Functional and organic

diseases of the Biliary

Tract.
Pancreatitis in Children

Lecture for 4 year students

Docent Dyedovych N.G.
 Plan of the Lecture

 Biliary Disturbance *
 Organic disordes of billiary system on
children of the late age*
 Pancreatitis in Children*
* ethyology, clinic, diagnostic, treatment
and prophylaxis.
• Biliary Disturbance (BD) is a
disorder of the sphincters’
tonus and kinetics of the
gallbladder and the bile ducts

• There are two basic forms of

BD: hypotonic-hypokinetic and
hypertonic-hyperkinetic
 Etiology
1. Vegetative neurosis
- Parasympathetic NS (n.vagus) hyperkinetic of
GB, hypotonic of sphincters’ tonus
- Sympathetic NS hypokinetic of GB, hypertonic
of sphincters’ tonus

2. Hormonal dysbalance
- Gastrin, cholecystokinin, secretin hyperkinetic
of GB, hypotonic of sphincters’ Oddy
- Glucagon, calcitonin, anticholecystokinin
hypokinetic of GB, hypertonic of sphincters’Oddy
 Predisposition factors
 Bad diet (as to regularity and quality of feeding-
fatty, spicy food)
 Hereditary load
 Infected diseases of GIT
 Hypodynamia
 Allergic diathesis is a state of readiness to
appearance of sensibilization, allergic reaction and
diseases because of hereditary , congenital or
acquired peculiarities of immunity, metabolism and
neuro-vegetative system.
 CLASSIFICATION
of Biliary Disturbance
Etiology  Primary (Vegetative neurosis,
Hormonal dysbalance)
 Secondary ( viscero-visceral reflex,
accompanying diseases of GIT

Clinical form • Hyperkinetic – hypertonic of

sphincters’Oddy
• Hypokinetic - hypotonic of
sphincters’Oddy
 Mixed form (hyperkinetic – hypotonic,
hypokinetic – hypertonic)
 Clinical Criteria of diagnosis
In hyperkinetic forms of BD:
 Pain syndrome: pain occurs 30-40 minutes after
meal, it is localized in the right hypochondrium or
round umbilicus,it is paroxysmal and cutting or
shooting, and it lasts for 5-15 minutes
 on palpation there is painfulness in the right
hypochondrium
 Signs of Ortner, Merphy, Boas, frenicus-symptom
are positive
 Dispeptic syndrome: nausea, vomiting, abdominal
distension.
 Astheno-vegetative syndrome (Parasympathetic
NS)- emotional lability, irritable, sweating)
 In Hypokinetic forms of BD
 Pain syndrome: pain occurs 1-1,5 hours after meal
(especially fatty) or after physical exertion, it is
localizedin the right hypochondrium.
 It is dull or pressing, and it lasts 1-2 hours, sometimes
accompanied by nausea.
 On palpation painfulness is revealed in the right
hypochondrium.
 Bladder signs are distinctly positive.
 Enlargement and tenderness of the liver are common.
 Dispeptic syndrome: nausea, belching, suppressed
appetite, constipation, bitterness in the mouth.
 Instrumental tests
 The most informative test for verification of
diagnosis is USE with use of cholekynetics
(egg yolk, sorbit) for functional
investigations.
 Changing of size of gall bladder helps to
evaluate its tonus and the rate of contraction
and in an indirect way to conclude about the
state of the sphincters.
 TREATMENT OF BD

Diet:
 Food intakes are more frequent (5-6

time a day) as it improves outflow of

bile.
 Restriction of nitrogenous extractive

substances and fats.

 Products rich in lipotropic substances

and methionine are desirable.

 Pharmacological therapy of
hyperkinetic forms of BD
 Spasmolytics: drotaverine (no-spa),
mebeverine, papaverine,
butilskopolamine,
 M- cholinolytics: priphiniya bromid
 Sedative therapy
 Phytotherapy (Mint, Barberry,
Celandine)
 Mineral waters
 Pharmacological therapy of
hypokinetic forms of BD
 Choleretics: allochol, cholenzyme,
flamine, hepabell (Cynara
scolymus), hepabene
 Cholekinetics :domperydon, sorbite,
xylite, magnesium sulfate, olive oil
 Phytotherapy: Mint, Barberry,
Celandine
 Intubation
 Mineral waters
CHOLECYSTITIS AND CHOLELITHIASIS

