Pulmonary collapse

Inability to breathe deeply and cough up bronchial secretions is the primary cause of pulmonary collapse after surgery. Contributory factors include paralysis of cilia by anaesthetic agents, impairment of diaphragmatic movement, over-sedation, abdominal distension and wound pain. When there is complete obstruction of a bronchus or bronchiole, air in the lung distal to the obstruction is absorbed, the alveolar spaces close (atelectasis), and the affected portion of the lung contracts and becomes solid. Small bronchioles (1 mm or less) are prone to close when lung volume reaches a critical point (closing volume). The closing volume is higher in older patients and in smokers, owing to the loss of elastic recoil of the lung, which increases the risk of atelectasis. The extent of collapse varies from closure of a small segment to collapse of a lobe or, when a main bronchus is obstructed, the entire lung. Atelectasis is a very common complication of surgery and usually occurs within 24 hours. It is of clinical relevance because it leads to increased work of breathing and impaired gas exchange; if untreated, secondary bacterial infection will supervene, causing lobar or bronchopneumonia.

The clinical signs of pulmonary collapse include rapid respiration, tachycardia and mild pyrexia, with diminished breath sounds and dullness to percussion over the affected segment. Arterial P_aO₂ is low and the chest X-ray shows areas of increased opacification.

Preoperative measures to reduce the risk of pulmonary collapse following surgery include stopping smoking before the operation, physiotherapy for patients with COPD, and deferring elective surgery for at least 2 weeks in patients with a chest infection. Practising with an incentive spirometer preoperatively will help.

Postoperatively, pulmonary collapse is prevented by encouraging the patient to breathe deeply, cough and mobilize. Adequate analgesia and regular chest physiotherapy are of great importance in the postoperative period. Placement of an epidural catheter in patients undergoing major abdominal surgery may help alleviate postoperative wound pain. Hypoxia is treated by giving oxygen by mask or nasal prongs, and bronchospasm is relieved by inhalation of salbutamol.

When hypoxia is severe, endotracheal intubation, assisted ventilation and repeated bronchial aspiration may be needed. Posture is important and the patient should initially be placed on the unaffected side to aid expansion of the collapsed lung. Bronchoscopy may be needed to suck out a plug of inspissated secretion.

Pulmonary infection

Pulmonary infection commonly follows pulmonary collapse or the aspiration of gastric secretions. Pyrexia, tachypnoea and green sputum are typical. The chest signs are those of collapse with absent or diminished breath sounds, often in association with bronchial breathing and coarse crepitations from surrounding areas of partial bronchial occlusion. Chest X-ray usually demonstrates patchy fluffy opacities.

The patient is encouraged to cough, and antibiotics are prescribed after sputum is sent for bacteriological examination. Most pulmonary infections are caused by the respiratory commensals, Streptococcus pneumoniae and Haemophilus influenzae, but many postoperative pulmonary infections are caused by Gram-negative bacilli acquired by aspiration of oropharyngeal secretions. Antibiotics provide the mainstay of treatment. Oxygen is given if there is hypoxia, and more intensive measures, including bronchoscopy and assisted ventilation, are instituted if respiratory function continues to deteriorate.

Respiratory failure

Respiratory failure is defined as an inability to maintain normal partial pressures of oxygen and carbon dioxide (P_aO₂ and P_aCO₂) in arterial blood. Blood gas determinations are the key to its early recognition and should be repeated frequently in patients with previous respiratory problems. The normal P_aO₂ is > 13 kPa at the age of 20 years, falling to around 11.6 kPa at 60 years; respiratory failure is denoted by a value of less than 6.7 kPa. Severe hypoxaemia may result in visible central cyanosis. In type 1 respiratory failure there is hypoxia and in type 2 there is hypercarbia with hypoxia.

Acute respiratory distress syndrome (ARDS)

ARDS is characterized by impaired oxygenation, diffuse lung opacification on chest X-ray and an increasing ‘stiffness’ of the lungs (decreased compliance). It may result from pulmonary or systemic sepsis, following massive blood transfusion, or as a consequence of aspiration of gastric contents. The syndrome displays a wide spectrum of severity. Many minor and transient cases recover spontaneously, whereas in a proportion of cases, progressive respiratory insufficiency occurs. Tachypnoea with increasing ventilatory effort, restlessness and confusion develop. Hypoxia initially responds to an increase in the oxygen content of inspired air, but progressively increasing concentrations are required to prevent the P_aO₂ from falling. The pathophysiology is unclear, but endotoxin-activated leucocytes are thought to be deposited in the pulmonary capillaries, releasing oxygen-derived free radicals, cytokines and other chemical mediators. Damage to the vascular endothelium results in increased capillary permeability and leakage of fluid, causing widespread interstitial and alveolar oedema. This is seen as bilateral diffuse fluffy opacities on chest X-ray (Fig. 9.2). The lungs become increasingly stiff and difficult to ventilate.

