Postoperative care and pain relief in vascular surgery

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VASCULAR ANAESTHESIA AND INTENSIVE CARE MEDICINE 8:6 244 © 2007 Published by Elsevier Ltd. Postoperative care and pain relief in vascular surgery David Yates Lawrence Caldicott Abstract Postoperative care of the vascular patient is the same as that for any major surgical patient. The aims are to provide adequate arterial oxy- genation and ensure adequate respiratory function, a normal cardiac output, an adequate circulating volume at an appropriate haematocrit, a good urine output and good analgesia. The high incidence of comorbidi- ties in this group of patients and the widespread nature of atheromatous disease predisposes to frequent complications. These complications and their management are described in general and with particular refer- ence to specific vascular procedures. Vigilant monitoring and attention to detail in the postoperative management of these patients is essential for successful outcome. Keywords pain relief; postoperative care; vascular surgery The postoperative care of the vascular patient is the same as any major surgical patient. The aims of postoperative care are to ensure: adequate arterial oxygenation and respiratory function normal cardiac output and cardiovascular parameters adequate circulating volume at an acceptable haematocrit good urine output good analgesia. Postoperative care can be more challenging in the vascular patient because of the high incidence of comorbidity. Sites for postoperative care Arterial vascular surgery could be considered as major surgery, and therefore patients should be managed in at least a highdependency unit. This type of unit is defined as a service provided for patients with actual or potential organ failure, who will benefit from inten sive nursing, observation and medical input, which cannot be pro vided on a general ward. Invasive monitoring may be used. The nurse to patient ratio on a highdependency unit is normally 2:1. David Yates, FRCA, is Specialist Registrar in Anaesthesia at York. He qualified at the University of Leeds, and trained as an SHO in the Yorkshire region. His research interests include perioperative optimization and the identification of high-risk surgical patients. Lawrence Caldicott, FRCA, is Consultant Anaesthetist at St James’s Hospital, Leeds. He qualified at St George’s Hospital, London, and trained in anaesthesia in Leeds and Sheffield. His interests include anaesthesia for vascular surgery and local anaesthetic techniques. Patients with more severe cardiovascular or respiratory failure, needing endotracheal intubation and/or inotropic support will require more intensive nursing input (nurse:patient ratio of 1:1), and for this reason are admitted to the ICU. Renal replacement therapy can also be provided. The exact placing of a postopera tive patient depends on the patient’s characteristics and the locally available resources and usual practices. Adherence to rigid policies (e.g. requesting an ICU bed before starting elective aortic aneurysm surgery) can result in cancellation of surgery. Recent evidence shows that selective admission to the ICU for aortic surgery may reduce occupancy, with little impact on outcomes and care. In fact, many elective aneurysm patients, if carefully chosen, can be extu bated and safely managed overnight in theatre recovery areas. 1 General considerations Postoperative myocardial infarction This condition is the most common cause of death after vascu lar surgery, and occurs in 2–5% of patients. It is probably due to rupture of an atheromatous coronary artery plaque, with sub sequent thrombosis and distal occlusion of the artery, or pro longed ischaemia. It carries a 25–50% mortality, and commonly occurs on the first or second postoperative day. Presentations include hypotension, chest pain, heart failure, confusion, pulmo nary oedema, ventricular arrhythmias and sudden death. It may be diagnosed clinically with sequential ECGs and measurement of cardiac enzymes such as creatine kinase (CKMB) or cardiac troponins. Treatment is as for myocardial infarction in medical patients, except thrombolysis is contraindicated. Cardiac tropo nin I (cTnI) is a very sensitive marker for myocardial necrosis. Studies measuring cTnI postoperatively have shown that raised concentrations may occur at two time points: early rises at 12–32 hours and late rises at 48–72 hours postsurgery. 2 Both are predictive of inhospital cardiac complications and poor long term outcome, and may be due to differing pathophysiologies. The early rise may follow a ruptured coronary artery plaque and a late rise may follow prolonged ischaemia. Aggressive use of βblockers, analgesia, and maintaining an adequate haematocrit may minimize the myocardial necrosis in these patients. The pathophysiology of perioperative myocardial infarction is multifactorial (Table 1). Pathophysiology of perioperative myocardial infarction Increased peripheral oxygen consumption requires increased cardiac output and therefore increased myocardial oxygen demand Increased likelihood of atheromatous plaque rupture in the perioperative period Hypercoagulable states postoperatively Nocturnal hypoxia secondary to opioids Inadvertent omission of cardiac medications due to patient being nil by mouth Deliberate cessation of antiplatelet agents for the perioperative period Table 1