 Acute acalculous cholecystitis is uncommon

in children and is usually caused by
infection. Pathogens include streptococci
(groups A and B), gram-negative organisms,
particularly Salmonella and Leptospira
interrogans. Parasitic infestation with
ascaris or Giardia lamblia may be found.
 Calculous cholecystitis may rarely follow
abdominal trauma or burn injury or is
associated with a systemic vasculitis, such
as periarteritis nodosa.
 CHOLECYSTITIS
 Clinical features include right upper quadrant or
epigastric pain
 The pain may radiate substernally or to the right
shoulder
 Right upper quadrant guarding and tenderness
are present.
 A positive inspiratory arrest (Murphy sign)
 Nausea,
 Vomiting,
 Fever,
 Jaundic, scleral icterus
CHOLECYSTITIS

 Ultrasonography discloses an
enlarged, thick-walled gallbladder,
without calculi.
 Serum alkaline phosphatase (ALP)
activity and direct-reacting
bilirubin levels are elevated.
 Leukocytosis is usual.
Cholelithiasis (Gallstones)
Cholelithiasis is relatively rare in otherwise healthy children,
occurring more commonly in patients with various predisposing
disorders
 Cholelithiasis (Gallstones)

 In children, >70% of gallstones are the

pigment type, 15–20% are cholesterol
stones, and the remainder are
composed of a mixture of cholesterol,
organic matrix, and calcium bilirubinate.
 Calcium carbonate stones have also
been described in children.
 The groups at risk for
gallstones include:

• patients with known or

suspected hemolytic disease,
• females,
• teenagers with prior
pregnancy,
• obese individuals, etc
 CLASSIFICATION

 Course of disease: acute, chronic,

latent
 Period of disease: exacerbation,
remission
 Presence of accompanying disease
 Diagnostic criteria

I. Anamnestic:
 typical complaints

 presence of other patients with

cholecystitis or cholelithiasis in the
family
 Diagnostic criteria
II. Clinical:
 Pain syndrome: attacks of biliary colics: acute
strong abdominal pains in the upper right quadrant
with irradiation to the right shoulder, lumbal
region, scapula, especially with ingestion of fatty
foods or after physical exertion
Tenderness is present in the right upper quandrant of
epigastrium, with a positive Murphy sign
 Dispeptic syndrome: nausea, vomiting,

sometimes jaundice because of obstruction of a bile

duct, decolorized fetid stool sometimes
 Intoxication syndrome: febrile t (39),headaches,
collapse, skin dry
 Diagnostic criteria
III. Laboratory:
 leucocytosis of neutrophilic origin, elevated ESR, rarely
anemia in exacerbation, in latent stage – leucopenia.
 Biochemical: liver’s functional tests (elevated alkaline
phosphatase, leucinaminopeptidase, 5-nucleotidase,
glutamiltranspeptidase),
 decreased cholato-cholesterin ratio (lower then 13),
 Amylase and lipase levels may be increased if stone
obstruction occurs at the ampulla hepatopancreatica.
 Proteinogram (dysproteinemia with an elevated level of
globulins),
 Analysis of urine (microhematuria,microalbuminuria,
leucocyturia)
 Coprogram
 Diagnostic criteria
IV. Instrumental:
 ultrasound investigation

 cholecystography and

hepatobiliscintigraphy
Ultrasound investigation
 TREATMENT OF CHOLECYSTITIS
Cholelithiasis

 Regimen depends on the period of the

desease
 I/v rehydration, dezintoxication therapy
 I/v Antibiotic therapy (ampicillin,
cefalosporins), nitrofurantoin
 Analgetics
 Spasmolytics: drotaverine (no-spa), galidor,
buskopan
 TREATMENT OF CHOLECYSTITIS
Cholelithiasis
 Urolesan
 Choleretics: allochol, chollagon,
cholenzyme, flamine
 Cholekinetics: intubation with sorbite,
xylite
 Mineral waters, phytotherapy
 Cholecystectomy is curative. Laparoscopic
cholecystectomy is routinely performed in
symptomatic children with cholelithiasis.
 Pancreatitis, the most common
pancreatic disorder in children
Etiology of Pancreatitis in Children
 DRUGS AND TOXINS: Valproic acid, Acetaminophen
overdose, 5-aminosalicytate, Corticosteroids, Enalapril,
Furosemide, Alcohol, Azathioprine, Tetracycline…
 HEREDITARY PANCREATITIS: Cystic fibrosis gene
 INFECTIOUS: Epstein-Barr virus, Coxsackie B virus,
Hepatitis A, B, Influenza A, B, Malaria, Measles, Rubella…
 OBSTRUCTIVE:Biliary tract malformations, Choleithiasis,
Sphincter of Oddi dysfunction, Tumor…
 SYSTEMIC DISEASE: Collagen vascular diseases, Crohn
disease, Diabetes mellitus, Malnutrition…
 TRAUMATIC
 PATHOGENESIS of Acute Pancreatitis

