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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5524_Библиотеки_им_академика_М_И_Перельмана.pdf
338 R. T. Stovall
• Multiple conditions are associated with the development of ACPO.
• TMC is the final common pathway of many inflammatory colon disease pro-
cesses.
{ Commonly described as a result of inflammatory bowel disease but other
inflammatory processes also can lead to TMC.
{ Perhaps fulminant Clostridium dificile is one of the more common
infectious etiologies that can cause TMC in the ICU setting.
Main Body
• Clinical Presentation of ACPO
{ Nausea, vomiting and/or pain in the awake patient.
{ Distended abdomen.
{ No stool output or possibly diarrhea.
{ Signs or symptoms of systemic toxicity should raise the suspicion of
another diagnosis.
{ The presence of peritonitis should raise of the suspicion of other diagnosis
or ACPO complicated by perforation.
• Diagnosis of ACPO
{ Need to maintain a high level of clinical suspicion.
{ To be ACPO must rule out mechanical obstruction and toxic mega colon.
{ History and physical exam.
Usually ongoing illness or recent surgery.
“Non-toxic.”
Abdominal distention without signs of peritonitis.
{ Labs
No diagnostic labs.
Assessment of electrolytes and acid base status can be helpful in both
diagnosis and additional supportive measures.
{ Abdominal plain films
Distended colon, specifically the cecum and transverse.
Possibly less distended left colon.
May show free air with perforation.
{ Contrast Enema evaluation
Less used with current generation CT scanners.
Colorectal 339
Can rule out distal obstruction.
In certain cases may have therapeutic benefit.
{ CT Scan of the Abdomen and pelvis
Will show distention of colon without evidence of distal obstruction.
Useful to rule out additional diagnoses such as abscess or perforation.
• Differential Diagnosis of ACPO
{ Large bowel obstruction (e.g. tumor, volvulus, stricture).
{ Toxic mega-colon (e.g. from Inflammatory bowel disease, infectious
etiology).
{ Both of these must be ruled out as ACPO is usually considered a diagnosis
of exclusion.
• Treatment of ACPO
{ Evidence of perforation, ischemia, and/or peritonitis necessitate urgent
surgical intervention.
{ Identify and correct likely underlying precipitating factors.
{ Nothing by mouth (NPO), nasogastric tube decompression, fluid resus-
citation.
{ Consider possible rectal tube or fecal management system.
{ Close monitoring with serial exams, radiographs and laboratory assessments.
{ Correct electrolyte abnormalities.
{ Discontinue narcotic usage as possible and other sedatives or anitcholin-
ergics.
{ Minimize all poly-pharmacy as possible.
{ Prone positioning and alternation of positioning may have benefits in the
more mobile patient.
{ Pharmacologic options (after assuring no distal obstruction or toxic mega-
colon).
First-line therapy often considered to be neostigmine.
Neostigmine — 2 mg IV given over 3–5 minutes with possible repeat
dose.
Ö Cardiovascular monitoring should be used during and following
administration. Atropine should be at the bedside.
Ö Usual response if fairly rapid after administration of drug.
Ö Timing of repeat dose a matter of debate.
Ö Relapse rate of around 15–40%.
Other possible pharmacological options or if neostigmine fails.
340 R. T. Stovall
Ö Repeat neostigmine or neostigmine drip.
Ö Polyethylene glycol has some support in preventing recurrence
after neostigmine has initially been successful.
Ö Pyridostigmine may have promise.
Ö 10 to 30 mg pyridostigmine two times a day.
Ö Increasing interest in peripheral opioid receptor antagonist but
unclear benefit at this time.
Ö Erythromycin, metoclopramide or cisapride have fallen out of
favor for the treatment of ACPO.
{ Endoscopic Therapies
Colonoscopic decompression with or without the placement of a
decompression tube.
Ö Used when there is a failure of pharmacologic intervention.
Ö Usual pre-colonoscopy bowel preparation is not used in ACPO.
Ö Complication rates and mortality rates after colonoscopy for
ACPO are higher than after colonoscopy for other indications.
Ö Initial success rate fairly high, but recurrence requiring repeat
decompression occurs in up to 40% of patients.
Ö Passing scope all the way to cecum not felt to be indicated, only to
hepatic flexure.
Ö Can leave a decompression tube in the transverse colon but not
clear that this improves outcome.
Ö No hard indications for when to attempt colonoscopic decom-
pression.
— Likely no definite size criteria as indication for colonoscopy
but more related to rate of increase in size and duration of
dilation.
— Usually after 9–12 cm consideration for colonoscopic decom-
pression should be entertained.
Colonoscopic decompression with the placement of a cecostomy tube
has been described.
