BOWEL OCCLUSION =the full and persistent Spastic adynamic obstructions: thin intestinal

block of the bowel transit at the level of the small loops + contracted walls + no lumen + pale serosa +
intestine / colon, that affects hemeostasis unapparent vascular pattern

Classification: Causes:
 Functional (adynamic*) occlusion: obstruction • Local(irritating): Foreign bodies, Irritating
with no obstacle foods, Intestinal parasites, Intestinal ulcerations
 Mechanical (dynamic*) obstruction: • Reflex
mechanical blockage by physical barrier which o Celiac plexus damage
prevents the advance of bowel contents o Abdominal contusions
 Intestinal subocclusion: incomplete obstruction • Central nervous
of the intestinal lumen→ could develop into full o Brain tumors
obstruction / restoration of intestinal transit o Mental disorders
Treatment based on type of obstruction o Lead intoxication (saturnine colic)
1. Functional (adynamic) occlusion o Tabes dorsalis
- Motility disorder→medical treatment o Non-determined
2. Mechanical (dynamic) obstruction
A. Non-ischemic→postponed emergency
Clinical manifestations
surgical treatment
 Abdominal pain,
B. Ischemic→immediate emergency
 Nausea and/or vomiting,
surgical treatment
 Blockage of gas and feces (absolute
Classification of obstructions
constipation indicates complete intestinal
• Topography:
obstruction)
o Upper obstruction: in the upper digestive
• Accompanied by:
tract (i.e., pylorus, duodenum, jejunum)
 Abdominal distension: dependent on the site
o Lower obstruction: ileum, colon or rectum
of the obstruction (the more distal the
 Evolution: Acute, Subacute, Chronic obstruction site, the greater the distention)
 Complete / partial  Systemic signs of dehydration
I.FUNCTIONAL (ADYNAMIC)
OBSTRUCTIONS Physiopathology Physical examination
Paralytic adynamic occlusion: distended intestinal Inspection
loops, thin-walled, filled with liquid and gas • Abdominal distension(meteorism):
Causes:  Specific sign
Metabolical  Frequently present, moderate and diffuse–in
 HypoK (Darrow syndrome), HypoNa, severe the paralytic ileum
hypoCa  Absent / minimum peristaltism
- Diabetic coma.  Evident – in later stages of the lower
- Uremia obstruction;
- Porphyria Palpation:
Reflex  Abdominal distention
- Biliary or renal colic  Rarely: signs of peritoneal irritation
- Organtorsions(ovary,testicle)  Signs of peritoneal irritation – late stages of
- Brain or spine injuries acute peritonitis.
- Acute pancreatitis, peritonitis, hemoperitoneum Percussion
- Abdominal,retroperitoneal injuries  Abdominal tympany
Other causes  Disappearance of liver dullness
- Abdominal surgical procedures – mixed causes: Auscultation
o Reflex, Electrolyte disorders, Peritoneal  Early stage: ↑ bowel sounds
irritation (hyperperistalsis)
- Intoxications:Heavy metals, Drug addiction  Advanced obstruction stages: reduced /
- Sepsis,shock absent bowel noises

