Ming Kon Yii
11.1 Introduction
Common postoperative problems occur despite the best of surgical care but can be minimised with adequate preoperative planning. Patient-related concurrent medical problems are identified prior to surgery and these conditions are optimised. This has been discussed in detail in Chapter 10.
Postoperative care starts before the patient is taken to operating theatre. For example, cessation of smoking at least one week prior to surgery is beneficial. Attention to symptoms and signs in the early postoperative period may detect small but vital changes and proper management could prevent further deterioration and hence avoid major complications. For example, inadequate pain relief in a patient who has abdominal surgery would lead to poor respiratory efforts with atelectasia, especially in a smoker. Good pain relief, and chest physiotherapy that can be learnt preoperatively, and early mobilisation can potentially prevent this and avoid the onset of pneumonia.
Pain starts from the time of surgery. Inadequate pain relief can potentially exacerbate other problems and this will be addressed during surgery (pre-emptive analgesia such as local anaesthetic infiltration of the wound) and provided for adequate immediately on completion of surgery.
Good postoperative care requires precise and comprehensive orders on completion of surgery. Instructions should include not just observable vital signs such as heart rate, blood pressure, respiratory rate, oxygen saturation and urine output. They should include the care of wounds and drains. Daily inspection of intravenous line, drain, urinary catheter and wound can detect problems before the onset of established sepsis. Fever is often the first sign pointing to a brewing problem.
A few days following surgery, thromboembolism, secondary haemorrhage or cardiac compromise can lead to sudden deterioration or collapse.
The most common postoperative problems are listed in Table 11.1.
Table 11.1 Postoperative complications
|
Wound |
Infection |
|
Haematoma |
|
|
Dehiscence |
|
|
Incisional hernia |
|
|
Fever |
Atelectasis |
|
Sepsis |
|
|
Thromboembolic disease |
|
|
Vomiting |
Anaesthesia |
|
Ileus |
|
|
Obstruction |
|
|
Shock |
Haemorrhage |
|
Myocardial infarction |
|
|
Sepsis |
|
|
Pulmonary embolus |
|
|
Haemorrhage |
Wound |
|
Concealed |
|
|
Gastrointestinal |
|
|
Secondary |
|
|
Jaundice |
Septicaemia |
|
Drug cholestasis |
|
|
Hepatitis |
|
|
Respiratory |
Atelectasis |
|
Aspiration |
|
|
Adult respiratory distress syndrome |
|
|
Pneumothorax |
|
|
Cardiovascular |
Arrhythmias |
|
Myocardial infarction |
|
|
Congestive cardiac failure |
|
|
Urinary |
Retention |
|
Infection |
|
|
Renal injury |
|
|
Psychiatric |
Delirium |
|
Vascular access |
Phlebitis |
|
Pneumothorax |
11.2 Pain
Planning is important in the control of postoperative pain. This starts before surgery and, depending on the amount of anticipated pain, the patient is counselled as to what to expect following surgery and the methods of pain relief.
Different surgeries produce varying amounts of pain. The size and site of the wound affect the amount of pain. Skin graft donor site, vertical upper abdominal, chest, hand and loin incisions typically require more analgesia. The cultural, age and emotional status of the patient may affect the amount of postoperative pain.
Effective pain relief reduces the metabolic stress response to surgery. This reduces the cardiac demand, improves respiratory effort and lessens sputum retention, atelectasis and pneumonia and promotes mobility. The end result is earlier discharge and fewer complications.
Pre-emptive analgesia is started at operation. This includes:
• oral or rectal or intravenous nonsteroidal anti-inflammatory drugs (NSAIDs) given before or during surgery (NSAIDs are contraindicated in patients with renal impairment, known allergy, severe asthma, bleeding disorders, hypovolaemia and pregnancy)
• oral or intravenous paracetamol with or without codeine and tramadol, which is effective in those with anticipated mild to moderate pain
• local anaesthetic infiltration into the wound edge or field and ring block at the start of operation with long-acting bupivacaine (this is the most common approach although a specially designed catheter can be left in the wound at the completion of surgery to allow a continuous infusion of the anaesthetic agent)
• regional nerve blocks such as brachial plexus or femoral nerve blocks for upper or lower limb surgery
• spinal or epidural analgesia for abdominal or pelvic surgery.
The role of pain relief after major surgery is often undertaken by the acute pain service as a continuation of the anaesthetic care. A multimodality approach is used to achieve the best results.
Intermittent intramuscular opiates given at three- to four-hourly intervals (or as required) gives poor pain relief. Patients differ widely in the amount of analgesia required after major surgery. Opiates given intravenously as a continuous infusion are more effective, but this can result in respiratory depression if a larger than necessary dose is given. A much better and effective way to administer intravenous opiates is the patient-controlled analgesia (PCA) device. This allows the patient to control the frequency of a given dose with a lockout to prevent excessive dosage over a given period of time. This technique improves pain relief with minimal respiratory compromise.
For major operations involving the abdomen, pelvic or lower limb, epidural analgesia using opiates and local anaesthetic agent such as bupivacaine gives excellent pain relief. An epidural catheter is left in situ to allow longer term administration of agents. This method requires a dedicated team and close observation in the high-dependency unit (HDU) to avoid toxicity, severe hypotension, dense motor block and respiratory depression.
Non-opiates such as NSAIDs are effective for moderate pain. They can be given in the oral, rectal or intramuscular form. They do not cause nausea or vomiting, sedation or depression of respiratory and bowel functions. When given in combination with opiates, they reduce the requirement of opiates and hence the associated side effects. NSAIDs can cause renal impairment, gastric irritation and bleeding and bronchospasm and their use are contraindicated as mentioned.
11.3 Nausea and vomiting
Nausea and vomiting are common in the immediate postoperative recovery. These are often due to anaesthetic-related agents and postoperative analgesia, especially opiates. The common causes are listed in Box 11.1. These include: early, postanaesthetic sickness;
Box 11.1
Causes of postoperative vomiting
Anaesthetic drugs and gases
Acute gastric dilatation
Paralytic ileus
Intraperitoneal abscess
Adhesive mechanical obstruction
Strangulation of bowel
Table 11.2 Commonly used analgesics and dosage guide
acute gastric dilatation within 48 hours; paralytic ileus from two to three days; and mechanical intestinal obstruction thereafter.
