Read Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice Online
Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (62 page)
There have been major developments in our understanding of intra-abdominal pressure (IAP) and intra-abdominal hypertension (IAH). Raised IAP has far-reaching consequences for the physiology of the patient.
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Clinically, the organ systems most affected include the cardiovascular, renal and pulmonary systems. A sustained IAP ≥ 20 mmHg associated with new organ dysfunction is known as abdominal compartment syndrome (ACS; see
Table 13.2
).With increasing awareness of the problem, reduced fluid resuscitation and more appropriate damage control, the incidence of ACS in trauma is decreasing. Failure to detect ACS in a timely fashion and treat it aggressively results in high mortality in such patients.
Table 13.2
Consensus definitions related to IAP, IAH and ACS
Reproduced with permission from the World Society for Abdominal Compartment Syndrome.
The first World Congress on ACS was held in 2005 and an internal consensus agreement relating to current definitions
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is shown in
Table 13.2
.
ACS is defined as a sustained IAP ≥ 20 mmHg (with or without an abdominal perfusion pressure < 60 mmHg) that is associated with new organ dysfunction/failure.
The incidence of increased IAP may be 30% of postoperative general surgery patients in intensive care and after emergency surgery the incidence is even higher. The causes of acutely increased IAP are usually multifactorial (see also
Chapter 18
). The first clinical reports of postoperative increased IAP were often after aortic surgery, with postoperative haemorrhage from the graft suture line. Peritonitis and intra-abdominal sepsis, tissue oedema and ileus are the predominant cause of increased IAP. Raised IAP in trauma patients is often caused by a combination of blood loss and tissue oedema. Causes of increased intra-abdominal pressure include:
tissue oedema secondary to insults such as ischaemia, trauma and sepsis;
paralytic ileus;
intraperitoneal or retroperitoneal haematoma;
ascites;
trauma with hypothermia, coagulopathy and acidosis.
Renal function
The most likely direct effect of increased IAP is an increase in the renal vascular resistance, coupled with a moderate reduction in cardiac output. The absolute value of IAP that is required to cause renal impairment is probably in the region of 20 mmHg. Maintaining adequate cardiovascular filling pressures in the presence of increased IAP also seems to be important.
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Increased IAP reduces cardiac output as well as increasing central venous pressure, systemic vascular resistance, pulmonary artery pressure and pulmonary artery wedge pressure. Cardiac output is affected mainly by a reduction in stroke volume, secondary to a reduction in preload and an increase in afterload. This is further aggravated by hypovolaemia. Paradoxically, in the presence of hypovolaemia, an increase in IAP can be temporarily associated with an increase in cardiac output. Venous stasis occurs in the legs of patients with IAP values above 12 mmHg. In addition, recent studies of patients undergoing laparoscopic cholecystectomy show up to a fourfold increase in renin and aldosterone levels.
In association with increased IAP, there is diaphragmatic splinting, exerting a restrictive effect on the lungs with reduction in ventilation, decreased lung compliance, increase in airway pressures and reduction in tidal volumes. The mechanism by which increased IAP impairs pulmonary function appears to be purely mechanical. As IAP increases, the diaphragm is forced higher into the chest, thereby compressing the lungs. Adequate ventilation can still be achieved, but only at the cost of increased airway pressures.
In critically ill, ventilated patients the effect on the respiratory system can be significant, resulting in reduced lung volumes, impaired gas exchange and high ventilatory pressures. Hypercarbia can occur and the resulting acidosis can be exacerbated by simultaneous cardiovascular depression as a result of the raised IAP. The effects of raised IAP on the respiratory system in the intensive care setting can sometimes be life threatening, requiring urgent abdominal decompression. Patients with true ACS demonstrate a remarkable improvement in their intraoperative vital signs following abdominal decompression.
Interest in visceral perfusion has increased with increased awareness of gastric tonometry, and there is an association between IAP and visceral perfusion as measured by gastric pH. In a study of 73 patients after laparotomy, it was shown that IAP and gastric pH are strongly associated, suggesting that early decreases in visceral perfusion are related to IAP at levels as low as 12 mmHg.
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Visceral reperfusion injury is a major consideration after a period of raised IAP, and may of itself have fatal consequences.
Raised IAP can have a marked effect on intracranial pathophysiology and cause severe rises in intracranial pressure.
The most common method for measuring IAP uses a urinary catheter.
