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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5524_Библиотеки_им_академика_М_И_Перельмана.pdf
348 C. C. Burlew
The technique as described by Kron et al. involves the installation of
25 cc of saline into the bladder via the aspiration port of a 3-way Foley
catheter with the drainage tube clamped; after waiting for 30–60 seconds to allow the detrusor musculature to relax, pressure measurement
with a manometer at the pubic symphysis is performed.
Although the manometer technique is a single measurement in time,
continuous monitoring is also an option.
There are several conditions in which the bladder pressure may not be
reflective of the intraabdominal pressure: external compression on the
bladder due to pelvic packs, bladder rupture, marked adhesive disease,
or neurogenic bladder.
{ A grading system based on bladder pressure measurements was devel-
oped to aid in the diagnosis and subsequent treatment of ACS (Fig. 2).
{ Abdominal perfusion pressure, defined as the mean arterial pressure
minus the intraabdominal pressure, has also been advocated to diagnose
IAH and ACS; to date, this has not been widely adopted in clinical
practice.
• Treatment
{ There is not a single IAH pressure that mandates intervention; organ fail-
ure can occur over a wide range of recorded bladder pressures.
{ If the patient has ACS, however, emergent decompression is indicated;
mortality is directly affected by decompression.
{ Patients with significant intraabdominal fluid, determined by bedside
ultrasound, as the primary component of their ACS may be candidates for
decompression via a percutaneous drain.
{ Abdominal decompression is typically performed via a midline laparot-
omy incision which allows egress of peritoneal fluid or blood as well as
evisceration of the edematous bowel (Fig. 3).
{ Following laparotomy, temporary coverage of the viscera is necessary;
one option for temporary abdominal closure is the use of a steri-drape and
occlusive Ioban (Fig. 4).
The bowel is covered with a fenestrated subfascial 1010 steri-drape
(3M Health Care, St. Paul, MN).
Small holes are cut in the plastic drape with a scalpel to allow intraab-
dominal fluid to pass through the drape.
The steri-drape is placed over the bowel and tucked under the fascia.
Two Jackson-Pratt drains are placed along the fascial edges to control
reperfusion-related ascitic fluid; the drain tubing should exit cephalad
to permit better occlusion between the Ioban and skin.
Abdominal Compartment Syndrome 349
The open abdomen, steri-drape, and drains are then covered using a
large ioban (3M Health Care, St. Paul, MN).
{ Despite temporary closure of the abdomen, a patient may develop recur-
rent ACS; leaving “expansion space” for the bowel in the temporary
covering is critical. Additionally, bladder pressures should be monitored
in at-risk patients.
Practical Algorithm(s) / Diagrams
Fig. 1. ACS affects multiple organ systems and physiologic parameters.
ICP = intracranial pressure; PA = pulmonary artery; CVP = central venous pressure; SV = stroke volume;
CO = cardiac output; SVR = systemic vascular resistance; UOP = urine output.
350 C. C. Burlew
ACS GRADE
I 10 –15 13 –20
II 16 –25 21 –35
III 26 –35 36 –47
IV >35 >48
Bladder Pressure
mm Hg cm H2O
Fig. 2. Grading system for intraabdominal pressure measurements in ACS.
Fig. 3. Midline laparotomy permits decompression with egress of intraabdominal fluid/
blood and edematous bowel.
Abdominal Compartment Syndrome 351
Fig. 4. Temporary abdominal closure using a fenestrated steri-drape, 2 JP drains,
and an occlusive Ioban covering.
352 C. C. Burlew
Review of Current Literature with References
• In 2013, Kirkpatrick et al. updated their 2006 consensus definitions of IAH
and ACS and included practice guidelines. Their recommendations include
intra-abdominal pressure measurement and protocolized monitoring, decompressive laparotomy for overt ACS, and negative pressure wound therapy to
promote fascial closure. Other topics in the article include medical management of IAH, percutaneous drainage for ACS management, and red cell to
plasma ratios (Intensive Care Med 2013; 39: 1190–1206).
• In a meta-analysis of 14 studies with 2,500 patients, multiple risk factors for
IAH and ACS were identified across a spectrum of patient populations; in
trauma and surgical patients, large volume resuscitation was the most common risk factor for ACS (Crit Care 2013; 17: R249). Madigan et al. had
previously identified early, large volume crystalloid administration as the
greatest predictor of secondary ACS (J Trauma 2008; 64: 280–285).
• Balogh et al. noted in their single institution study that not only can ACS be
predicted early but the rates of multiple organ failure in this population are
markedly higher, >50% versus 12% in a non-ACS comparative group
(J Trauma 2003; 54: 848–859). Cotton et al. suggest that the rates of both
multiple organ failure and the incidence of open abdomen management may
be mitigated by the use of a massive transfusion protocol early in the patient’s
hospital course (J Trauma 2009; 66: 41–48).
• In this single institution study, Cheatham et al. demonstate that percutaneous
catheter decompression is effective in decreasing intraabdominal pressure; in
their evaluation, a significant proportion of patients avoided decompressive
laparotomy, particularly those with >1000 mL of drain output in 4 hours
(Chest 2011; 140: 1428–1435).
9. Hematology
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Chapter 9-(i)
Intensive Care Unit Anemia
and Packed Red Blood Cell Transfusion
Fredric M. Pieracci, MD, MPH *
* Acute Care Surgeon, Denver Health Medical Center
Take Home Points
• Intensive care unit (ICU) anemia is nearly universal; 95% of patients who
spend at least three days in the surgical ICU become anemic.
