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234
Abdominal Compartment Syndrome
Figure 1. Massive colonic dilatation exacerbating IAH and ACS following multitrauma due to a fall.
Reducing Gastrointestinal Ileus and Promoting Gastrointestinal
Decompression
Ileus is common in most critically ill patients and in particular in those who have had
abdominal surgery, peritonitis, major trauma, massive fluid resuscitation, electrolyte abnormality and the administration of narcotic and sedative drugs. These factors characterise the
patients commonly at risk from ACS. Measures to counter and prevent the adverse effects of
ileus include gastric and rectal decompression with tubes, or in more advanced cases of colonic
distention an endoscpic decompression may be required. Correcting electrolyte abnormalities,
particularly potassium and magnesium is important. Prokinetic agents may be useful and erythromycin (200 mg IV 8 hourly) has a direct contractile effect via the motilin receptor. It has
been shown to be an effective prokinetic in the critically ill and is the drug of choice.
Metoclopromide (10 mg IV 8 hourly) as an alternative may promote gastric emptying by
235Medical Management of Abdominal Compartment Syndrome
dopamine antagonism. Neostigmine (2 mg diluted in up to 50 mL IV given slowly by infusion) is not a true prokinetic but may be an effective therapy for pseudo-obstruction (Ogilvie’s
syndrome, Fig. 1), which can cause massive bowel dilatation and worsen or generate IAH and
4
ACS.
Because the bowel may be significantly compromised by these processes there is small
but significant risk of bowel perforation associated with the use of neostigmine and other
decompressive procedures.
Constipation may also be so severe that it adds to IAH and ACS and aggressive use of
aperients and enemas are required. While cases of massive faecal impaction and constipation
are rarely reported they are seen in clinical practice and may be associated with rectal and
colonic necrosis.
5,6
Percutaneous Tube Decompression of Ascites and Blood
Drainage of tense ascites by insertion of a small tube may result in a reduction in IAH.
Cirrhotic patients with tense ascites may develop a circulatory dysfunction syndrome after
massive paracentesis, manifested by an increase in plasma rennin activity, a decrease in systemic
vascular resistance and peripheral arterial vasodilatation. If IAP is maintained at its original
level, during the process of paracentesis these haemodynamic changes may be avoided despite
large volume paracentesis.
Haemoperitoneum large enough to cause IAH and ACS may be seen in patients for whom
a major surgical decompression may be a poor option. For example, from the authors (MP)
recent experience, an oncology patient with a highly malignant lymphoma while being staged
for aggressive chemotherapy had a liver biopsy. This was followed by a slow haemorrhage with
pathological coagulopathy that failed to respond to conventional therapy but which eventually
responded to treatment with recombinant activated factor VII (rFVIIa, Novoseven). He received a massive transfusion and IAH with ACS and oliguric then anuric renal failure ensued.
A large laparotomy and leaving the abdomen open in this situation would have almost certainly resulted in his being too unwell for the chemotherapy he urgently required or death from
the septic consequences following chemotherapy. He was managed with a small tube drainage
of the intraperitoneal haemorrhage, his ACS and renal function improved and aggressive chemotherapy directed at the lymphoma was commenced. Other cases of percutaneous decompression have been reported as case reports and pilot studies and are described as a safe and
effective modality for intra-abdominal hypertension and abdominal compartment syndrome
in burn patients with less than 80% of total body surface area, and without inhalation injury.
7
7,9
Externally Applied Continuous Negative Abdominal Pressure
Externally applied continuous negative pressure has been applied in the clinical setting and
is the subject of Chapter 20.
10
Octreotide and Melatonin in Secondary Abdominal Compartment
Syndrome
Octreotide is a long-acting somatostatin analog widely used in the treatment of metastatic
neuroendocrine tumors, acute pancreatitis, and gastrointestinal and pancreatic fistulas. The
impact of somatostatin and octreotide on intestinal microcirculation has not been studied in
relation to IAP-induced oxidative multiorgan damage. Reperfusion of the ischaemic tissue may
release reactive oxygen metabolites that can mediate the microvascular abnormalites that precede organ damage induced by ischaemia and reperfusion These mediators also trigger and
activate leukocytes which generate oxygen free radicals that cause further tissue injury. Preventing this sequence with agents such as octreotide may have a protective effect against reperfusion
11
injury.
