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General surgical operations are now performed on patients who are older, more frail and with significant and often multiple (medical) comorbidities, so it becomes even more important to appreciate and consider these ‘medical’ conditions. Detailed reports of emergency abdominal surgery outcome audits have been published by the UK National Emergency Laparotomy Audit (see: http://www.nela.org.uk/reports ). A high-risk patient is usually defined as one whose estimated risk of mortality is greater than 5%, and includes any patient over the age of 65 years undergoing major gastrointestinal or vascular surgery, and any patient over 50 years with diabetes mellitus or renal impairment. Recommendations include preoperative risk assessment with a tailored management plan. This was traditionally directed by consultant surgeons and anaesthetists, but increasingly for older patients, a specialist geriatrician is involved. This was pioneered with orthogeriatricians working with anaesthetists and orthopaedic surgeons in management of hip fracture. In many centres, geriatricians with expertise in perioperative management of general surgical problems are being appointed. A major role for the team is rapid identification and treatment of postoperative infection and potential sepsis.
Medical disorders appear in surgical practice in four main ways:
A preexisting medical condition may precipitate a surgical admission because of exacerbation, progression or complications of the condition: for example, foot problems in diabetes.
A preexisting medical condition may be made worse by operation. In chronic obstructive pulmonary disease (COPD), for example, general anaesthesia and postoperative sputum retention may precipitate life-threatening pneumonia.
A surgical condition may be complicated by an unrelated medical disorder. For example, a patient with rheumatoid arthritis on steroid therapy is vulnerable to impaired healing and recurrent infection.
An occult condition can become manifest under the stress of anaesthesia and operation. For example, perioperative or postoperative myocardial infarction can be caused by occult ischaemic heart disease.
A new medical problem may be precipitated by a surgical complication. For example, new onset rapid atrial fibrillation (AF) occurring after anastomotic leakage.
Emergency surgery in patients with cardiac disease is about four times more likely to result in death than the same operation done electively. Thus preoperative assessment is vitally important in emergency patients, so any cardiac condition can be recognised and stabilised, electrolyte imbalances corrected and appropriate anaesthesia, surgical technique, monitoring and aftercare used to minimise risk.
The clinical manifestations of ischaemic heart disease are:
chronic stable exertional angina; previous myocardial infarction
acute coronary syndrome (ACS)
cardiac failure
arrhythmias (e.g., AF)
conduction system disturbances (e.g., complete heart block)
asymptomatic atherosclerotic coronary artery disease
Asymptomatic coronary artery disease may progress to infarction under anaesthetic and surgical stresses, including laryngoscopy and endotracheal intubation, pain, hypoxia, rapid blood loss, anaemia, hypotension, hypocarbia and fluid overload. For major operations, general anaesthesia and spinal anaesthesia carry similar risks. Local anaesthesia, when practicable, is much safer.
There is usually little increased risk during operation and exercise tolerance is by far the most important indicator of the patient’s ability to tolerate anaesthesia and surgery. This can be assessed in the history (remembering that exercise tolerance may be limited by mobility problems rather than cardiorespiratory problems). A convenient measure is the MET (metabolic equivalent of a task). A patient with 4 METs can climb a flight of 18 stairs, walk at 4 mph on level ground, run short distances, use a vacuum cleaner, lift heavy furniture, play golf or doubles tennis. Such patients have a low risk of cardiac events. Formal assessment on a treadmill may be helpful; if patients are immobile, pharmacological cardiac perfusion imaging may be helpful. Occasionally coronary angiography is required to fully assess cardiac risk. The indications are the same for nonsurgical patients, that is, unstable angina, limiting stable angina or adverse noninvasive test results.
In general, all cardiac medication should be continued perioperatively. Nitrates, which dilate the coronary arteries and reduce preload and left ventricular (LV) work, may reduce cardiac ischaemia during general anaesthesia and should not be stopped in the perioperative period. A transdermal nitrate patch is a useful alternative to tablets or sprays. Beta-adrenergic blockers, which reduce cardiac work and oxygen demand, should be continued unless non ischaemic cardiac failure develops. Most patients will be taking aspirin (and some clopidogrel in addition, see bleeding disorders, later). Angiotensin-converting enzyme (ACE) inhibitors may be continued, though hyperkalaemia can be a risk especially if co-prescribed with nonsteroidal anti-inflammatory medications. ACE inhibitors should be stopped if acute kidney failure occurs. Statin medications can be discontinued for a few days perioperatively without detriment.
