Preventing, Recognizing and Treating Postoperative Complications

POSTOPERATIVE MANAGEMENT

oxygen and glucose to meet their energy demands. This occurs when blood is oxygenated adequately and the heart can produce enough systolic pressure to perfuse the tissues. Patients must be assessed preoperatively to identify those at increased risk of postoperative hypoxaemia or organ hypoperfusion, so that their condition can be optimized and appropriate postoperative monitoring instituted (e.g. admission to an HDU). Prompt identification of postoperative hypoxaemia or organ hypoperfusion, followed by appropriate intervention, limits the severity of complications and prevents the spiral into multi-organ failure. This contribution discusses postoperative complications by reference to common scenarios.

Preventing, Recognizing and Treating Postoperative Complications Ingrid Wilkins Dan Wheeler Complications can occur after any operation, but are most likely after major surgery or in patients with significant cardiac or respiratory comorbidity. They range from distressing or inconvenient to life-threatening. Complications causing failure of a single body organ or system can lead to multiple system failure or even death. Investigating and treating complications (and litigation) cost the UK NHS billions of pounds every year. For example, a simple wound infection delays discharge from hospital by an average of 7 days, and costs an extra £1700. Surgery injures and kills cells, causing inflammatory mediators (e.g. cytokines, thromboxanes, leukotrienes, prostaglandins, nitric oxide) to be released. The inflammatory response prevents introduction of infection into the body and promotes healing. An uncomplicated recovery from surgery relies on the body being able to increase its metabolic rate to maintain its normal homeostatic mechanisms and mount an adequate inflammatory response. The normal source of energy for a cell is derived from adenosine triphosphate (ATP), created during the metabolism of glucose in the presence of oxygen. Aerobic respiration, utilizing the citric acid cycle and oxidative phosphorylation inside mitochondria, liberates sufficient energy to create 36 ATP molecules per glucose molecule. Without oxygen, only 2 ATP molecules and 2 pyruvate molecules are created per glucose molecule; pyruvate is converted to lactate. If oxygen or glucose is in short supply during or after surgery, cells switch to anaerobic metabolism, producing such small amounts of energy that membrane pumps fail. The cell swells and is eventually irreversibly damaged or ruptures. Cells with a high demand for oxygen (e.g. myocardial cells, neurons) are especially susceptible. Most postoperative complications develop when organs fail to function correctly because oxygen supply to their cells does not meet demand. The prevention of complications is paramount and, on a physiological level, can be thought of as providing cells with sufficient

The patient with chest pain From history and examination alone, it can be difficult to distinguish between chest pain arising from the cardiovascular, respiratory or gastrointestinal systems. Myocardial causes of chest pain Preoperative identification of patients at risk of myocardial ischaemia is important: baseline investigations will need to be performed, pre-emptive treatment given and appropriate monitoring used (see Arrowsmith and Mackay, Surgery 2002; 20(4): 91–6). Myocardial ischaemia occurs when myocardial oxygen demand outstrips supply. Most coronary blood flow occurs in diastole, so that oxygen supply to the heart depends on: • adequate saturation of haemoglobin with oxygen • adequate flow within the coronary arteries relying on adequate coronary perfusion pressure (= diastolic blood pressure – left ventricular end diastolic pressure) and adequate time in diastole for blood to flow. Therefore hypoxaemia, hypotension, and tachycardia decrease myocardial oxygen supply and cause ischaemia, especially in patients with pre-existing coronary artery disease. If oxygen demand remains unfulfilled, ischaemia may progress to infarction, which carries a mortality rate of 50% postoperatively. Classically, myocardial infarction is said to occur on the third postoperative night. It is thought that hypoxaemia due to lung atelectasis or pneumonia and dehydration causing hypoperfusion are most severe 72 hours after surgery. In fact, asymptomatic or ‘silent’ myocardial ischaemia is common during and immediately after surgery. ‘Textbook’ central crushing chest pain radiating down the arms and up to the jaw is rarely so clearly described postoperatively. Patients at risk of perioperative myocardial ishaemia should be nursed in an HDU or ICU, where continuous electrocardiogram (ECG) and peripheral oxygen saturation (SpO2) or more specialist cardiac monitoring can be instituted, daily 12-lead ECGs can be performed and continuous supplemental oxygen administered (see Arrowsmith and McKay, Surgery 2002; 20(4): 91–6). There is strong evidence that perioperative β-adrenoceptor blockade significantly reduces ischaemic episodes in patients with heart disease, probably by reducing myocardial oxygen demand. T-wave inversion, ST segment changes or new left bundle branch block on a 12-lead ECG indicate myocardial ischaemia or infarction. Serum creatine kinase rises after surgery as a result

