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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_901_Библиотеки_им_академика_М_И_Перельмана
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210
L. Amodu et al.
Complications and their treatment
Complications Characteristics
Peritonitis s/p
adhesiolysis
Wound infection Pain and redness in the incision Open the incision and check if the midline fascia is
Most commonly caused by an
unrecognized enterotomy during
surgery
Return to operating room (run the bowel from
ligament of Treitz to ileocecal value to assess for any
missed enterotomies)
intact
Bedside irrigation and debridement+packing in a
“wet-to-dry” fashion
If cellulitis or purulent drainage→antibiotics
Treatment
Recurrent SBO Recurrence rates of SBO increase
with repeated episodes of SBO
Patient with recurrent SBO→laparoscopic
adhesiolysis
Small Intestinal Bacterial Overgrowth/Blind Loop Syndrome
Small intestinal bacterial overgrowth/blind loop syndrome
Predisposing
factors
Pathophysiology
Presentation Chronic diarrhea, steatorrhea, excessive atulence, abdominal distention, malnutrition, and
Diagnosis Positive carbohydrate breath test (d-xylose breath test)
Previous abdominal surgery with bypassed small intestinal loops, large diverticula, stula,
stricture, or motility disorders (Crohn’s disease, radiation enteritis, and diabetes)
Most commonly associated with antecolic Billroth II loop reconstructions with a long
(>30cm) afferent limb
Most common bacterial species include Escherichia coli and Klebsiella pneumonia
Blind loop→stagnation and proliferation of aerobic and anaerobic
bacteria→malabsorption, disordered digestion
megaloblastic anemia (due to bacterial overconsumption of vitamin B
Jejunal aspirate culture→bacterial concentration of >103 colony forming units/mL
Dietary modications: Medium-chain triglyceride diets→do not require digestive enzymes
12)
Management
Vitamin B12 supplementation
Antibiotics: Rifaximin for 14days
Small bowel resection, bypass creation, or stricturoplasty
7 Small Bowel
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Meckel Diverticulum
Meckel’s diverticulum
Meckel’s diverticulum is a persistent remnant of the omphalomesenteric duct
Anatomy
Meckel’s diverticulum may contain two types of tissue: Gastric and pancreatic
Most common congenital malformation of the gastrointestinal tract
Epidemiology
Rule of 2s mnemonic: 2% of the population, 2 inches long, 2feet from ileocecal valve, 2/3 have
ectopic mucosa (most common gastric and pancreatic), 2% become symptomatic
Presentation Bleeding which can be acute and massive or chronic
Intestinal obstruction
Acute inammation of the diverticulum
Diagnosis Meckel’s scan—Nuclear medicine study with 99m technetium pertechnetate, which has an afnity
for gastric mucosa, performed to identify areas of ectopic gastric mucosa
211
Management
Symptomatic→resect simple diverticulectomy versus segmental small bowel resection and
primary anastomosis
Asymptomatic Meckel’s diverticulum→controversial
Case scenarios
Case scenarios
Incidentally discovered Meckel’s diverticulum
in older individual or patient with comorbidities
Young patient (<50years of age) with
asymptomatic Meckel’s diverticulum
incidentally found intraoperative
Symptomatic Meckel diverticula or patient with
palpable lesion in Meckel’s diverticulum
Diverticulum containing visual or palpable
mass
Management
Incidentally found Meckel should not be electively resected
because the risk of developing complications related to the
diverticulum is very low except if there is a palpable
abnormality
Resect the Meckel’s diverticulum if there is a palpable
abnormality or the Meckel’s diverticulum is longer than 2cm,
or diverticulum has a brous band
Diverticulectomy or segmental small bowel resection if lumen
is in jeopardy, palpable abnormality is present at the base of
diverticulum, or neck of diverticulum >2cm
A broad-based Meckel diverticulum is best managed by
segmental resection
Resect because there is a relationship between Meckel
diverticulum and GI malignancy
212
Research
Reference
Shah K, Khiria L, Desai P, Vora H, Bhavsar
M.Surgically inverting an incidentally detected
Meckel’s diverticulum—Wrong method. Int J Surg
Case Rep. 2015;6C:289–91
L. Amodu et al.
Findings
Meckel diverticulum is the most common cause of
non-idiopathic intussusception. Simple diverticulectomy is
preferred since malignancy rate is low over resection with
anastomosis
Lequet J, Menahem B, Alves A, Fohlen A, Mulliri
A.Meckel’s diverticulum in the adult. J Visc Surg.
2017;154(4):253259
Kabir SA, Raza SA, Kabir SI.Malignant neoplasms
of Meckel’s diverticulum; an evidence based review.