This is a term applied to a spectrum of conditions from unstable angina to non-ST-elevation myocardial infarction to ST-elevation myocardial infarction (STEMI). ACS associated with surgery usually occurs during the first few days after operation, particularly on the second to fourth postoperative nights, rather than during the operation. Typical chest pain is not always a feature and postoperative ACS may present ‘silently’ (i.e., painlessly) with otherwise unexplained hypotension, cardiac failure, arrhythmias or cardiac arrest, particularly in patients with diabetes. Diagnosis is made on the basis of at least two of the following: appropriate symptoms (particularly typical cardiac ischaemic pain); a significant rise in a cardiac biomarker, usually troponin; and electrocardiogram (ECG) changes consistent with ischaemia (dynamic changes including ST depression, T-wave flattening or inversion) or infarction (ST elevation). It is always helpful to have a preoperative ECG for comparison, which should be performed on all patients over 50 years of age and any with cardiac symptoms or signs.
Troponin is a very specific marker of myocardial damage, but be aware that this damage may result from conditions other than ischaemia or infarction caused by coronary artery disease, for example, sepsis, hypotension or heart failure, and therefore the management may differ from that of ACS.
The medical treatment of ACS includes aspirin, clopidogrel (for antiplatelet activity) and fractionated heparin given subcutaneously. These drugs adversely affect clotting in the perioperative period and are discussed under bleeding disorders later. Other treatments, such as nitrate and beta-adrenergic receptor blockade are less likely to have adverse ‘surgical’ effects. STEMI is ideally treated by emergency primary angioplasty but this depends on the surgical stability of the patient, and on how close the nearest coronary intervention centre is. Thrombolysis is obsolete except where there are no facilities for primary angioplasty. In these circumstances, it remains an option, but the potential salvage of myocardium has to be weighed against the serious risk of major haemorrhage.
This is a complex clinical syndrome with symptoms and signs resulting from impairment of the heart as a pump owing to structural or functional abnormalities. The severity of heart failure correlates poorly with objective measurements of heart function (such as ejection fraction), such that up to 50% of patients presenting with symptoms and signs of heart failure will have ‘preserved ejection fraction’ (previously called diastolic heart failure ). This is especially common in older patients. Assessment of severity is based on clinical features, particularly when exercise tolerance is limited (New York Heart Association classification: http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classes-of-Heart-Failure_UCM_306328_Article.jsp ). Patients with renal impairment or electrolyte abnormalities have a poorer prognosis and tend to decompensate more readily with operative stress.
Most patients will be taking diuretics, an ACE inhibitor and a beta-blocker as first-line treatment, and nitrates and digoxin if the condition is more severe, and these treatments should be continued if possible.
Patients with chronic heart failure (CHF) should be optimised before major surgery, but there is still an increased mortality of up to 5%. The causes, symptoms and signs of cardiac failure are shown in Fig. 8.1 .
Surgery should be postponed until treatment has been optimised and the clinical condition stabilised. Hasty preoperative diuretic therapy is dangerous because it may provoke intravascular volume depletion, hypotension and electrolyte abnormalities. Patients taking diuretics (and often ACE inhibitors or angiotensin-receptor antagonists in addition) may have abnormalities such as:
Hypokalaemia (usually caused by potassium-losing diuretics prescribed without potassium supplements).
Hyponatraemia.
Raised plasma urea and creatinine with hyperkalaemia (particularly if taking an ACE inhibitor and spironolactone)—the urea is often raised to a greater extent than creatinine, indicating intravascular volume depletion. However, in severe cardiac failure, the glomerular filtration rate falls causing urea and creatinine to rise. Clinical assessment by an experienced physician may be needed to differentiate dehydration from overload in patients with cardiac failure and a raised urea and creatinine.
Postural hypotension.