{ Surgical Options
Always indicated for evidence of perforation or ischemia.
May be indicated if diagnosis is not clear.
Outside of these indications, used in extreme circumstances.
Pharmacologic and endoscopic decompression should be entertained
prior to operative intervention.
Colorectal 341
Options include
Ö Cecostomy to the skin.
Ö Cecostomy tube.
Ö Colectomy.
— If performed, usually recommended that end ostomy and
mucous fistula are created and anastomosis avoided.
Ö Laparoscopic or open approaches are described. Depending on the
size of the colon, laparoscopic is made more difficult.
• Clinical Presentation of TMC
{ Affects all ages and sexes.
{ History of IBD common, but can be first presentation.
{ Antecedent diarrhea usually bloody, abdominal pain, cramping, distention.
{ Ongoing resistant colitis may have been present leading up to the devel-
opment of TMC.
{ Patient will appear ‘toxic’
Altered mental status.
Fever, tachycardia, possibly lower blood pressure.
Peritonitis may or may not be present.
Consider ongoing treatments and how they may affect presentation.
• Diagnosis of TMC
{ High index of suspicion.
{ Diagnosis is clinical in the setting of dilated, non-obstructed colon and a
toxic patient.
{ History
May include IBD, chronic diarrhea, acute diarrhea, known infections,
recent travel.
Current and recent therapies should be evaluated — recent antibiotics,
steroids or other immunosuppressant drugs or diseases.
{ Physical Exam
May or may not have peritonitis.
Will have distention, and possible tenderness, abdominal pain.
Fever, tachycardia, hypotension, altered mental status.
{ Labs
Should be drawn as parts of the work-up of the toxic patient, but no
diagnostic lab test, all support the overall picture.
342 R. T. Stovall
Labs will be consistent with an inflammatory picture.
Stool cultures should be sent to work-up the diarrhea for infectious
etiologies (including C. difficile).
Other cultures such as blood and urine should likely also be drawn in
the workup.
{ Radiology
Plain radiographs of the abdomen are crucial early to evaluate colonic
source of abdominal distention.
Ö Colon dilated (dilation > 6 cm).
Ö Usual haustra may be present but are often disturbed.
Ö Small bowel dilation and possible large and small bowel fluid
levels.
Computed Tomography
Ö Can be helpful in assessing the colon and may help rule out
mechanical causes of colonic dilation.
Ö Colon will be thickened, may have “accordion or target signs.”
Ö Pericolonic fat stranding.
Ö May help evaluate other intra-abdominal processes and compli-
cations of mega colon.
Literature is developing on the use of ultrasound to help diagnosis TMC.
{ Endoscopy
May have a limited role in the diagnosis of TMC if diagnosis is
unclear.
Usually felt that full colonoscopy in this setting is high-risk and thus
limited exams only may be indicated.
• Treatment of TMC
{ Multi-disciplinary approach is critical from an early stage.
{ Medical treatment
Depends on the underlying cause (e.g. IBD or C. diff. or CMV).
Includes fluid resuscitation, bowel rest, correction of lab abnor-
malities and treatment of underlying cause.
Minimize any drugs that may decrease colonic activity.
Goals to reduce inflammatory source and prevent complications of
severe colitis and to prevent death.
Early surgical consultation is critical for a multi-disciplinary
approach.
Colorectal 343
Some have advocated patient positioning changes in the more mobile
patient.
{ Surgical treatment
Subtotal colectomy with end ileostomy is preferred when surgery
indicated.
Ö Some lavage and diversion procedures for C. difficile have been
advocated and are situation dependent (See section on treatment of
C. difficile).
Earlier surgery (especially prior to perforation) has been shown to
decrease mortality.
The decision for when to proceed to surgery is very challenging and
the overall status of the patient must be considered as must the underlying diagnosis and underlying comorbidities of the patient.
Practical Algorithm(s) / Diagrams
Fig.1. Suspected TMC.
344 R. T. Stovall
Fig.2. Suspected ACPO.
Review of Current Literature with References
• Jain A, MD, Vargas, D. Advances and challenges in the management of acute
colonic pseudo-obstruction (ogilvie syndrome). Clin Colon Rectal Surg 2012;
25: 37–45.
{ Overview of Ogilvie’s syndrome, pathophysiology, diagnosis and treatment.
• Autenrieth DM, Baumgart DC. Toxic mega colon. Inflamm Bowel Dis 2012;
18: 584–591.
{ Recent review of TMC.
Chapter 8-(vi)
Abdominal Compartment Syndrome
Clay Cothren Burlew, MD*
*Director of Surgical Intensive Care Unit, Denver Health Medical Center,
Professor of Surgery, University of Colorado School of Medicine
Take Home Points
• Abdominal compartment syndrome (ACS) is defined as the combination of
intraabdominal hypertension (IAH) with end organ dysfunction.
