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52 Moshe Schein · Sai Sajja · Hans Ulrich Elben
Fig. 5.20. Abdominal CT: perforation of a Meckel’s diverticulum. Note the central
structure, which lacks luminal contrast and is surrounded by tissue reaction
Fig. 5.21. Abdominal CT: acute sigmoid diverticulitis. Note the thickened loop of
sigmoid with almost absent lumen and the tissue stranding around it, denoting
inflammation
Free Fluid
Watch for free fluid between the intestinal loops and elsewhere. The fluid
density gives a clue to its nature: for ascites, it is like water, 0–20 HU; for pus, it is
between 15 and 30 HU; and for blood, it is about 50 HU, but be aware that these
specifications do not always allow an exact differentiation.
5 Abdominal Imaging 53
Fig. 5.22. Abdominal CT. Appendagatis: acute inflammation of the appendix epiploica
of the sigmoid colon. See the inflammatory process compressing the lumen of the colon
An abscess shows an annular enhancement, and gas inclusions inside will
prove it. Diffuse peritonitis is not easy to diagnose, but helpful signs include fluid
collections between intestinal loops and in the pouch of Douglas and a thickened
base of the small bowel mesentery.
Retroperitoneum, Big Vessels, and Abdominal Wall
Watch the lumen of the aorta and the pelvic vessels to find a ruptured aneu-
>
rysm (
Fig. 5.23). Look for free gas or a collection suggesting an abscess due to
retroperitoneal perforation of a viscus such as the colon or duodenum.
Looking at the abdominal wall, try to find pathological changes like subcutaneous abscesses, rectus sheath hematomas, or abdominal wall hernias (> F ig . 5.24).
And be nice to your radiologists … they can be your best friends.
Final Words
Moshe Schein
Unfortunately or fortunately—depending on one’s viewpoint—in the United
States, where I practice, the decision about whom and when to scan is no longer in
our surgical hands. The fact of the matter is that most (if not all) patients have
already undergone a CT scan before surgeons are called on to assess them. Typically,
such scans are ordered by ER physicians or other specialists before consulting the
54 Moshe Schein · Sai Sajja · Hans Ulrich Elben
Fig. 5.23. Abdominal CT: leaking abdominal aortic aneurysm. See the aortic aneu-
rysm and large retroperitoneal hematoma on the left
Fig. 5.24. Abdominal CT: incisional hernia. Note a loop of small bowel incarcer-
ated within an incisional abdominal wall defect
surgeon. In most hospitals in the United States, even the tiny rural ones, high-tech
CT images are much easier to obtain than a gourmet meal or even a cup of real
coffee. And, radiologists are always readily available to interpret the images online.
No wonder then that physicians confronted with the acute abdomen feel compelled to get a CT, which is as easily procured as junk food. Is this practice of (almost) routine CT scanning, imposed on us by others and impossible for us to
modify or reverse, “good” or “bad” for our patients? It is very difficult, if not impossible, to prove scientifically that this increased use of CT scanning is beneficial
overall. But, what about the individual patient?
5 Abdominal Imaging 55
Luckily, gone are the days when the acute abdomen represented a totally
black box—days I remember well from my training—when peritoneal signs on
examination mandated a laparotomy, which often proved to be “negative” or
“nontherapeutic” and therefore unnecessary. The gradual introduction of CT
imaging (and ultrasound) has made that abdominal black box much more penetrable and less mysterious. In the individual patient, it helps us to be more selective and more conservative; helps us to decide when not to operate, when to
choose alternative modalities (e.g., percutaneous drainage); and guides us to the
choice of incision. Equally important—for those of us who take emergency
calls—CT lets us sleep better and longer at night.
So, from the individual patient’s and surgeon’s perspective, I believe that
liberal use of abdominal CT in the setting of the acute abdomen reflects a positive
trend, with two caveats: First, we have to try to prevent repeated exposures to CT
radiation, particularly in younger patients; most importantly, an experienced
abdominal surgeon must be the one interpreting the CT images (together with
the radiologist) and deciding how to proceed. An abdominal image without an
abdominal surgeon is only an image, but together, the surgeon and the CT, they
represent the best modern surgical judgment—the human one supplemented
and made more accurate.
Optimizing the Patient
James C. Rucinski
When physiology is disrupted, attempts at restoring anatomy are futile.
The preparation of the patient for surgery may be as crucial as the operation itself.
