No abstract

Summary The pressure within the abdominal cavity is normally little more than atmospheric pressure. However, even small increases in intra‐abdominal pressure can have adverse effects on renal function, cardiac output, hepatic blood flow, respiratory mechanics, splanchnic perfusion and intracranial pressure. Although intra‐abdominal pressure can be measured directly, this is invasive and bedside measurement of intra‐abdominal pressure is usually achieved via the urinary bladder. This cheap, easy approach has been shown to produce results that correlate closely with directly measured abdominal pressures. Significant increases in intra‐abdominal pressure are seen in a wide variety of conditions commonly encountered in the intensive care unit, such as ruptured aortic aneurysm, abdominal trauma and acute pancreatitis. Abdominal compartment syndrome describes the combination of increased intra‐abdominal pressure and end‐organ dysfunction. This syndrome has a high mortality, most deaths resulting from sepsis and multi‐organ failure. Detection of abdominal compartment syndrome requires close surveillance of intra‐abdominal pressure in patients thought to be at risk of developing intra‐abdominal hypertension. The only available treatment for established abdominal compartment syndrome is decompressive laparotomy. Prevention of abdominal compartment syndrome after laparotomy by adoption of an open abdomen approach may be preferable in the patient at significant risk of developing intra‐abdominal hypertension, but this has not been demonstrated in any large trials. Most surgeons prefer to adopt a ‘wait and see’ policy, only intervening when clinical deterioration is associated with a significant increase in intra‐abdominal pressure.

Septic shock, the most severe complication of sepsis, accounts for approximately 10% of all admissions to intensive care. Our understanding of its complex pathophysiology remains incomplete but clearly involves stimulation of the immune system with subsequent inflammation and microvascular dysfunction. Cardiovascular dysfunction is pronounced and characterized by elements of hypovolaemic, cytotoxic, and distributive shock. In addition, significant myocardial depression is commonly observed. This septic cardiomyopathy is characterized by biventricular impairment of intrinsic myocardial contractility, with a subsequent reduction in left ventricular (LV) ejection fraction and LV stroke work index. This review details the myocardial dysfunction observed in adult septic shock, and discusses the underlying pathophysiology. The utility of using the regulatory protein troponin for the detection of myocardial dysfunction is also considered. Finally, options for the management of sepsis-induced LV hypokinesia are discussed, including the use of levosimendan.

Despite widespread awareness of IAH and the ACS, many intensive care units never measure the IAP. When it is measured, the intravesical route is used exclusively. No consensus exists on optimal timing of measurement or when decompressive laparotomy should be performed.

Hospital acquired or nosocomial infections continue to be an important cause of morbidity and mortality. The critically ill patient is at particular risk of developing intensive care unit acquired infection, with the lungs being especially vulnerable. Nosocomial bacterial pneumonia occurring after two days of mechanical ventilation is referred to as ventilator associated pneumonia, and is the most common nosocomial infection seen in the intensive care unit. Intubation of the trachea and mechanical ventilation is associated with a 7-fold to 21-fold increase in the incidence of pneumonia and up to 28% of patients receiving mechanical ventilation will develop this complication. Its development is associated with an attributable increase in morbidity and mortality. The establishment of an accurate diagnosis of ventilator associated pneumonia remains problematic and as yet there is still no accepted “gold standard” for diagnosis. The responsible pathogens vary according to case mix, local resistance patterns, and methodology of sampling. However, there is general agreement that rapid initiation of appropriate antimicrobial therapy improves outcome.