Transcript of Postoperative care and pain relief in vascular surgery

Page 1: Postoperative care and pain relief in vascular surgery

Vascular

Postoperative care and pain relief in vascular surgeryDavid Yates

lawrence caldicott

AbstractPostoperative care of the vascular patient is the same as that for any

major surgical patient. The aims are to provide adequate arterial oxy­

genation and ensure adequate respiratory function, a normal cardiac

output, an adequate circulating volume at an appropriate haematocrit,

a good urine output and good analgesia. The high incidence of comorbidi­

ties in this group of patients and the widespread nature of atheromatous

disease predisposes to frequent complications. These complications and

their management are described in general and with particular refer­

ence to specific vascular procedures. Vigilant monitoring and attention

to detail in the postoperative management of these patients is essential

for successful outcome.

Keywords pain relief; postoperative care; vascular surgery

The postoperative care of the vascular patient is the same as any major surgical patient. The aims of postoperative care are to ensure:• adequate arterial oxygenation and respiratory function• normal cardiac output and cardiovascular parameters• adequate circulating volume at an acceptable haematocrit• good urine output• good analgesia.Postoperative care can be more challenging in the vascular patient because of the high incidence of comorbidity.

Sites for postoperative care

Arterial vascular surgery could be considered as major surgery, and therefore patients should be managed in at least a high-­dependency unit. This type of unit is defined as a service provided for patients with actual or potential organ failure, who will benefit from inten-­sive nursing, observation and medical input, which cannot be pro-­vided on a general ward. Invasive monitoring may be used. The nurse to patient ratio on a high-­dependency unit is normally 2:1.

David Yates, FRCA, is Specialist Registrar in Anaesthesia at York.

He qualified at the University of Leeds, and trained as an SHO in

the Yorkshire region. His research interests include perioperative

optimization and the identification of high-risk surgical patients.

Lawrence Caldicott, FRCA, is Consultant Anaesthetist at St James’s

Hospital, Leeds. He qualified at St George’s Hospital, London, and

trained in anaesthesia in Leeds and Sheffield. His interests include

anaesthesia for vascular surgery and local anaesthetic techniques.

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Patients with more severe cardiovascular or respiratory failure, needing endotracheal intubation and/or inotropic support will require more intensive nursing input (nurse:patient ratio of 1:1), and for this reason are admitted to the ICU. Renal replacement therapy can also be provided. The exact placing of a postopera-­tive patient depends on the patient’s characteristics and the locally available resources and usual practices. Adherence to rigid policies (e.g. requesting an ICU bed before starting elective aortic aneurysm surgery) can result in cancellation of surgery. Recent evidence shows that selective admission to the ICU for aortic surgery may reduce occupancy, with little impact on outcomes and care. In fact, many elective aneurysm patients, if carefully chosen, can be extu-­bated and safely managed overnight in theatre recovery areas.1

General considerations

Postoperative myocardial infarctionThis condition is the most common cause of death after vascu-­lar surgery, and occurs in 2–5% of patients. It is probably due to rupture of an atheromatous coronary artery plaque, with sub-­sequent thrombosis and distal occlusion of the artery, or pro-­longed ischaemia. It carries a 25–50% mortality, and commonly occurs on the first or second postoperative day. Presentations include hypotension, chest pain, heart failure, confusion, pulmo-­nary oedema, ventricular arrhythmias and sudden death. It may be diagnosed clinically with sequential ECGs and measurement of cardiac enzymes such as creatine kinase (CK-­MB) or cardiac troponins. Treatment is as for myocardial infarction in medical patients, except thrombolysis is contraindicated. Cardiac tropo-­nin I (cTnI) is a very sensitive marker for myocardial necrosis. Studies measuring cTnI postoperatively have shown that raised concentrations may occur at two time points: early rises at 12– 32 hours and late rises at 48–72 hours post-­surgery.2 Both are predictive of in-­hospital cardiac complications and poor long-­term outcome, and may be due to differing pathophysiologies. The early rise may follow a ruptured coronary artery plaque and a late rise may follow prolonged ischaemia. Aggressive use of β-­ blockers, analgesia, and maintaining an adequate haematocrit may minimize the myocardial necrosis in these patients. The pathophysiology of perioperative myocardial infarction is multifactorial (Table 1).

