Acute Intestinal

Obstruction
Epidemiology

 Accounts for 1-3% of all hospitalizations and

25% of all urgent and emergent general
surgery admissions
 80% involve small bowel
 1/3 present with significant ischemia
 Mortality rate for strangulation operated on
within 24-30h of onset: 8%  TRIPLES after
Types
 Extent of mechanical obstruction:
 Partial
 High-grade
 Complete
 Presence/absence of vascular insufficiency and intestinal
ischemia:
 Simple
 Strangulated
 Mechanisms:
 Mechanical – blockage: extrinsic, intrinsic, intraluminal
 Functional – intestinal dysmotility
Most common causes of acute intestinal
obstruction
EXTRINSIC INTRINSIC INTRALUMINAL
ABNORMALITIES
Adhesions Congenital (malrotation, atresia, Bezoars
stenosis, intestinal duplication,
congenital bands)
Internal or external hernias Inflammation (IBD, diverticulitis, TB, Feces
schistosomiasis)
Neoplasms (carcinomatosis, Neoplasia Foreign bodies
extraintestinal malignancies)
Endometriosis Traumatic (hematoma, anastomosis Gallstones
strictures)
Intraperitoneal abscess Intussussception, volvulus, Enteroliths
Hirschsprung disease
Idiopathic sclerosis Radiation or ischemic injury
 Smallbowel
obstruction
 MCC: extrinsic
diseases
(adhesions,
carcinomatosis,
herniation of
anterior abdominal
wall)
 Colonic obstruction
 Cancer of
descending colon
and rectum in 2/3
of cases
 Adhesions and
hernias rare
 Functional
obstruction
 AKA ileus or pseudo-
obstruction
 Dysmotility prevents
intestinal contents from
moving distally
 MCC: post-
intraabdominal surgery
Functional obstruction
 Other causes:
 Ogilvie syndrome: colonic pseudoobstruction from
autonomic NS abnormalities
 Intraabdominal procedures, lumbar spinal injuries, or
surgery of lumbar spine and pelvis
 Metabolic: hypokalemia, hypomagnesemia,
hyponatremia, uremia, severe hyperglycemia
 Intestinal ischemia
 Drugs: opiates, antihistamines, anticholinergic agents,
psychotropics (haloperidol, TCAs)
 Intraabdominal/retroperitoneal inflammation/hemorrhage
 Systemic sepsis
 Hyperparathyroidism
Pathophysiology

 Manifestations depend on nature of underlying process,

location, changes in blood flow
History and PE

 Cardinal signs:
 Colicky abdominal pain
 Abdominal distension
 Emesis (feculent if with bacterial overgrowth)
 Obstipation
 Distal obstruction: more distension and discomfort,
delayed emesis
 More proximal obstruction: less distension, more vomiting
 Important in history: prior surgery, cancer, IBD
History and PE
 Most appear critically ill
 Severe intravascular depletion  oliguria, hypotension,
tachycardia
 Strangulation or systemic inflammation  fever
History and PE
 Bowel sounds are difficult to interpret
 early SB obstruction: high-pitched, musical, tinkling bowel sounds
and perisltaltic rushes (borborygmi)  Late SB obstruction:
absent or hypoactive
 Ileus: absent/hypoactive from beginning
 Partial blockage: continues to pass flatus/stool
 Complete blockage: evacuates contents of bowel downstream
beyond obstruction
History and PE
 Examine all surgical incisions
 Tender abdominal/groin mass  highly suggestive of
incarcerated hernia causing obstruction
 Tenderness  ischemia, necrosis, peritonitis
 Localized severe pain/peritoneal irritation  strangulated
or closed-loop obstruction
 Discomfort may be out of proportion to PE (mimics acute
mesenteric ischemia)
History and PE
 Colonic volvulus
 Severe abdominal pain
 Vomiting obstipation
 Asymmetric abdominal distension
 Tympanic mass
 Ileus or pseudo-obstruction
 Similar to SBO
 Abdominal distension
 Pain typically absent
 May not have nausea or emesis
 Regular discharge of stool/latus  help distinguish from CGO
Labs and Imaging
 Complete blood count
 Mild hemoconcentration
 Slight WBC elevation
 Serum electrolytes and Creatinine
 Hypokalemia, hypochloremia, hyponatremia, elevated BUN-Crea
ratio, metabolic alkalosis
 Guaiac positive stool and IDA  strongly suggestive of
malignancy
 Higher WBC and metabolic acidosis  possible severe
volume depletion, ischemic necrosis, sepsis
Labs and Imaging
 Do not delay surgical consult and operative intervention
if strongly suggest high grade or complete obstruction of
bowel compromise
 Abdominal xray
 Must include upright or cross-table lateral views
 Quick to complete
 Labs and Imaging

 Abdominal x-ray
 Small bowel obstruction
 staircasing pattern
 Dilated air and fluid-filled SB
loops
 >2.5 cm diameter
 Little/no air in colon
 Labs and Imaging

