Curmrr A~weshesicr curd Criricul 0 1999 Harcourt Publishers LIP
Cure
( 1999)
10. 207-2
I4
Focus on: Anaesthesia in non-cardiac vascular surgery
Postoperative care of the vascular surgery patient
E. Wennberg
and H. HaljamGe
The patient undergoing peripheral vascular surgery is at increased operative risk owing to overt or occult manifestations of coexisting atherosclerotic disease mainly affecting cardiac and renal function. Common problems in the postoperative period are related to hyper-/hypotension, hypothermia, tachycardia, hypoxaemic episodes, hypercapnia, myocardial ischaemia/infarction and renal functional disturbances. Relevant strategies for prevention of postoperative morbidity and mortality should include monitoring of cardiac performance, central and peripheral haemodynamics (including graft function), systemic oxygenation and renal function. Increased cardiac workload and oxygen requirements are commonly caused by increased stress owing to hypothermia, pain or nausea. Therefore, therapeutic measures for adequate sedation and pain alleviation are essential in the postoperative period for reducing stressassociated increases in cardiovascular work load and oxygen requirements. 0 Harcourt Publishers Ltd
Introduction In an extensive study of I8 380 patients subjected to general anaesthesia, Rose et al.’ noted that in the postanaesthesia care unit, the major cardiovascular events associated with unplanned critical care admission or mortality were hypertension or tachycardia. Specific choices in anaesthetic management during surgery were not found to contribute significantly to the occurrence of these cardiovascular events while patient factors, as well as surgical factors, i.e. factors beyond the control of the anaesthesiologist, were considered of primary etiological importance.’ The vascular surgery patient. however, commonly suffers from generalized atherosclerotic cardiovascular involvement resulting in a high prevalence of hypertension, heart disease, cerebrovascular disease and renal functional impairment. Diabetes and chronic obstructive Dr E. Wennberg Chairman. Sahlgrenska
MD,
Departmenr University
Correspondence
PhD.
Professor
Dr H. Haljamle
MD,
ol’ Anaesthesiology and Intensive Care. Hospital. S-413 45 Giiteborp. Sweden
IO: H. H.
PhD,
lung disease may further complicate the postoperative course. Therefore, in the postoperative phase the patient having undergone non-cardiac vascular surgery may be considered a relatively high-risk patient. The goals of the postoperative care of these patients are, consequently,
to minimize the risk of potentially severe complications by the use of proper prophylactic and therapeutic strategies. It should be remembered that the effects of most anaesthetic techniques are not limited to the duration
of the surgical intervention, but may extend far into the postoperative period. Intensive postoperative monitoring and immediate access to experienced medical advice is, therefore, essential for an uneventful outcome, especially after major (aortic aneurysm) non-cardiac vascular surgery.’
Postoperative surgery
concerns
following
vascular
Common reasons for postoperative morbidity and mortality in vascular surgery patients are summarized in Table I.”
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Table
1
patients
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Potential perioperative complications in vascular surgery resulting in increased postoperative morbidity and mortality.’ .
Major
cardiovascular
-
angina myocardial arrhythmias congenstive
infxclion heart
Failure
Pulmonary
- respiratory - prolonged
failure intubation/respiratory
Rena!
- renal failure - uraemic symptoms
Neurologic
-
Gastrointestinal
- bowel dysfunction - gastrointestinal haemorrhage
Infectious
- pneumonia - wound infection
support
sensory abnormalities disturbed motor function cognitive disturbances/delirium stroke
Postoperative cardiovascular conlplications Adverse postoperative cardiac events may either be caused by disturbed coronary artery perfusion or be secondary to hypoxaemic episodes. Ischaentic myocardial episodes - In vascular surgery patients with coronary risk factors, the occurrence of ischaemic myocardial episodes is much more common in the postoperative period than during anaesthesia and surgery. After surgery there is usually an increased stress load on cardiovascular function, which, in combination with activation of humoral inflammatory mediators and the coagulation cascade, may disturb myocardial perfusion and oxygen supply. Cardiac complications account for most perioperative morbidity and mortality, one-third of all postoperative complications, and more than one-half of the deaths.’ As recently stated by Cohen.’ research into perioperative myocardial ischaemia used to be preoccupied with preoperative and intraoperative risk factors and their modification. It has been suggested by Landesberg et al.6 that cardiac morbidity in patients undergoing major, non-cardiac surgery may be best predicted by the occurrence of postoperative myocardial ischaemia rather than by the traditional clinical predictors. Coronary blood flow is regulated by metabolic, myogenie, neuronal and endothelial factors. A matching of myocardial oxygen supply and consumption is essential for the prevention of ischaemic episodes and myocardial infarction. It seems that patients with severe coronary artery disease (CAD) have diminished endogenous nitric oxide activity owing to endothelial cell dysfunction.’ Angiographic evidence of CAD seems, for example, to be associated with a reduced metabolic coronary dilatation of resistance vessels in response to pacing.x Such reduced responsiveness of the coronary circulation could be a contributing factor to the occurrence of cardiac ischaemia in vascular surgery patients. It seems that myocardial infarction usually occurs between 12 and 32 h following surgery and is preceded by episodes of ischaemia.6