Modern anaesthetic techniques and the use of antiemetics such metoclopramide, ondansetron and dexamethasone routinely in combination with opiates, have reduced the incidence of this early postoperative period. Potentially lethal aspiration may occur, especially in patients with gastrointestinal obstruction or bleeding, and in those who are extubated before the respiratory and cough reflexes have adequately recovered from anaesthesia.
Nausea and vomiting in the early and late postoperative recovery are often related to delayed gastrointestinal function. Acute gastric dilatation is nowadays a rare complication. Copious volumes are lost by effortless vomiting and there is a grave danger of pulmonary aspiration. The problem occurs mainly in the debilitated, depleted patient, with a persistent atonic defect of gastric emptying after surgery. Immediate nasogastric intubation and aspiration is warranted to prevent potential aspiration.
Paralytic ileus is much more common and is assumed to be present when gastrointestinal function has not returned within three days of surgery. The gastric and small intestinal function recovers quickly after operation. The large bowel takes longer to recover. Normal recovery of bowel function is heralded by hunger, return of bowel sounds and the passage of flatus. Ileus is more common after large bowel surgery or retroperitoneal aortic surgery. Ileus may be contributed to by operative trauma such as rough bowel handling, by electrolyte disturbance (especially hypokalaemia) and by severe systemic illness. Most cases will spontaneously resolve. Persistent vomiting and distension in the patient with ileus (with persistent X-ray signs of distended, fluid-filled small and large bowel) suggest that an intra-abdominal complication such as abscess may have occurred and this may require intervention.
A later onset of vomiting and distension, with colicky pain, in a patient who otherwise appears to be recovering satisfactorily suggests that mechanical adhesive obstruction has developed. Ileus and mechanical obstruction, however, may be very difficult to differentiate in the postoperative period. Patients with suspected adhesive obstruction are also treated conservatively initially. This consists of intermittent nasogastric aspiration and drainage, correction of fluid and electrolytes, and analgesia. But, if tenderness or a mass develop, if pain is severe or becomes continuous or if symptoms and signs persist for more than two to three days, laparotomy is indicated because of the danger of strangulation.
Ileus of the large bowel (pseudo-obstruction) can occur in a debilitated and ill patient who has severe illness other than an abdominal cause. The presentation is often vomiting, abdominal distension and pain. The treatment is colonoscopic decompression to prevent colonic rupture.
11.4 Tachycardia
Tachycardia is defined as rapid heartbeat of more than 100 beats per minute. This may be a feature of inadequate pain relief, anxiety, a cardiovascular disorder, infection or thyrotoxicosis.
Effective pain relief reduces the metabolic stress response to surgery and this reduces the cardiac demand and anxiety level of the patient. The stress response is characterised by tachycardia.
Hypovolaemia either from excessive loss, as in haemorrhage or gastrointestinal loss, or dehydration from inadequate fluid replacement is manifested by tachycardia unless the cardiac response is suppressed by beta-blockers. Treatment is rapid correction of coagulopathy, seeking the source of haemorrhage and intravascular volume replacement. A central venous line along with a urinary catheter are helpful in monitoring the progress of treatment (Ch 11.9).
Cardiovascular disorders that produce tachycardia include cardiac failure, myocardial infarction and cardiac arrhythmias such as atrial fibrillation or flutter. Medical consultation is required and appropriate therapy should be instituted.
One of the signs of severe sepsis is tachycardia with or without hypotension. In postoperative abdominal surgery, gastrointestinal anastomotic leakage must be suspected and treated appropriately.
11.5 Fever
Postoperative fever is common and often is part of the body response to trauma/surgery. The fever is mild but should be closely monitored on the daily ward round. Early diagnosis of the cause and treatment prevents its progression to a major problem.
A number of factors are helpful in determining the possible causes of fever. These include the timing of fever in relation to surgery, the pattern of temperature changes and the type of surgery with its specific complications. Table 11.3 provides a summary of the common causes of postoperative fever and Figure 11.1 provides a visual summary of the timing and pattern of fevers.
Table 11.3 Causes of postoperative fever
|
Diagnosis |
Days after operation |
|
Reaction to blood products |
0–1 |
|
Atelectasis |
1–2 |
|
Pneumonia |
2–4 |
|
Infusion thrombophlebitis |
2–5 |
|
Wound infection |
5–30 |
|
Thromboembolism |
5–15 |
|
Less common causes |
|
|
Tissue necrosis — myocardial infarction |
0–5 |
|
Malignant hyperpyrexia |
0–5 |
|
Neoplasm |
– |
|
Acute gout |
5–10 |
|
Fat embolism syndrome |
2–5 |
|
Drug allergy |
– |
|
Endocrine — thyroid or adrenal crisis |
2–5 |
|
Iatrogenic-overheating patient |
– |
|
Faking of fever by patient |
– |
Figure 11.1 Causes of fever and onset
Fever appearing soon after surgery, at about 24–48 hours, is often related directly to the surgery and anaesthesia. These include: basal lung atelectasis and aspiration pneumonitis, which may progress to pneumonia; intravenous blood or fluid administration, such as transfusion-related reaction or from pyrogenic contaminants; drug-related fever or a nonspecific inflammatory response to surgery.
In the early postoperative period (from day 2 to 5), infections become an important contribution to fever. These include chest infection, urinary tract infection, which is often related to a urinary catheter, intravenous cannulation site sepsis and thrombophlebitis and may include central venous catheter infection and wound infection/cellulitis.
Fever occurring more than 5–10 days postoperatively may be related to septic collections such as a wound abscess, intra-abdominal abscess from a gastrointestinal anastomotic leak or infected pelvic collection and deep vein thrombosis.
The pattern of fever can often gives a clue to the possible cause. A low-grade ‘grumbling’ fever of 37.5–38°C is seen in early basal lung atelectasis, early wound infection, intravenous cannula-related infection and later deep vein thrombosis. A high swinging fever of 39–40°C is seen with collection of pus such as wound abscess, intra-abdominal abscess (often pelvic or subphrenic abscess) or empyema in the chest.