This problem results from poor tolerance of intravenous fluids, unaccustomed supine posture, myocardial infarction or ischaemia in the perioperative period, or arrhythmias (particularly AF) induced by the stresses of surgery and anaesthesia. Prompt and vigorous diuretic therapy with intravenous furosemide and nitrate is required to prevent worsening cardiac failure, hypoxia, renal failure or other potentially lethal complications. In addition, treatment of any precipitating factors should be instituted, such as reducing cardiac stress by giving good pain relief. Postoperative cardiac failure is best managed in an intensive care unit, using a central venous pressure line to guide fluid replacement.
Chest x-ray may demonstrate cardiomegaly and there may be signs of pulmonary oedema including upper lobe diversion, hilar congestion, septal Kerley B lines and pleural effusions (see Fig. 8.1 ). ECG may show an arrhythmia, myocardial ischaemia, ventricular hypertrophy, left bundle branch block or loss of R waves.
LV function can be assessed by echocardiography and documented more precisely by radionuclide studies using multiple-gated acquisition, but the best assessment is a clinical one based on exercise tolerance. Measurement of blood urea and electrolytes is important as baseline and also indication of severity of the condition. A preoperative body weight is crucial but is sadly often omitted.
If there is any doubt about the fitness of a patient for operation, a cardiological opinion should be sought ideally well before planned surgery.
Preexisting (preoperative) AF is very common and affects 2% of the population overall, rising to 10% to 17% among over 80s. In many patients, the heart is structurally normal, but AF may indicate underlying cardiomyopathy, ischaemic heart disease, thyrotoxicosis or (in the developing world) mitral stenosis. It is often associated with hypertension. Acute onset AF postoperatively may be caused by a major surgical complication (e.g., anastomotic leakage after bowel resection) or medical complication (e.g., pneumonia) (see Fig. 8.2 ). If the onset of atrial arrhythmia (particularly AF) is associated with right bundle branch block on the ECG, this suggests a diagnosis of pulmonary embolism.
AF with a controlled ventricular rate (i.e., a pulse rate of less than 90 beats per minute at rest) causes minimal extra risk. An uncontrolled ventricular rate may cause perioperative heart failure. Adequate control of ventricular rate should be achieved before operation with beta-blocker and digoxin, occasionally supplemented with verapamil or amiodarone. Digoxin can be given intravenously if rapid control is necessary but potassium levels need to be monitored closely as digoxin given in the presence of hypokalaemia can lead to further arrhythmias. AF (even with a controlled ventricular response) increases the risk of arterial embolism from any thrombus present in the left atrium. For this reason, all patients with intermittent or permanent AF should be considered for anticoagulation.
The aim here is to maintain necessary anticoagulation but to reduce the risk of surgical bleeding. Warfarin should be stopped for 5 days before major elective surgery and the international normalised ratio (INR) checked on the day of surgery. Patients with recent venous thromboembolism (VTE) or recurrent VTE on anticoagulation should have ‘bridging’ therapeutic low-molecular-weight (LMW) heparin, with the last dose 24 h before operation. Bridging is also recommended for patients with most mechanical heart valves and for patients with AF who have had a stroke or transient ischemic attack (TIA) in the previous 3 months; also for patients with a previous stroke and three or more of these risk factors: congestive cardiac failure, hypertension (>140/90 mmHg or on medication), age over 75 years or diabetes. Prophylactic LMW heparin is used for other situations, that is, VTE over 3 months before, patients with AF that are not high risk and those with bi-leaflet aortic valves. For emergency surgery, 5 mg of phytomenadione intravenously reverses warfarin within 6 to 8 h. If surgery cannot wait that long, four-factor prothrombin complex concentrate should be given in consultation with the on call consultant haematologist. Warfarin can be restarted on the evening of surgery owing to its slow onset of action.