The stress sensitivity of the individual patient may be of importance for induction of adverse cardiovascular events leading to postoperative cardiac morbidity and mortality. Stress seems to be one major causative factor for cardiovascular complications for the relatively highrisk vascular surgery patient. Silent rather than symptomatic myocardial ischaemic episodes are common’ and have been reported by McCann et al.“’ to occur in 38% of patients undergoing peripheral vascular surgery. Preoperative silent myocardial ischaemia has, by perioperative Holter ECG monitoring, been found to be strongly associated with postoperative silent myocardial ischaemia.” A history of hypertension, indicated by treatment with antihypertensive drugs, was also found to be associated with postoperative silent myocardial episodes.” Tachycardia, being a major determinant of myocardial oxygen consumption, seems often associated with the occurrence of ischaemic cardiac episodes and may induce acute myocardial infarction. It is consequently of major importance to reduce postoperative stress and the circulatory effects of increased sympathetic tone.” Postoperative hymramic episodes - Hypoxaemic episodes seem to occur rather commonly in a postanaesthesia care unit. Russel and Graybeal” noted that 15% of surgical patients were experiencing episodes of desaturation on admission to the recovery room. In spite of 40% oxygen administration during the postanaesthetic recovery period, late desaturations (about 30 min after admission; SaO, ~92%) were still observed in 25% of the patients. Factors associated with the occurrence of hypoxaemic episodes were found to be low admission saturation, patient age and body weight. ASA-class, general anaesthesia and intraoperative intravenous fluid infusion of volumes > 1500 mL. Hypoxaemic episodes influencing oxygen availability are common not only in the immediate postanaesthetic period, but may also continue to occur until the fourth to fifth postoperative day.” After major abdominal surgery, hypoxaemia, especially episodic hypoxaemia at night-time, has been observed by Rosenberg et al.“,‘” to last for 2-5 days postoperatively. Therefore, it is likely that postoperative hypoxaemia is a factor of importance in the pathogenesis of ischaemic cardiac complications (arrhythmias and myocardial infarction) also in the late postoperative period.” Causes of postoperative hypoxaemia may be inhomogenity of pulmonary ventilation and perfusion, reduced functional residual capacity with increased closing volume and postoperative increase in venoarterial shunting. Administration of narcotics may be an additional factor resulting in respiratory depression and modified ventilatory response to hypercapnea and hypoxaemia. Additional mgocardial ischaemia evoking factors - In addition to stress, other perioperative states that contribute to the risk of postoperative myocardial ischaemic episodes are pain, hypothermia, hypovolaemia or hyper-
POSTOPERATIVE
volaemia, anaemia, blood viscosity changes, hypercoagulability and electrolyte disturbances.
Measures for prevention cardiac complications
of postoperative
Myocardial ischaemia resulting in infarction is the most serious postoperative cardiac complication and may compromise short- as well as medium-term life expectancy.J Therefore, proper postoperative measures for prevention, detection and treatment of myocardial ischaemic episodes are essential for the reduction of cardiac morbidity and mortality after vascular surgery. Monitoring alternatives and therapeutic measures of potential importance are summarized in Table 2. Crrrdiovnsculcrr monitoring and therapeutic measures Maintenance of haemodynamic stability is of importance to avoid problems associated with either arterial hypotension or hypertension. Therefore. continuous monitoring of blood pressure (preferably invasive) and heart rate is essential, and disturbances should be treated aggressively. The clinical value of a pulmonary artery catheter in the postoperative period has been questioned following abdominal aortic aneurysm surgery.“.” Myocardial ischaemia monitoring in patients undergoing peripheral vascular surgery has been stressed by Pasternack et al.“’ Continuous ST-segment analysis for detection of myocardial ischaemia seems essential since it provides immediate evidence of ongoing ischaemia with direct implications for the management of the patient.“‘.” As shown by Raby et al.,” silent ischaemic events usually precede clinical cardiac events in vascular surgery patients. In the study by Landesberg et al.’ continuous ECG recordings (including ST-trend analysis) were started 1 day before surgery and continued during the operation and 72 h postoperatively. Most (77%) adverse cardiac events were found to start within 24 h of surgery. In 58% of the patients 342 episodes of ST Table
2
for reduction mortality.
Postoperative management of the vascular surgery patient of the risk of postoperative cardiac morbidity and
Monitoring - blood
Therapeutic pressure.
heart rate
- pulse oximetry - ECG.