The management of postoperative fever demands a careful history and examination of the patient. Particular attention is paid to the various potential septic sites and if necessary, specimens are taken for microbiological analysis including any wound discharge, urine, sputum, blood and central venous catheter tip culture. Appropriate imaging is requested, such as duplex ultrasound for deep vein thrombosis, chest X-rays for chest complications, abdominal ultrasound or CT scanning for intra-abdominal collections
Not all fevers require antibiotic treatment. Provided the patient is not unwell, these can be withheld until it is clear that there is a septic focus. Exceptions are in instances where prosthetic implants have been used, such as in vascular and orthopaedic surgery. For patients who are unwell, and for those with potentially serious complications, a broad-spectrum intravenous antibiotic is started as soon as the septic screen has been performed. The antibiotic is refined once microbiological culture and antibiotic sensitivity results are available.
Basal lung atelectasis is by far the most common cause of postoperative fever. It results from sputum retention in patients with an ineffective cough and can produce a high fever within 24 hours of surgery. This is discussed in Ch 11.6.
Thrombophlebitis at the intravenous cannula site unfortunately is common and in the early stage is the result of chemical and mechanical irritation rather than bacterial infection. Even when the infusion is buffered and heparin in small doses is used to prevent the intravenous catheter from becoming blocked, phlebitis is inevitable after several days of infusion via the same peripheral vein. Thrombophlebitis is prevented by routinely changing the cannula site every 72 hours.
Urinary tract infections are most common after pelvic operations and in patients who have been catheterised during and after surgery for monitoring purposes. Inspection of urine and regular urine cultures should be routine if there is any suspicion of such.
Wound infections are usually obvious by the fifth day after surgery; in most cases signs develop insidiously from the second or third day. These are discussed in Ch 11.10.
All septic collections are treated by either percutaneous drainage with or without imaging guidance or by open surgery if this is unsuccessful.
11.6 Shortness of breath and tachypnoea
Patients who are at risk for respiratory complications are often easily identified prior to surgery. These patients usually smoke and have chronic obstructive and restrictive lung diseases. The severity of the condition and the respiratory reserve are monitored with respiratory function tests (peak expiratory flow, vital capacity and forced expiratory flow in one second), blood gas analysis, chest X-ray and chest CT scan. Improvement can be achieved with cessation of smoking in advance of surgery, active physiotherapy and antibiotics if indicated from positive sputum culture.
In the postoperative period respiratory complications often manifest as shortness of breath, tachypnoea and cough. These complications are more common in those with inadequate pain relief and in those with respiratory depression.
Common causes
1. Basal lung atelectasis, bronchitis and bronchopneumonia: ‘the postoperative chest’
2. Adult respiratory distress syndrome (ARDS)
3. Tension pneumothorax
4. Pulmonary embolism
5. Acute pulmonary oedema
6. Cardiac failure
1 Basal lung atelectasis, bronchitis and bronchopneumonia: ‘the postoperative chest’
Atelectasis implies collapsed airless lung tissue and is unfortunately a very common complication of surgery — particularly after upper abdominal surgery. It usually presents within 24–48 hours of surgery (Fig 11.2) and, if untreated, will progress to bronchitis, bronchopneumonia and hypoxaemic respiratory failure.
Figure 11.2 ‘The postoperative chest’
A: breathing is impeded centrally and peripherally by wound pain, opiates and anaesthetics; B: ciliary action is depressed by anaesthetics, smoking and chronic bronchitis; C, D: atelectasis results from sputum retention
Mucus is normally carried proximally from the smaller air passages by ciliary action into the segmental lobar and main bronchi and is then coughed up. Ciliary action is depressed during anaesthesia and is rendered less effective if the membrane becomes dry or if mucus secretion is excessive or tenacious. Wound pain, excessive narcosis and debility depress the depth of respiration and the ability to cough forcibly. This aggravates any predisposition to sputum retention. Patients with chest disease (and smokers) are at much greater risk. Deficiency of surfactant may also occur after anaesthesia. Surfactant normally coats the alveolar epithelium and reduces surface tension and thus the stickiness of the alveolar walls. Together, these lead to sputum involving small or large plugs of mucus, occluding one or more segments of the bronchial tree. Distal to the plugs the gas is absorbed, leaving collapsed airless lung. The clinical effect and its severity depend upon the area of lung affected.
Massive collapse of a whole lung is possible but more often the collapse is segmental (lobular or lobar atelectasis). Collapsed segments with stagnant secretions predispose to pulmonary infection. Intrapulmonary blood flow is shunted through the collapsed airless segments and results in hypoxia of moderate or profound degree; PaO2 falls from the normal 100 mmHg breathing air to 70 mmHg or less. Diffusion of CO2 is more efficient than that of O2 and the PaCO2 is usually normal or slightly subnormal because hypoxia causes overbreathing. Clinically the patient develops shortness of breath, rapid breathing, a rapid pulse and fever — usually within 24–48 hours of operation. The respiratory symptoms are generally proportional to the degree of atelectasis, as are the lung signs on examination. Minor degrees of lobular atelectasis without clinically apparent chest signs are very common and are the most usual cause of fever and tachycardia within the first day or two of surgery. Chest X-rays in the early postoperative period often reveal areas of basal lung atelectasis as streaky linear areas that were unsuspected clinically.
Treatment of established atelectasis is mechanical. Chest physiotherapy with good analgesia encourages coughing and uses postural drainage to expel the obstructing mucus. Inhalation therapy using positive pressure ventilation of humidified air, with added oxygen, is also helpful. For major collapse, flexible or rigid bronchoscopy may occasionally be required with suction and instrumental clearing of major inspissated plugs.
2 Adult respiratory distress syndrome — acute respiratory failure
A variety of factors, including complications of surgery or trauma, can cause severe generalised acute respiratory insufficiency. A plethora of names for the syndrome (‘shock lung’, ‘acute posttraumatic or postoperative pulmonary insufficiency’, ‘adult respiratory distress syndrome — ARDS’) reflects the confusion surrounding its aetiology. The syndrome may follow any one of several widely different clinical situations (Box 11.2). Clinical features are impaired arterial oxygenation (diminished PaO2), diffuse lung opacification on chest X-ray and an increasing ‘stiffness’ of the lungs (decreased compliance).