 Abdominal x-ray
 Large bowel obstruction
 Colon dilation
Labs and Imaging

 Abdominal x-ray
 Perforation
 free air
 Labs and Imaging

 Abdominal x-ray
 Volvulus
 gas-filled, coffee bean-shaped
dilated shadow
Labs and Imaging
 Computed tomography
 May be time-consuming and expensive
 Beneficial in unclear diagnosis
 95% sensitivity and 96% specificity for high-grade obstruction
 Lower accuracy for closed-loop obstruction (60%)
 Contrast appearing in cecum within 4-24h of oral water-soluble contrast
 expected to improve (95% sens and spec)
 Ultrasound
 Difficult to interpret
 Appropriate for pregnant patients/xray exposure contraindicated
 Barium studies
 Contraindicated in complete/high-grade bowel obstruction
 NEVER give barium orally in patient with possible obstruction
Treatment

 Stabilization as quickly as possible reduces mortality

 Fluid resuscitation
 Electrolyte repletion
 Nasogastric tube decompression
 Urine output/CVP measurement
 Antibiotics: controversial, prophylaxis may be needed for OR
 Ileus
 Treatment is supportive: IV fluids, nasogastric decompression
 Treat underlying pathology
Treatment

 60-80% of patients with mechanical bowel obstruction can

be treated conservatively
 Decision to operate is based on clinical judgment and
sometimes imaging
 Defining feature of bowel obstruction intra-op: dilation
proximal to site of blockage with distal collapse
 Intraoperative strategies depend on underlying problem
(adhesiolysis vs. resection with diversion or anastomosis)
Acute Appendicitis and
Peritonitis
Acute Appendicitis: Epidemiology

 Most common emergency general surgical disease

affecting the abdomen
 MC age group: 10-19 yo
 70% of patients <30 yo
 Mostly affects men
 Higher perforation rates in patients <5 yo and >65yo
Acute Appendicitis: Pathogenesis

 Etiology not completely understood

 Important step in some cases: obstruction of appendiceal
lumen
 Bacterial overgrowth and luminal distension  Increased luminal
pressure  inhibits lymph and blood flow  vascular thrombosis and
ischemic necrosis  distal appendix perforation
 Etiology: fecaliths found in ~50% of perforated gangrenous
appendicitis
 Others with association: incompletely digested food, lymphoid
hyperplasia, intraluminal scarring, tumors, bacteria, viruses, IBD
Acute Appendicitis: Pathogenesis

 After perforation  leak contained by omentum or

surrounding tissues
 Abscess formation
 Severe peritonitis
 Infective suppurative thrombosis of portal vein, intrahepatic
abscess (rare, poor prognosis)
 Simple cases may resolve spontaneously or with
antibiotics
 Fecaliths rarely identified in simple disease
Acute Appendicitis: History
 Consider appendicitis in ANY age group
with abdominal pain unless previously
removed
 Presentation dependent on anatomical
location
Acute Appendicitis: History
Acute Appendicitis: History
 Classic History
 Initial:
nonspecific complaints – bowel habit changes, malaise,
vague/intermittent/crampy abdominal pain
 Migration of pain to right lower quadrant over 12-24 hours
 sharper, localized
 Local muscle rigidity and stiffness (parietal peritoneal irritation)
 Nausea develops AFTER abdominal pain
 Distinguishes from AGE (nausea first)
 Mild/scant emesis (also AFTER pain)
 Anorexia: question the diagnosis if this is absent!
Acute Appendicitis: History

 Patient lies still to avoid movement causing peritoneal

irritation
 Some report discomfort with bumpy car ride, coughing,
sneezing, Valsalva
 Diagnosis more challenging with atypically located appendix,
women of childbearing age, very young, elderly
 Children: smaller omentum  less likely to wall off perforation
 Elderly: subtle presentation, minimal reaction compared to younger
patients, nausea/anorexia/emesis more predominant
 Consider other diagnosis or perforation/phlegmon/abscess if
temp >38.3C or if with rigors
Acute Appendicitis: History

 Pelvic appendicitis:
 Dysuria
 Urinary frequency
 Diarrhea
 Tenesmus
 Pain may only be present on palpation of suprapubic region or
rectal/pelvic examination
 Rectocecal appendix/below pelvic brim: little tenderness in
anterior abdomen
 Simple appendicitis: Mildly ill
Acute Appendicitis: PE
 Examine WHOLE abdomen
 Classical tenderness found at McBurney’s point
One-third along line from anterior iliac spine to umbilicus
Acute Appendicitis: PE
 Rovsing’s sign: gentle pressure in LLQ elicits pain in RLQ
Acute Appendicitis: PE
 Obturator sign: pain with hip internal rotation (pelvic
appendicitis)
 Iliopsoas sign: pain along posterolateral back and hip with
R hup extension (retrocecal appendicitis)
Acute Appendicitis: PE
 ALL patients must undergo rectal examination
 Pelvic examination mandatory in women (rule out
urogynecologic etiology: PID, ectopic pregnancy, ovarian
torsion)
Acute Appendicitis: Laboratory Testing