Ingrid Wilkins is a Specialist Registrar in Anaesthetics at Addenbrooke's Hospital, Cambridge, UK. She qualified from St Bartholomew's Hospital, London, UK, and trained in anaesthetics in Nottingham, Cambridge and Norwich, UK. Her research interests lie in paediatric anaesthesia and medical education. Dan Wheeler is the Clinical Lecturer in Anaesthesia at the University of Cambridge, UK. He trained in accident and emergency and general medicine in Oxford and Poole, Dorset, UK. His research interests are based in the neurosciences and modelling of human respiration.

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Obstructed airway: when the airway is obstructed, stimulation of the respiratory muscles by the respiratory centre is normal or increased, but results in no air movement. There is a characteristic ‘seesaw’ movement of the chest and abdomen associated with respiratory effort. Simple airway opening manoeuvres (head tilt/ chin lift or jaw thrust) must be performed. Snoring represents a partially obstructed airway that may be improved by nursing the patient on his side, allowing the tongue to fall forward away from the soft palate. Patients with pre-existing obstructive sleep apnoea may require continuous positive pressure oxygen postoperatively. Obesity and over-sedation are strong risk factors. A completely obstructed airway is silent, and is a medical emergency.

of tissue damage and so is unhelpful as a marker of myocardial damage. Creatine kinase MB isoenzyme (CK-MB) or troponin I are better markers. Immediate care consists of sitting the patient up, giving 100% oxygen and opioid analgesia (e.g. i.v. morphine sulphate 0.1 mg/kg titrated slowly). More complex treatment and evaluation requires specialist help, especially in the presence of hypotension. Although thrombolysis is contraindicated after surgery, treatment with nitrates, aspirin, β-blockers, and heparin may be appropriate. Intestinal causes of chest pain Indigestion or acid reflux is classically described as a ‘burning retrosternal pain with an acid taste in the throat’. It is common in patients with hiatus hernia, smokers or the obese. Such patients are often taking H2-receptor antagonists or proton pump inhibitors and these drugs should be continued perioperatively if possible. Symptoms are treated with antacids or alginates. Because myocardial pain is so atypical postoperatively, it is very difficult to distinguish from intestinal-related chest pain. Therefore, a patient with chest pain postoperatively should have a 12-lead ECG performed even if the pain is eased by antacids or alginates.

Hypoxaemia with breathlessness: the patient may be attempting to improve ventilation by sitting forward in the tripod position using accessory muscles to breathe. He may be too breathless to complete his sentences, and is usually restless. Examination may reveal tachypnoea, i.e. respiratory rate above normal range (15–20 minutes), tracheal tug or subcostal recession. Cyanosis is clinically detectable in the presence of 5 g/dl of unsaturated haemoglobin and may therefore be absent in severe anaemia. Central cyanosis (blue lips and tongue) is very serious. Breathlessness may result from deficits in lung volumes, gas exchange, or lung perfusion, and the causes are summarized in Figure 1.

Respiratory causes of chest pain Chest pain arising from the lungs or pleura (pleuritic pain) is usually sharp in nature and worse on deep breathing or coughing. Pleuritic chest pain of clinical significance will usually be associated with hypoxia (see below).

Lung volumes If secretions or debris block small airways, gas distal to the blockage is slowly absorbed and the alveoli collapse, decreasing the lung volume available for gas exchange. The absence of gas exchange from part (or all) of the lung is termed atelectasis. There are several factors that predispose to atelectasis in the perioperative period: • high airway pressures generated during artificial ventilation are traumatic • general anaesthetics suppress the mucociliary escalator (and granulocyte function in vitro)

Musculoskeletal chest pain Musculoskeletal chest pain is a diagnosis of exclusion. It is treated with mild to moderately strong analgesics, such as paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs).