Box 11.2
Factors contributing to the development of acute postoperative respiratory failure (adult respiratory distress syndrome)
Sepsis, massive trauma and prolonged shock
Fluid overload with crystalloid
Pre-existing chronic lung disease (smoking, COAD)
Chest injury
Sputum retention and atelectasis
Massive blood transfusion
Aspiration of gastric content
The syndrome displays a wide spectrum of severity. Many minor and transient cases recover spontaneously after early diagnosis and treatment of contributing causes. In a minority of cases, progressive pulmonary insufficiency occurs. Tachypnoea with increasing ventilatory effort, restlessness and confusion, hypoxia and hypocapnia develop. Hypoxia initially responds to increasing the oxygen content of inspired air, but progressively increasing concentrations are required to prevent the PaO2 from falling further. The lungs become increasingly stiff and difficult to ventilate. Widespread fluffy opacities caused by interstitial oedema coalesce until the lungs become totally opaque and hazy. Alveolar hypoventilation and a diffusion defect cause PaO2 to fall. Intrapulmonary arteriovenous shunting occurs through blood vessels not exposed to alveolar gas. This substantial physiological shunt makes the hypoxia worse.
Treatment is to identify and manage the contributory factors, with respiratory (such as pressure mask) and ventilatory (e.g. noninvasive or endotracheal) support as necessary. If mechanical ventilation needs to be prolonged for more than a week, percutaneous or open tracheostomy is usually necessary. If ARDS persists for more than a few days, the likelihood of established sepsis is high and appropriate antibiotics should be administered. The associated effects of systemic sepsis may include chronic disseminated intravascular coagulation (DIC). If this occurs, haematological monitoring is necessary and heparin administration may be required.
3 Tension pneumothorax
A central venous cannula may be inserted prior to or during surgery by the percutaneous infraclavicular route to the subclavian vein. Inadvertent injury of the underlying lung can cause a pneumothorax, which is usually small and resorbs spontaneously. Under general anaesthesia with positive pressure ventilation a tension pneumothorax can develop. This is a rare, but potentially lethal, complication. Acute cardiorespiratory failure can occur with hypotension and cyanosis. The condition, once diagnosed, is easily correctable by insertion of an intercostal (size 20 French) catheter. This is best done through the anterior chest wall in the second interspace or an alternate approach through the fourth or fifth interspace in the mid-axillary line. The drain must be left in and connected to a sealed suction drainage system.
4 Pulmonary embolism
The classical presentation of pulmonary embolism is a sudden onset of dyspnoea, shock followed by pleuritic chest pain, haemoptysis and pleural rub. This generally appears a few days after surgery. This must be diagnosed and treated rapidly to prevent fatal outcome (Ch 11.9 and Ch 4).
5 Acute pulmonary oedema
Acute pulmonary oedema manifests as shortness of breath and tachypnoea with or without pink frothy sputum. It is usually the result of fluid overload and left ventricular failure, often in a patient with pre-existing cardiac disease. Acute myocardial infarction should be considered. Basal crepitations are present and the jugular venous pressure is elevated. Treatment consists of oxygen administration, morphine, diuretics and ventilatory support if necessary.
Other causes of shortness of breath and tachypnoea include septic shock, acute hypovolaemia with haemorrhage, and anaemia.
11.7 Confusion and altered mental state
Confusion is a common problem in the postoperative patient and may range from minor disturbances, such as disorientation, clouding of consciousness and incoherent speech, to severe agitation and violent behaviour, including pulling out cannulas and catheters.
Patients who are particularly at risk of confusion are those with early dementia, the elderly and those with multiple medical comorbidities. The patient is often in pain, disorientated from the usual familiar home environment, sleep deprived due the activities in the ward and has mild metabolic disturbances. Most of the episodes are mild and settle with reassurance.
It is important to establish an accurate history of the onset of confusion, including the background mental state, medication (prescribed and non-prescribed) usage and alcohol intake. The most common causes are hypoxia, medication and alcohol withdrawal, infection and metabolic disturbances.
Hypoxia may be related to sedative and analgesic medications used in the postoperative period, respiratory compromise such as basal lung atelectasis, pneumonia, pulmonary oedema or thromboembolism. The medication chart should be reviewed and the diagnosis clarified with a physical examination. Arterial blood gases are measured and all confused patients should have supplemental oxygen.
Anaesthetic agents and opiates are frequent causes of confusion. Non-prescription drug and alcohol withdrawal should be considered with or without an obvious previous history. Signs of alcoholic liver disease, such as palmar erythema, hepatic tremor, spider naevi, parotid enlargement, ascites and abnormal liver enzymes, may support the diagnosis. In some cases prescribed sedatives may have been withheld unnecessarily, leading to confusion.
Sources of infection leading to confusion include the surgical wound, urinary tract, chest or intra-abdominal collections and gastrointestinal anastomotic leak. These often occur in conjunction with a fever.
Common metabolic causes of confusion include hyponatraemia, uraemia, dehydration or fluid overload and hypo- or hyperglycaemia.
In a confused patient, the vital signs are checked. The medication list should be reviewed. Chest, abdominal and neurological examinations are performed and a septic focus excluded. Investigations include urinary microscopy and culture, full blood count and electrolyte determination, blood gases and cultures as necessary.
Once the cause is determined and actions taken to address it, sedatives may be administered. One useful sedative in the postoperative period is haloperidol, which can be given intramuscularly or intravenously.
11.8 Low urine output
Minor physiological low urine output, oliguria, is not uncommon for the first 24 hours after surgery and requires no special treatment. Surgery induces the normal ‘stress response’ and the magnitude depends on the type of surgery. Urine output is calculated according to body weight and a minimum output of 0.5 mL/kg per hour is generally regarded as acceptable. A total urine volume of 700–1000 mL in the first 24 hours after surgery is usually quite normal.
Early diagnosis of postoperative oliguria is extremely important because incipient acute renal injury may be recognised early and reversed. A urethral catheter is necessary to monitor urine output in a patient who is severely ill or shocked and has under gone major surgery.