It’s 4 a.m., and you assess your patient as having an “acute abdomen”—
probably due to a perforated viscus. Clearly, your patient needs an emergency
laparotomy; what is left to decide is what efforts, and how much time, should be
invested in the patient’s optimization before the operation.
Optimization is a double-edged sword: wasting time trying to “stabilize”
an exsanguinating patient is an exercise in futility for the patient will die.
Conversely, rushing to surgery with a hypovolemic patient suffering from intestinal obstruction is a recipe for disaster.
The issues to be discussed here are:
Why preoperative optimization at all?
What are the goals of optimization?
Who needs optimization?
How to do it?
6
Why Is Preoperative Optimization Necessary?
Simply, preoperative optimization is necessary because volume-depleted
patients do not tolerate anesthesia and operation. The induction of general anesthesia and muscle relaxation causes systemic vasodilatation, depressing the compensatory antishock physiologic mechanisms. On opening the abdomen,
intraperitoneal pressure suddenly declines, allowing pooling of blood in the venous system, which in turn decreases venous return and thus depresses cardiac
output. An emergency laparotomy in an underresuscitated patient may result in
cardiac arrest even before the operation is started. In addition, the intraoperative fluid requirements are unpredictable: Do you want to start with a volumedepleted patient, having to chase your tail?
James C. Rucinski
New York Methodist Hospita l, Brooklyn, NY, USA
M. Schein et al. (eds.), Schein’s Common Sense Emergency Abdominal Surger y,
DOI: 10.1007/978-3-540-74821-2_6, © Springer-Verlag Berlin Heidelberg 2010
57
58 James C. Rucinski
What Are the Goals of Optimization?
Patients awaiting an emergency laparotomy need optimization for two
main reasons: hypovolemia or “sepsis.” Both conditions cause underperfusion of
the tissues and both are treated initially with volume expansion. The chief goal
of preoperative optimization is to improve the delivery of oxygen to the cells.
There is a direct relationship between cellular hypoxia and subsequent cellular
dysfunction, systemic inflammatory response syndrome (SIRS), organ failure,
and adverse outcome (> Chap. 54).
In sick surgical patients, unlike the medical ones, optimization means volume
and more volume—a lot of fluids. (This is, however, not true in actively bleeding
patients; here, optimization means immediate control of the hemorrhage, and
until this is achieved you should restrict fluids and keep the patient moderately
hypotensive.)
Who Needs Optimization?
Surgical patients often “look” sick. The appearance of the patient usually
gives an important first impression even before factoring in tachycardia, tachypnea, hypotension, mental confusion, and poor peripheral perfusion.
Only basic laboratory studies are necessary. Hemoconcentration, reflected in
an abnormally high hemoglobin and hematocrit, implies either severe dehydration
or extracellular “third-space” fluid sequestration. Ur ine ana lys is with a high specific
gravity (>1.039) provides similar information. Electrolyte imbalance and associated
prerenal azotemia (with a >20:1 ratio of BUN [blood urea nitrogen] to creatinine),
again imply volume depletion. Arterial blood gas measurement gives critical information regarding respiratory function and tissue perfusion. Note that in the emer-
gency surgical patient metabolic acidosis almost always means lactic
acidosis—associated with inadequate tissue oxygenation and anaerobic metabolism
at the cellular level. Other causes of metabolic acidosis such as renal failure, diabetic
ketoacidosis, or toxic poisoning are possible but extremely unlikely. A base deficit of
more than 6 (base excess [BE] less than −6) is a marker of significant metabolic acidosis and adverse prognosis and indicates a need for aggressive resuscitation.
All patients with any degree of these physiological abnormalities need
optimization. Naturally, the magnitude of your efforts should correlate with the
severity of the disturbances.
Measurement of the Severity of Illness
An experienced surgeon can “eyeball” his or her patient and estimate how
sick the patient is by assessing “the glare in his eye and the strength of the grip.”
6 Optimizing the Patient 59
Fig. 6.1. APACHE II (Acute Physiological and Chronic Health Evaluation II)
60 James C. Rucinski
Fig. 6.2. Eventual morbidity and mortality in emergency abdominal surgery
But, terms such as “very sick,” “critically ill,” or “moribund” mean different things
to different people. We recommend therefore that you become familiar with a universal physiological scoring system that gives an objective measure of “sickness.”
