In the 1980s and early 1990s, the treatment of the critically ill patient was seen to be becoming increasingly expensive with little evidence that this expensive care improved outcome. This applied particularly to surgical patients in whom techniques originally pioneered in a healthy population are expanded to include patients who are more elderly with co- existing diseases. These high - risk patients have a higher mortality and morbidity rate and frequently die from multiple organ dysfunction syndrome (MODS), a syndrome that once established has proved largely resistant to therapeutic intervention . New evidence suggests that treatment targeted towards optimising cardiovascular function might improve outcome. To understand the principles involved, this paper discusses normal physiological changes around the time of surgery, surgical mortality, and the pathophysiology of MODS, before discussing evidence that manipulating cardiac function to increase blood flow reduces mortality and morbidity , this manipulation is known generically as ' goal - directed' therapy .
PHYSIOLOGICAL CHANGES IN THE PERI - OPERATIVE PERIOD
IT has been known for some time that there are changes in cardiovascular function at the time of surgery . In patients undergoing thoracotomy,' low cardiac index and arterial hypoxia were indicators of non- survival . Following the development of the balloon- tipped , flow- directed pulmonary artery catheter, , it was shown that patients who survived major surgery had higher cardiac index , lower systemic vascular resistance, and higher oxygen delievery than non - survivors. It was found that the commonly monitored vital signs ( heart rate, temperature, central venous pressure and haemoglobin) were the poorest predictors of survival , while perfusion- related variables ( such as oxygen delievery and oxygen consumption ) and cardiac index ( which express the interrelationship between oxygen transport and red cell volume and flow ) were the best . Furthermore , oxygen transport values change before the more commonly monitored variables , and , in patients who die or have complications , vital signs usually remain in the normal range until the terminal event , while oxygen transport variables had started to change some hours previously .
It has been hypothesised that a rise in oxygen transport requirements after surgery may be necessary to pay back an oxygen debt that has accumulated during the surgical procedure. Furthermore, if the cumulative tissue oxygen debt is calculated during the period of operation, it is found that patients who survive have the smallest oxygen debt and patients who fail to survive have the biggest; patients with organ failure who survive have intermediate oxygen debts.
In summary , cardiovascular changes around the time of surgery produce an increase in tissue perfusion; if this compensatory mechanism fails, patients are more likely to die and have complications.
SURGICAL MORTALITY AND MORBIDITY
Assessing mortality rates in higher risk patients is difficult ; the 1991 Acute Physiology and Chronic Health Evaluation database gives a 10.3% mortality for patients admitted directly to intensive care from the operating theatre in US centres; in the South West Thames ICU database mortality was higher (9.4% for elective surgery and 28.7% for emergency surgery in 1993-1994), and this is similar to data from the Intensive Care National Audit and Research Council database . Furthermore, the National Confidential Enquiry into Peri- Operative Deaths (NCEPOD ) in England and Wales 1992-1993 showed that the median day of death was day 6 and that patients did not usually die soon after operation. Postoperative mortality is increased in older patients with pre- existing disease and more severe surgery, and this has recently been highlighted by the Society of Cardiothoracic Surgeons of Great Britain and Ireland. Studies have also shown that thoracic and abdominal procedures have higher mortality and complication rates ; in elderly patients undergoing non- cardiac surgery , mortality is more related to factors such as a history of cardiac disease and signs of low CI around the time of surgery than factors such as the type of operation performed.
In general, patients with non- elective admissions ( mortality rate 30% versus 5% for elective admissions), ASA grade 3+ (mortality rate 27% versus 8% for ASA <3 ), age over 75 years ( mortality rate 20 % versus 11% for patients aged 65-74 years ) and major surgery (mortality rate 25% versus 10 % for non- major surgery) are associated with much higher mortality, and these factors are more important than the type of surgery.
MODS AND THE SURGICAL PATIENT
A syndrome in which there was multiple failure of a number of organ systems was first described in the 1970s in a group of surgical patients. This was initially termed multiple organ failure syndrome (MOF) , but recently the terminology has been standardised and it is now called multiple organ dysfunction syndrome (MODS). MODS carries a high mortality which increase as the number of organ systems fail. The incidence of MODS in surgical intensive care unit ( ICU) patients can be as high as 44.3% , and is associated with prolonged illness , death and increased cost. IT is currently estimated that MODS accounts for 60-80% of all surgical ICU death, and disappointingly there appears to have been little improvement in prognosis of established MODS over the last 20 years.
There are a number of factors which acting independently or in combination trigger the onset of MODS but the final common pathway is that of cytokine activation; first a local production of cytokines in response to an injury or infection which is a physiological response , then a release of a small amount of cytokines into the body's circulation , and finally a massive systemic reaction where cytokines turn destructive by compromising the integrity of the capillary walls and flooding end-organs. The triggers that lead from a normal response to an unregulated pathological response probably involve genetic factors and the priming of the inflammatory system by other stimulants. One can imagine in the surgical situation multiple stimulants to the inflammatory pathways been present in any one individual; these could include trauma, ischaemia, reperfusion injury, and infective and chemical insults. One of the major factors intiating cytokine activation appears to be alterations in microcirculatory flow, and others are related to tissue damage and the stimulation of inflammatoy mediators. Shoemaker and colleagues reported the link between failure of the normal postoperative responses of increased cardiac index and oxygen delievery maintaining flow and perfusion , and the development of MODS and death. This is probably the result of the activation of nuclear factor-kB, but demonstrating this in humans undergoing surgery and then relating this to the pathogenic processes of MODS and patient outcome has been more complicated. However , the frequency and magnitude of postoperative organ dysfunction after thoraco- abdominal aneurysm and abdominal aneurysm repair is associated with an increased concentration of the cytokines tumor necrosis factor-a and interleukin -6 and this is related to extended visceral ischaemia times.
In summary , pathophysiological evidence shows a direct link between surgery and trauma and the development of MODS in some patients; there is also an implication that the degree of surgery makes this chain of events more likely. Moreover, evidence above suggests that this is also more likely to occur when physiological reserve is limited
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