Ann Med Surg (Lond). 2019;43:75–81
Meckel’s diverticulum is the most frequent gastrointestinal
congenital malformation, lifetime risk 4%. Surgery is not
indicated in the absence of risk factors for complications,
including male gender, age<40, diverticulum >2cm
Meckel’s diverticulum primary malignancy is extremely
rare, only 0.5–3.2%, with the most common being
carcinoid (33–44%)
Enterocutaneous Fistula
Enterocutaneous stula
Enterocutaneous stulae are anomalous connections between the gastrointestinal tract
and the skin
Characteristics
Common anatomic locations of enterocutaneous stulas: Stomach, small intestine, colon,
and rectum
Predisposing factors Most commonly iatrogenic (85%) (enterotomy, anastomotic leakage, erosion of foreign
material), Crohn’s disease, radiation enteritis, diverticulitis, trauma, and malignancy
Low output stula (<200mL/24h)→more likely to close spontaneously
Classication
Intermediate output stula (200–500mL/24h)
High output stula (>500mL/24h)→proximal stulae (stomach, small intestine) tend to
have high output
Fever, leukocytosis, and wound erythema
Sepsis is common and is the most common cause of death
Presentation
High output stula→increased risk of metabolic derangements
Patients with enteroenteric and enterocolonic stulae may have diarrhea
Diagnosis Fistulogram to determine anatomy of a stula tract
7 Small Bowel
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Enterocutaneous stula
Fluid resuscitation, electrolyte replacement, sepsis control, nutritional support (TPN),
wound care, control of output (proton pump inhibitors [PPIs] and histamine 2 receptor
antagonists to help decrease gastric secretions, antimotility agents and somatostatin),
prevention of skin breakdown
Management
If concerns for infection→antibiotics
Abscesses or intra-abdominal uid collections→percutaneous or operative drainage
High output stulas, stula length <2cm, lateral bowel wall location, the presence of
multiple stulas, and adjacent inammation→poor prognostic indicators for
spontaneous closure of an ECF
Indications for surgery: Failure of 8–12weeks of nonoperative management
213
Key principles for
enterocutaneous stula
resection
Attempt a single-stage procedure
Ensure careful adhesiolysis
Address compromised tissue with wedge excision or intestinal resection
Attempt at covering suture lines with viable tissue
Research
Reference
de Vries FEE, Reeskamp LF, van Ruler O,
etal. Systematic review: Pharmacotherapy
for high-output enterostomies or enteral
stulas. Aliment Pharmacol Ther.
2017;46(3):266–73
Gribovskaja-Rupp I, Melton
GB.Enterocutaneous stula: Proven
strategies and updates. Clin Colon Rectal
Surg. 2016;29(2):130–7
Adaba F, Vaizey CJ, Warusavitarne
J.Management of intestinal failure: The
high-output enterostomy and enterocutaneous
stula. Clin Colon Rectal Surg.
2017;30(3):215–22
Findings
This paper found evidence for the following medical therapies to
be effective: Omeprazole, loperamide and codeine, ranitidine, and
cimetidine
They proposed an algorithm for standard of care which consists
of high-dose proton pump inhibitors combined with high-dose
loperamide as the rst step followed by addition of codeine in
case of insufcient output reduction
Denitive repair of the ECF should be planned if no spontaneous
closure occurs by 12weeks after sepsis control, nutritional
optimization, and establishing wound cares
Management of enterocutaneous stula involves an approach
described as SNAPP:
• Sepsis control
• Nutrition
• Determining anatomy
• Protection of skin (wound care)
• Planned denitive surgery
214
Ileostomy andIleostomy Closure
Ileostomy
Indications Advantages and disadvantages
Loop ileostomy Temporary diversion Easier to reverse
L. Amodu et al.
Loop versus end
ileostomy
Ileostomy marking
Key steps for
ostomy creation
End ostomy
Lower incidence of parastomal and
incisional hernias, stomal prolapse,
and stula formation
End ileostomy Very little distal bowel remains
(after total abdominal colectomy)
Preoperative stoma marking and teaching→fewer ostomy complications
It should protrude and come through the rectus muscle
The patient should be able to visualize the stoma and access it without difculty
In obese patients, can place above umbilicus through rectus sheath for visualization
Be 5cm away from skin crease or bony prominence
All stomas should be externalized through the rectus abdominis to mitigate parastomal
hernias
A disk of skin is removed
Muscle-splitting technique is used to approach the fascia
A fascial incision is created allowing two ngerbreadths to easily slide through
A Babcock is used to pull the stoma through, and the bowel is visualized again for adequate
perfusion.