Rectal exam
 Vacuity of the rectal ampulla
 Occlusive rectal tumor mass
 Fecal impaction (fecaloma)
 Visible / occult sanguinolent secretions
(malignant descending colon and rectal
tumors)
• Abdominal pain: Sudden onset, Colicky(each
episode:3-5min), general and permanent
• Vomiting – with biliary aspect
• Absence of transit of faeces and gases: significant
and defining clinical sign.
Systemic manifestations
• Less obvious than in the mechanical (dynamic)
obstruction:
 Vomiting
 Altered general state (of patient)
 Hypotension
 Tachycardia
 Oliguria
 Facies – “toxic” appearance
Paraclinical tests
Laboratory tests
 Hemoconcentration
 Leukocytosis
 Diselectrolytemia - Na, Cl
 Initially – hypoK → final stage: hyperK
 ↑ urea & blood creatinin
 Mixed acidosis (predominantly alkaline
losses)
Imagistic investigations:
Simple abdominal Rx:
 First 3-5h from onset: intestinal gaseous
distension
 In advanced stages: numerous hydroaeric levels
 Small-intestine obstruction: multiple, central
hidroaeric levels + long horizontal diameter
 Large-intestine obstruction: a few, peripheral
hidroaeric levels + long vertical diameter
Abdominal Rx with oral contrast agent: perioral
administration of hydrosoluble contrast agent with
management of its progress at short, 30-minute
intervals (Pansdorf test)
 Small-bowel obstruction: central dilated loops
(>3 cm diameter)
 Large-bowel obstruction: contrast enema
(barium / gastrogaffin)
 the progress of the substance does not show
digestive lumen.
– Abdominal CT-scan with contrastagenti.v./oral
 The contrast agent progress does not show
bowel obstruction
 Used to detect the surgical causes of
dynamic obstruction
 Used for the differential diagnosis with
mechanical obstruction / entero-mesenteric
infarction
 Must not postpone surgery
 Mandatory if the patient’s condition allows
– Abdominal ultrasound:
 Bowel inspection → gaseous distension,
significant / absent peristalsis
 Intraluminal
obstacles(tumors,foreignbodies)or
extraluminal (compressive tumors)
 Highlights the intraperitoneal fluid
Positive diagnosis
 Clinical obstruction signs
 In the presence of etiological factors of
dynamic obstruction
 Abdominal Rx on an empty stomach with
gaseous distension and diffuse hidroaeric
levels
Differential diagnosis
 Mechanical obstructions
 Diffuse peritonitis
 Ascites
 Acute gastric distension
 Habitual constipation
 Pregnancy
Treatment
 Medical treatment
 Restoration of initial hydroelectrolytic
and acid-base balance
 Broad-spectrum antibiotic therapy
 Nil by mouth (nothing by mouth –
NBM) & intestinal decompression (NG
tube, rectal tube, enema)
 Venous & urinary catheters (the “3
catheters” rule)
 GI (drug) stimulants of intestinal transit
(Neostigmine, Debridate)
 Treatment of the medical causes
 Anti-emetics
 Painkillers (analgesia)
 Surgical treatment: in case of an etiology
which requires surgical treatment (e.g. organ
torsion, acute pancreatitis, etc.)
Objectives:
 Bowel decompression–evacuation of bowel
contents by:
 Retrograde purge through NG tube
 Direct, by pouch enterotomy
 Intrinsic intestinal obstacle (tumor) removal,
exteriorization of the proximal intestinal end
(ileostoma / colostoma)
 Shunting by internal derivation
 If it’s opted for intestinal transit restoration at
the colic level → anastomoses protection by
stomas is recommended.

Post-operatory ileum

- functional (paralytic) occlusion occurs

consecutive to opening the peritoneal cavity.
- 12-72h intestinal transit resumes normal
- Persistence of postop ileum >72h -> no
resumption of digestive transit, significant
gastric stasis, abdominal distention, electrolyte
disorders.

II. MECHANICAL OBSTRUCTION

A. Non ischemic mechanical obstruction -
based on location of the obstruction in
the intestinal
2. Intramural (intrinsic):  Cardiovascular, respiratory, septic disorders
 Intestinal atresia & stenosis, (e.g. bronchopneumonia, etc.)
 Tumors
 Peritoneal carcinomatosis,
 Intestinal stenosis (Crohn’s disease,
diverticulitis, etc.)
 Intestinal tuberculosis
 Intramural hematoma (injuries,
coagulopathies)
 Volvulus
 Intussusception (one segment of the intestine
”telescopes” inside of another)
3. Extramural (extrinsic):
 Peritoneal adhesions
 Incarcerated hernia / eventration
 Compression by large tumors
 Intraperitoneal foreign bodies
 Superior mesenteric artery syndrome
(Wilkie’s syndrome)
Intestinal obstacle physiopathology
 Counter intestinal contractions
upstream the obstacle
 Bowel distention above the obstacle
 Intense peristalsis→↓ later→abolished
peristaltis
 ↑ intraluminal pressure
 Venous and capillary stasis; ↑
permeability and plasmatic dehydration

 Intestinal parietal edema
 Significant intraluminal fluid retention
proximal to the location of the obstacle
 Peritoneal effusion
 Vomiting

 Hydroelectrolytic losses in pathological

space

 Acid-base balance disorders

 Respiratory acidosis (alteration of
ventilation with CO2 accumulation)
 Metabolicacidosis
 Microbial proliferation exacerbation
 Altered mucosa barrier
 Microbial translocation
 Altered microvascularization of the
intestinal wall (intestinal ischemia) →
necrosis → perforation → peritonitis