Urine output below 700 mL in 24 hours (or less than 30 mL hourly for several hours on catheter drainage) should be considered as pathological oliguria and a cause should be sought.
Common causes
1. Prerenal: acute vascular insufficiency such as hypovolaemia, water depletion or extracellular fluid depletion
2. Renal: acute intrinsic renal injury (from acute tubular necrosis)
3. Post-renal: obstructive renal injury
Clinical features and management plan
1 Prerenal: acute vascular insufficiency
Poor urine output is often due to hypotension during surgery or inadequate fluid replacement in a fasting patient. The clinical circumstances are suggestive, with gradually diminishing urine output in association with clinical signs of intravascular volume depletion. A patent urethral catheter must be in place to ensure that urinary retention has been excluded. Urine analysis may show an elevated specific gravity (>1015) or osmolality, a high urea (>20 g/L) or creatinine content, a low sodium content (<25 mmol/L) and high urinary/plasma ratios of creatinine, urea or osmalolity (Table 11.4).
Table 11.4 Acute renal injury: urine analysis
|
Prerenal acute vascular insufficiency |
Renal acute intrinsic renal injury |
|
|
Specific gravity |
High (>1015) |
Low |
|
Osmolality |
High |
Low |
|
Urea |
High (>20 g/L) |
Low |
|
Creatinine |
High |
Low |
|
Sodium |
Low (<25 mmol/L) |
High |
|
Urinary/plasma ratio of creatinine, urea and osmolality |
High |
Low |
In a patient with suspected hypovolaemia, judicial intravenous fluid challenge can help with the diagnosis and restore the renal perfusion. A cardiac assessment should be made. Those with poor cardiac function, such as ischaemic heart disease, cardiac arrhythmia and known pulmonary hypertension, are more prone to acute pulmonary oedema when a fluid challenge is given. A bolus dose of 250 mL or 5 mL/kg of intravenous fluid (e.g. normal saline) is given and the urine output monitored. A repeat challenge can be given after half an hour if necessary. If hypotension and low output persist, a central venous pressure estimation is helpful to further assess intravascular volume status. If urine output does not increase and hypovolaemia has been excluded, intravenous mannitol (12.5 g) and frusemide (40 mg) may avert incipient oliguric renal failure. High-dose frusemide and dopamine infusions are reserved for those in the intensive care setting. If there is no response to fluid loading and diuretics, established acute renal injury has been confirmed.
2 Renal: acute intrinsic renal failure (from acute tubular necrosis)
Acute postoperative renal failure occurs when the reversible stage of acute renal circulatory insufficiency progresses to acute tubular necrosis.
Renal damage may be worsened by toxic breakdown products from muscle or blood (ischaemic or crushed tissues, burns or incompatible transfusion), by nephrotoxic antibiotics or by severe systemic sepsis.
Reversible renal insufficiency must be distinguished from established renal failure. Volume loading is curative in the former but potentially dangerous in the latter. Urine volume is low — usually 100–400 mL in 24 hours — and the urine may contain red cells, epithelial casts and protein. The specific gravity and osmolality are low, as are creatinine and urea content, and the sodium content is high (>50 mmol/L). Urinary/plasma ratios of creatinine, urea or osmolality are also low.
Once the patient has established acute renal failure, the aim of management is to maintain fluid and electrolyte balance. Fluid restriction is combined with specific measures to replace renal function (peritoneal dialysis, haemodialysis, haemofiltration). The causes of the acute renal injury (ischaemic, nephrotoxic or obstructive) must be treated.
Acute renal failure may not be associated with oliguria. Clinical vigilance is required to diagnose nonoliguric renal injury (high-output renal failure). This type is common in patients with septic shock, multisystem failure and burns.
3 Post-renal: obstructive renal failure
In all instances of severe oliguria or anuria, mechanical causes must first be considered and excluded.
Total anuria very strongly suggests obstruction. The most common cause is urinary retention in the male. The patient may have suprapubic pain and tenderness with a palpable mass arising from the pelvis which is dull to percussion. This is easily confirmed with an ultrasound scan.
For those without an enlarged bladder, upper urinary tract obstruction is excluded by an abdominal ultrasound.
Simple passage of the urinary catheter resolves the issue of urinary retention but a subsequent failure of a trial of voiding after urinary catheter removal will require a urological consultation.
11.9 Sudden collapse or rapid deterioration
A patient who collapses suddenly or deteriorates rapidly has shock, that is, an acute clinical syndrome resulting in generalised cellular hypoxia. Clinical features include hypotension, tachycardia, poor peripheral perfusion and oliguria.
The four most common causes in the postoperative period are:
• concealed haemorrhage that occurs within 24 hours
• myocardial infarction or cardiac arrhythmias from the first to the third day
• septic shock after the fourth or fifth day
• pulmonary embolism about a week after surgery.
Less common causes include anaphylaxis and incompatible transfusion, tension pneumothorax, stroke, hypoxia and drug-induced respiratory depression, metabolic derangements (hypokalaemia, hyponatraemia, hypo- or hyperglycaemia) and acalculous cholecystitis (Table 11.5).
Table 11.5 Causes of postoperative shock and collapse
|
Time after operation |
|
|
Hypovolaemia: concealed haemorrhage |
0–48 hours |
|
Myocardial infarction |
1–3 days |
|
Cardiac arrhythmia |
|
|
Septic shock: local surgical complication |
4–5 days |
|
Pulmonary embolus |
5–10 days |
|
Less common causes |
|
|
Anaphylaxis |
|
|
Drug reaction |
Variable |
|
Incompatible transfusion |
Early |
|
Tension pneumothorax |
Variable |
|
Acalculous cholecystitis |
First week |
In shocked patients, the diagnosis proceeds in parallel with resuscitation and definitive treatment. A quick but methodical approach is required: airways, breathing, circulation, drugs administered or omitted, temperature, fluid balance and urine output are assessed. Investigations include ECG, blood glucose, blood gases, chest X-ray and full blood count, and electrolytes are ordered. Large-bore cannula intravenous access is established and oxygen is administered by facial mask.