 The classic etiologic theory suggests

that after an initial insult, such as
ductal disruption or obstruction,
lysosomal hydrolases co-localize with
pancreatic proenzymes within the
acinar cell.
 Pancreastasis (similar in concept to
cholestasis) with continued synthesis
of enzymes occurs.
 PATHOGENESIS of Acute Pancreatitis

 Trypsinogen is activated to trypsin,

which then activates other pancreatic
proenzymes, leading to autodigestion,
further enzyme activation, and release
of active proteases.
 Lecithin is activated by phospholipase
A2 into the toxic lysolecithin.
Prophospholipase is unstable and can
be activated by minute quantities of
trypsin.
 CLINICAL MANIFESTATIONS

 The patient with acute pancreatitis has

severe abdominal pain, persistent vomiting,
and fever.
 The pain is epigastric or in either upper
quadrant and steady, often resulting in the
child's assuming an antalgic position with
hips and knees flexed, sitting upright, or
lying on the side.
 CLINICAL MANIFESTATIONS

 The child is very uncomfortable and

irritable and appears acutely ill.
 The abdomen may be distended and
tender. A mass may be palpable.
 The pain increases in intensity for 24–
48 hr, during which time vomiting may
increase and the patient may require
hospitalization for dehydration and
may need fluid and electrolyte therapy.
 DIAGNOSIS
 Acute pancreatitis is usually diagnosed by
measurement of serum amylase and lipase activities.
 The serum amylase level is typically elevated for up
to 4 days.
 The serum lipase rises by 4–8 hr, peaks at 24–48 hr,
and remains elevated 8–14 days longer than serum
amylase.
 Other laboratory abnormalities: leukocytosis,
hyperglycemia, glucosuria, hypocalcemia, elevated γ-
glutamyl transpeptidase, and hyperbilirubinemia.
 DIAGNOSIS

 Ultrasound and, more specifically, CT

scanning have major roles in the diagnosis
and follow-up of children with pancreatitis.
 Findings can include pancreatic
enlargement, a hypoechoic, sonolucent
edematous pancreas, pancreatic masses,
fluid collections, and abscesses
 DIAGNOSIS

 Endoscopic retrograde
cholangiopancreatography (ERCP) or more
often magnetic resonance
cholangiopancreatography (MRCP)
are essential in the investigation of
recurrent pancreatitis, and disease
associated with gallbladder pathology.
 TREATMENT

 The aims of medical management are

to relieve pain and restore metabolic
homeostasis.
 Analgesia should be given in adequate
doses.
 Fluid, electrolyte, and mineral balance
should be restored and maintained.
 Nasogastric suction is useful in patients
who are vomiting.
 TREATMENT

 Prophylactic antibiotics
(imipenem/cilastatin) are controversial but
are used in severe cases to prevent infected
pancreatic necrosis or to treat infected
necrosis. Recovery is usually complete
within 4–5 days.
 Refeeding can commence when vomiting
has resolved, the serum amylase is falling,
and clinical symptoms are resolving.
 The treatment of severe acute
pancreatitis can gastric acid
suppression, and peritoneal lavage to
reduce the risk of secondary infection.
 Enteral alimentation is superior to
parenteral nutrition.
 Surgical therapy of acute pancreatitis is
rarely required, but may include
drainage of necrotic material or
abscesses.
 PROGNOSIS

 Children with uncomplicated acute

pancreatitis do well and recover within
4–5 days.
 When pancreatitis is associated with
trauma or systemic disease, the
prognosis is typically related to the
associated medical conditions.