 No laboratory test identifies appendicitis

 Mild-moderate WBC elevation in 70% of simple appendicitis
cases (10-18k)
 Left shift to immature PMNs in >95%
 Amylase, lipase
 Urinalysis to exclude GU conditions
 Sterile pyuria/hematuria CAN BE PRESENT  inflamed appendix
abutting ureter or bladder
Acute Appendicitis: Laboratory Testing

 Pregnancy test in women of childbearing age

 Cervical cultures in suspected PID
 Anemia and guaiac-positive stools: suggestive of other
diseases or complications (e.g. cancer)
Acute Appendicitis: Imaging

 Plain films
 not routine
 r/o intestinal obstruction, perforated viscus, ureterolithiasis
 Ultrasound
 operator-dependent (86% sensitivity, 81% specificity)
 Findings: wall thickening, increased appendiceal diameter,
free fluid
 Current practice: used as first-line imaging (use others if
findings are equivocal)
Acute Appendicitis: Imaging

 CT scan
 94% sensitivity, 95% specificity
 Useful if diagnosis is doubtful
 Helps assess severity of appendicitis in the absence of
peritoneal findings
 Suggestive: dilatation >6mm with wall thickening, lumen
not filled with enteric contrast, fatty tissue stranding, air
surrounding appendix
Appendicitis: Treatment

 Most patients with strongly suggestive medical histories and

PE with supportive labs are candidates for appendectomy
 Repeat abdominal exam over 6-8h for uncertain diagnosis
 Correct fluid status and electrolytes prior to OR
 Either laparoscopic or open appendectomy for
uncomplicated appendicitis
 Phlegmon or abscess
 Broad-spectrum antibiotics
 Drainage if abscess >3cm
 Parenteral fluids
 Bowel rest
 Appendectomy after 6-12 weeks
Appendicitis: Treatment

 Laparoscopic appendectomy
 Accounts for majority of procedures in Western world
 Useful in uncertain diagnosis, obese patients
 Less post-operative pain
 Shorter length of stay
 Faster return to normal activity
 Fewer superficial wound complications
 Higher risk of intraabdominal abscess formation
 Common complications: fever, leukocytosis (>5 days:
consider intraabdominal abscess)
Appendicitis: Treatment

 Uncomplicated nonperforated appendicitis mortality rate:

0.1-0.5%
 Perforated appendicitis or other complicated disease
mortality rate: 3%-15% (elderly)
Acute Peritonitis
Acute Peritonitis

 Inflammation of the visceral and parietal peritoneum

 Most often but not always infectious in origin
 Secondary to perforation of hollow viscus
 Primary peritonitis vs. secondary peritonitis
 Primary: spontaneous, no source identified
 Secondary: underlying cause (e.g. infection)
 Localized vs. diffuse
Acute Peritonitis: Etiology

 Primary or spontaneous bacterial peritonitis: patients with

ascites or hypoproteinemia
 Secondary: Infective organism contaminates peritoneal
cavity
 Spillage from hollow viscus
 Most common: perforation of appendix, colonic diverticuli, stomach,
duodenum
 Others: bowel infarction/incarceration, cancer, IBD, intestinal
obstruction, volvulus
 Penetrating abdominal wound
 Introduction of foreign object (e.g. PD catheter or port)
Acute Peritonitis: Etiology

 Aseptic peritonitis
 Abnormal presence of physiologic fluids (gastric juice, bile,
pancreatic enzymes, blood, urine) or sterile foreign bodies
(surgical sponges, instruments)
 Complication of SLE, porphyria, familial Mediterranean fever
Acute Peritonitis: Clinical Features
 Cardinal signs and symptoms
 Acute, severe abdominal pain
 Tenderness
 Fever
 Less response in elderly and immunosuppressed patients
 Generalized peritonitis
 Diffuse abdominal tenderness
 Local guarding
 Rigidity
Acute Peritonitis: Clinical Features
 Localized presentation in specific region of abdomen if
intraperitoneal inflammatory process is limited or
contained
 Bowel sounds absent to hypoactive
 Signs of volume depletion: tachycardia, hypotension
Acute Peritonitis: Labs

 Significant leukocytosis
 Severe acidosis
 Radiographs
 Dilation of bowel and associated bowel wall edema
 Free air: possible surgical emergency
 Diagnostic paracentesis in stable patients with ascites
 Test for protein, LDH, cell count
Acute Peritonitis: Therapy and Prognosis

 Treatment:
 Correct electrolyte abnormalities
 Restore fluid volume and stabilization of cardiovascular system
 Appropriate antibiotic therapy
 Surgical correction of underlying abnormalities
 Mortality rate:
 Uncomplicated localized peritonitis in reasonably healthy patients:
<10%
 Elderly/immunocompromised: >40%