Octreotide has been studied primarily in animals and has shown ability to control
neutrophil infiltration and improve the reperfusion-induced oxidative damage after decompression of intra-abdominal hypertension.
Following the same principles for the use of octreotide, experimental studies have focused
on melatonin, a secretory product of the pineal gland known to have free radical scavenging
12
236
Abdominal Compartment Syndrome
A
Figure 2A,B. Massive oedema is a frequent complication of aggressive fluid resuscitation, may be increased
with some forms of goal directed therapy and increase the risk of all forms of ACS.
B
and antioxidative properties. It was recently shown that melatonin can reduce lipid peroxidation
in cell membranes, a process that promotes cell death as the functional integrity of these structures is damaged. Melatonin also has anti-inflammatory effects and inhibits the activation of
neutrophils by free radicals. In rats melatonin reduces reperfusion-induced oxidative organ
13
damage.
Diuretics, Dialysis and/or Ultrafiltration to Remove Excess Edema
Because of the nature of the illness and injury associated with ACS these patients retain
large volumes of sodium and water, which exacerbates tissue oedema, IAP and ACS. In the
early stages diuretic therapy is often not a viable option because the patients are intravascularly
depleted secondary to large capillary leakage due to systemic inflammatory response syndrome
(SIRS) and despite their grossly oedematous states. Administration of large volumes of fluid
resuscitation is usually unavoidable in the early stages (Figs. 2A, 2B). As the acute SIRS resolves
the use of diuretics may be appropriate to reduce oedema and perhaps IAP. For many patients
as IAH progresses oliguria and then anuria occur as renal blood flow is reduced. The further
administration of fluid in this situation will clearly add to tissue oedema and worsen the IAP,
and it becomes mandatory to initiate renal replacement therapy with fluid removal if a secondary or tertiary ACS is to be avoided despite the abdomen being left open.
Targeted Abdominal Perfusion Pressure (APP)
In a similar manner to targeting cerebral perfusion pressure it may be appropriate to target
abdominal perfusion pressure (APP), where APP = MAP - IAP, to a level that reduces the risk of
worsened splanchic perfusion and subsequent organ dysfunction. Clear guidance on this subject is currently lacking as are levels for APP that should be targeted. It is likely that individual
variation and requirements will be different and patients with preexisting hypertension and
splanchnic arterial disease (e.g., renal artery stenosis and mesenteric arterial disease) are likely
to be high risk groups. There may also be a valid argument for suggesting a role for gastric
tonometry as a monitor of the splanchnic circulation.
onstrated by this strategy and when used as part of a oxygen delivery goal directed therapy there
is also the potential to increase adverse effects.
14
An outcome benefit is yet to be dem-
15
237Medical Management of Abdominal Compartment Syndrome
General Support (Intensive Care) of the Critically Ill Patient
Management of a patient with an open abdomen mandates high quality intensive care to
manage the pulmonary, cardiovascular, splanchnic, urinary and central nervous system effects.
Given the clinical scenarios of most patients with raised IAP and ACS most will already be in a
critical care facility. If the patient is not intubated it is likely to be appropriate to intubate and
ventilate. The administration of appropriate levels of sedation and neuromuscular blockade
will then allow accurate assessment of the IAP and optimise ventilation and the patient status
for any advanced intervention. This will allow appropriate selection of patients for surgical
intervention or further decompression of an already open abdomen. Once abdominal decompression is achieved, it is the usual practice to leave the abdominal fascia and skin open with
foreign material at skin level to prevent evisceration. These have the problems of secondary
infection, fluid shifts from the exposed bowel and peritoneum, and injury to the bowel.
The nature of acute respiratory failure in these patients may be multifactorial and high
airway pressures may be required to achieve satisfactory oxygenation and carbon dioxide elimination. As many of the patients are at high risk for acute lung injury and acute respiratory
distress syndrome a protective strategy of ventilation should also be considered.
airway pressure while potentially increasing the risk of volume and barotraumas may also increase IAP.
The haemodynamic consequences of IAH must be addressed. As mentioned above NMB
may improve haemodynamic status but the true role of muscle relaxant and compliance of the
abdominal wall in patients with ACS has not been studied.
3,17
Hypotension due to hypovolaemia
requires rapid correction. Fluid resuscitation may consist of natural or artificial colloids or
crystalloids and blood products. As the volume of distribution for crystalloids is larger than for
colloids, crystalloid resuscitation needs more fluid to achieve the same end-points and results
in more edema. There is however little evidence to support one type of fluid over another. The
safety of colloids and albumin in particular has been questioned in patient groups at risk of
IAH and ACS.