Haemorrhage is the most common cause of postoperative shock and differs from cardiogenic shock in that hypovolaemia is associated with a low central venous pressure, a falling haemoglobin (may be normal in an acute haemorrhage) and a normal ECG, apart from tachycardia. Poor peripheral skin perfusion is common in both hypovolaemic and cardiogenic shock.
Perioperative haemorrhage is of three main types: primary during operation, reactionary within 24 hours and secondary about a week later (Box 11.3). Most cases of reactionary (and primary) haemorrhage are from an unligated vessel or a slipped ligature or clip and are not secondary to a coagulation disorder. The bleeding in secondary haemorrhage is due to erosion of an artery from spreading infection. Secondary haemorrhage is seen mainly when a heavily contaminated wound is closed primarily and can often be prevented by delayed wound closure.
Box 11.3
Characteristics of postoperative haemorrhage
Types
Primary — at operation
Reactionary — <24 hours, due to unligated vessel
Secondary — 1–2 weeks, due to infective erosion
Causes
Local vessel
General haemostatic defect
Site of bleeding
Wound
Haematoma
External haemorrhage
Intraperitoneal
Often concealed
Necrotising pancreatitis
Gastrointestinal
Duodenal ulcer
Stress ulcer syndrome
Diffuse bleeding tendency
Haemostatic deficit
Postoperative haemorrhage following abdominal surgery can also be classified according to its clinical presentation. The most common forms are wound bleeding, concealed intraperitoneal bleeding, gastrointestinal haemorrhageand the diffuse ooze of disordered haemostasis.
A wound haemorrhage presents as a blood-soaked dressing. The tendency is to apply another dressing in an attempt to achieve control by pressure. The wound dressing should be taken down and the wound inspected. In most instances, a single bleeding point can be located and controlled.
Most instances of concealed intraperitoneal haemorrhage are reactionary, occurring within 24 hours. Shock develops and the patient is noted to have a falling haemoglobin. The fall in haemoglobin may offer an important clue to the diagnosis. Physical examination and girth measurement are unreliable in the postoperative patient and drainage tubes often block with clot and so may prove to be of little diagnostic assistance. Secondary intraperitoneal haemorrhage is most commonly seen as a delayed complication of acute pancreatitis. In such inaccessible sites temporary control of bleeding can sometimes be achieved by arterial embolisation under angiographic control, before infection is definitively controlled by thorough debridement and drainage.
Haematemesis in the postoperative period may be from a pre-existing chronic ulcer but is often from the stress ulcer syndrome. Associated uncontrolled systemic sepsis is also present in most instances.
Sometimes primary or reactionary haemorrhage is caused by a haemostatic disorder. Most cases follow inadequate reversal of oral anticoagulants, undetected thrombocytopenia or liver failure. Massive transfusion can lead to a dilutional coagulopathy that may compound an established defect in coagulation.
The principles of treatment include rapid intravascular fluid restoration to maintain cardiovascular stability, oxygen administration and stopping the haemorrhage by pressure, surgery or percutaneous angiographic embolisation.
Hypotension with peripheral vasodilatation (‘warm hypotension’) suggests the early stage of septic shock. Septic shock is often accompanied by an acute brain syndrome, which makes diagnosis more difficult.
Septic shock is due to the action of various bacterial toxins and kinins on cardiovascular function. It can complicate Gram-positive, Gram-negative or anaerobic infection at any site. In surgical patients it usually follows Gram-negative infections of the gastrointestinal, biliary or urinary tract. Common organisms are E. coli, K. pneumonia, P. aeruginosa and Proteus, Enterobacter and Bacteroides species.
Early clinical presentation of septic shock may be with a normal or high cardiac output and a low peripheral resistance (‘warm hypotension’). This phase is usually transient and quickly progresses to the classic shock picture with a low cardiac output and high peripheral resistance. The skin is pale, cold and sweating. Tachycardia is present and arrhythmias may occur. The venous pressure is often low in the early stages when associated hypovolaemia is present. Later, progressive myocardial failure occurs with high central venous pressure. Lack of adequate vital organ and tissue perfusion, together with the action of circulating toxins and kinins, causes widespread capillary thrombosis leading to multisystem organ failure (MOF).
A high index of clinical suspicion is required; abdominal examination supplemented by CT scan will often confirm the diagnosis of a localised collection causing systemic sepsis and shock.
The principles of treatment are the control of sepsis, adminstration of oxygen, cardiovascular support and correction of acidosis. Operative intervention is the most effective therapy and many patients will require surgical re-exploration and drainage.
Pulmonary embolism can cause shock or sudden collapse in the postoperative period. The classical presentation is sudden onset of dyspnoea, shock followed by pleuritic chest pain, haemoptysis and a pleural rub. One in 10 events is fatal. Only half the patients with pulmonary embolism have signs of peripheral deep venous thrombosis. Shock in these patients is classically obstructive with a raised central venous pressure, severe dyspnoea, central chest pain, tachypnoea, right heart failure and cyanosis. The ECG changes are different from those of myocardial infarction. Sinus tachycardia is the most common finding. The classic ECG changes of S wave in lead 1, Q wave and inverted T wave in lead 3 (S1, Q3, T3) are less common. Chest X-ray and ECG are, however, often nonspecific. Multislice CT pulmonary angiography with contrast is the quickest and most reliable method of confirming the diagnosis. This has largely replaced the radioisotope ventilation/perfusion scan. Apart from supportive cardiorespiratory measures, the immediate infusion of heparin can be life-saving. This is followed by oral anticoagulation with warfarin. The pulmonary embolus may occasionally be retrieved by mechanical means, including angiographic embolectomy and open surgery.
11.10 Wound care problems
Wound complications are often the result of technical error. A common end result is infection. Sound technique ensures that blood supply to the wound is adequate by avoiding incisions parallel to previous scars, avoiding haematoma formation by gentle tissue handling and careful haemostasis, by the removal of devitalised tissue and by tension-free closure while maintaining surgical asepsis and antisepsis throughout the operation.
Contamination is prevented or controlled by wound adhesive draping, copious lavage and by delaying wound closure when necessary. Appropriate prophylactic perioperative antibiotic administration may minimise the impact of contamination.