Fig. 9.2 Chest X-rays showing features of ARDS.

Management includes supportive measures in the form of ventilation with positive end-expiratory pressure (PEEP) and treatment of the underlying condition, i.e. control of infection by antibiotics, drainage of any source of pus and correction of hypovolaemia. The mortality rate of severe ARDS is approximately 50%.

Pleural effusion

Small pleural effusions (Fig. 9.3) are not uncommon following upper abdominal surgery, but are usually of no clinical significance. They may be secondary to other pulmonary pathology, such as collapse/consolidation, pulmonary infarction or secondary tumour deposits. The appearance of a pleural effusion 2–3 weeks after an abdominal operation may suggest the presence of a subphrenic abscess. Small effusions may be left alone to reabsorb if they do not interfere with respiration. Alternatively, pleural aspiration is performed and the fluid sent for bacteriological culture.

Fig. 9.3 Postoperative right-sided pleural effusion.

Pneumothorax

The most common cause of postoperative pneumothorax is the insertion of a central venous line, and a chest X-ray is necessary after this procedure to exclude this potential complication. There is also an enhanced risk of pneumothorax in patients on positive-pressure ventilation, presumably owing to rupture of pre-existing bullae. The insertion of an underwater seal drain is usually followed by rapid expansion of the lung.

Myocardial ischaemia/infarction

Although in most cases there is a history of preceding cardiac disease, myocardial ischaemia or cardiac arrest can occur in an otherwise fit patient. Patients with ischaemia may complain of gripping chest pain, but this is not invariable (particularly in the elderly diabetic patient or in the early postoperative period) and hypotension may be the only sign. The absence of symptoms after operation is thought to be due to the residual effects of anaesthesia and to the administration of postoperative analgesia. If ischaemia is suspected, an ECG is performed urgently and arrangements are made for cardiac monitoring. A sample of blood is withdrawn to estimate concentrations of cardiac enzymes. One-third of postoperative myocardial infarctions are fatal.

Cardiac failure

Although acute cardiac failure occurs most often in the immediate postoperative period, patients with ischaemic or valvular heart disease, arrhythmias or major surgical insult can also go into failure in the subsequent recovery period. Clinical manifestations are progressive dyspnoea, hypoxaemia and diffuse congestion on chest X-ray. Excessive administration of fluid in the early postoperative period in patients with limited myocardial reserve is a common cause, which can be avoided by monitoring CVP. Treatment consists of avoiding further fluid overload, and the administration of diuretics and cardiac inotropes.

Arrhythmias

Sinus tachycardia is common and may be a physiological response to hypovolaemia or hypotension. It is also caused by pain, fever, shivering or restlessness. Tachycardia increases myocardial oxygen consumption and may decrease coronary artery perfusion. Sinus bradycardia may be due to vagal stimulation by neostigmine, pharyngeal irritation during suction, or the residual effects of anaesthetic agents. Atrial fibrillation is the most common postoperative arrhythmia. Fast atrial fibrillation may result in haemodynamic disturbances and may require pharmacological intervention. Refractory cases may require cardioversion.

Postoperative shock

Shock is defined as a failure to maintain adequate tissue perfusion. The three main types are hypovolaemic, cardiogenic and septic shock. Hypovolaemic shock may be caused by inadequate replacement of pre- or perioperative fluid losses or postoperative haemorrhage, whereas cardiogenic shock is usually secondary to acute myocardial ischaemia/infarction or an arrhythmia. Hypovolaemic and cardiogenic shock are characterized by tachycardia, hypotension, sweating, pallor and vasoconstriction. Septic shock is characterized in the early stages by a hyperdynamic circulation with fever, rigors, a warm vasodilated periphery and a bounding pulse. Later features include hypotension and peripheral vasoconstriction. Without appropriate management, shock will result in oliguria and the development of multisystem organ failure, and may lead to death.