18,19
A recent large prospective randomized trial of albumin versus saline for fluid resuscitation
(the SAFE study) while demonstrating no excess mortality associated with albumin use found
an excess mortality in the albumin group for patients with multitrauma and a head injury. The
study also suggests that the current teaching of a 1:3 ratio of volume equivalence is incorrect
and that a ratio of 1:1.3 for saline versus albumin.
20
If following correction of hypovolaemia there is still evidence of hypotension then inotropic/vasopressor administration is appropriate. Human and animal studies suggest potential
adverse effects of epinephrine on the splanchnic circulation. Dobutamine, dopamine and noradrenaline have been advocated to improve splanchnic perfusion but there is no good human
evidence in IAH and ACS to recommend any particular agent. There is no evidence to support
the use of low-dose dopamine for renal protection in a large study that included patients at risk
of IAH and ACS.
21
The aggressive management of acidosis, coagulopathy and hypothermia is required and this
is particularly the case for patients who are undergoing damage control surgery. This is recently
covered elsewhere.
In the past arguments have been made for trying to achieve supranormal resuscitation levels, aiming for oxygen delivery index higher than 600 mL/min/m
22
2
. In a retrospective analysis
however, Balogh found that a supranormal resuscitation strategy was associated with more
fluid infusion (Ringers lactate), decreased intestinal perfusion, intra-abdominal hypertension,
abdominal compartment syndrome incidence, multiple organ failure and mortality.
mon with the management of septic patients the current goal of resuscitation should instead be
to achieve adequate levels of oxygen delivery while avoiding flow dependant tissue hypoxia.
Much of what has been recently described as the basis for evidence based intensive care management of patients with sepsis will apply to patient who is at risk of IAH and ACS and this
document acts as a useful resource.
23
16
Excessive
15
In com-
23
238
Abdominal Compartment Syndrome
Optimisation after Surgical Decompression to Counteract Adverse
Effects Associated with Decompression and Prevent Recurrence
Reperfusion syndrome refers to the damage done by restoration of blood flow to ischaemic
tissues and is distinct from the original ischaemic insult itself. Reperfusion syndrome may
occur at the time of abdominal decompression in some patients with ACS. During decompression, abdominal organs reperfusion may produce arterial hypotension and asystole.
ment or treatment with mannitol and bicarbonate infusions has been recommended. It is likely
that this can be avoided if decompression is performed at lower levels of IAP.
24
Pretreat-
25
Management of ACS by opening the abdomen and temporary abdominal closure does not
prevent the development of recurrent ACS and the mortality is high when ACS occurs in this
scenario.
26
Optimal medical management may reduce this potential. From what has been pre-
sented above some key strategies to prevent ACS or its recurrence would include:
• prevent ileus
• reduce excessive fluid resuscitation
• avoid resuscitative strategies that may increase the incidence of ACS (some forms of goal
directed therapy)
• therapy to reduce the inflammatory response
Conclusion
Although medical management of abdominal compartment syndrome may lower
intra-abdominal hypertension, reduce systemic effects, and prevent a secondary ACS, surgical
decompression currently represents definitive treatment. As there is morbidity and mortality
associated with the decompression procedures, temporary abdominal closure and abdominal
wall reconstruction, assessment of nonsurgical treatment options is warranted. Some progress
has been made in describing the medical and surgical management of ACS but further studies
are needed to fully understand the clinical implications and appropriate management.
Commentary
Michael Sugrue
The non-operative medical management of abdominal compartment syndrome (ACS) remains in its infancy. Surgeons have led the crusade relating to ACS and this is reflected in the
international literature. Between 1994 and 2003, 28 review articles relating to perioperative
renal failure identified only one article that makes reference to intra-abdominal hypertension
1
(IAH).
The medical management of the ACS is of crucial importance in optimising abdominal perfusion, and yet avoiding the adverse effects of fluid overload. The abdominal compartment syndrome occurs in medical patients albeit less frequently than in surgical patients. Recognition is vital for early treatment modalities such as aggressive gastrointestinal decompression
and facilitation of release of rectal gaseous and faecal material. The role of diuretics and inhibitors of the angiotensin renal vascular system remain to be verified and further exciting research
will help in this area. Continuously applied negative abdominal pressure may have a role in a
certain sub-group of patients. Until randomised control trials identify key issues in relation to
fluid resuscitation and surgery it is important that at least the concept of ACS is recognised in
our medical ICUs and that common sense prevail ensuring avoidance of abdominal distension
through known basic treatment modalities.