Pathophysiology of perioperative myocardial infarction

• Increased peripheral oxygen consumption requires increased

cardiac output and therefore increased myocardial oxygen

demand

• Increased likelihood of atheromatous plaque rupture in the

perioperative period

• Hypercoagulable states postoperatively

• Nocturnal hypoxia secondary to opioids

• Inadvertent omission of cardiac medications due to patient

being nil by mouth

• Deliberate cessation of antiplatelet agents for the

perioperative period

Table 1

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Postoperative respiratory failureRespiratory failure occurs relatively infrequently following elective vascular surgery. If ICU admission is required, a prolonged period of weaning, possibly necessitating tracheostomy, may be required. This can greatly increase hospital stay, but is rarely a cause of increased mortality. The causes of respiratory failure are:• chest infection• pulmonary oedema secondary to myocardial ischaemia or

fluid overload• deterioration of pre-­existing lung disease (e.g. COPD, pul-­

monary fibrosis)• pulmonary embolus• aspiration pneumonitis• transfusion-­associated lung injury• acute respiratory distress syndrome.

Treatment of respiratory failure is directed at the under-­lying cause. Antibiotics, bronchodilators and physiotherapy, with the provision of adequate analgesia, are used in the first instance. Oxygen is administered and non-­invasive or invasive ventilation may be needed. This should occur in the critical-­care setting.

ThromboembolismVenous (deep vein thrombosis) and arterial (graft occlusion) thromboses occur more frequently in the postoperative period in vascular patients. Patients become more hypercoagulable postoperatively. Standard regimens of low molecular weight heparins (e.g. enoxaparin, 40 mg once daily) are effective in reducing thromboses. ‘TED’ stockings and pneumatic compres-­sion devices have also been shown to reduce the incidence. Despite these measures the incidence of deep vein thrombosis in the vascular surgical population is 3–8%. The use of epidural an-­algesia may reduce thromboembolism, but its effect on improv-­ing graft patency rates in peripheral vascular surgery is unclear and unproven.

HaemorrhageFollowing vascular surgery may be torrential and quickly life-­threatening. Control via direct pressure and the restoration of an adequate circulating volume are the aims of treatment. Bleeding may also be more diffuse, as after aortic aneurysm repair, with large blood transfusion. A bleeding point may not be identified, and measures should be taken to ensure tests of coagulation are within normal limits. This may involve the use of fresh frozen plasma, platelets or cryoprecipitate. Aprotinin has not been shown to be of use in reducing transfusion requirements in vascular surgery.

Thromboelastography is increasingly available, and can be used to guide appropriate treatment and monitor therapy. The need for fresh frozen plasma, cryoprecipitate and platelets can be observed, and results are often available before those of labor-­atory tests.

Compartment syndromeRestoration of blood flow to ischaemic tissues, either acutely or after chronic ischaemia, can cause a reperfusion injury. This is mediated by the release of free radicals and causes cellular oedema and rhabdomyolysis. If swelling occurs in a fascial compartment, the pressure may rise above that of the venous

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bed, causing capillary blood flow to cease, which results in cell death and further oedema. Myocyte death releases myoglobin and creatine kinase. Clinically the limb is very tender (pain can theoretically ‘break through’ an epidural block), and urine is of low volume and dark. Distal pulses may still be present. Myoglobin precipitates in renal tubules in acidic urine and will cause renal failure. Treatment includes fasciotomies to reduce the compartment pressure, and forced alkaline diuresis using sodium bicarbonate, mannitol and large volumes of crystalloid. A urine output of 300 ml/hour with a pH greater than 6.5 should be maintained. Invasive monitoring and a critical-­care setting will be needed.