Other factors that may interfere with wound healing include alcoholism, malignancy, malnutrition, diabetes, chronic renal injury, steroid and antineoplastic drug treatment, smoking, chronic obstructive airways disease, hypotension and shock, systemic sepsis, dehydration and anaemia and prolonged surgery.
In brief, wound healing starts immediately with surgery.
In the early phase, there is establishment of haemostasis and onset of inflammatory changes from days one to four. The intermediate phase is characterised by mesenchymal cell migration and proliferation, angiogenesis and epithelialisation over two to five days. In the late phase, collagen and other matrix proteins are laid down and the wound contracts over one to four weeks. The final phase of wound healing involves scar formation and remodelling over many months.
The wound complications encountered in the early postoperative period are: haematoma, seroma, ischaemia, infection and dehiscence. Later complications are wound sinus; painful, hypertrophic or keloid scar; and incisional hernia (Box 11.4).
Box 11.4
Postoperative wound problems
Early
Haematoma, seroma
Ischaemia
Dehiscence — subcutaneous or total
Late
Wound sinus
Painful scar
Hypertrophic or keloid scar
Incisional hernia
Haematomas and seromas figure prominently as precursors of infection. They may of themselves cause serious morbidity by, for example, causing respiratory obstruction after thyroidectomy or by lifting skin flaps and increasing the risk of skin ischaemia. Wound ischaemia is also seen when a new abdominal incision is made parallel to or impinging at an acute angle with an old scar, leading to an inadequate blood supply to the bridge of tissue between the two wounds. This leads to skin necrosis. Infection of minor or major degree is the most common complication of the operative wound and is seen especially in the obese diabetic patient and after colorectal surgery, where margins for technical error are much reduced. Wound infection is usually obvious by the fourth or fifth day (although sometimes presentation may be delayed for some weeks after surgery), as a painful tender wound with surrounding cellulitis and low-grade temperature. Pus forms early and must be drained. Treatment is to remove sutures to allow free drainage of pus. Deep seated infection may require antibiotics treatment.
Wound dehiscence usually occurs about a week after surgery, especially in the cachectic patient with increased postoperative intra-abdominal pressure from cough and ileus (Box 11.5). Sutures too widely spaced, of the wrong material, with too small bites and/or under too much tension are the faulty technical factors of most importance in the pathogenesis of burst abdomen. The usual scenario is of a sudden ‘pop’ in the wound after coughing, followed by pain, a serosanguinous discharge or evisceration. Other factors such as wound infection or erosion by a fistula can contribute to dehiscence but more often cause gradual separation of the wound depths and a subsequent hernia. The wound and eviscerated bowel should be covered with moist occlusive dressing to prevent excessive fluid loss from the bowel. Surgical repair of acute dehiscence under general anaesthesia is carried out as soon as possible. Interrupted nonabsorbable sutures with wide bites of all layers, including the skin (‘tension’ sutures), are usually employed for such secondary wound closure.
Box 11.5
Causes of wound dehiscence
Technical error
Inappropriate suture (absorbable, calibre too small)
Inappropriate suturing: too far apart, bites too close, bites too small, too much tension
Local factors
Postoperative distension and increased intra-abdominal pressure: ileus, coughing, straining
Wound infection
Erosive alimentary fistula
General factors
Malignant cachexia
Steroids
Renal injury
Nutritional deficiency
Wound problems can also arise after discharge from hospital. A wound sinus can persist after a preceding wound infection. Wound healing will not occur until the infected deep non-absorbable suture is removed. In patients with underlying prosthetic materials, such as artificial joints or vascular grafts, a sinus may indicate prosthetic infection. The inflammatory markers, such as C-reactive proteins (CRP) and erythrocyte sedimentation rate (ESR), are often raised. Some patients develop a painful or sensitive scar after surgery. In most instances resolution of pain occurs within six months. In the meantime pain may need to be controlled with nonspecific local measures such as massage, local steroid and anaesthetic injections and local ultrasound. Hypertrophic and keloid scars are caused by tension, infection or ischaemia, but can be idiosyncratic. Dark-skinned patients are more prone to keloid scars than those with fairer skins. The majority of patients who develop an incisional hernia have had a previous wound infection. Most appear within three months of surgery, but hernias can appear years later after initially sound primary healing. Unless a definite contraindication to surgery exists, the incisional hernia should be repaired soon after diagnosis, before the hernia becomes so large that a sound repair is difficult to achieve. A mesh is often necessary to reduce any tension on the repair.
11.11 Abnormal investigations
Hypokalaemia
Potassium is the main intracellular cation. The total exchangeable potassium measured isotopically gives an accurate expression of body cell mass. Of a total body potassium of about 3000 mmol in the adult, 98% is in the intracellular compartment and the extracellular fluid contains only about 60 mmol of potassium in a concentration of 4.0–5.0 mmol/L. Normal daily intake is also about 60 mmol. Most excretion is in the urine. Hypokalaemia implies a plasma level below 3.5 mmol/L and hyperkalaemia a level over 5.5 mmol/L. A patient receiving nothing by mouth in the postoperative period should have daily estimations of serum sodium and potassium levels.
Hypokalaemia usually indicates potassium depletion. Common postoperative causes include inadequate potassium replacement, malnutrition, excessive intestinal loss (vomiting, diarrhoea, sequestration, fistulas) or excessive urinary loss (metabolic and respiratory alkalosis, effects of diuretics and steroids). Potassium deficiency, metabolic alkalosis, hypocalcaemia and hypomagnesaemia are commonly associated. Prolonged administration of potassium-free intravenous fluids in a patient who is losing potassium will cause or exacerbate potassium deficiency, as will inadequate potassium supplements in enteral or parenteral nutrition.
The other common surgical causes of hypokalaemia are:
• pyloric stenosis with metabolic alkalosis and malnutrition
• inflammatory bowel disease with chronic diarrhoea
• irritable colon and ingestion of potassium-losing diuretics
• small-bowel fistula with malnutrition
• villous adenoma of the colorectum
• long-term steroid treatment for chronic disease.
Hypokalaemia causes muscles weakness, paralytic ileus, cardiac arrhythmias and ECG changes and sensitivity to digitalis.