References
1. Reddy VG. Prevention of postoperative acute renal failure. J Postgrad Med 2002; 48:64-70.
1A. Decker G. Abdominal compartment syndrome. J Chir 2001; 138:270-6.
2. Walker J. Criddle LM. Pathophysiology and management of abdominal compartment syndrome.
Am J Crit Care 2003; 12(4):367-71, quiz 372-3.
3. Macalino JU, Goldman RK, Mayberry JC. Medical management of abdominal compartment syndrome: Case report and a caution. Asian J Surg 2002; 25:244-6.
4. van der Spoel JI, Oudemans-van Straaten HM, Stoutenbeek CP et al. Neostigmine resolves critical
illness-related colonic ileus in intensive care patients with multiple organ failure-a prospective,
double-blind, placebo-controlled trial. Intensive Care Med 2001; 27:822-7.
5. Gorecki PJ, Kessler E, Schein M. Abdominal compartment syndrome from intractable constipation. J Am Coll Surg 2000; 190:371.
6. Lohlun J, Margolis M, Gorecki P et al. Fecal impaction causing megarectum-producing colorectal
catastrophes. A report of two cases. Digestive Surgery 2000; 17:196-8.
7. Cabrera J, Falcon L, Gorriz E et al. Abdominal decompression plays a major role in early
postparacentesis haemodynamic changes in cirrhotic patients with tense ascites. Gut 2001; 48:384-9.
8. Corcos AC, Sherman HF. Percutaneous treatment of secondary abdominal compartment syndrome.
J Trauma 2001; 51:1062-4.
9. Latenser BA, Kowal-Vern A, Kimball D et al. A pilot study comparing percutaneous decompression with decompressive laparotomy for acute abdominal compartment syndrome in thermal injury. J Burn Care Rehabil 2002; 23:190-5.
10. Bloomfield G, Saggi B, Blocher C et al. Physiologic effects of externally applied continuous negative abdominal pressure for intra-abdominal hypertension. Journal of Trauma-Injury Infection &
Crit Care 1999; 46:1009-14.
11. Kaçmaz A, Polat A, User Y et al. Octreotide: A new approach to the management of acute abdominal hypertension. Peptides 2003; 24:1381-6.
12. Kaçmaz A, Polat A, User Y et al. Octreotide improves reperfusion-induced oxidative injury in
acute abdominal hypertension in rats. J Gastrointest Surg 2004; 8:113-9.
13. Sener G, Kaçmaz A, User Y et al. Melatonin ameliorates oxidative organ damage induced by acute
intra-abdominal compartment syndrome in rats. J Pineal Res 2003; 35:163-8.
14. Ivatury RR, Porter JM, Simon RJ et al. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: Prophylaxis, incidence, and clinical relevance to gastric mucosal pH
and abdominal compartment syndrome. J Trauma 1998; 44:1016-21.
15. Balogh Z, McKinley BA, Cocanour CS et al. Supranormal trauma resuscitation causes more cases
of abdominal compartment syndrome. Arch Surg 2003; 138:637-42.
16. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342:1301–1308.
17. De Waele JJ, Benoit D, Hoste E et al. A role for muscle relaxation in patients with abdominal
compartment syndrome? Intensive Care Medicine 2003; 29:332.
18. Cochrane injuries group albumin reviewers human albumin administration in critically ill patients:
Systematic review of randomised controlled trials. Br Med J 1998; 317:235-40.
19. Schierhout G, Roberts I. Fluid resuscitation with colloid or crystalloid solutions in critically ill
patients: A systematic review of randomized trials. Br Med J 1998; 316:961–964.
20. The SAFE study investigators. A comparison of albumin and saline for fluid resuscitation in the
intensive care unit. N Engl J Med 2004; 350:2247-56.
21. Bellomo R, Chapman M, Finfer S et al. Australian and New Zealand intensive care society clinical
trials group. Low dose dopamine in patients with early renal dysfunction: A placebo controlled
randomised trail. Lancet 2000; 356:2139-2143.