Specific vascular operations

Carotid endarterectomyAfter general anaesthesia, analgesia can be improved with the addition of a superficial cervical plexus block, with good patient satisfaction and reduced morphine requirements.3 If the procedure is carried out under regional/local anaesthesia, oral analgesics such as paracetamol or codeine are sufficient. After carotid endarterectomy mortality is mostly attributable to stroke and myocardial infarction.

Cardiovascular problems: both hypertension and hypoten-­sion occur frequently after carotid endarterectomy. The physi-­ology behind this is not entirely clear. The baroreceptor in the carotid sinus may become denervated during surgery, leading to a brain-­ stem mediated reflex tachycardia and an increase in systemic vascular resistance. Hypertension can cause increased bleeding from the arteriotomy site, intracerebral bleeds and myocardial ischaemia, and must be controlled aggressively. Labetolol infusions can be used to avoid tachycardia associated with nitrates. Exposing the carotid sinus baroreceptor to the full force of the systolic blood pressure may result in a vagally mediated bradycardia and hypotension. If this is a problem intra-­operatively the surgeon may instil local anaesthesia around the carotid sinus. Postoperatively, infusions of dopamine or nor-­epinephrine can be used to maintain blood pressure. Invasive blood pressure monitoring should ideally continue for 6 hours postoperatively. If a high-­dependency unit bed is not available, the patient can stay in the recovery ward for this period before being taken to the ward. If a patient requires vasoactive drugs postoperatively, central venous access and a high-­dependency unit bed will be needed. Baroreceptors normally ‘reset’ 24 hours postoperatively, and at this stage the frequency of monitoring may be reduced.

Neurological problems: postoperative stroke may be due to ischaemia or bleeding. About 60–70% of neurological deficits following endarterectomy occur peroperatively and are due to intraoperative embolization or hypoperfusion. Postoperatively, neurological observations should be carried out every 15 minutes for at least the first 4 hours. Any deterioration should prompt quick Doppler examination of the carotid artery because speedy surgical evacuation of thrombus can ameliorate or even reverse a developing hemiplegia secondary to carotid thrombosis. Cra-­nial and laryngeal nerve palsies have been reported in more than 50% of patients (when looked for on ENT examination). Most

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are minor and resolve quickly; voice or swallowing rehabilitation is only rarely necessary. The risk of motor cranial nerve injury persisting up to hospital discharge is about 4%, with most of these resolving within the year following surgery.

Hyperperfusion syndrome is due to a sudden increase in blood flow to the brain with a loss of autoregulation. It usually pre-­sents several days postoperatively, with headaches, facial pain, seizures, confusion, cerebral oedema or even haemorrhage. The underlying mechanism is not clear but may be caused by restora-­tion of blood flow to a brain suffering loss of autoregulation due to chronic ischaemia. Transcranial Doppler ultrasound is useful for diagnostic purposes. High blood flows postoperatively can lead to cerebral oedema and should be treated with aggressive control of the associated high blood pressure. Mannitol and dexa-­methasone are also used.

Airway: postoperative bleeding is normally venous and control-­lable with direct pressure. Haematoma formation rarely causes airway obstruction (as with thyroid surgery), but usually leads to lymphatic obstruction and oedema of the airway. Obstruction in these circumstances will not be immediately relieved by evacua-­tion of the haematoma, and a period of endotracheal intubation will be needed. Immediate exploration of the wound may be necessary to identify and stop further bleeding.

Abdominal aortic aneurysmOpen surgical repair of an aortic aneurysm is a significant insult in terms of blood loss, aortic cross-­clamping, and hypothermia, in a group of patients who have significant comorbidity pre-­operatively. The average mortality following elective aortic an-­eurysm surgery is about 7%, but, as mentioned before, an ICU bed is not always needed for elective surgery. Unforeseen surgical complications or prolonged operation, resulting in a cold patient, or large blood loss may necessitate ICU admission. Endovascular repair via groin incisions is better tolerated, and recovery occurs quickly. It can be performed under epidural or even local anaes-­thesia with good results and early discharge.

Renal failurePostoperative renal failure increases mortality and is linked with preoperative renal impairment, suprarenal clamping for more than 40 minutes, blood transfusions more than 5 units, and rhabdomyolysis. Meticulous fluid balance is vitally important. Dopamine has no effect on mortality or the need for renal replace-­ment therapy. Fenoldopam, a dopamine-­1 receptor agonist, has shown some improvement in renal outcomes in small studies for both elective and emergency surgery.

