Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_785_Библиотеки_им_академика_М_И_Перельмана
.pdf
40 The Abdominal Compartment Syndrome 437
CVP + wedge pressure
Thoracic + airway
pressures
Respiratory failure
Venous return
Venous stasis
Urinary output
Cardiac output
Craniospinal
pressure
Fig. 40.1. The abdominal compartment syndrome
Because the Trendelenburg position (or its reverse) may affect intrabladder pressure, accurate measurements are best achieved in the supine position.
mal, but hepatic arterial blood flow falls significantly; an IAP of 15 mmHg produces adverse, but spontaneously correctable, cardiovascular changes; an IAP of
20 mmHg may cause renal dysfunction and oliguria, and an increase to 40 mmHg
induces anuria. In an individual patient, the effects of increased IAP are not isolated but usually superimposed on multiple underlying and coexistent factors, the
most notable being hypovolemia, which aggravates the effects of increased IAP.
(> Fig. 40.2). Any increase in the volume of any of the contents of the abdomen
or the retroperitoneum elevates IAP. Clinically significant elevation of IAP has
been observed in a variety of contexts (> Table 40.2), such as postoperative intra-
abdominal hemorrhage; after complicated abdominal vascular procedures or major operations like hepatic transplantation; in association with severe abdominal
Deleterious Consequences of Raised IAP Appear Gradually
At pressures less than 10 mmHg, cardiac output and blood pressure are nor-
Why Didn’t We Notice IAHT and ACS Before?
Because you—or your mentors—did not know that this entity exists!
438 Moshe Schein
Fig. 40.2. “What? Abdominal compartment syndrome? Never heard of it!”
Table 40.2. Etiology of increased intra-abdominal pressure
Condition Etiology
ACUTE
Spontaneous Peritonitis, intra-abdominal abscess, ileus, intestinal
Postoperative Postoperative peritonitis, paralytic ileus, acute gastric
Post-traumatic Intra-/retroperitoneal bleeding, postresuscitation visceral
Iatrogenic Laparoscopic procedures, pneumatic antishock garment,
CHRONIC Ascites, large abdominal tumor, chronic ambulatory
The list cannot be considered “complete” as any increase, of any etiology, in the volume of the
intra- or retroperitoneal space will increase intra-abdominal pressure
obstruction, ruptured abdominal aortic aneurysm, tension
pneumoperitoneum, acute pancreatitis, mesenteric venous
thrombosis, fecal impaction
dilatation, intraperitoneal hemorrhage
edema
abdominal packing, reduction of a massive parietal or
diaphragmatic hernia, abdominal closure under excessive
tension
peritoneal dialysis, pregnancy, morbid obesity
trauma accompanied by visceral swelling, hematoma, or the use of abdominal
packs; severe peritonitis; necrotizing pancreatitis; the use of the pneumatic antishock garment; tense ascites in cirrhotic patients; or even extreme distension of
40 The Abdominal Compartment Syndrome 439
the colon (e.g., colonic pseudo-obstruction). Peritoneal insufflation during laparoscopic procedures is currently the most common (iatrogenic) cause of IAHT.
Note that severe intestinal edema causing IAHT has been described following
massive fluid resuscitation for extra-abdominal trauma. The combination of se-
vere abdominal wall burns (producing a tight-constricting eschar) and fluid resuscitation causing visceral edema could lead to ACS in the burned patient.
Be aware that morbid obesity (> Chap. 31) and pregnancy (> Chap. 33) are
“chronic” forms of I AHT; various manifestations associated with such conditions (e.g.,
hypertension, pre-eclampsia) are attributed to IAHT. Note that anything can cause
IAHT and ACS—irrespective of the ingredients used in the “stuffing” or its flavor.
The stuffing can even be composed of feces (definitely not recommended in turkeys).
An elderly lady presented with poor peripher al perf usion, blood pre ssure of 70/40, a nd
re spi ra tor y ra te o f 36 /mi n. Her abd ome n wa s ve ry di ste nde d and di ff usel y te nde r w ith g ua rding. Rectal examination revealed a large amount of soft impacted feces. Blood urea nitrogen
(BUN) and creatinine levels were 30 mg% and 2 mg%, respectively. Arterial blood gases
showed a metabolic acidosis with pH 7.1. Her IAP was 25 cmH
hugely distended rectosigmoid. She survived following a decompressive laparotomy and resection of the partially ischemic and massive rectosigmoid (
can cause ACS.
O. Abdominal X-ray showed a
2
>
Fig. 40.3). So , yo u se e: e ven s **t
Fig. 40.3. Abdominal X-ray showing a massively dilated rectosigmoid and the corresponding findings at operation
440 Moshe Schein
Only a few years ago, we would have described this patient as suffering
from “septic shock” due to “colonic ischemia.” We would have attributed the
cardiovascular collapse and acidosis to the consequences of endotoxemic sepsis.