• The etiology of ICU anemia is multi-factorial; the most common contributing
factors in critically ill surgical patients are hemorrhage, serial phlebotomy,
hemodilution, impaired erythropoiesis, decreased erythrocyte lifespan, and
deranged iron metabolism.
• Inflammation results in anemia via alterations in erythropoietin synthesis and
sensitivity, decreased erythrocyte longevity, and hepcidin-mediated induction
of a functional iron deficiency, in which iron is shunted from the bone marrow
into storage as ferritin. This constellation of effects is termed the anemia of
inflammation, and occurs within hours of ICU admission.
Contact information: Denver Health Medical Center, 777 Bannock Street, MC 0206, A388,
Denver, CO 80206. Email: Fredric.Pieracci@dhha.org
355
356 F. M. Pieracci
• Although ICU anemia is associated with adverse outcomes, correction of
anemia via allogeneic packed red blood cell (pRBCs) transfusion does not
improve oxygen consumption, morbidity, or mortality, except in cases of
either severe (hemoglobin < 7.0 g/dL) anemia or hemorrhagic shock.
• Despite these observations, pRBCs transfusion for stable ICU anemia remains
a common practice in surgical ICUs; transfusions for stable ICU anemia
outnumber those for hemorrhagic shock approximately five-fold at most
academic trauma centers.
• Blood product transfusions are toxic: they induce an acute inflammatory
response, are pro-thrombotic, and cause immunosuppression.
• Patients in hemorrhagic shock should receive pRBCs transfusions until the
bleeding has stopped. Clinical markers of resuscitation should take precedence over an arbitrary hemoglobin transfusion trigger.
• For all other ICU patients, level I evidence exists to support a hemoglobin
transfusion trigger of 7.0 g/dL, including patients in non-hemorrhagic shock,
those with cardiac comorbidities, those with tachycardia, and those with traumatic brain injury.
• One exception may be patients with acute coronary syndromes [Chapter 5-(vii)],
for which level II evidence exists supporting a hemoglobin transfusion trigger
of 8.0 g/dL.
• Current data do not support routine supplementation of anemic ICU patients
with recombinant erythropoietin, although important limitations to the literature should be recognized.
• Current data do not support routine iron supplementation (either enteral or
parenteral) of anemic, critically ill surgical patients.
Background
• ICU anemia is exceedingly common: nearly all critically ill surgical patients
become anemic within 72 hours of ICU admission.
• The etiology of ICU anemia is multi-factorial, including hemorrhage from
trauma or surgical procedures, hemodilution with resuscitative fluids, serial
phlebotomy, and the effects of inflammatory cytokines on erythropoiesis.
• Daily serial phlebotomy may exceed 250 mL of blood in some surgical ICU
patients.
• Transfusion of pRBCs is also a common occurrence in the surgical ICU.
Approximately one half of critically ill surgical patients receive at least one
pRBCs transfusion during their ICU stay. Approximately 85% of all pRBCs
transfusions in surgical ICUs are for ICU anemia (the other 15% are for acute
hemorrhage).
Intensive Care Unit Anemia and Packed Red Blood Cell Transfusion 357
• Although ICU anemia is correlated with adverse outcomes, a causal relation-
ship has been difficult to demonstrate. Many confounders, such as severity of
injury, comorbidities, and number of procedures, exist. In general, mild to
moderate anemia (Hgb 7 – 12 g/dL) is well-tolerated, and may even be beneficial rheologically. Furthermore, there are no convincing data that correction
of mild to moderate anemia with pRBCs transfusion improves outcomes.
• The inflammatory response associated with critical illness has a profound
effect upon both erythropoiesis and erythrocyte longevity; these changes persist for months after ICU discharge.
• Inflammatory cytokines decrease erythropoietin synthesis and the sensitivity
of the bone marrow to erythropoietin. Furthermore, these same cytokines
decrease erythrocyte longevity. This results in inhibition of bone marrow
erythropoiesis, and accelerated hemolysis.
• Inflammation also causes cytokine-mediated alterations in iron metabolism;
specifically, iron is shunted from bone marrow sites of erythropoiesis into
storage as ferritin within the reticuloendothelial system.
• This shunting is believed to be secondary to upregulation of the hepatic acute
phase reactant hepcidin, which in turn down-regulates ferroportin, trapping
iron within both duodenal enterocytes and macrophages.
• These changes result in a functional iron deficiency, in which little iron is
available for incorporation into erythrocytes, although total body iron in storage is markedly elevated.
• The characteristic pattern of iron markers seen in inflammatory-mediated,
functional iron deficiency is: (1) hypoferremia (serum iron concentration <50
ug/dL); (2) decreased transferrin saturation (<20%); (3) hyperferritinemia
(serum ferritin concentration > 400 ng/mL, and often markedly elevated to
>1000 ng/mL); and (4) increased byproducts of iron-deficient erythropoiesis,
including erythrocyte zinc protoporphyrin and hypochromic erythrocytes.
• This pattern is also frequently observed in patients with chronic inflammatory
conditions, such as systemic lupus erythematous, and was formally termed
“anemia of chronic disease.” However, because it is now appreciated that
these changes occurs within hours of the inflammatory insult, the term “ anemia of inflammation” has been adopted, and is more representative of the
pathophysiology.
• Laboratory derangements seen in functional iron deficiency are nearly identical
to those seen in absolute iron deficiency anemia, with the exception of the serum
ferritin concentration (low in IDA and normal or high in functional iron deficiency), and the serum transferrin receptor concentration (low in IDA and normal
in functional iron deficiency). The clinical scenario will also help differentiate
between IDA and functional iron deficiency secondary to inflammation.