The hypoxaemic patient An SpO2 of 93% or lower is worrying, especially if the patient is receiving supplemental oxygen. Hypoxaemia is defined as an arterial pO2 below 12 kPa (90 mmHg) measured on an arterial blood gas (ABG) sample, checked without removing the supplemental oxygen. Hypoxaemic patients are often agitated, restless or confused.

Causes of postoperative hypoxaemia Lack of alveolar ventilation • Hypoventilation (airway obstruction, opioids) • Atelectasis • Bronchospasm • Pneumothorax

Hypoxaemia without breathlessness Hypoventilation: this may result from low respiratory rate or poor inspiratory effort resulting in low tidal volumes. Intravenous opioid infusion or intrathecal opioid administration is more likely to cause respiratory depression than oral, intramuscular or patient-controlled opioid regimens. Modern anaesthetic drugs are so rapidly excreted that opioids are the most likely culprit on the ward. Protocols to detect hypoventilation should be in place for patients receiving perioperative opioids, to trigger emergency anaesthetic referral or administration of the opioid receptor antagonist, naloxone. The very young, the very old or those with concurrent conditions (e.g. obesity, intracranial pathology) are most at risk. Hypoventilation due to low tidal volumes may be caused by pain from thoraco-abdominal wounds, cerebrovascular accident or weakness of the respiratory muscles from underlying neuromuscular disease.

Decreased diffusion across alveolar membrane • Pneumonia • Pulmonary oedema • ARDS and inflammation Lack of alveolar perfusion • Ventilation–perfusion mismatch (PE) • Shunting (alveolar collapse, atelectasis) • Tension pneumothorax • Cardiac failure ARDS, Adult respiratory distress syndrome; PE, pulmonary embolism

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• breathing non-humidified oxygen dries protective secretions. Lung volumes are further decreased postoperatively, especially after thoracic and major abdominal surgery. Diaphragmatic splinting and wound pain (which discourages coughing) reduces vital capacity by 45% and functional residual capacity by 20%. Lung volumes are decreased in pneumothorax, which often causes pleuritic chest pain and should be considered if an attempt has been made to gain central venous access.

across the alveolar membrane. Simultaneously, reduced cardiac output results in decreased blood flow through pulmonary capillaries. Hypoxaemia due to pneumonia and heart failure can be difficult to distinguish and may coexist. Pulmonary embolus: when a deep vein thrombosis (DVT) embolizes to the pulmonary artery, symptoms and signs vary widely, and are shown in Figure 2. The easiest investigations to perform are the least specific. ECG may show the classical ‘SIQIIITIII’ right ventricular strain pattern or more frequently simply sinus tachycardia. Arterial blood gases may demonstrate ventilation–perfusion mismatching as hypoxaemia in the presence of hypocapnoea, but are frequently normal. Chest radiographs seldom show oligaemic lung fields. Ventilation–perfusion scanning can be diagnostic, but atelectasis and pneumonia can make interpretation difficult. Pulmonary angiography is the ‘gold standard’, but is not widely available. Anticoagulation with heparin then warfarin is the mainstay of treatment or, very rarely, thrombolysis or embolectomy.

Gas exchange Free diffusion of oxygen and carbon dioxide from alveoli to blood relies on a functioning alveolar membrane. The trauma of alveolar collapse and re-inflation, the accumulation of debris and desiccation causes inflammation and oedema of the alveolar membrane. Subsequent impaired gas exchange causes hypoxaemia. Bronchopneumonia: this is common after major surgery secondary to atelectasis and impaired immune defences. Additional secretions and pus worsen airway blockage. Lobar infections tend to be caused by aspiration; causative organisms are atypical and difficult to treat (e.g. Pseudomonas aeruginosa, anaerobes).