Gastrointestinal systemEarly enteral feeding has become popular, with sips of water allowed at day 1, progressing to a regular diet on day 3–4. This is aided by epidural anaesthesia, which reduces the duration of ileus and promotes stomach emptying. Colonic ischaemia occurs rarely, but carries a high mortality (up to 90%). It can be dif-­ficult to diagnose but presents with a continuing acidosis and sometimes blood in the faeces. It is related to emergency surgery with prolonged hypotension and cross-­clamp times. Diagnosis is made by colonoscopy.

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Emergency aortic surgeryMortality from emergency repair of aortic aneurysms is about 50%. This is due to the severity of the initial insult and the high incidence of multi-­organ failure secondary to prolonged hypoperfusion. Surviving patients can require a protracted stay on the ICU. In the ICU the initial postoperative management is aimed at establishing haemodynamic stability, reversing or preventing coagulopathy, correcting metabolic acidosis, warm-­ing the patient and optimizing fluid filling to maintain renal blood flow.

AnalgesiaIn addition to the normal analgesic ‘ladder’, many local anaes-­thetic techniques are applicable to the vascular patient.

EpiduralThoracic and lumbar epidurals are frequently used for aortic and peripheral vascular surgery (Anaesthesia and intensive care medicine 7:11: 422). Although benefits in terms of reduced mortality are lacking, excellent analgesia, reduced respiratory complications, fewer deep vein thromboses and, in the case of

Local anaesthetic techniques for vascular surgery

Technique Advantages Disadvantages

spinal rapid, intense

analgesia

Bilateral effects, short

lasting, coagulation and

infection considerations

Epidural

(lumbar)

catheter top­ups

for prolonged

peripheral surgery

Epidural haematoma/

abscess, bilateral,

impairs mobilization

Epidural

(thoracic)

Excellent analgesia,

reduced ileus and

chest infections

Epidural haematoma/

abscess

sciatic nerve

block

Easy, prolonged

analgesia, unilateral

Prolonged onset, not

easy to use as sole

technique for surgery

Femoral

nerve block

Easy, adjunct to

sciatic for leg

surgery/amputation

Not for foot surgery

ankle block Foot surgery, avoids

general anaesthesia,

prolonged analgesia

Difficult if oedema/

infection present

Metatarsal

block

as an adjunct to

ankle block, easy

Deep cervical

plexus block

sensory and motor

block to neck

Vertebral artery

injection/damage, not

strictly needed, phrenic

nerve block, recurrent

laryngeal nerve block

superficial

cervical

plexus block

Easy, good

analgesia after

surgery with general

anaesthesia

External jugular vein

injection

Table 2

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thoracic epidurals, reduced postoperative ileus have been shown when compared with general anaesthesia alone (Table 2). ◆

KEy REfEREnCES

1 callaghan cJ, lynch aG, amin I, et al. Overnight intensive recovery:

elective open aortic surgery without a routine Icu bed. Eur J Vasc

Endovasc Surg 2005; 30: 252–8.

2 longhitano s, coriat P, agro F. Postoperative myocardial infarction:

patho­physiology, new diagnostic criteria, prevention. Minerva

Anestesiol 2006; 72: 965–83.

3 Messner M, albrecht s, lang W, et al. The superficial cervical plexus

block for postoperative pain therapy in carotid artery surgery.

aNaEsTHEsIa aND INTENsIVE carE MEDIcINE 8:6 24

a prospective randomised controlled trial. Eur J Vasc Endovasc Surg

2007; 33: 50–4.

fuRTHER READinG

Kirk lawlor D, lovell M, Derose G, et al. Is intensive care necessary

after elective abdominal aortic aneurysm repair? Can J Surg 2004;

47: 359–63.

Monini s, Tauino M, Barbara M, et al. laryngeal and cranial nerve

involvement after carotid endarterectomy. Acta Otolaryngol 2005;

125: 398–402.

Papia G, Klein D, lindsay T. care of the patient following open

abdominal aortic surgery. Curr Opin Crit Care 2006; 12: 340–5.

7 © 2007 Published by Elsevier ltd.