ST-segment
- blood
gas analysis
- haemoglobin - graft
function
- pain/sedation
level
amplitude
measureS
- prevention of hypo-/hypertension and tachycardia - optimization of oxygen administration - reduction of stress/cardiac workload - optimization of oxygenation/ ventilation/acid-base level - optimization of haemoglobin level - haemorheological enhancement of blood flow/sympathetic blockadelantithrombotic treatment - pain therapy (parenteral. epidural. patient controlled (PCA))
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depression were observed. Patients with cardiac events were noted to have more and longer ischaemic episodes. Postoperative ischaemia of more than 2 h duration was found to be significantly associated with cardiac events. All patients suffering postoperative myocardial infarctions were found to have had cumulative ischaemia times lasting for more than 5 h. Therefore, in case of appearance of ST segment depression in the postoperative period, the condition may, in the early phases, be treatable with proper anti-ischaemia therapy and more severe myocardial ischaemic consequences leading to permanent heart damage can thereby be prevented. Postoperative tachycardia and increased sympathetic activation are factors of importance for the development of disturbed oxygen availability and the occurrence of myocardial ischaemia. Heart rate control for 48 h after surgery and administration of a P-blocker when indicated has been suggested to reduce the risk of postoperative myocardial ischaemia after vascular surgery in this high-risk group of patients.‘3 Even preoperative start of the therapy could be considered. In a study by Wallace et aLZJ it was considered that perioperative myocardial ischaemia occurs in 20-40% of patients at risk for cardiac complications, and that the ischaemia was associated with a ninefold increase in risk for perioperative cardiac death, myocardial infarction or unstable angina, and a twofold long-term risk. Prophylactic atenolol was given for 1 week to patients with, or at risk for, coronary artery disease. Atenolol administration could be shown to reduce significantly the incidence of myocardial ischaemia. In addition, a reduced risk for death at 2 years after surgery was observed. Therefore, it has been claimed that P-adrenergic blocking drugs are probably underutilized considering their beneficial effects on cardiovascular function in the perioperative period.25 Also after myocardial infarction the protective effects of P-adrenergic blocking drugs against reinfarction are of importance. It is possible that women run a higher risk of perioperative myocardial infarction than men after lower extremity arterial bypass grafting.‘6 The reason seems to be that women more often have unrecognized cardiac disease that adversely affects perioperative, as well as long-term, outcome. Prolonged oxygen therapy is indicated in the postoperative period to reduce the risk of increased morbidity and mortality.” The risk of tissue hypoxia in spite of a normal PaOz should be considered, especially in the case of postoperative hypovolaemia, hypotension or anaemia. Therefore, oxygen therapy should be considered routine practice during the postoperative recovery period. Determination of cardiac myocardial injury - In patients with a prior history of cardiac ischaemic disease or intraoperative cardiovascular instability, assessment of plasma levels of myocardial enzymes and isoenzymes should be carried out in the postoperative phase. In recent years new serum markers for acute myocardial infarction have been introduced.‘*.‘9 The cardiac troponin level in plasma may be considered a highly specific
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marker for myocardial necrosis since it is not affected by the surgery, as such. 3o Also in unstable angina both troponin T and troponin I may be elevated. There is a correlation between the plasma troponin levels measured postoperatively and the incidence of cardiac complications in the months following surgery.“’ Patients with raised troponin levels preoperatively seem to be at a higher risk for myocardial infarction, left ventricular failure and increased mortality.3’~3’ Troponin is, consequently, the biological marker that should be determined whenever mypcardial ischaemic injury is suspected. Optimal haemoglobin level - The acceptable postoperative haemoglobin level of the high-risk vascular surgery patient has remained a matter of controversy. Recently, a restrictive strategy of red-cell transfusion in critically ill patients has been advocated by HCbert et alJ3 Not even in patients with clinically significant cardiac disease could a major difference in mortality be demonstrated between patients with haematocrit levels in the range of 70-90 g/L as compared with patients with haemoglobin levels the range of 100-120 g/L. Nelson et al.,jJ on the other hand, studied the implications of postoperative anaemia for the development of myocardial ischaemia and morbid cardiac events (cardiac death, myocardial infarction, unstable angina, ischaemic pulmonary oedema) in high-risk patients undergoing elective infrainguinal arterial bypass surgery. A haematocrit of about 28%, i.e. a haemoglobin level in the range of 90-100 g/L, was considered a safe lower threshold value. A haematocrit value of lower than about 28% was found to be associated with an increased incidence of cardiac ischaemia and complication rates. Consequently, Nelson et al.3J suggested that anaemia may play a role in postoperative myocardial ischaemia and cardiac morbidity in high-risk vascular patients. Monitoring of graffimction - Early detection of graft failure is essential for prevention of limb loss and myoglobinuria-associated renal failure. Temperature, colour, capillary filling and peripheral pulses should, therefore, be checked repeatedly (doppler ultrasound). In the case of a deteriorating pulsatile flow the vascular surgeon should immediately be contacted to allow rapid revascularization so that fasciotomy may be avoided. Furthermore, graft function is influenced by blood viscosity and coagulability. Arterial disease is characterized by hypercoagulability and the success of bypass grafting is dependent on high graft blood-flow velocity, and prevention of platelet and leukocyte deposition onto the prosthetic materials.