Increasingly direct oral anticoagulants (DOACs) are replacing warfarin; they do not require monitoring blood tests, have fewer interactions and are less likely to cause intracranial bleeding than warfarin. They are also rapidly acting and do not need ‘bridging’ heparin. However, patients on a DOAC may not be aware they are on anticoagulants because of the variety of trade and generic names without the familiarity of warfarin. Reversing DOACs is more problematic than warfarin. If renal function is normal, DOACs should not be taken for 24 h before elective procedures and 48 h if the procedure is high risk. If renal function is abnormal, this interval is calculated according to the individual DOAC and the creatinine clearance. Anticoagulation can normally be restarted 6 to 12 h postprocedure but not until 48 h if the patient is at risk of bleeding. In patients with higher thrombosis risk, prophylactic doses of DOAC can be given earlier. Clotting studies are unpredictable in assessing DOAC effect, but a normal thrombin time indicates minimal circulating dabigatran. For emergency surgery with a significant bleeding risk, andexanet alfa can be used for urgent reversal. Tranexamic acid can also reduce bleeding in those with residual anticoagulant effect. Drugs, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and colloids that impair haemostatic mechanisms, should be avoided in patients on DOACs.
Bradycardia is common in young fit athletic patients and is not a problem. In patients taking beta-blockers or digoxin, if the apex rate is below 60 beats per minute, that day’s dose should be omitted and the regular dose reviewed.
Bradycardia may be caused by complete heart block , which should be easily diagnosed on the ECG. This may require urgent temporary transvenous pacing , particularly when there is significant haemodynamic compromise or syncope (‘Stokes Adams attacks’).
If a patient has a cardiac pacemaker , it is important to know the reason for its insertion: is the patient pacemaker-dependent, has the pacemaker been checked recently, what type of pacemaker has been inserted? Surgical diathermy, particularly monopolar diathermy, can interfere with the pacemaker if the current flows close to the heart. Ideally, bipolar diathermy should be used if diathermy is required. In addition, a strong magnet should be available; if placed over the pacemaker this will return the rate to 100 beats/min In certain cases within the abdomen ultrasonic shears can be an alternative energy source for dissection and haemostasis.
Bifascicular block , in which conduction is impaired down two of the three main fascicles (right bundle plus anterior or posterior divisions of the left bundle, manifest by right bundle branch block and left axis deviation on the ECG), may progress to complete heart block (and low cardiac output) under anaesthesia. For these patients, a prophylactic temporary transvenous pacemaker should be considered before operation.
About one in four patients coming to surgery is either hypertensive or is receiving antihypertensive therapy. Most have ‘essential’ hypertension , but causes, such as renal artery stenosis and phaeochromocytoma must be considered in patients presenting with raised blood pressure (BP) which has not been appropriately investigated. (For other causes see Fig. 8.3 .) Undiagnosed renal artery stenosis puts the patient at risk of severe acute kidney injury if there is an episode of hypotension, and phaeochromocytoma of potentially fatal hypertensive crisis.
Patients with a systolic pressure of less than 180 mm Hg and a diastolic pressureless than 110 mmHg are at minimal risk of cardiac complications, unless there is some other cardiovascular disease. Sometimes, anxiety about the operation contributes to the hypertension. A labile BP or systolic hypertension at any time may, however, indicate widespread atherosclerosis.
Most common antihypertensive drugs are ‘cardioprotective’ and should not be stopped before general anaesthesia. Despite the patient being ‘nil by mouth’ in the immediate preoperative period, the normal dose of oral antihypertensive drugs should usually be given with a small amount of water. Sudden withdrawal of antihypertensive drugs may cause rebound hypertension. Withdrawal of beta-blockers may trigger autonomic hyperactivity and lability of BP. Postural hypotension may occur after operation, especially if there is dehydration.
If the BP is greater than180/110 mmHg, then treatment needs to be instituted and any non urgent operative procedure delayed. During anaesthesia the untreated hypertensive patient has a very labile BP and is at high risk of perioperative myocardial infarction, cardiac failure or stroke.
Chest x-ray may identify cardiomegaly or cardiac failure, both of which increase the perioperative morbidity and mortality. An ECG may reveal signs of ventricular hypertrophy and ischaemia. Plasma urea and electrolytes should be measured in all patients taking diuretics or ACE inhibitors and in any patient with suspected chronic renal impairment.
A patient has cerebrovascular disease if there is a history of stroke or TIAs . Cerebral atherosclerosis may render the blood flow to the brain precarious, with an increased risk of perioperative stroke from hypoxia, hypotension or increased blood viscosity resulting from dehydration.