But today, it is clear to us that the mass effect created by the extreme dilatation
of the rectum produced severe IAHT, causing cardiovascular and respiratory
collapse and renal dysfunction—representing a typical ACS. This further decreased splanchnic perfusion, thus aggravating colorectal ischemia. Rectal disimpaction and abdominal decompression rapidly reversed the adverse
physiological manifestations of the intra-abdominal hypertension. Being more
aware that IAHT is a “real problem” and liberally measuring IAP, we are recognizing it with increasing frequency in our daily clinical practice.
The Mechanisms Culminating in ACS Are Usually Multiple
The typical scenario of ACS occurs in a multiple-trauma or post- emergency
laparotomy patient who receives a large volume of fluid for resuscitation,
causing an increase in interstitial fluid volume. The ensuing visceral and retroperitoneal edema is aggravated by shock-induced visceral ischemia and reperfusion edema as well as by temporary mesenteric venous obstruction caused by
surgical manipulation or the employment of hemostatic packs. The edematous
abdominal wall is closed over the bulging abdominal contents under extreme
tension.
The Clinical Syndrome
The clinical syndrome of ACS consists of:
Increased airway pressure
Decreased cardiac output
Decreased urinary output
Abdominal distension
These abnormalities are often present despite apparently normal cardiac
filling pressures because transmission of increased IAP to the thorax elevates
central venous pressure (CVP), right atrial pressure, and pulmonary capillary
wedge pressure. Cardiovascular, respiratory, and renal dysfunction become progressively difficult to manage unless IAP is reduced. Rarer consequences of ACS
have been described, such as intestinal ischemia following laparoscopic cholecystectomy or spinal cord infarction in the setting of IAHT following perforation
of a gastric ulcer.
40 The Abdominal Compartment Syndrome 441
When Should You Consider Abdominal Decompression?
The decision to decompress the abdomen should not be taken based on isolated measurements of IAP without taking into account the whole clinical picture.
Early or mild physiological abnormalities caused by IAHT can be managed by
fluid administration or afterload reduction. (Note, however, that increasing cardiac
filling offers only a temporary solution, and that fluid administration may in fact
increase tissue edema and thus aggravate IAHT.) In patients receiving mechanical
ventilation, muscle paralysis may decrease IAP by relaxing the abdominal wall.
Established ACS, however, mandates an emergency decompressive laparotomy, which, when performed in the well-resuscitated patient, should promptly
restore normal physiology. To prevent hemodynamic decompensation during the
laparotomy, intravascular volume should be restored, oxygen delivery maximized,
and hypothermia and coagulation defects corrected. Following decompression,
the abdominal skin and fascial edges are left open using one of the temporary
abdominal closure devices (TACD) described in > Chap. 52.2.
Prevention
To avoid IAHT and ACS, forceful closure of the abdomen in patients having
massive retroperitoneal hematoma, visceral edema, severe intra-abdominal infection, or a need for hemostatic packing should be avoided (> Chap. 43). Leaving the
fascia open, closing only the skin with sutures to protect the bulging viscera, is a
good option! Occasionally, however, the skin closure alone may produce IAP of 50
mmHg or more. Certainly, leaving both fascia and skin unsutured offers maximal
reduction in IAP but may result in fistula and evisceration. Bridging the fascial gap
with a TACD circumvents most these problems (> Chaps. 43, 52, and 53).
Would Decompression Benefit Patients with Only Moderate IAHT?
That the “extreme” case of ACS as described necessitates an urgent abdominal
decompression is obvious. But, what about a less-extreme case? Would decompression benefit a postoperative patient in whom the moderately increased IAP of 20
mmHg is compensated by appropriate fluid and ventilatory therapy? We believe
that the available evidence suggests that the detrimental effects of IAHT take place
long before the manifestations of ACS become clinically evident—just as nerve and
muscle ischemia begins long before neuromuscular signs of the extremity compartment syndrome are evident. IAHT may cause gut mucosal acidosis at relatively
low pressures long before the onset of clinical ACS. Uncorrected, it may lead to
442 Moshe Schein
splanchnic hypoperfusion, distant organ failure, and death. Prophylactic nonclosure
of the abdomen may facilitate prevention of IAHT and reduce these complications.
It seems sensible therefore that if postoperative IAHT seems likely, then delayed
abdominal closure should be considered. It appears that “borderline” IAHT contributes to the overall morbidity, but in patients in whom the abdomen has already
been closed, the risk-benefit ratio of abdominal decompression is not yet clear.
Conclusion
Intra-abdominal hypertension is yet another factor to consider in the overall
management of the patient needing emergency abdominal care. It may be obvious—“crying” for abdominal decompression. More commonly, however, it is relatively silent but contributing to your patient’s SIRS (systemic inflammatory
response syndrome), organ dysfunction, and death. So, now you know better; you
know that your patient is not a “dead turkey to be stuffed.” Bon appetit!