“-” Although the choice of general or regional anaesthesia for peripheral vascular surgery may not significantly influence cardiac outcome, it still seems advantageous for postoperative graft function by influencing blood flow as well as coagulation.’ Infusion of a plasma volume expander will also reduce blood viscosity and enhance microvascular blood flow. Dextran, especially 10% Dextran 40 000, has been shown of value for prevention of early postoperative
thrombosis following lower extremity bypass.“’ The deposition of platelets and leukocytes onto prosthetic materials is reduced by Dextran, which, together with haemorheological effects, will favour graft patency. Hydroxyethyl starch (HES) has also been reported to induce beneficial effects on endothelial cell activation, microvascular permeability and reperfusion injury.““ Postoperative stress modulatiorl and pain relief Hypothermia is a stress factor that may cause potential adverse physiological effects including cardiac arrhythmias, coagulopathies, altered levels of consciousness, decreased drug metabolism. impaired renal function and a leftward shift in the haemoglobin oxygen saturation curve reducing the delivery of oxygen to tissues. Elderly patients are considered to have a decreased ability to maintain normal body temperature during anaesthesia. In addition, the rewarming rate of the elderly patient is slower so that a prolonged rewarming period is needed.‘” Hypothermic vascular surgical patients have in the postoperative period been shown to have decreased arterial oxygen tension, increased incidence of electrocardiographic changes consistent with myocardial ischaemia and angina.J’ Myocardial ischaemia has been noted in 36% of the hypothermic patients undergoing lowerextremity vascular reconstruction as compared to 13% in the normothermic patients. Since unintentional hypothermia increases the risk of cardiac ischaemic events in the early postoperative period it is consequently, essential always to take necessary measures to prevent intraoperative hypothermia, especially in the elderly vascular surgical patient. In cases of hypothermia there is a risk of hypertension followed by hypotension during rewarming, when blood vessels dilate and systemic vascular resistance decreases. The vasodilatation may enhance third-space fluid losses. Therefore, in the early postoperative phase there is usually a need for additional fluid infusion to maintain adequate cardiac filling pressures and haemodynamic stability. Proper sedation and pain alleviation are considered of major importance for reduction of the stress load and the risk of stress-associated complications. The use of analgesic techniques in the early postoperative period which decrease postoperative stress. e.g. continuous epidural block with local anaesthetics and/or opioids may, by modulation of blood flow and coagulability, reduce the risk of postoperative myocardial ischaemia.’ Regional anaesthesia for postoperative analgesia appears to have several advantages over traditional techniques. Epidural infusion of opioids in combination with dilute local anaesthetics seems to produce good analgesia without the drawbacks of motor blockade. By efficient modulation of postoperative sympathetic hyperactivity and hypercoagulability, the risk of myocardial ischaemic episodes will be diminished.‘,” Therefore. epidural anaesthesia prolonged into the postoperative period may, in addition to stress alleviating effects, prevent platelet hyperaggregability after peripheral vascular surgery.”
POSTOPERATIVE
Diebel et al.““ have claimed that epidural analgesia after aortic reconstructions will attenuate the postoperative increase in total body oxygen consumption and thereby the haemodynamic demands on the heart. Thoracic epidural anaesthesia (TEA) allows specific blockade of nociceptive reflex arcs and may exert beneficial effects on stress-induced alterations of organ function in patients undergoing aortic surgery. In patients with coronary artery disease it has been shown that TEA may increase the diameter of stenotic epicardial coronary artery segments without causing dilation of coronary arterioles.” Myocardial blood flow to areas at risk is, consequently, improved and paradoxical reactions of atherosclerotic coronary arteries after symphatetic stimulation are suppressed. During stress-induced myocardial ischaemia in patients with coronary artery disease TEA has been found to improve global and regional left ventricular function.J” Pulmonary function is improved owing to pain relief allowing the patient to breathe and cough adequately. Lumbar epidural analgesia in the postoperative period has been reported to increase haemodynamic stability and reduce the incidence of postoperative respiratory failure.J7 Cardiac arrest caused by coronary spasm has, however, been reported in vascular surgery patients during the recovery period from lumbar epidural bupivacaine anaesthesia.