22. Parr MJA, Alabdi T. Damage control surgery and intensive care. Injury 2004; 35:713-722.
23. Dellinger RP, Carlet JM, Masur H. Surviving sepsis campaign guidelines for management of severe
sepsis and septic shock. Intensive Care Med 2004; 30:536–555.
24. Wysocki A. Abdominal compartment syndrome: Current view. Przeglad Lekarski 2001; 58:463-5.
25. Morris Jr JA, Eddy VA, Blinman TA et al. The staged celiotomy for trauma. Issues in unpacking
and reconstruction. Ann Surg 1993; 217:576-86.
26. Gracias VH, Braslow B, Johnson J et al. Abdominal compartment syndrome in the open abdomen.
Arch Surg 2002; 137:1298-300.
239Medical Management of Abdominal Compartment Syndrome
240
Abdominal Compartment Syndrome
CHAPTER 20
Continuous Negative Abdominal Pressure
Franco Valenza* and Luciano Gattinoni
Abstract
n this chapter we will focus on the possibility of artificially decreasing intra-abdominal pres
I
sure by applying a continuous negative pressure around the abdomen.
We will start from the rationale of this potential noninvasive tool to treat intra-abdominal
hypertension, to subsequently describe our initial experience with the use of continuous negative extra abdominal pressure (NEXAP).
The results of a trial conducted using different levels of NEXAP on 30 patients admitted to
our intensive care unit will be presented and discussed together with the insights of animal
studies we and others conducted to investigate the cardio-respiratory effects of NEXAP.
The bulk of data will be put together so to give to the reader a general view of our understanding of the possibility of using NEXAP to treat the abdominal compartment syndrome.
Rationale
There is an increasing appreciation of the importance of intra-abdominal hypertension
(IAH) in critically ill patients. In fact, as many as 50% of patients in the ICU present with an
intra-abdominal pressure (IAP) higher than 12 mm Hg, 8% of which are characterized by the
abdominal compartment syndrome.
and increasingly recognized by physicians who treat critically ill patients.
At higher levels of pressure surgical decompression is an accepted treatment,
where in between 12 and 25 mm Hg the detrimental consequences of IAH are present but
surgical decompression is not indicated. Patients with these values of IAP represent the great
majority of those labeled as having IAH, however there is no definite treatment modality for
these patients, except for supportive therapy for failing organs.
Recently non surgical decompression of the abdomen has been proposed to treat intracranial hypertension associated with abdominal compartment syndrome: a decrease of IAP with
the use of a continuous application of negative pressure around the abdomen of experimental
animals has been described.
The rationale and the initial knowledge to treat non invasively IAH in critically ill patients
was posed. However, the appealing possibility of using negative extra abdominal pressure
(NEXAP) in the ICU setting was not yet tested.
Fascinated by this hypothesis, we set out to test if NEXAP could decrease IAP in critically ill
patients and if there were major side effects in this population. The data obtained left us with
open questions on the cardio-respiratory effects of NEXAP, that prompted us to a subsequent
animal study.
In this chapter, after having briefly presented the protocols of the human and animal studies, we will take each of the following questions into consideration:
10,11
2
The effects of IAH on organ function are well known
6-8
3,6,9
while some-
3-5
*Corresponding Author: Franco Valenza —Universita degli Studi di Milano, Istituto
di Anestesia e Rianimazione, Ospedale Maggiore di Milano, Milano, Italy.
Email: Franco.valenza@unimi.it
Abdominal Compartment Syndrome, edited by Rao R. Ivatury, Michael L. Cheatham,
Manu L. N. G. Malbrain and Michael Sugrue. ©2006 Landes Bioscience.
241Continuous Negative Abdominal Pressure
Table 1. Patient demographics
Number of patients 30
Age (years) 57 ± 17
Sex (M/F) 18/12
Body Mass Index (kg/m2) 26.1 ± 4
SAPS II 41.8 ± 17
Ramsay score 4.6 ± 1.8
Muscle relaxation 6
Vasoactive drugs 7
Outcome (D/S) 4/26
1. Does NEXAP decrease intra-abdominal pressure?
2. Are there problems with NEXAP application in the critically ill?
3. Does NEXAP alter general hemodynamics, and to what extent?
4. Does NEXAP alter respiratory mechanics?
We will discuss these questions taking into consideration the bulk of data coming from ours
and others’ investigations.