The hypotensive patient Hypotension is defined as inadequate perfusion of vital organs. If a patient’s normal blood pressure is 190/100 then the ‘textbook’ normal value of 120/80 may represent hypotension in that patient. Patients with mild hypotension feel dizzy, nauseated and may vomit. As the hypotension worsens they may become anxious, confused or even unconscious. Whatever the cause of the hypotension (hypovolaemia, cardiac failure, arrhythmias, drugs, spinals or epidurals) the outcome is the same. Persistent hypoperfusion of vital organs causes irreversible damage leading to kidney, brain or gut failure, hence the need to recognize hypotension and treat it appropriately.

Exacerbation of existing obstructive airways disease: mucosal damage, pneumonia and drugs that inhibit prostaglandin synthesis (e.g. NSAIDs) or release histamine (e.g. morphine, rarely) can trigger bronchospasm and cause hypoxaemia in asthmatic or emphysematous patients perioperatively. Some patients with chronic obstructive pulmonary disease who retain CO2 rely on hypoxaemia for respiratory drive. Such patients can be rendered apnoeic by high oxygen concentrations. Most patients with chronic lung disease are under-treated with oxygen for this reason. Regular ABGs will detect the onset of hypercapnoea under these circumstances.

Hypovolaemia Hypovolaemia is relatively common postoperatively, although

Treatment: a hypoxaemic patient should be treated with supplemental oxygen delivered continuously by fixedperformance mask. Other masks and nasal prongs deliver varying concentrations of oxygen dependent on respiratory pattern, which makes ABGs more difficult to interpret. If hypoxaemia does not improve (or the patient is tiring), artificial ventilation may be required. Comfortable patients who can move and cough postoperatively are less likely to develop atelectasis, so good analgesia is important. Lung expansion techniques also help; physiotherapists use a variety of means to improve respiratory muscle function, and prevent atelectasis and pneumonia. If a causative organism is isolated from blood or sputum cultures, it should be treated with an appropriate antibiotic. Pneumothorax should be treated by aspiration or formal drainage.

Symptoms and signs of pulmonary embolus Symptoms Dyspnoea Chest pain Haemoptysis Classic triad of all three symptoms Signs Tachycardia Fever Tachypnoea Signs of deep vein thrombosis Raised jugulovenous pressure Shock Accentuated second pulmonary heart sound Cyanosis Pleural friction rub

Lung perfusion Heart failure will reduce perfusion throughout the lung, whereas a pulmonary embolus will cause a local deficit. Left ventricular failure: when a diseased left ventricle cannot match preload and afterload, cardiac output is embarrassed and pulmonary oedema may develop. Two processes contribute to hypoxaemia. Secretions in the airways decrease gas exchange

Percentage (%) 77 63 26 14

59 43 38 23 18 11 11 9 8

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Cardiogenic shock Cardiogenic shock (pump failure) exists when, despite normovolaemia, the heart cannot maintain sufficient blood pressure to perfuse vital organs. Admission to an ICU for invasive pressure monitoring and positive inotropes is needed, but mortality remains around 90% for this condition.

the cause may not be immediately obvious. Bleeding into drains is easy to see, but occult bleeding into the thoracic or abdominal cavities or into the retroperitoneal space can cause hypovolaemia. Many litres of fluid can be sequestered in the bowel in ileus or bowel obstruction. The hypotensive response to hypovolaemia in a patient with an epidural infusion or spinal block is exaggerated because of inhibition of reflex sympathetic vasoconstriction. Similarly, tachycardia (the normal reflex response to hypovolaemia) may be abolished by β-blockers, high spinal regional nerve block and in ischaemic or valvular heart disease. Blood loss should be measured and the degree of hypovolaemia judged using the parameters shown in Figure 3. Confounding factors, such as the suppression of reflex tachycardia by β-blockers or early decompensation in the elderly or ill, should be noted. Oxygen must be administered while the degree of hypovolaemia is being assessed. The calculated volume should be replaced with a fluid appropriate to the clinical situation (i.e. blood or colloid for blood loss, crystalloid for gastrointestinal losses) at an appropriate rate via a peripheral wide bore cannula. Choice of fluid remains controversial; crystalloids have short intravascular half-lives, colloids may exacerbate oedema in the long term, blood transfusion risks transfusion reaction and infection. Pulse, blood pressure and urine output should be recorded frequently to assess adequacy of resuscitation. Central venous pressure monitoring may be helpful in some situations when co-existing medical conditions (e.g. heart or renal failure) complicate matters.