“” Coronary spasm caused by an altered balance between sympathetic and parasympathetic nervous activity was suggested to induce myocardial ischaemia followed by malignant dysrythmias. The study stresses the importance of close cardiac monitoring during the entire postoperative period of patients operated on under epidural anaesthesia. Epidural analgesic drugs and segmental site of infusion should be chosen so that blockade of motor neurons to the lower extremity is absent or minimaLJY With TEA, efficient analgesia can be obtained after aortic surgery while more peripheral vascular surgery will benefit from a lumbar epidural block. Lumbar epidural analgesia may impair postoperative ambulation unless agents with minor motor blocking effects, e.g. ropivacaine, and/or epidural opioids, are used. For safe epidural analgesia, monitoring of leg motor function and sensibility must be performed for early detection of complications (epidural haematoma, infection).‘” Such monitoring is of utmost importance in vascular surgery since anticoagulants are routinely used which may increase the risk of epidural haematoma. Moreover, diabetes is a common complication in patients scheduled for peripheral vascular surgery and diabetic disease will increase the risk of infectious complications including epidural infections. Safe routines for regular review of patients with epidural analgesia are, consequently, necessary in the postoperative period.“” Once the patient leaves the postanaesthesia care unit, the optimal use of postoperative epidural analgesia may be limited by lack of safe routines in the surgical wards. Patient-controlled epidural analgesia with bupivacaine (0.05%) and fentanyl (4 pg/ml) has been found an alternative approach for providing effective and safe
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postoperative analgesia on hospital wards.” Side effects of epidural local anaesthetic combined with opioids are, in order of frequency: pruritus, nausea, sedation, hypotension and motor block.” Prophylactic inclusion of antiemetics may reduce the incidence of nausea.52 Respiratory depression was, however, found to be a rather uncommon adverse effect (0.3%). Intestinal function and permeability may be affected after major vascular surgery.53 Gastrointestinal function is recovered faster when TEA is used which may reduce the risk of nausea as well as of gastrointestinal ischaemia leading to bacterial translocation and risk of septic systemic organ dysfunction. Respiratory and neurological function A recent cumulative meta-analysis of randomized controlled studies comparing the effects of different analgesic therapies on pulmonary outcome indicate that postoperative epidural pain control can significantly decrease the incidence of pulmonary morbidity.54 The time of intubation, duration of stay in the intensive care unit and incidence of cardiac and pulmonary complications can be reduced by epidural analgesia for postoperative pain relief after elective repair of abdominal aortic aneurysms.5s Compared with systemic opioids, epidural opioids or local anaesthetics were observed by Ballantyne et a1.54to decrease the incidence of atelectasis (opioids) and pulmonary infections and overall complications (local anaesthetics). It is obvious that with respect to lung function the epidural route allows a better recovery of respiration when opioids are administered. Combination of opioids with low concentration of local anaesthetics is also an acceptable pain alleviation approach while high-dose local anaesthetics may paralyse chest muscles and impair respiratory function. Ropivacaine (0.2%) in combination with sufentanil (1 pg/mL) may be a better choice than a bupivacaine (0.175%)-sufentanil mixture, owing to ropivacaine’s lesser effects on motor function.56 Respiratory depression resulting in hypoxaemic episodes may also influence cognitive function and the occurrence of confusional states or overt delirium.57~s* Experience from climbing to extremely high altitude indicates that changes in cognitive function may provide the most sensitive and specific evidence of impaired oxygen delivery.59 High postoperative pain scores at rest have been shown to be associated with an increased risk of delirium over the first 3 postoperative days.m The method of postoperative analgesia was not found to affect the risk of delirium. Therefore, effective control of postoperative pain according to the accepted pain treatment regimes seems essential for reducing the incidence of postoperative delirium. A rare neurological complication of elective abdominal aortic aneurysm repair is spinal cord ischaemia owing to injury or blood-flow disturbance in the artery of Adamkiewicz supplying the anterior spinal artery.