Human Study
We recruited 30 consecutive patients the characteristics of which are presented below in
Table 1. To generate NEXAP, we used a shell (Life Care – Nev 100, Respironics) traditionally
used to apply negative pressure around the thorax. To fit the shell over the abdomen, it was
rotated by 180˚. The apparatus used for the study is described in Figure 1.
Patients were investigated in the supine position. Once basal measurements were taken
(Basal), NEXAP was applied on the abdomen, in a random order, at a pressure equal to IAP
(NEXAP0), 5 cm H
Measurements included IAP (bladder pressure) and cardio-respiratory parameters. These
measurements were taken at each of the four steps after 30 minutes of stabilization.
O (NEXAP-5) or 10 cm H2O (NEXAP-10) more negative than NEXAP0.
2
Animal Study
Eight pigs were sedated and paralysed. They were randomized with respect to abdominal
insufflation: four animals had their abdomen insufflated with heium (intra-abdominal hypertension - IAH), while basal (basal) measurements were taken afterwards. Four animals followed
the reverse order.
Cardio-respiratory measurements were taken in both basal and IAH condition before NEXAP
was applied (pre), immediately after the transition to NEXAP (NEXAP 1), 15 minutes after
NEXAP was applied (NEXAP 2), and 15 minutes after NEXAP was relieved (post).
The figure shows the experimental protocol (Fig. 2).
To generate NEXAP (-20 cm H
O), we used a shell similar to that of the human study, but
2
smaller (Life Care – Nev 100, Respironics) (Fig. 3).
Does NEXAP Decrease Intra-Abdominal Pressure?
Saggi et al10 and Bloomfield et al11 found in animal models that negative pressure around
the abdomen significantly decreased IAP. However, to generate negative pressure around the
abdomen they used a “large poncho connected to a vacuum into which the entire animal was
11
placed”.
decribed above.
below:
6.0 ± 4.2 (Basal vs. NEXAP0, P<0.001). Changes were greater when more negative pressure
This is somewhat difficult to obtain in humans; therefore we decide to use the shell
The effects of NEXAP on IAP in critically ill patients we found are shown in Figure 4
Basal IAP ranged from 4 to 22 mm Hg. NEXAP decreased IAP from 8.7± 4.3 mm Hg to
242
Abdominal Compartment Syndrome
Figure 1. NEXAP applied by shell on abdomen. Reprinted with permission from Valenza F, Bottino N,
Canavesi K et al. Intra-abdominal pressure may be decreased non-invasively by continuous negative extraabdominal pressure (NEXAP). Intensive Care Med 2003; 29(11):2063-7. ©2003 Springer Science and
Business Media.
Figure 2. Animal study protocol. Helium for creating IAH.
243Continuous Negative Abdominal Pressure
Figure 3. Smaller shell used to create NEXAP in animal model. Reprinted with permission from Valenza
F, Irace M, Guglielmi M et al. Effects of continuous negative extra-abdominal pressure on cardiorespiratory
function during abdominal hypertension: an experimental study. Intensive Care Med 2005; 31(1):105-11.
©2005 Springer Science and Business Media.
was applied (P<0.001). Average decrease of IAP with NEXAP-10 was 4.5 ± 2.9 mm Hg (maxi-
mum decrease 11 mm Hg).
Therefore, as clearly shown, the first of our questions was answered: yes, NEXAP may be
used to decrease IAP in critically ill patients.
Are There Problems with NEXAP Application?
The application of NEXAP was well tolerated by patients and there were no major side
effects. At the end of the protocol, there was mild and reversible erythema on the skin of the
abdomen where the shell was applied. Awake patients suffered some degree of discomfort at
higher levels of NEXAP, but only one patient was clearly uncomfortable. However, at NEXAP
levels equal to baseline IAP (NEXAP0), all patients were comfortable.
These results are similar to those reported by Sugerman et al who used negative pressure to
treat headhache in obese patients affected by pseudotumor cerebri. Patients were intermittently treated several hours a day without major complaints or adverse effects.
12
Does NEXAP Alter General Hemodynamics, and to What Extent?
The third question we were interested in originated from the kind of patients we were about
to treat with NEXAP (ICU patients) and the knowledge that, in animal models, cardiac index
remained essentially unchanged during IAH,
We found that NEXAP did not cause any severe impairment of cardiovascular function:
MAP did not change, so did HR, if not for a slight significant increase at highest levels of
11
but decreased when IAP was normal.
10
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