Creating some protrusion of the bowel above the skin level leads to easier stoma pouching
The marginal artery should not be disrupted during mobilization
End ostomy: Created with one end of transected bowel
The transected end is then brought through the abdominal wall, the staple line removed, and
matured by suturing the edges of bowel to the skin
Loop ostomy
Ostomy reversal
key steps
Loop ostomy is created by bringing an entire loop of colon through the abdominal wall and
making a transverse incision on the antimesenteric wall of the bowel
The cut edges are then folded back and sutured to the skin, opening both lumens to allow for
decompression
A supporting rod or looped catheter is placed below the common edge of bowel to keep it
from retracting
Circumferential peristomal incision is made at mucocutaneous junction and dissected to the
level of the fascia
All adhesions to the fascia should be dissected for later fascial closure
Loop ostomies should have the edges freshened and closed transversely with running sutures
or reestablish continuity with a side-to-side stapled anastomosis
Looped bowel reversals can often be performed solely through the stoma incision
End ostomies often require the same mobilization and further intra-abdominal dissection to
mobilize the bowel requiring an open or laparoscopic mobilization of the bowel to reach the
anastomosis site
Left colostomy reversal: A colorectal anastomosis is performed using a circular stapler most
commonly or a handsewn anastomosis after taking down of the ostomy
7 Small Bowel
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Research
Reference
Luglio G, Pendlimari R, Holubar SD, Cima RR,
Nelson H.Loop ileostomy reversal after colon
and rectal surgery: a single institutional 5-year
experience in 944 patients. Arch Surg.
2011;146(10):1191–6.
This large, single institution study of outcomes after
ileostomy reversal surgery demonstrated that, despite an
overall complication rate of 21.5%, grades III and IV
complications with ileostomy reversal surgery were observed
relatively infrequently (5%)
The following surgical complications were described after
ileostomy reversal: Ileus/partial small-bowel obstruction,
small-bowel obstruction requiring reoperation, volvulus
requiring reoperation, anastomotic leak, abdominal abscess,
and wound complications
Complications of ileostomy creation and their management
Complications Characteristics
Retraction of
stoma
Ischemia result in late-term stoma
stenosis and retraction
Caused by inadequate mobilization of
stoma conduits
Mild retraction→conservative management
Retraction of stoma below fascia→emergent
operation to prevent intra-abdominal contamination
215
Findings
Management
Stoma necrosis
Mucocutaneous
separation
Ileostomy
prolapse
Parastomal
hernia
High output
ileostomy
Poorly perfused stomas can necrose in
the early postoperative period
Arterial insufciency is the most
common cause of stoma necrosis;
however, venous ischemia can rarely
arise from fascial obstruction within
the trephine
Ileal mucosa pulls away from the edge
of the skin
The length of the segment of ileum
outside the skin increases
Common complication after ileostomy
creation
May be asymptomatic or may present
with obstruction
High ileostomy output is dened as
>1200mL/d→which results in
volume depletion and electrolyte
abnormalities
Identify the proximal extent of mucosal ischemia with
a bedside “test-tube” examination
Any stoma with early evidence of sub-fascial ischemia
(i.e., posterior to abdominal wall fascia)→should be
revised (deep ischemia may progress to perforation)
Topical wound care
Minimally symptomatic→conservative management
Signicantly symptomatic→revision
Asymptomatic parastomal hernia→does not mandate
repair
Mildly symptomatic→appliance modications or a
modied abdominal binder or stomal support belt
Patients with intermittent obstructions, intolerable
discomfort, and signicant pouching
difculties→elective repair
Incarcerated hernias causing complete obstruction or
worrisome for strangulation→immediate surgery
Dietary and lifestyle changes, ber supplements,
antidiarrheal agents (loperamide), and antisecretory
agents
Electrolyte abnormalities (especially hyponatremia)