Postoperative urinary retention

Inability to void postoperatively is common, especially after groin, pelvic or perineal operations, or operations under spinal/epidural anaesthesia (Fig. 9.4). Postoperative pain, the effects of anaesthesia and drugs, and difficulties in initiating micturition while lying or sitting in bed may all contribute. Males tend to be more commonly affected than females. When its normal capacity of approximately 500 ml is exceeded, the bladder may be unable to contract and empty itself. Frequent dribbling or the passage of small volumes of urine may indicate overflow incontinence, and examination may reveal a distended bladder. The management of acute urinary retention is catheterization of the bladder, with removal of the catheter after 2–3 days (see Chapter 8).

Fig. 9.4 Postoperative urinary retention.

Urinary tract infection

Urinary tract infections are most common after urological or gynaecological operations. Pre-existing contamination of the urinary tract, urinary retention and instrumentation are the principal factors contributing to postoperative urinary infection. Cystitis is manifested by frequency, dysuria and mild fever, and pyelonephritis by high fever and flank tenderness. Treatment involves adequate hydration, proper drainage of the bladder and appropriate antibiotics.

Renal failure

Acute renal failure after surgery results from protracted inadequate perfusion of the kidneys. The most common cause of postoperative oliguria is pre-renal vascular insufficiency from hypovolaemia, water depletion or extracellular fluid depletion. Hypoperfusion of the kidney may be aggravated by hypoxia, sepsis and nephrotoxic drugs. Patients with pre-existing renal disease and jaundice are particularly susceptible to hypoperfusion, and are more likely to develop acute renal failure.

The complication can largely be prevented by adequate fluid replacement before, during and after surgery, so that urine output is maintained at 0.5 ml/kg/hr or more. The importance of monitoring hourly urine output means that bladder catheterization is needed in all patients undergoing major surgery, and in those at risk of renal failure. Early recognition and treatment of bacterial and fungal infections is also important in the prevention of renal failure.

Urine output below 700 ml in 24 hours (or less than 0.5 ml/kg/hr for several hours on catheter drainage) should be considered pathological oliguria. Management involves the restoration of an adequate circulating intravascular compartment by the administration of intravenous fluids. A CVP line is usually required to measure circulating blood volume. Diuretics may be administered only if the patient is well hydrated; however, they should not be continually prescribed if the patient remains oliguric.

Acute postoperative renal failure occurs when the reversible stage of acute renal insufficiency progresses to acute tubular necrosis. Volume loading becomes potentially dangerous with established renal failure, and the mainstays of treatment at this stage are the replacement of observed fluid loss, plus an allowance of approximately 500 ml/day for insensible loss, and restriction of dietary protein intake to less than 20 g/day. Biochemical status is checked by frequent estimations of serum urea and electrolytes. Hyperkalaemia can be treated by intravenous administration of insulin and glucose, or cation exchange resins. Haemofiltration or haemodialysis may be indicated if conservative measures fail to prevent rapid rises in serum concentrations of urea and potassium. Recovery from acute tubular necrosis can be anticipated in survivors after 2–4 weeks. The patient will then enter a polyuric phase, in which fluid and electrolyte balance requires careful monitoring. The mortality rate in patients who develop postoperative renal failure is 50%.

Cerebrovascular accidents (CVA)

These are usually precipitated by sudden hypotension during or after surgery in elderly hypertensive patients with severe atherosclerosis. They are a specific complication of carotid endarterectomy, occurring in 1–3% of cases, but may also complicate cardiac surgery.

Neuropsychiatric disturbances

These occur frequently and cover a wide spectrum of disorders. The most common is mental confusion with agitation, restlessness and disorientation, and is known as delirium. It usually occurs in the elderly and may arise on a background of dementia due to cerebral atrophy, but is often precipitated by the use of sedative or hypnotic drugs. Acute toxic confusion state is a well-recognized acute psychiatric disorder that occurs in some patients during a serious illness or after a major surgical intervention. Many factors can contribute, and it is important to look for a treatable cause, such as hypoxia, sepsis, or a metabolic disturbance such as uraemia or electrolyte imbalance. Sleep deprivation, particularly in intensive care units, can also cause severe mental disturbance.

Delirium tremens (acute alcohol withdrawal syndrome)

Delirium tremens occurs in alcoholics who stop drinking suddenly. In most instances, this can be predicted from a detailed history. Prodromal symptoms include personality changes, anxiety and tremors. The fully developed condition is characterized by extreme agitation, visual hallucinations, restlessness, confusion and, rarely, convulsions and hyperthermia. If symptoms are mild, treatment involves the prescription of oral diazepam and vitamin B (thiamine). Control of extreme agitation may require intravenous administration of diazepam, or haloperidol.