One scoring system, which has been validated in most emergency surgical situations, is the APACHE II (Acute Physiological and Chronic Health Evaluation II) (>
Fig. 6.1). It measures the physiological consequences of acute disease while taking
into consideration the patient’s premorbid state and age. The scores are easily
measured from readily available basic clinical and laboratory variables and correlate with a prediction of morbidity and mortality (> Fig. 6.2). A score of 10 or
below represents a relatively mild disease; a score above 20 signals a critical illness.
Instead of telling your chief resident that this patient is “really sick,” you would say
“his APACHE II is 29.” Now, it is clear to everyone involved that the patient is
moribund. [Next everyone will ask you: “What the **** is APACHE? A horse?” So
now you will have the chance to teach them and appear smart! —The Editors]
How to Do It? (> Fig. 6.3)
Principles of optimization: air goes in and out; blood goes round and round;
oxygen is good.
Despite the high-tech intensive care unit (ICU) environment, which may or
may not be available to you, optimization of the surgical patient is simple. It can
6 Optimizing the Patient 61
Fig. 6.3. “Let me optimize you…”
be accomplished anywhere and requires minimal facilities. All you want is better
oxygen delivery, that is, increased oxygenation of arterial blood and enhanced tissue perfusion. You do not need a five-star ICU, but you do have to stick around
with the patient. Writing orders and going to bed (until the operation) will unnecessarily prolong the optimization and delay the operation. So, stay with the
patients, monitor their progress, and be there to decide when enough is enough.
Oxygenation
Hypoxia not only stops the motor, it wrecks the engine.
Any patient who requires optimization should at least receive oxygen by
mask. Look at the patient and the patient’s pulse oximetry or arterial blood gases;
evidence of severe hypoventilation or poor oxygenation may be an indication for
endotracheal intubation and mechanical ventilation. Do not temporize; the patient
will need intubation anyway, so why not now? Remember, pain and distension
associated with any abdominal catastrophe impede ventilation. Effective analgesia
impairs ventilation still further. If a nasogastric (NG) tube is not already in situ,
this may be the time to insert one. The advantage of NG tube insertion before
intubation is to decompress the distended stomach and reduce the risk of aspiration during the procedure. The disadvantage is that the presence of a tube through
the cricopharyngeus may allow regurgitation during rapid sequence induction of
anesthesia.
62 James C. Rucinski
Restoration of Volume
The major cause of shock is decreased circulatory volume. Replace body fluids by
the best means at hand. (Alfred Blalock, 1899–1964)
Now, after your patient is well oxygenated you must see to it that the oxygen
arrives where it is needed by restoring blood volume. This is accomplished by intravenous infusion of crystalloids such as normal saline or Ringer’s lactate. Forget
about the much more expensive colloids such as fresh frozen plasma, albumin, or
solutions containing synthetic organic macromolecules such as Hemastarch or
low molecular weight dextran; their theoretical advantages have never been translated to better results. Hypertonic saline resuscitation may theoretically be advantageous, but it remains an investigational therapy at present. [It has been
experimental since we finished medical school! —The Editors] Blood and blood
products are given if necessary as discussed below.
How much crystalloid to infuse? An old rule of thumb was that the hypov-
olemic surgical patient needs more volume than you think he or she needs and
much more than the nursing staff thinks he or she needs. [But, this rule seems to
be outdated; see “editorial comment” below.] We assume that your patient
already has a large-bore intravenous catheter in situ, so just hook it up to the
solution, open the valve, and let it run. You run in a liter and hang up another.
But, how much is enough? At this stage, you need to assess the effectiveness of
what you do.
Measurement of Effectiveness of Treatment
The principal goal of nonoperative treatment in the emergency surgical
patient is the restoration of adequate tissue oxygenation. This endpoint is recognized by physical examination and measurement of urinary output in conjunction with the information provided by selective invasive monitoring and
laboratory studies.
With fluid resuscitation, one hopes to see improvement of tissue oxygenation
by normalization of vital signs and improvement in the visible peripheral circulation. Resolution of hypotension, mental confusion, tachypnea, and tachycardia
may be seen either partially or fully. Postural hypotension reflects a significant def-
icit in the circulating blood volume. Remember that the usual response to a change
in position from supine to upright is an increase in the systolic blood pressure, a
widening of the pulse pressure. Consequently, if a narrowing of the pulse pressure
is seen when the patient sits up, then postural hypotension is present. With fluid
resuscitation, mottling of the skin and the palpable temperature of the fingers and
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