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The patient is positioned flat in the bed and a standard Foley catheter is used with a T-piece bladder pressure device attached between the urinary catheter and the drainage tubing. This piece is then connected to a pressure transducer, which is placed in the mid-axillary line and the urinary tubing clamped. Approximately 50 mL of isotonic saline is inserted into the bladder via a three-way stopcock. After zeroing, the pressure on the monitor is recorded.
The following factors are important in achieving effective IAP measurements:
A strict protocol and staff education on the technique and interpretation of IAP is essential.
Very high pressures (especially unexpected ones) are usually caused by a blocked urinary catheter.
The size of the urinary catheter does not matter.
The volume of saline instilled into the bladder is not critical, but it should be enough to overcome the resistance of the contracted bladder; usually, not more than 50 mL is adequate.
A central venous pressure manometer system can be used but it is more cumbersome than online monitoring.
Elevation of the urine catheter and measuring the urine column provides a rough guide and is simple to perform.
If the patient is not lying flat, IAP can be measured from the pubic symphysis.
IAP is not a static measurement and should be measured continuously. In addition, whether IAP is measured intermittently or continuously, consideration of abdominal perfusion measurement should be given (see below). Real-time continuous monitoring of IAP is effective and shows trends as well as actual pressures.
Intra-abdominal hypertension (IAH) is defined by a sustained or repeated pathological elevation of IAP > 12 mmHg.
Like the concept of cerebral perfusion pressure, calculation of the ‘abdominal perfusion pressure’ (APP), which is defined as mean arterial pressure (MAP) minus IAP, assesses not only the severity of IAP present, but also the adequacy of the patient's abdominal blood flow. A retrospective trial of surgical and trauma patients with IAH (mean IAP 22 ± 8 mmHg) concluded that an APP > 50 mmHg optimised survival based upon receiver operating characteristic curve analysis.
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APP was also superior to global resuscitation end-points such as arterial pH, base deficit, arterial lactate and hourly urinary output in its ability to predict patient outcome.Three subsequent trials in mixed medical–surgical patients (mean IAP 10 ± 4 mmHg) suggested that 60 mmHg represented an appropriate resuscitation goal.
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–
49
Persistence of IAH and failure to maintain an APP ≥ 60 mmHg by day 3 following development of IAH-induced acute renal failure was found to discriminate between survivors and non-survivors.
General support
In general, the best treatment is prevention, both by minimising the causative agents and early appreciation of the potential complications.
There are a number of key principles in the management of patients with potential ACS:
regular (< 8-hourly) monitoring of IAP;
optimisation of systemic perfusion and organ function in the patient with IAH;
institution of specific medical procedures to reduce IAP and the end-organ consequences of IAH/ACS;
early surgical decompression for refractory IAH.
The second aspect of management is to correct any reversible cause of ACS, such as intra-abdominal bleeding. Maxwell et al. reported on secondary ACS, which can occur without abdominal injury, and stated that, again, early recognition could improve outcome.
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Massive retroperitoneal haemorrhage is often associated with a fractured pelvis, and consideration should be given to measures that would control haemorrhage, such as pelvic fixation or vessel embolisation. In some cases, severe gaseous distension or acute colonic pseudo-obstruction can occur in patients in intensive care. This may respond to drugs such as neostigmine but if it is severe, surgical decompression may be necessary (see also
Chapter 10
). Ileus is a common cause of raised IAP in patients in intensive care. There is little that can be actively done in these circumstances apart from optimising the patient's cardiorespiratory status and serum electrolytes.
Abdominal evaluation for sepsis is a priority and surgery is obviously the mainstay of treatment in patients whose rise in IAP is caused by postoperative bleeding.
Management of IAH and ACS is summarised in
Figs 13.2
and
13.3
.
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,
48
,
49
Figure 13.2
Intra-abdominal hypertension (IAH)/abdominal compartment syndrome (ACS) management algorithm. ACS, abdominal compartment syndrome; APP, abdominal perfusion pressure (MAP − IAP); IAH, intra-abdominal hypertension; IAP, intra-abdominal pressure; Primary ACS, a condition associated with injury or disease in the abdomino-pelvic region that frequently requires early surgical or interventional radiological intervention; Recurrent ACS, the condition in which ACS redevelops following previous surgical or medical treatment of primary ACS; Secondary ACS, ACS due to conditions that do not originate from the abdomino-pelvic region.
Figure 13.3
Medical management options to reduce intra-abdominal pressure (IAP). ACS, abdominal compartment syndrome; APP, abdominal perfusion pressure; IAH, intra-abdominal hypertension.