After a stroke , operation should be avoided for at least 2 months if practicable. This is because autoregulation of cerebral BP becomes disrupted, so that cerebral arterial pressure becomes directly related to systemic arterial pressure. Brain perfusion thus loses the buffering effect of autoregulation on peaks and troughs of BP that tend to occur during anaesthesia and surgery. If operation cannot be delayed, it is important to prevent hypertension and hypotension in the perioperative period.
Patients with cerebrovascular disease will usually be on platelet inhibitors (see bleeding disorders, later).
The common valvular abnormalities are mitral regurgitation, aortic stenosis and aortic regurgitation. Any of these may dangerously alter cardiovascular dynamics, but stenotic lesions are more serious than regurgitant ones, as the cardiac output tends to be fixed.
Under perioperative stress, valvular disease may precipitate acute myocardial ischaemia, hypotension, cardiac failure, arrhythmias or thromboembolism. Valvular heart disease also predisposes to infective endocarditis (IE).
Aortic stenosis is potentially the most serious valvular disorder in a surgical patient because it limits the cardiac output and reduces blood flow to the coronary arteries. Indeed, the patient may already be functioning close to the limit with almost no reserve. Perioperative hypotension and tachycardia can be life threatening in such cases. Aortic ‘sclerosis’ produces a similar ejection systolic murmur and is caused by fixed, rigid valve leaflets, usually with systolic hypertension but does not have a significant transvalvar gradient. The perioperative risk is that of the hypertension and arterial disease.
In a patient with an ejection systolic murmur, any associated cardiac symptoms may help identify the murmur as pathological, for example, a history of syncope, angina or shortness of breath on exertion. Note, however, that any systolic murmur is difficult to categorise clinically, particularly in the elderly, and an echocardiogram including colour Doppler must be performed to identify the valvular cause and offer an assessment of severity. A specialist cardiology assessment may also be required.
Clinical signs of aortic stenosis are:
Slow rising upstroke of the carotid pulse.
A harsh ejection systolic murmur radiating into the neck.
Hyperdynamic apex beat indicating LV hypertrophy. (Note: the apex beat is only displaced laterally if aortic stenosis coexists with aortic regurgitation or is complicated by cardiac failure.)
LV hypertrophy on ECG.
If aortic stenosis is suspected, an echocardiogram and Doppler will confirm the diagnosis and aid assessment of severity by measuring the aortic valve area, the gradient across the valve and an estimate of LV systolic function. A mean pressure gradient of >40 mmHg, a valve area of <1.0 cm 2 and impaired LV function all imply severe aortic valve disease.
Nonurgent surgery may be best delayed until after operative intervention to the aortic valve. This may now be carried out percutaneously in frail or elderly patients (transcatheter aortic valve implantation [TAVI]) in whom previously the risk of valve replacement was prohibitive.
Symptomatic valvular disease is potentially dangerous and requires full preoperative assessment and treatment. Major valvular heart disease may be discovered in recent immigrants from developing countries where rheumatic heart disease is prevalent. Patients with valvular heart disease require cardiac monitoring during operation and usually intensive care afterwards. For management of anticoagulation for patients with artificial heart valves, see the surgical patient on anticoagulants, earlier.
In all cases, it is advisable to involve the haematologist in discussion for advice on management, and in anticipation of specific treatment.
Valvular disease, and in particular prosthetic replacement valves, carry a risk of IE . When blood is forced under pressure through a narrow orifice, laminar flow is disrupted and eddy currents predispose to local thrombus formation and deposition of circulating bacteria. The vegetations of IE thus form on the low-pressure side of the jet of blood passing through a damaged valve or a ventricular septal defect. The left side of the heart is more susceptible than the right because of the higher pressures and greater potential for turbulence.