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Bilateral hypogastric artery occlusion or profound shock may also cause cord ischaemia. If pa,raplegia develops the prognosis is usually very poor, while partial or even complete recovery can be expected after partial motor or sensory loss. Monitoring of leg sensibility and motor function in the postoperative phase is of importance for the diagnosis of this complication and the possible alternative of epiduraVintraspina1 haematoma should be kept in mind. Monitoring of’renal function In vascular surgery patients, especially patients undergoing aortic aneurysm repair, there is a considerable risk of postoperative renal dysfunction. Acute renal failure may be caused by prolonged ischaemia owing to hypovolaemia, extended periods of suprarenal aortic crossclamping, atheroembolization of renal arteries or in response to nephrotoxins.6’ Rhabdomyolysis with release of myoglobin from ischaemic muscle may occur in the vascular patient when arterial blood flow to muscle is compromised and result in renal functional impairment. Preoperative signs of left ventricular dysfunction seems predictive of postoperative renal failure, especially in patients of advanced age.6’ Routine measurement of urine output on an hourly basis should always be carried out in the postoperative period. In case of low urine output a fluid challenge should be tried, especially when cardiac filling pressure is low. Lack of response to fluid challenge in spite of increased filling pressures necessitates additional supportive measures. Low doses of dopamine infusion (3 pg/kg/min) after abdominal vascular surgery in patients with renal functional impairment have been shown to increase urinary output and the diuretic effect seems related to the plasma dopamine concentration.” Patients not responding to the dopamine infusion were found to have prolonged clamping and operation times. The value of dopamine for improving renal function in the periopertive setting is presently a matter of controversy and questioned by many clinicians. Furosemide, owing to its rapid onset of action, is the loop diuretic most often given in case of low urine output and may also be needed to avoid left ventricular failure in patients with reduced cardiac reserve and nephrosclerosis. Increasing creatine and urea levels in combination with consistently low urine output may make it necessary to start haemofiltration therapy to cope with a transient renal failure situation. Postoperative bleeding, colon ischaemia and antibiotic prophylaxis In vascular surgery patients, especially in those undergoing aortic surgery, it is important to monitor the coagulation status and observe for signs of postoperative bleeding complications. Signs of hypovolaemia and transfusion requirements, in combination with increasing abdominal girth, are pathognomic for ongoing intra-
abdominal bleeding. Postoperative bleeding may be surgical or non-surgical. Patients with a non-surgical bleeding may present with general oozing from wound sites and cannulae. Blood tests for diagnosis of the haemostatic disturbance may be needed for decisions on proper therapeutic measures. Monitoring of the thromblastographic pattern may provide useful information on the functional status of the haemostatic capacity.hJ Signs indicating colon ischaemia should also be sought in the postoperative period. This severe complication may occur in response to intraoperative splanchnic hypoperfusion, atherosclerosis, thrombosis, embolization or ligation of the primary or collateral blood supply to the left colon. Colon ischaemia may present with bloody diarrhoea and intense abdominal pain in combination with leukocytosis, metabolic acidosis, fever, tachycardia and excessive nasogastric tube retentions. Peritoneal inflammatory signs may occur secondary to transmural necrosis and perforation. Massive intensive care efforts and surgical interventions may be necessary to cope with this ischaemic complication. Antimicrobial prophylaxis is of importance in vascular surgery for the prevention of wound infection. Usually single or only a few repeated prophylactic doses are given. It has recently been suggested, however, that optimal prophylaxis is achieved by a multiple-dose antibiotic regimen rather than single-dose therapy.” Furthermore, it was suggested that the antimicrobial prophylaxis should be continued in the postoperative period until lines/drain tubes are removed, but not for more than 5 days.
References I. Rose D K. Cohen M M, DeBoer D P. Cardiovascular events in the postanesthesia care unit. Contribution of risk factors. Anesthesiology 1996; 84: 772-78 I. 2. Campbell W B, Ballard P K. Goodman D A. Intensive care after abdominal aortic surgery. Eur J Vast Surg I99 I : 5: 665-668. 3. Tuman K J. McCarthy R J, March R J et al. Effects of epidural analgesia on coagulation and outcome after major vascular surgery. Anesth Analg 199 I: 73: 696-704. 4. Mangano D T. Perioperative cardiac morbidity. Anesthesiology 1990; 72: 153-164. 5. Cohen A T. Prevention of perioperative myocardial ischaemia and its complications. Lancet 1998: 35 I : 385-366. 6. Landesberg G, Luria M H, Cotev S et al. Importance of longduration postoperative ST-segment depression in cardiac morbidity after vascular surgery. Lancet 1993: 34 I : 7 IS-7 19. 7. Zeiher A M. Krause T, Schachinger V. Minners J. Moser E. Impaired endothelium-dependent vasodilation of coronary resistance vessels is associated with excercise-induced myocardial ischemia. Circulation 1995; 9 I : 2345-2352. 8. Nabel E G, Selwyn A P. Ganz P. Paradoxical narrowing of artheroslerotic coronaly arteries induced by increases in heart rate. Circulation 1990: 8 I : 850-859. 9. Epstein S E, Quyyumi A A, Bonow R 0. Myocardial ischemia silent or symptomatic’? N Eng J Med 19X8: 318: 1038-1043. IO. McCann R L, Clements F M. Silet myocardial ischemia in patients undergoing peripheral vascular surgery: incidence and association with perioperative cardiac morbidity and mortality. J Vast Surg 1989: 9: 583-587. I I. Howell S J. Hemming A E, Allman K G et al. Predictors of postoperative myocardial ischaemia. The role of intercurrent hypertension and other cardiovascular risk factors. Anaesthesia 1997; 52: 107-I I I. 12. Fleisher L. Tuman K. What can we learn from provoking ischemia? Anesth Analg 1997; 84: I 177-I 179.