Be as aware of intra-abdominal hypertension as you are of arterial hypertension.
It is much more common and clinically relevant than you have suspected.
[We asked Dr. Sugrue, who is a leading international authority on ACS, to
comment.—The Editors]
Invited Commentary
Michael Sugrue
The World Society of the Abdominal Compartment Syndrome (www.wsacs.
org) defines ACS as sustained IAP >20 mmHg (with or without an abdominal
perfusion pressure [APP] <60 mmHg) that is associated with new organ dysfunction or failure (Malbrain et al. 2006) and occurs in between 5% and 8% of intensive
care patients. Not all hospitals have sophisticated transducers and monitoring
equipment to measure IAP, so simple bedside monitoring can be undertaken;
however, the more reliable gold standard is the modified Kron technique of instilling 25 ml into the urinary bladder, which is connected via a T piece and pressure
transducer to the bedside monitor. Alternatively, commercial devices are available;
simple ones are the Holtec or the Advisor. Alternatively, continuous IAP measurement can be undertaken using a three-way Foley catheter.
Recognition of ACS is increasing, although many units do not routinely
measure IAP. This is now changing with the introduction of guidelines and
40 The Abdominal Compartment Syndrome 443
recommendations (Cheatham et al. 2007). The formation of the World Society of
the Abdominal Compartment Syndrome and the success of the four initial world
congresses will ensure greater worldwide awareness of ACS. The prevention of ACS is
increasingly coming to the fore with greater emphasis on hemorrhage control rather
than over zealous resuscitation—thus avoiding massive visceral and abdominal wall
edema causing IAHT. Some units are reporting a reduction in secondary ACS due
to fluid overload. And, prophylactic abdominal decompression remains a popular
preventive option among trauma surgeons in particular (Ivatury et al. 1998).
The key to the management of both medical and surgical patients with impending ACS is treating the underlying cause, be it intra-abdominal hemorrhage
or sepsis. Alternative techniques such as negative pressure and prone ventilation
are unproven. In a significant number of patients, however, percutaneous drainage of intraperitoneal fluid has a role to play. Newer techniques (e.g., laparoscopic
decompression of the fascia and linea alba [laparoscopic abdominal fasciotomy])
are being tried.
One of the greatest challenges, however, is managing the open abdomen.
Early closure will reduce complications, particularly fistula. Currently, vacuumassisted dressings offer the most manageable option for the open abdomen.
There is increasing use of dynamic closure systems to apply “gradual” tension,
which prevents further divarication of muscle mass (see > Chap. 52.2).
In conclusion, the keys are prevention through timely hemorrhage control,
excellence in elective and emergency abdominal surgery, and consideration for
prophylactic decompression, particularly in trauma, aortic, and pancreatic patients. We must recognize the need for IAP monitoring as an adjunct to the diag-
nosis of ACS: no IAP, no ACS. The future will enlighten us further and provide
greater understanding into the side effects of intra-abdominal hypertension
since it was first described in 1865.
1
References
Cheatham ML, Malbrain ML, Kirkpatrick A, et al. (2007). Results from the international
conference of experts on intra-abdominal hypertension and abdominal compartment
syndrome. II. Recommendations. Intensive Care Med 33:951–962.
Ivatury RR, Porter JM, Simon RJ, Islam S, John R, Stahl WM. (1998). Intra-abdominal hyper-
tension after life-threatening penetrating abdominal trauma: prophylaxis, incidence,
and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J
Trauma 44:1016–1021.
Malbrain ML, Cheatham ML, Kirkpatrick A, et al. (2006). Results from the international
conference of experts on intra-abdominal hypertension and abdominal compartment
syndrome. I. Definitions. Intensive Care Med 32:1722–1732.
1
For information about the history of abdominal compartment syndrome, access http://www.
docschein.com/Compartment.html.
Abdominal Aortic Emergencies
Paul N. Rogers
Abdominal/back pain and hypotension = a ruptured AAA unless proven otherwise.
Urological and orthopedic wards are a cemetery for ruptured AAA cases.
Presentation
The diagnosis of a leaking abdominal aortic aneurysm (AAA) is usually
not difficult to make. Typically, the patient presents with a sudden onset of acute
lumbar backache, abdominal pain, and collapse associated with hypotension.
On examination, the presence of a pulsatile abdominal mass confirms the diagnosis. In this situation, the patient proceeds directly to the operating room with
a delay only to allow cross-matched blood to become available if the patient is
stable.