Drugs Almost all anaesthetic drugs cause some degree of hypotension, either by decreasing systemic vascular resistance or by directly depressing myocardial contractility, and so reducing cardiac output. Residual anaesthetic drugs are present immediately after an operation. However, any problems they may cause should have been resolved in the recovery area before discharge to the ward. Epidural infusions Epidural infusions (or residual spinal block) are a common cause of hypotension on the ward. The local anaesthetic not only blocks pain fibres, but also sympathetic nerves to blood vessels, which normally maintain vasoconstrictor tone. This causes a relative hypovolaemia. The patient may be slightly tachycardic with warm, well-perfused peripheries and little or no pain from the operative site. A fluid challenge or small dose of peripheral vasoconstrictor (e.g. i.v ephedrine, 3 mg ) should restore blood pressure, but the level of the epidural block and adequacy of analgesia should be monitored. If the patient is in pain with an inadequate block, then the hypotension is unlikely to be due to the epidural. Conversely, if he is very comfortable, the upper limit of the block may be too high and the epidural infusion should be reduced or stopped briefly. A block above the level of the cardiac sympathetic fibres (C6) will prevent a compensatory tachycardia occurring, further exacerbating the hypotension. A block above C4 will paralyse the diaphragm and the patient will become apnoeic (but not necessarily unaware). This is an emergency and the patient requires artificial ventilation immediately until the block subsides.

Clinical assessment of hypovolaemia in the adult (70 kg) Grade of hypovolaemia

1 Minimal

2 Mild

3 Moderate

4 Severe

% blood volume lost

10

20

30

>40

Volume lost (ml)

500

1000

1500

>2000

120–140

>140

<100

<80

20–30 (ml/hr)

10–20 (ml/hr)

Nil

Pulse (min-1)

Normal

100–120

Systolic pressure (mmHg)

Normal

Orthostatic hypotension

Urine output

Normal (0.5–1.0 ml.kg-1. min-1)

Conscious level

Normal

Normal

Anxious, confused

Drowsy– coma

Peripheral circulation

Normal

Cool, pale

Cold, pale

Cold, clammy, cyanosis

Capillary refill

Normal Normal (2 seconds)

Delayed

Very delayed

The patient with an arrhythmia Arrhythmias are common intraoperatively. Nodal rhythms and ventricular ectopics are the most commonly seen, but are usually benign and self-limiting. They occur because general anaesthetics sensitize the myocardium to the effects of circulating catecholamines. Some arrhythmias are persistent or compromise blood pressure and these require further investigation and treatment (e.g. atrial fibrillation with a rapid ventricular response rate or ventricular tachycardia). The common causes of perioperative arrhythmias are listed in Figure 4. Tachycardias increase myocardial oxygen demand and reduce myocardial oxygen supply. Left ventricular blood supply occurs during diastole. As the heart beats faster, diastole is shortened, coronary artery filling time is reduced and the myocardium becomes ischaemic. Loss of co-ordinated atrial contraction reduces cardiac output by 20% and increases risk of thromboembolism. Bradycardias and ventricular ectopics may also compromise cardiac output. Supplemental oxygen should be administered, pulse identified

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digoxin levels and hypokalaemia may contribute to tachycardia in atrial fibrillation. Patients who have developed new atrial fibrillation in the perioperative period should be considered for cardioversion.

Causes of perioperative arrhythmias • • • • • • • •

Hypercapnoea Hypoxaemia Electrolyte imbalance (especially K+ abnormalities) Acidosis Pain Myocardial ischaemia or infarction Drugs Local anaesthetic toxicity

The hypertensive patient A combination of any of the causes shown in Figure 6 can be responsible for postoperative hypertension. Pain or exacerbation of existing primary hypertension is the usual cause of postoperative hypertension. Analgesia should be optimized, after which the blood pressure can be compared to the preoperative value. Oxygen should be administered, and blood pressure controlled with the patient’s normal therapy. A substitute may be needed if the patient is unable to absorb oral medication. Treating hypertension can unmask hypovolaemia and some patients may require more fluids. The patient’s normal antihypertensive medication should be continued throughout the perioperative period. The ‘nil by mouth’ preoperative fast is not a reason for normal cardiovascular medication to be omitted.