may be exacerbated by patient attempts to make up for
high ileostomy output by taking in hypotonic uids
216
Ileal arteries
L. Amodu et al.
Mesenteric Ischemia: Acute (Arterial, Venous, andNonocclusive)
Mesenteric ischemia
Arterial supply to the small intestine consists primarily of SMA (except proximal duodenum)
Superior mesenteric artery branches:
Superior mesenteric
Inferior
pancreaticoduodenal
arteries
Middle colic artery
Right colic artery
Ileocolic artery
artery
Superior
mesenteric
artery branches
1-inferior pancreaticoduodenal artery
2-middle colic artery
3-ileal and jejunal branches
4-right colic artery
5-ileocolic artery
Jejunal
arteries
The venous system parallels the arterial system
Presentation Acute abdominal pain, pain out of proportion to exam, metabolic acidosis. Very high suspicion if
patient has A-b and subtherapeutic
Diagnosis CT scan with intravenous contrast or
contrast angiography with delayed venous
phase images
Sagittal maximum intensity projection CT
image with IV contrast demonstrates abrupt
lling defect in the proximal superior
mesenteric artery (arrow). Not shown, on other
images, is hypoenhancing small bowel wall,
indicating acute mesenteric ischemia
7 Small Bowel
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Mesenteric ischemia
Resuscitation/pain control/broad-spectrum antibiotics/NPO/NGT/systemic anticoagulation
(heparin)
Indications for exploratory laparotomy: Any patient suspected of having intestinal infarction or
Management
perforation (peritonitis, worsening abdominal examination or metabolic acidosis). Proximal
thromboembolic disease on CTA
Patient with thromboembolism to SMA SMA embolectomy±patch angioplasty
Patient with thrombosis to SMA Open SMA bypass with antegrade inow from the
217
Case Management
aorta or retrograde from the iliac artery
Key steps
Venous mesenteric ischemia
Nonocclusive mesenteric ischemia Circulatory support and increased cardiac output
Exploratory laparotomy
Inspection of the entire bowel
Exposure of the SMA (retract transverse colon superiorly and small bowel inferiorly)
If thromboembolism to SMA→embolectomy
If thrombosis to SMA→bypass (retrograde versus antegrade)
Resect nonviable bowel
Second-look laparotomy with temporary abdominal closure within 24–48h
Anticoagulation→if persistent
symptoms→venous thrombolysis
Mesenteric Ischemia
Acute
Acute venous
mesenteric
Cause Acute arterial mesenteric ischemia
Arterial embolism Arterial thrombosis
Incidence 40–50% 20–30% 5–15% 15–20%
ischemia
nonocclusive
mesenteric
ischemia
Etiology Due to a dislodged emboli
from the left atrium, left
ventricle, cardiac valves,
or proximal aorta
Mechanism Occlusion in the SMA
occurs distal to the takeoff
with sparing of proximal
branches (proximal jejunal
sparing)→jejunum
unaffected
Due to an acute
thrombus (history of
chronic intestinal
ischemia from
atherosclerotic
disease)
Occlusion is at the
takeoff of the artery
with associated
calcications along
the SMA
Hypercoagulable states
or from secondary
causes (malignancy or
prior abdominal
surgery)
Venous occlusion of
SMV
Due to splanchnic
hypoperfusion and
vasoconstriction
Hypoperfusion of
splanchnic
circulation
218
Celiac artery
Super
Celiac artery
L. Amodu et al.
Mesenteric Ischemia
Acute
Acute venous
mesenteric
Cause Acute arterial mesenteric ischemia
Presentation Acute catastrophic Insidious onset Subacute Acute or subacute
ischemia
nonocclusive
mesenteric
ischemia
Risk factors Arrhythmia, myocardial
Atherosclerosis
infarction, endocarditis
Diagnosis CT angiogram CT angiogram CT angiogram with
venous phase
Findings: Target sign of
SMV
Management SMA
embolectomy±patch
angioplasty
Open SMA bypass
with antegrade inow
from the aorta or
retrograde from the
Anticoagulation→if
persistent
symptoms→venous
thrombolysis
iliac artery
Mesenteric arterial embolism versus thrombosis
ior mesenteric artery
Middle colic artery
Thrombus
Embolus
Middle colic artery
Thrombus
CT angiogram
Circulatory support
and increased
cardiac output
Atherosclerotic plaque
Superior mesenteric artery
Paralytic Ileus
Ileus
Risk factors Abdominal or pelvic surgery, delayed enteral nutrition, open surgery, intra-abdominal infection,
intra-abdominal bleeding, opioids use, electrolyte derangements
Presentation Abdominal distention, abdominal pain, nausea, vomiting, obstipation, intolerance to oral diet
7 Small Bowel
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Ileus
219
Diagnosis is usually clinical based on symptoms or signs after exclusion of mechanical bowel
obstruction
If cannot distinguish ileus from small bowel obstruction→perform computed tomography of the
abdomen and pelvis
Diagnosis
Diagnostic modality Characteristics Radiology
Dilated loops of small
bowel and colon in
patients with
postoperative ileus
Abdominal radiograph
Should demonstrate
air in the colon and
rectum without
transition point
Differentiates
between ileus and
obstruction
CT of abdomen and pelvis
Identies secondary
causes of ileus (such
as a pelvic abscess or
postoperative
bleeding)
(A) Axial abdominal CT image with IV
contrast demonstrates dilated colonic
(arrow) and small bowel loops
(arrowhead). There was no transition
point to suggest mechanical obstruction.
(B) Scout radiograph from the same
patient demonstrates gaseous dilation of
the colon (arrow) and small bowel loops
(arrowhead) without an abrupt transition
point
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