Streptococcus viridans is the most common causative organism of IE. Other bacteria, such as coliforms or fungi, for example, Candida , may also be responsible. Many types of operation and some invasive investigations cause transient bacteraemia. Although the incidence of IE following such procedures is small, the consequences can be catastrophic. In recent years, recommendations for prophylaxis against IE have radically changed and the current consensus is that antibiotic prophylaxis should be confined to those at highest risk. These are patients with prosthetic heart valves or prosthetically repaired valves; those with previous IE; and those with untreated cyanotic congenital heart disease or congenital heart disease with palliative shunts, conduits or other prostheses. Other valvular heart disease patients need no prophylaxis but should have good dental and cutaneous hygiene. These downgraded recommendations result from the following considerations: overuse of antibiotics encourages resistance and there are no randomised controlled trials of antibiotic effectiveness. The risk following dental procedures is now known to be low with low-grade bacteraemia being common after tooth brushing (and even chewing), especially in those with poor dental health, and does not seem to cause IE. For patients at high risk, prophylaxis is indicated for dental scaling, root canal treatment and manipulation of gingival or periapical regions of the teeth or perforation of the oral mucosa. For all other procedures on respiratory, gastrointestinal, urogenital tract (including foetal delivery), skin or musculoskeletal system prophylaxis is not recommended. Since the main target for prophylaxis is oral streptococci, oral amoxicillin or clindamycin in case of penicillin allergy is recommended.
Respiratory complications (mainly atelectasis and pneumonia) occur in as many as 15% of surgical patients and are the leading cause of postoperative mortality in the elderly. The risk of a respiratory complication increases with the increasing duration of anaesthetic and is amplified by preexisting respiratory disease, such as COPD, asthma or bronchiectasis. Other important factors include smoking, cardiac failure, obesity, old age and general debility. Good postoperative pain relief allows the patient to breathe deeply and cough, which, along with effective physiotherapy, helps reduce the risk of respiratory complications.
COPD (smoking-related lung disease—chronic bronchitis and emphysema) is common and strongly predisposes to postoperative respiratory complications, particularly bronchopneumonia, lobar collapse and pneumothorax. There is often a degree of reversible bronchoconstriction , and this can be assessed before operation by measuring peak expiratory flow before and after bronchodilator treatment, if necessary using a low-reading instrument. Many patients will already have had spirometry and vitalography in family practice or in specialist hospital COPD services and their treatment optimised. Otherwise preoperative assessment by the hospital ‘chest team’ will help bring the patient into optimum health. The forced expiratory volume in 1 second (FEV 1 ) is perhaps the single most useful assessment of severity of chronic lung disease.
Other chronic lung diseases include bronchiectasis, pneumoconiosis, pulmonary fibrosis, sarcoidosis and pulmonary tuberculosis.
Smokers of cigarettes have a fivefold greater risk of postoperative respiratory problems than nonsmokers. This is partly caused by preexisting smoking-related respiratory disease but also because smokers have a highly reactive airway. This increases the intraoperative risk of laryngeal spasm and bronchospasm.
Smoking should be stopped at least 4 weeks before operation and ideally 8 weeks before if any early benefit is to be achieved. This gives time for recovery of physiological respiratory functions, such as bronchial ciliary activity. Stopping smoking just before surgery may actually be detrimental because it causes an increase in bronchial mucus production.
Acute upper respiratory tract infections (usually viral) are common and these patients have reduced resistance to surgical trauma and infection. This alone may be grounds for postponing an elective operation.
Conditions associated with chronic infection, such as bronchiectasis and cystic fibrosis are more difficult. Elective operations should be carried out during remissions where possible, with intensive physiotherapy and perioperative prophylactic antibiotics.
Asthma is common in children and adolescents but may occur later in life, particularly as a component of COPD. The main elements of asthma are airway hyperreactivity (with constriction), bronchial wall oedema, excessive mucus production and airway plugging. All these factors predispose to atelectasis, infection and hypoxia.
Asthmatic problems can be exacerbated by the following factors associated with general anaesthesia and surgery:
Endotracheal intubation—increases airway sensitivity.
Increased airways secretions—caused by intubation or the autonomic side-effects of anaesthetic drugs, such as muscle relaxants.
Dehydration—increases mucus viscosity.
Limitation of movement and posture because of pain—inhibits coughing to clear secretions
The direct effects of other drugs, for example, bronchoconstriction caused by beta-blockers or morphine-associated respiratory depression.
In patients with asthma, the usual medication should be continued in the perioperative period, given via a nebuliser if necessary. Operations should be postponed during acute exacerbations.
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