Transient during operation: • Vagal manoeuvres (laryngoscopy, irritation of carina) • General anaesthetics (sensitize myocardium to circulating catecholamines and cause nodal rhythms) 4

and blood pressure measured, and continuous cardiac monitoring commenced. The diagnosis can be confirmed with a 12-lead ECG and specialist advice sought. The principles behind treatment algorithms are summarized in Figure 5.

The unconscious or confused patient after surgery Coma and unconsciousness In recovery, metabolism and elimination of anaesthetic drugs continues until the patient is alert, pain is controlled and observations are stable before discharge to the ward. Drugs with longer half-lives (e.g. barbiturates) or with active metabolites (e.g. benzodiazepines) may delay ‘alertness’ and ‘orientation’. A decreased level of consciousness on the ward should not automatically be attributed to anaesthetic drugs, especially if the patient was alert on discharge from recovery. If a patient becomes unresponsive postoperatively, immediate action is required to maintain a safe airway and ensure adequate breathing and circulation. Figure 7 summarizes possible causes of altered conscious level.

Conduction defects Atrioventricular nodal conduction is decreased by general anaesthetics, electrolyte imbalances and local anaesthetic toxicity. Therefore, there is a risk of pre-existing heart block developing into complete heart block during surgery. The preoperative ECG will identify susceptible patients. Patients with symptomatic heart block or asymptomatic Mobitz type II, third-degree or coexisting bifascicular and first-degree blocks should be fitted with a pacemaker before surgery. Rapid ventricular response rate in patients with chronic atrial fibrillation should be controlled preoperatively with digoxin. Digoxin and potassium levels should be measured. Subtherapeutic

Confusion and agitation The elderly are particularly prone to postoperative confusion. They metabolize and excrete drugs more slowly, are prone to hypoxia and may have co-existing dementia. Being removed from their normal environment can cause acute confusion in some elderly patients. Almost any diagnosis can present with confusion, thus it is important to have a logical approach to excluding correctable or serious causes (Figure 7). The most common causes (hypoxaemia, pain and electrolyte disturbance) are the most easily treated. Lipid-soluble drugs (e.g. atropine, cyclizine) can cause a central anticholinergic syndrome. Alcohol and benzodiazepine withdrawal should also be considered.

Principles behind the treatment of arrhythmias Basic action • Feel for pulse • Administration of supplemental oxygen Diagnosis • Blood pressure compromised? • 12-lead ECG and rhythm strip • Tachycardia or bradycardia? • Supraventricular or ventricular? Urgency of treatment • Cardiopulmonary resuscitaion needed? • Help needed? • Time to treat easily reversible cause?

Causes of postoperative hypertension • • • • • •

Cardioversion • Direct current cardioversion • Cardioversion with drugs • Rate control 5 SURGERY

Pain Urinary retention Pre-existing hypertension, especially if poorly controlled Hypoxaemia Hypercapnoea Positively-inotropic drugs

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nephrotoxic drugs (e.g. NSAIDs, gentamicin, ACE inhibitors) discontinued. Patients with existing renal impairment, renovascular disease, diabetic nephropathy, sepsis or hypotension are most at risk and need careful monitoring postoperatively, possibly in an HDU. Giving frusemide to a patient with low or no urine output is controversial. It is detrimental if hypovolaemia has not been corrected. In patients with adequate circulating volume, there is no evidence that the improved urine flow leads to a better outcome. Dialysis may be necessary if hyperkalaemia or fluid overload exists.

The patient with poor urine output Urinary retention Inability to adopt the normal position for micturition, pain or dislike of using bedpans are common causes of urinary retention. Other causes include residual spinal or epidural blockade, administration of anticholinergic drugs or opioids, and prostatic hypertrophy. If simple encouragement (privacy, running taps) is ineffective, catheterization may be required. Urinary retention is very uncomfortable and can cause hypertension, agitation and confusion.