Atypical Presentation
41
Not infrequently, however, the diagnosis can be difficult to make. There may
be no history of collapse, and the patient may be normotensive on admission. The
only clue may be nonspecific back or abdominal pain. A pulsatile mass may not be
palpable. Ruptured AAA patients are frequently obese; thinner patients tend to
notice their AAA and present early for an elective repair. A leaking AAA may be
mislabeled as “ureteric colic,” but the absence of microscopic hematuria should
alert one to the possibility that a leaking aneurysm is responsible for the symptoms. A high index of suspicion is important to prevent the diagnosis of a leaking
AAA being overlooked. In appropriate individuals, particularly men in latemiddle and old age, if significant and unexplained abdominal or back pain causes
the patient to present acutely, abdominal aneurysms should be excluded by means
of ultrasound or computed tomography (CT).
Paul N. Rogers
Department of Surgery, Gartnaval General Hospita l, Glasgow, Scotland, UK
M. Schein et al. (eds.), Schein’s Common Sense Emergency Abdominal Surger y,
DOI: 10.1007/978-3-540-74821-2_41, © Springer-Verlag Berlin Heidelberg 2010
445
446 Paul N. Rogers
The Diagnostic Dilemma
A different diagnostic dilemma occurs in the patient who is known to
have an aneurysm and who presents with abdominal or back pain, which may
or may not be related to the aneurysm. The difficulty here is that a small, contained, “herald” leak from an aneurysm might produce pain without any hemodynamic instability. Examination in these patients may be unhelpful in that the
aneurysm may not be tender. These patients are at high risk of a further bleed
from the aneurysm, and this could be sudden and catastrophic. For this reason,
it is important that they are identified appropriately and have an operation before a major, possibly fatal, hemorrhage occurs. The difficulty, of course, is that
such a patient might easily have another cause for the symptoms, mechanical
backache for example, that is unrelated to the aneurysm. Here, an operation is
clearly not in the patient’s best interests, particularly if his or her general health
is poor. This dilemma, of operating without delay in patients who require it yet
avoiding operation in those in whom it is not necessary, is a difficult one, sometimes even for experienced clinicians, to resolve. An emergency CT scan is in-
dicated in this situation to delineate the AAA and presence of any associated
leak, usually into the retroperitoneum. In general, however, in this situation it
is safer to err on the side of operating on too many rather than too few
patients.
Who Should Have an Operation?
A useful rule of thumb regarding who should have an operation is that the
chances of survival in a patient with a ruptured AAA are directly proportional to
the blood pressure on admission. Profoundly shocked patients rarely survive; sure,
they may survive the operation but usually do not leave hospital through the front
door. Consequently, it has been proposed that operating on shocked ruptured
AAA patients is futile and a waste of resources. Another view is that you should
proceed with the operation unless the patient is clearly “agonal” or known to suffer
from an incurable disease. You may be able to save the occasional patient and gain
additional experience, which may help you to save the next rupture patient. These
issues of philosophy of care are for the individual surgeon to resolve with his or
her God, patients, and their families. A scoring system has been devised that aims
to help with this decision making. The so-called Hardman criteria relate the presence of several easily determined variables to the likelihood of survival from surgery from a ruptured aneurysm.
41 Abdominal Aortic Emergencies 447
The Hardman Criteria (Hardman et al. 1996)
Age >76 ✓
History of unconsciousness ✓
Hemoglobin <9.0 g/dl ✓
Creatinine >190 ✓ mmol/l
Electrocardiographic evidence of ischemia ✓
If three or more criteria are present, the mortality is 100%.
If two are present, mortality is 72%.
If one, mortality is 37%.
Perhaps not surprisingly, since these criteria were published other workers
have demonstrated that it is possible to operate successfully on patients with three
Hardman criteria (confirming the rule of “never say never”). Nevertheless, the
criteria are a useful adjunct to the decision-making process in these patients.
The Operation
Once the diagnosis of aortic rupture has been established or strongly suspected, the patient should be rushed to the operating theater without delay. Do not
even bother with additional lines and intravenous fluids as what you pour in will
pour out, and increasing the blood pressure will only increase the bleeding. Aim
for stable hypotension in resuscitation.
Preparation “Prep and drape” (including the groins in case aorto-femoral
bypass is necessary) for surgery while the anesthetic team establishes the appropriate monitoring lines. Do not allow them, however, to waste time by inserting
unnecessary gimmicks such as the pulmonary arterial catheter. Anesthesia
should not be induced until you are ready to make the skin incision; not infrequently, the administration of muscle relaxants at induction, and the subsequent
relaxation of the abdominal wall, is sufficient to permit a further bleed from the
aneurysm with an immediate hemodynamic collapse. Remember: your clamp on
the aorta proximal to the aneurysm is more important than anything else.
Incision Open the abdomen through a long midline incision extending
from the xiphisternum to a point midway between the umbilicus and the symphysis pubis. Occasionally, if the distal iliac arteries are to be approached, the
Соседние файлы в папке Библиотека им академика М.И. Перельмана