• Clinical indices of end-organ derangement such as decreased urine output,
increased pulmonary pressures, decreased preload, cardiac dysfunction, and
elevated intracranial pressure are fundamental to the identification of ACS.
• ACS is typified by IAH due to either intraabdominal injury (primary) or fol-
lowing massive resuscitation (secondary).
• Increasing abdominal pressure may develop before, during or after surgery,
typically within the first 24–48 hours after injury.
• Physical examination cannot definitively diagnose IAH or its severity; a diag-
nosis of IAH can be obtained by measuring the patient’s bladder pressure.
Contact information: Department of Surgery, Denver Health Medical Center, 777 Bannock Street, MC 0206, Denver, CO 80204; Tel.: 303-436-6558, Fax: 303-436-6572, email:
clay.cothren@dhha.org
345
346 C. C. Burlew
• With the recognition that ACS is a late event in the evolution of IAH, monitor-
ing at-risk patients is advocated; this permits intervention in patients with
IAH in an attempt to prevent the sequelae of ACS.
• Trauma patients that develop the “bloody vicious cycle” of hypothermia,
acidosis, and coagulopathy are particularly susceptible to ACS and damage
control operative technique should be considered.
• Once a patient is diagnosed with ACS, emergent decompression is indicated;
this is typically accomplished via a midline laparotomy incision with evisceration of the bowel and egress of the accumulated peritoneal fluid or blood.
• Patients with marked intraperitoneal fluid as the primary component of their
ACS may be effectively decompressed via a percutaneous drain placed using
bedside ultrasound.
Background
• In the late 1800’s, physicians identified the entity of increased abdominal
pressure, and recognized that this increase in abdominal pressure could have
systemic effects.
• The impact of intraabdominal pressure was largely ignored until the 1940s
when Dr. Gross and his colleagues recognized that early forced closure of
omphalocele defects, with reduction of the abdominal contents under extreme
pressure, would lead to an infant’s cardiovascular collapse.
• Despite this recognition, 35 additional years lapsed before the concept of
intraabdominal hypertension (IAH) and its associated end-organ sequelae
were discussed in the literature again with regularity.
• Kron et al. made the significant clinical contribution, that abdominal pressure,
itself, could be used to determine need for abdominal decompression, and that
this intervention could be lifesaving.
• Although Kron et al. are often credited with coining the term abdominal com-
partment syndrome (ACS), the first report of this term in the literature was not
until five years later.
• The original description of ACS was in four patients who had undergone
ruptured abdominal aortic aneurysm repair; postoperatively, when the
patients’ abdominal distension, increased airway pressures, increased central
venous pressure, and oliguria, the surgeons reopened the patients’ abdomen
with resolution of the end-organ derangements.
Abdominal Compartment Syndrome 347
Main Body
• Etiology and physiology
{ The etiology of ACS is multifactorial, typified by IAH due to either
intraabdominal injury (primary) or following massive resuscitation (secondary).
{ The most common scenario for ACS is the multiply injured trauma patient
who requires a large volume resuscitation, including both crystalloid and
blood products; IAH in these patients is due to resuscitation-associated
bowel edema, retroperitoneal edema, and large quantities of ascitic fluid
combined with any associated intraabdominal pathology.
{ Increased abdominal pressure affects the cardiovascular system (decreased
venous return to the right heart, decreased preload, decreased cardiac
output, increased systemic vascular resistance, diminished stroke volume,
decreased hepatic and intestinal perfusion), the pulmonary system (cephalad displacement of the diaphragm, increased intrathoracic pressures,
decreased thoracic compliance, elevated airway pressures, hypoxemia),
the renal system (relative obstruction to renal venous drainage, increased
renal vascular resistance, decreased urine output), and the central nervous
system (increased intracranial pressures) (Fig. 1).
• Diagnosis
{ Evidence of end-organ derangement such as decreased urine output,
increased pulmonary pressures, decreased preload, cardiac dysfunction,
and elevated intracranial pressure should herald the development of ACS.
{ With a multitude of etiologies that could cause a patient to have low urine
output and cardiopulmonary woes, screening at-risk patients for IAH is
paramount.
{ Patients identified to be at risk for IAH include those who have received
10 units of packed red cells or 10 L of crystalloid.
{ Physical examination cannot definitively diagnose IAH or its severity, as
the patient’s exam maybe reliable only about 40% of the time.
{ A diagnosis of IAH is typically obtained by measuring the patient’s blad-
der pressure.
The bladder acts as a passive reservoir, hence transmitting intraab-
dominal pressure without imparting any additional pressure from its
own musculature.