Treatment for either prophylaxis or acute depletions is by oral potassium effervescent tablets or intravenous potassium. As a general rule, intravenous potassium supplements should not be started until it is clear that renal function is adequate.
Potassium should not be given intravenously at concentrations greater than 40 mmol/L or in amounts exceeding 40 mmol over a four-hour period. With severe depletion up to 10% of total body potassium may be lost and up to 200 mmol may be required in 24 hours.
Hyperkalaemia
The common causes are renal failure and shock.
Significant quantities of intracellular potassium are released into the extracellular space in response to the stress of surgical injuries, acidosis, sepsis and any catabolic state. Dangerous hyperkalaemia (>6 mmol/L) is rare if renal function is normal. Hyperkalaemia is only seen when renal failure and shock interfere with renal handling of potassium. The dangerous effects are confined to the heart and cause ECG changes, arrhythmias and death. Treatment is urgent and may include dialysis.
Emergency treatment of hyperkalaemia (>7 mmol/L) involves the following two procedures.
• Add to a litre flask of 10% dextrose: 20 units of soluble insulin, 20 mL of 10% calcium gluconate, 20 mmol of sodium bicarbonate and 500 units of heparin. This mixed cocktail may be slowly administered via a peripheral intravenous line for temporary control of hyperkalaemia.
• A retention enema of sodium or calcium cation exchange resin (50 g) is given.
The combined effects of these two measures last for several hours.
Dialysis will be required for all severe cases of acute renal failure when renal function is not likely to recover in the short term. Insertion of a silicone acute peritoneal dialysis catheter (Tenckhoff) at the time of the initial abdominal operation is simple and good prophylactic practice in high-risk patients.
Haemodialysis is used if peritoneal dialysis is ineffective or inappropriate. Venous access can be provided by insertion of a large central venous cannula (internal jugular vein or femoral vein) for venovenous dialysis using a pump.
Haemofiltration is an alternative technique using pressure ultrafiltration causing transfer of large volumes of fluid and electrolyte across a membrane. It is often used as an alternative to haemodialysis and requires careful monitoring of water and ECF balance and intravenous replacement of the large volumes of crystalloid fluid removed. This is done in the HDU or intensive care setting (Ch 12).
Hydrogen ion (acid–base) disorders
These may be of respiratory (gaseous) or metabolic (non-gaseous) origin. The hydrogen ion content of arterial blood is normally kept constant at about 40 nanomolar (between 36 and 44 nmol/L, which coincidentally equals pH 7.44–7.36) by a combination of respiratory and renal mechanisms with extracellular and intracellular buffers. The range of extracellular hydrogen ion content compatible with life is about 20–160 nmol/L (pH about 7.8–6.8).
The reversible reaction is:
This forms the basis of renal and respiratory control of acid–base disorders. The left side of the equation is governed by the balance between production of hydrogen ion by tissue perfusion and metabolism and its excretion by the kidney; the right side by balanced excretion of CO2 via the lungs under the influence of the respiratory centre. Thus CO2 elimination is equivalent to the elimination of acid. In the renal tubules, filtered NaHCO3 is converted to carbonic acid. Sodium ions are replaced by hydrogen ions excreted by the tubular cell. Dissociation of carbonic acid to CO2 and H2O allows CO2 to diffuse back into the tubular cells to there form fresh bicarbonate equivalent to the hydrogen ions excreted. Normally 50–100 mmol of hydrogen ion is excreted daily by the kidney and 15 000 mmol (approximately 300 L) of CO2 by the lungs. Metabolic and respiratory disturbances primarily affect the left and right sides respectively of the equation (Table 11.6).
Table 11.6 Changes in arterial blood chemistry with hydrogen ion disturbances
If the ratio of bicarbonate to CO2 remains unchanged, pH remains constant.
or
The contrast between the quantitative effects of renal and respiratory controls is dramatically illustrated by considering what happens if they fail. Suppression of renal H+ excretion for 30 minutes would cause no detectable change of the ECF hydrogen ion content; suppression of respiratory CO2 excretion for 30 minutes would cause the hydrogen ion content to exceed 100 nmol/L (pH <7).
Metabolic acidosis
Addition of hydrogen ion or loss of base causes metabolic acidosis. Metabolic acidosis after surgery is usually secondary to hypoxia and inadequate tissue perfusion with lactic acidosis. Shock and circulatory arrest are the major contributors. Treatment is directed at restoring the circulation and diagnosing and treating the cause(s) of shock. Persistent renal failure also causes metabolic acidosis. The unexcreted H+ forces the reaction to the right, serum HCO3falls and serum PCO2 rises, stimulating overventilation (acidotic breathing). Other causes of metabolic acidosis include diabetic ketoacidosis and loss of alkaline gastrointestinal fluid (e.g. pancreatic fistula).
Administration of base (as NaHCO3) can correct the acidosis, but treating the cause is paramount — the acidosis will then spontaneously revert to normal.
Metabolic alkalosis
The common cause is loss of acid because of obstruction of the gastric outlet (‘pyloric’ stenosis). Deficiencies of water, sodium, chloride and potassium in addition to alkalosis result from combined gastrointestinal and urinary losses of water and electrolytes. The renal response is initially to secrete an alkaline urine containing Na, K and HCO3; however, the urine subsequently becomes acid as hydrogen ion is secreted by the tubular cells in the face of severe depletion of the cations sodium and potassium.
Correction is by isotonic saline with added potassium, which almost always suffices to restore hydrogen ion status, provided that continuing losses are averted by correcting the obstruction.
Respiratory acidosis and alkalosis
These are the result of hypoventilation and hyperventilation respectively and are dealt with by adjusting ventilation. Common causes of respiratory acidosis and attendant hypoxia in the postoperative patient include wound pain, which can reduce vital capacity by up to two-thirds after laparotomy or thoracotomy. Basal lung atelectasis, sputum retention and bronchospasm exacerbate the lesion and if hypoxia persists and tissue oxygen supply is lower than basal requirements, metabolic acidosis will ensue as well.
Respiratory alkalosis often follows emotional overbreathing and anxiety. It can be exacerbated by alkalotic tetany due to a fall in ionised calcium level. Rebreathing a mixture of CO2 and O2 is usually curative.