The patient with pyrexia

Renal failure An adequate urine output is usually 0.5–1 ml.kg-1.hour-1. Renal failure (Figure 8) can develop despite adequate urine output, so serum urea and creatinine levels should also be measured regularly in patients at risk. Renal tract obstruction should be excluded with renal ultrasound, hypotension corrected, and

Pyrexia is a core body temperature above 38 oC. Up to 40% of children are pyrexial after surgery. Pyrexia in the first 24 hours is thought to be due to the inflammatory process from tissue damage and haematoma formation in the wound, or may be a reaction to blood transfusion. Classically, infection is said to cause pyrexia on the third postoperative day. The likely sources are chest, wound, urinary tract, catheter or cannula. A careful examination should be made and microbiological specimens taken (preferably before administration of antibiotics) to identify the source and causative organism. Early treatment with the correct antibiotics may prevent abscess formation, bronchopneumonia or septicaemia. Non-infective causes of postoperative pyrexia include myocardial infarction, pulmonary embolus and connective tissue disease.

Causes of altered conscious level after surgery Hypoxaemia

Cerebral ischaemia Coma due to hypoxaemia is a pre-terminal sign

Hypercapnoea

Arterial CO2 tensions of >9 kPa (68 mmHg) lead to coma

Hypotension

Hypoperfusion exacerbates cerebral ischaemia

Cerebrovascular accident

Intracranial haemorrhage Thrombo-embolic infarction Raised intracranial pressure in presence of head injury, tumour

Endocrine

Hypoglycaemia Hyperglycaemia Hypothyroidism Addisonian crisis

Hypo-osmolar syndrome

Hyponatraemia due to absorption of water during bladder or rectal irrigation with glycine-containing fluids

Drugs

Residual anaesthetic drugs Opioid analgesics Benzodiazepines Intracranial spread of local anaesthetic from epidural or interscalene block Impaired drug metabolism or excretion

Toxins

Malignant hyperthermia (MH) General anaesthetics and suxamethonium trigger this rare, inherited disorder. These drugs cause a massive increase in metabolic rate and body temperature (>40 oC). Rhabdomyolysis and hyperthermia cause hypoxaemia, fits and renal failure up to 8 hours post-exposure. Mortality can be reduced from 70% to 20% with prompt cooling, administration of dantrolene and supportive care in an ICU. The patient’s relatives will be invited to undergo genetic testing and notified if they are susceptible. An anaesthetic that avoids these triggering events can be administered for future surgery.

Causes of postoperative renal failure

Alcohol Illicit drugs Ammonia (hepatic encephalopathy, renal failure)

Epilepsy

Post-ictal

Hypothermia

Hypothermia is profound if it causes coma

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Prerenal (hypoperfusion)

Shock (hypovolaemia, cardiogenic, septic) Renal artery disease (aortic dissection)

Renal (direct injury)

Acute tubular necrosis (follows prerenal, aminoglycosides, contrast medium, myoglobin) Glomerulonephritis Interstitial nephritis (antibiotics)

Postrenal (obstruction)

Bladder outflow (enlarged prostate, urethral stricture) Single ureter (calculus, tumour, iatrogenic, papilla) Both ureters (bladder, iatrogenic, malignancy)

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Neurological complications of epidurals, spinals and nerve blocks Incorrect positioning of the patient is much more likely to cause nerve injury than peripheral nerve blocks, epidurals and spinals. Nerves may be injured either by direct trauma with a needle, compressed by an adjacent haematoma or by infection. Nerve blocks are performed with blunt-ended stimulator needles, allowing the anaesthetist to gauge proximity to the nerve to be blocked; the blunt bevel pushes nerves aside rather than transecting them. Needles in the epidural space can pierce the epidural venous plexus and the resultant haematoma can very rarely compress the spinal cord or cauda equina. Severe pain and pressure at the epidural site, urinary retention and distal lower motor neurone deficit may be masked by subsequent epidural infusion. CT or MRI scanning are diagnostic. The haematoma requires emergency evacuation to prevent permanent damage. Epidurals are contraindicated in coagulopathy, thrombocytopaenia and full anticoagulation. Prophylactic heparin should be withheld before insertion and removal of the catheter, the exact length of time depends on local protocols. Epidural abscess is serious but very rare, developing days or weeks after epidural or spinal anaesthesia. Symptoms are similar to those described above, but examination may reveal an inflamed, hot, tender or discharging epidural site. Imaging, then surgical evacuation and antibiotics, are the mainstays of treatment. Permanent neurological damage can also be caused by development of meningitis, transverse myelitis or cauda equina syndrome.