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13. Russel G B, Graybeal J M. Hypoxemic episodes of patients in a postanesthesia care unit. Chest 1993; 104: 899-903. 14. Powell J F. Menon D K. Jones J G. The effects of hypoxaemia and recommendations for postoperative oxygen therapy. Anaesthesia 1996; 5 I : 769-772. IS. Rosenberg J, Dirkes W, Kehlet H. Late postoperative episodic oxygen desaturation and heart rate variations following major abdominal surgery. Br J Anaesth 1989: 63: 652-654. 16. Rosenberg J. Ullstad T. Rasmussen J et al. The time course of postoperative hypoxaemia. Eur J Surg 1994: 160: 137-143. 17. Pateman J A, Hanning C D. Postoperative myocardial infarction and episodic hypoxaemia. Br J Anaesth 1989; 63: 648-650. 18. Sandison A J. Wyncoll D L, Edmondson R C et al. ICU protocol may affect the outcome of non-elective abdominal aortic aneurysm repair. Eur J Endovasc Surg 1998: 16: 356-36 I. 19. Valentine R J. Duke M L. Inman M H et al. Effectiveness of pulmonary artery catheters in aortic surgery: a randomized trial. J Vast Surg 1998: 27: 203-2 I I. 20. Pasternack P F. Grossi E A. Baumann F G et al. The value of silent myocardial ischemia monitoring in the prediction of perioperative myocardial infarction in patients undergoing peripheral vascular surgery. J Vast Surg 1989;lO: 617-625. 2 I. Clemets F M. McCann R L. Levin R I. Continuous ST segment analysis for detection of perioperative myocardial ischemia. Crit Care Med 1988: 16: 710-71 I. 22. Raby K E, Barry J. Creager M A et al. Detection and significance of intraoperative and postoperative myocardial ischemia in peripheral vascular surgery. JAMA 1992; 268: 222-227. 23. Raby K E. Brull S 1, Timimi F et al. The effect of heart rate control on myocardial ischemia among high-risk patients after vascular surgery. Anesth Analg 1999: 88: 477482. 24. Wallace A. Layug B. Tateo I et al. Prophylactic atenolol reduces postoperative myocardial ischemia. McSPl research group. Anesthesiology 1998; 88: 7-l 7. 25. Warltier D C. Beta-adrenergic-blocking drugs: Incredibly useful, incredibly underutilized. Anesthesiology 1998; 88: 2-5. 26. Mays B W. Towne J B, Fitzpatrick C M et al. Women have increased risk of perioperative myocardial infarction and higher long-term mortality rates after lower extremity arterial bypass grafting. J Vast Surg 1999: 29: 807-8 12. 27. Hanning C D. Prolonged postoperative oxygen therapy. Br J Anaesth 1992; 69: 115-l 16. 28. Hamm C W. New serum markers for acute myocardial infarction. Editorial. N Engl J Med 1994: 33 I: 607-608. 29. Adams III J E, Sigard G A, Allen B T et al. Diagnosis of perioperative myocardial infarction with measurement of cardiac troponin I. N Engl J Med 1994; 330: 67&674. 30. Metzler H, Gries M. Rehak P. Lang T. Fruhwald S. Toller W. Perioperative myocardial cell injury: the role of troponins. Br J Anaesth 1997: 78: 386-390. 3 I. Prellwitz W. Hafner G. Pupprecht H J. Meyer J. Diagnostic and differential diagnostic value of troponins. Med Klin 1996; 9 I : 336-342. 32. Munzer T. Heim C. Riesen W. Perioperative myocardial infarction and cardiac complications after noncardiac surgery in patients with prior myocardial infarction. Anaesthetist 1996: 45: 225-230. 33. Hebert PC, Wells G, Blajchman M A et al. A multicenter, randomized. controlled clinical trial of transfusion requiremens in critical care. N Engl J Med 1999; 340: 409-417. 34. Nelson A H. Fleisher L A, Rosenbaum S H. Relationship between postoperative anaemia and cardiac morbidity in high-risk vascular patients in the intensive care unit. Crit Care Med 1993: 2 I : 860-866. 35. Bandyk D F. Cato R F, Towne J B. A low flow velocity predicts failure of femoropopliteal and femorotibial bypass grafts. Surgery 1985; 98: 799-809. 36. Shoenfeld N A. Eldrup-Jorgensen J, Conolly R et al. The effect of low molecular weight dextran on platelet deposition onto prosthetic materials. J Vast Surg 1987; 5: 76-82. 37. Al-Huneidi W. Qwunwanne A. Christenson J T. Adhesion of leucocytes onto polytetrafluoroethylene (PTFE) vascular grafts and the effect of low molecular weight dextran (LMWD). hit Angiol 1990; 9: 16-19. 38. Rutherford R B. Jones D N, Bergentz S-E et al. The efficacy of dextran 40 in preventing early postoperative thrombosis following difficult lower extremity bypass. J Vast Surg 1984; I: 765-773. 39. Zirkia B A, Subbarao C, Oz M C et al. Macromolecules reduce abnormal microvacular permeability in rat limb ischemiareperfusion injury. Crit Care Med 1989; 17: 1306-1309.
