitis and primary peritonitis
– Hepatobiliary disease
– Pancreatic pseudocyst
 Differentials
• Biliary Colic
• Colonic Obstruction
• Pancreatitis, Acute
• Pneumonia, Community-Acquired
 Hookworm infection
• Hookworm infection is acquired through skin exposure to
larvae in soil contaminated by human feces
• Soil becomes infectious about 9 days after contamination and
remains so for about 2 weeks.
• Ancylostoma larvae may also infect via ingestion, but they do
not migrate into the body in this instance. dormant in
tissues and later be transmitted through breast milk
• Necator has a 5-year lifespan; Ancylostoma has a 1-year
lifespan.
• Infection is widely distributed throughout tropical and
subtropical areas, with prevalence in some communities as
high as 90%
• hookworm infection is uncommon in young children
 History
• Necator produces a local irritation, termed ground
itch, at the site of skin invasion.
• Severe infection with either A duodenale or N
americanus may produce pneumonitis (Loefflerlike
syndrome) that manifests as cough, fever, and
malaise.
• As worms mature in the jejunum, patients may
experience diarrhea, vague abdominal pain, colic,
and/or nausea
• Patients with severe iron deficiency anemia may
present with lassitude, headache, palpitations,
dyspnea, and edema
Physical
• Skin and pulmonary findings are minimal.
• Signs of iron deficiency anemia are often
insensitive.
Laboratory Studies
• Direct microscopic stool examination for ova
and parasites
• Anemia is confirmed by CBC count and
peripheral blood smear
Imaging Studies
• Chest radiography
 Medical Care
• Albendazole (Albenza)A single dose of
albendazole is the treatment of choice for
hookworm
• Mebendazole (Vermox)
Prognosis
• Most patients become reinfected within
months unless they are relocated to an area of
significantly improved sanitation.
Prevention
• Successful programs have included economic,
sanitary, and mass-treatment components.
 Differentials
• Eosinophilia
• Gastroenteritis, Bacterial
• Hemolytic Anemia
• Hypersensitivity Pneumonitis
• Iron Deficiency Anemia
• Plummer-Vinson Syndrome
• Pneumonia, Bacterial