Deep venous thrombosis (DVT)

The pathogenesis of venous thrombosis involves stasis, increased blood coagulability and damage to the blood vessel wall (Virchow’s triad). The incidence of DVT varies with the type of operation and the associated risk factors, which include increasing age, obesity, prolonged operations, pelvic and hip surgery, malignant disease, previous DVT or pulmonary embolism (PE), varicose veins, pregnancy, and use of the oral contraceptive pill.

Measures to prevent DVT include taking care to avoid prolonged compression of the leg veins during and after the operation; the use of graded compression support stockings (TED stockings); mechanical or electrical compression of the calf muscles during surgery; and low molecular weight heparin (LMWH).

DVT is frequently asymptomatic, but may present with a painful, tender swollen calf. It may be the cause of a postoperative fever. Duplex ultrasonography is now the investigation of choice for diagnosing DVT.

Nowadays, most DVTs are treated with LMWH injected subcutaneously once daily rather than by means of an unfractionated heparin infusion. Heparin therapy is stopped once the patient is fully anticoagulated with warfarin, which is then normally continued for 3–6 months. The dose of warfarin is adjusted to maintain an international normalized ratio (INR) at 2–3 times normal.

Pulmonary embolism

Massive pulmonary embolus with severe chest pain, pallor and shock demands immediate cardiopulmonary resuscitation, heparinization and urgent CT pulmonary angiography. Fibrinolytic agents, such as streptokinase or urokinase, can be infused intravenously to encourage clot lysis if it is at least 6 days after surgical intervention, or in extreme cases the clot can be removed at open pulmonary embolectomy under cardiopulmonary bypass.

If a PE is suspected in a patient complaining of chest pain, sometimes in association with tachypnoea, haemoptysis and a pleural rub and effusion, a chest X-ray and ECG should be undertaken, mainly to rule out alternative causes of the symptoms. If these are negative, a CT pulmonary angiogram should then be performed and if this reveals lobar or segmental perfusion defects, the patient is heparinized and monitored carefully (Fig. 9.5). In such cases, it is also important to search for the source of the embolus; warfarin therapy is recommended in all patients who have sustained a pulmonary embolus, and therapy is normally continued for 6 months. If the patient cannot be anticoagulated, or sustains further PE despite anticoagulation then consideration can be given to placing an inferior vena caval (IVC) filter.

Fig. 9.5 CT pulmonary angiograms showing pulmonary embolus.

Infection

Infection (Fig. 9.6) is the most common complication in surgery. The incidence varies from less than 1% in clean operations to 20–30% in dirty cases. Subcutaneous haematoma is a common prelude to a wound infection, and large haematomas may require evacuation. The onset is usually within 7 days of operation. Symptoms include malaise, anorexia, and pain or discomfort at the operation site. Signs include local erythema, tenderness, swelling, cellulitis, wound discharge or frank abscess formation, as well as an elevated temperature and pulse rate. If a wound becomes infected, it may be necessary to remove one or more sutures or staples prematurely to allow the egress of infected material. The wound is then allowed to heal by secondary intention. Antibiotics are only required if there is evidence of associated cellulitis or septicaemia. If the wound infection is chronic, the presence of a suture sinus or an enterocutaneous fistula must be excluded.

Fig. 9.6 Wound infection.

Dehiscence

The incidence of abdominal wound dehiscence should be less than 1%. Wound dehiscence (Fig. 9.7) may be partial (deep layers only) or complete (all layers, including skin). A serosanguinous discharge is characteristic of partial wound dehiscence. The extrusion of abdominal viscera through a complete abdominal wound dehiscence is known as evisceration. This rare complication usually occurs within the first 2 weeks after operation. Risk factors include obesity, smoking, respiratory disease, obstructive jaundice, nutritional deficiencies, renal failure, malignancy, diabetes and steroid therapy; however, the most important causes are poor surgical technique, persistently increased intra-abdominal pressure, and local tissue necrosis due to infection. The wound should be resutured under general anaesthesia. Incisional herniation complicates approximately 25% of cases.

Fig. 9.7 Wound dehiscence.

Postoperative fever

Fever in a patient who has had surgery can be due to a variety of causes related to the primary disease or complications related to the surgical intervention or general anaesthesia. The common conditions that cause fever are listed in Box 9.3. The cause must be diligently identified and treated appropriately.