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40. Frank S M. Beattie C, Christopherson R et al. Epidural versus general anesthesia, ambient operating room temperature, and patient age as predictors of inadvertent hypothermia. Anesthesiology 1992; 77: 252-257. 41. Frank S M, Beattie C, Christopherson R et al. Unintentional hypothermia is associated with postoperative myocardial ischemia. Anesthesiology 1993; 78: 468476. 42. Breslow M J. Jordan D A, Christopherson R et al. Epidural morphine decreases post-operative hypertension by attenuating sympathetic nervous system hyperactivity. JAMA 1989; 26 I : 3577-358 I. 43. Naesh 0, Haljamle H. Hindberg I et al. Epidural anaesthesia prolonged into the postoperative period prevents stress response and platelet hyperaggregability after peripheral vascular surgery. Eur J Vast Surg 1994; 8: 395400. 44. Diebel L N. Lange M, Schneider F et al. Cardiopulmonary complications after major surgery: a role for epidural analgesia? Surgery 1987; 102: 660-666. 45. Blomberg S. Emanuelsson H, Kvist H et al. Effects of thoracic epidural anesthesia on coronary arteries and arterioles in patients with coronary artery disease. Anesthesiology 1990; 73: 840-847. 46. Koch M. Blomberg S, Emanuelsson H et al. Thoracic epidural anesthesia improves global and regional left ventricular function during stress-induced myocardial ischemia in patients with coronary artery disease. Anesth Analg 1990.7 1: 625-630. 47. Her C. Kizelshteyn G, Walker V, Hayes D, Lees D E. Combined epidural and general anesthesia for abdominal aortic surgery. J Cardiothorac Anesth 1990: 4: 552-557. 48. Sprung J, Lesitsky M A, Jagetia A et al. Cardiac arrest caused by coronary spasm in two patients during recovery from epidural anesthesia. Reg Anesth 1996; 2 I: 253-260. 49. Breivik H. Safe perioperative spinal and epidural analgesia: importance of drug combinations, segmental site of injection, training and monitoring. Acta Anaesthesiol Stand 1995; 39: 869-87 I. 50. Burstal R, Wegener F. Hayes C, Lantry G. Epidural analgesia: prospective audit of 1062 patients. Anaesth Intens Care 1998; 26: 165-172. 5 I. Liu S S. Allen H W, Olsson G L. Patient-controlled epidural analgesia with bupivacaine and fentanyl on hospital wards Prospective experience with 1,030 surgical patients. Anesthesiology 1998; 88: 688-695. 52. Tramer M R, Walder B. Efficacy and adverse effects of prophylactic antiemetics during patient-controlled analgesia therapy: a quantitative systematic review. Anesth Analg 1999; 88: 1354-1361. 53. Roumen R M H, van der Vliet J A, Wevers R A, Goris R J A. Intestinal permeability is increased after major vascular surgery. J Vast Surg 1993: 17: 734-737. 54. Ballantyne J C, Carr D B, deFerranti S et al. The comparative effects of postoperative analgesic therapies on pulmonary outcome: cumulative meta-analyses of randomized, controlled trials. Anesth Analg 1986; 86: 598-612. 55. Major Jr C P, Greer M S, Russel W L, Roe S M. Postoperative pulmonary complications and morbidity after abdominal aneurysmectomy: a comparison of postoperative epidural versus parenteral opioid analgesia. Am Surg 1996; 62: 45-5 I. 56. Broder G, Mertes N. Van Aken H et al. Epidural analgesia with local anesthetics after abdominal surgery: earlier motor recovery with 0.2% ropivacaine than 0.175% bupivacaine. Anesth Analg 1999; 88: 128-133. 57. Akerlund LP, Rosenberg J. Postoperative delirium: treatment with supplementary oxygen. Br J Anaesth 1994; 72: 286-290. 58. Marcantonio E R, Goldman L, Mangione C M et al. A clinical prediction rule for delirium after elective noncardiac surgery. JAMA 1994; 271: 134-139. 59. Hornbein T F. Townes B D, Schoene R B, Sutton J R. Houston C S. The cost to the central nervous system of climbing to extremely high altitude. N Engl J Med 1989; 321: 1714-1719. 60. Lynch E P, Lazor M A Gellis J E et al. The impact of postoperative pain on the development of postoperative delirium. Anesth Analg 1998; 86: 781-785. 61. Hemreck AS. Prevention and management of surgical complications during repair of abdominal aortic aneurysms. Surg Clin North Am 1989; 69: 869-894. 62. Novis B K, Roizen M F, Aronson S, Thisted R A. Association of preoperative risk factors with postoperative acute renal failure. Anesth Analg 1994; 78: 143-149.
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ANAESTHESIA
AND
CRITICAL
CARE
63. Pavoni V, Vetri M, Ferraro L et al. Plasma dopamine concentration and effects of low dopamine doses on urinary output after major vascular surgery. Kidney Int Suppl 1998: . 66: S75-S80. 64. Gibbs N M, Crawford G P M, Michalopoulos N.
Thromboelastographic patterns following abdominal aortic surgery. Anaesth lntens Care 1994; 22: 534-538. 65. Hall J C, Christiansen K J, Goodman M et al. Duration of antimicrobial prophylaxis in vascular surgery. Am J Surg 1998; 175: 87-90.