The hypothermic patient Anaesthetics interfere with normal thermoregulatory homeostasis. In addition, patients lose heat (to the atmosphere and with body fluids) in various ways in the operating theatre. Lost fluids are often replaced with room temperature fluid or cold blood. Hypothermia decreases cardiac output, diminishes peripheral perfusion and deranges coagulation. Children and the elderly are at particular risk. Active patient and fluid warming with core temperature measurement are standard in long cases and in paediatric practice. Shivering Shivering is relatively common postoperatively and is caused by volatile anaesthetic agents and epidurals (as well as hypothermia). Shivering increases skeletal muscle activity, thereby increasing oxygen consumption, which may cause hypoxaemia. It is treated by administering high-concentration oxygen and maintaining (or attaining) normothermia.

The patient with a headache Mild headache is an inconvenient complication of general anaesthesia and responds to simple analgesics. Dural puncture and subsequent cerebrospinal fluid (CSF) leakage following spinal or epidural anaesthesia can cause severe, intractable headache. It is characteristically described as postural: worse on sitting or standing and associated with nausea and vomiting, but significantly improved by lying flat. It is occipital or frontal and has a ‘dragging’ quality. It usually occurs within 1 or 2 days of the dural puncture, but can occur weeks later and persist for months. Treatment is rest, hydration and simple analgesics. Caffeine is recommended, but not of clinically proven benefit. If symptoms are prolonged or intolerable, an epidural blood patch is required. This involves the anaesthetist injecting 15–20 ml of the patient’s own blood into the epidural space using a strict aseptic technique. The fibrin in the blood theoretically ‘patches’ the hole, preventing further CSF from escaping.

The nauseated or vomiting patient This is a very common complication following surgery. It is unlikely to cause any long-term problems unless it is secondary to hypotension. It is the most common cause for delayed discharge in day surgery. Risk factors include being female, prior history of postoperative nausea and vomiting or motion sickness. Long operations, gynaecological, middle ear, gastrointestinal procedures, and squint surgery are associated with increased risk. Opioid analgesia, especially when administered by means of patient-controlled analgesia, is another culprit. Careful rehydration and temperature control, use of antiemetics and anaesthetic technique all have some impact on incidence. Use of more than one class of antiemetic has a cumulative effect, but some patients will continue vomiting despite optimal therapy. u

The weak patient Cerebrovascular accident Neurons have a very high metabolic demand. If oxygen and glucose delivery to the brain is insufficient to meet this demand, neurons are irreparably damaged, resulting in global or focal brain injury. Thrombo-embolic or haemorrhagic stroke may also occur perioperatively, especially in patients with arteriosclerosis, atrial arrhythmia or poorly controlled hypertension.

FURTHER READING Auerbach A D, Goldman L. Beta-blockers and reduction of cardiac events in non-cardiac surgery: scientific review. JAMA 2002; 287(11): 1435–44. Jin F, Chung F. Minimizing perioperative adverse events in the elderly. Br J Anaesth 2001; 87(4): 608–24. Rodgers A, Walker N, Schug S, McKee A et al. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results from overview of randomised trials. BMJ 2000; 321(7275): 1493.

Nerve palsies Nerve palsies usually result from poor positioning of the patient on the operating table. The ulnar nerve is particularly likely to be injured by over flexion or pressure at the elbow. Incorrect litho-tomy positioning can cause common peroneal nerve neuropraxia, which may be severe enough to cause foot drop. Patients with pre-existing nerve damage should have care-ful documentation of the extent of their lesion before their operation.

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