Postoperative Care

Published on 27/02/2015 by admin

Last modified 27/02/2015

Print this page

This article have been viewed 1633 times

Postoperative Care

In modern anaesthetic practice, the patient is monitored and supervised closely and continuously during induction and throughout the operative procedure. However, many problems associated with anaesthesia and surgery may occur in the immediate postoperative period, and it is essential that supervision by adequately trained and experienced personnel is continued during the recovery period. In addition, some major and minor complications of anaesthesia and surgery may occur at any time in the first few days after operation.

THE EARLY RECOVERY PERIOD

Most hospitals have a recovery ward (or postanaesthesia care unit, PACU) within, or in close proximity to, the operating theatre suite (see Ch 20). The Association of Anaesthetists of Great Britain and Ireland (AAGBI) recommends that fully staffed recovery facilities must be available at all times in hospitals with an emergency surgical service. Some locations where anaesthesia is provided (e.g. the X-ray department) may not have a recovery ward. This section describes common problems which occur in the immediate postoperative period and refers specifically to their management in a recovery ward; however, the same principles are applicable to recovery in other locations.

The recovery period starts as soon as the patient leaves the operating table and the direct supervision of the anaesthetist. All the complications described below may occur at any time, including the period of transfer from operating theatre to recovery ward; in some operating theatre suites, the transfer to the recovery ward may last for several minutes, and it is essential that the standard of observation does not diminish during the journey. The patient must be supervised and monitored closely at all times.

The patient is nursed in a bed if available or if a prolonged stay is anticipated, but sometimes on a trolley (Fig. 40.1). All beds and trolleys must have the facility to be tipped head-down. Suction apparatus, including catheters, an oxygen supply with appropriate face mask, a self-inflating resuscitation bag and anaesthetic mask, a pulse oximeter and an automated non-invasive blood pressure monitor must be available for each patient. In addition, there should be a complete range of resuscitation equipment within the recovery area; this includes an anaesthetic machine, a range of laryngoscopes, tracheal tubes, bougies, intravenous (i.v.) cannulae, fluids, emergency drugs, electrocardiogram (ECG) monitor and defibrillator. Facilities for emergency airway management including surgical airways should also be available (see Ch 22).

FIGURE 40.1 Part of a recovery ward. Many patients are nursed on a trolley, but a bed is used if available, and particularly for those who have undergone major surgery and those who need to stay for several hours.

A wide range of drugs should be stored in the recovery area for the treatment of common complications and also emergency events (Table 40.1).

TABLE 40.1

Drugs Which Should be Available in the Recovery Room

On arrival in the recovery ward, the anaesthetist should give the nurse full details of pre-existing medical problems, surgical procedure, anaesthetic technique, drugs, regional blocks, fluids, blood loss/replacement, any untoward events and any anticipated problems during recovery. All patients should be monitored by measurement of pulse rate, arterial pressure, arterial oxygen saturation and respiratory rate, and by assessment of level of consciousness, peripheral circulation and adequacy of ventilation. Depending on the nature of work undertaken in the theatre suite, a proportion of bed stations should have the facility for monitoring ECG, systemic and pulmonary arterial pressures and central venous pressure (CVP) continuously; this may be required in high-risk patients or those who have undergone major surgery. Capnography should be available for use in patients who require tracheal intubation. At least one mechanical ventilator should be available, although more may be required depending on the workload. Urine output should be measured routinely in patients who have undergone major surgery. Wounds and surgical drains should be inspected regularly for signs of bleeding.

It is important that the handover from anaesthetist to recovery nurse is systematic and undertaken in an unhurried way when both anaesthetist and nurse can concentrate on the handover. In general this will be after essential monitoring, such as pulse oximetry and blood pressure, has been reapplied and checked. The anaesthetist should not leave the patient until he or she is satisfied that there are no immediate problems, particularly with regard to the airway, and respiratory and cardiovascular systems.

A record should be made of pulse rate, arterial pressure and arterial oxygen saturation, respiratory rate, level of consciousness, pain score, sensory level (if regional anaesthesia has been used), and any other relevant information (such as complications, and drug and fluid administration) obtained while the patient is in the recovery area. In most units, recordings of physiological measurements are made every 5 min until consciousness has returned and then at intervals of 10–15 min.

The patient should not be discharged to the surgical ward until the following criteria have been met.

Consciousness has returned fully, a patent airway can be maintained and protective reflexes are present.

Ventilation and oxygenation are satisfactory.

The cardiovascular system is stable with no unexplained cardiac irregularity or persistent bleeding. Consecutive measurements of pulse rate and arterial pressure should approximate to the patient’s normal preoperative values or be at an acceptable level commensurate with the planned postoperative care. Peripheral perfusion should be adequate.

Pain and nausea are controlled.

Temperature is within acceptable limits.

High-risk patients or those who have undergone major surgery may stay in the recovery ward for up to 24 h. If this is not feasible, or if instability persists for longer than 24 h, the patient should be transferred to a high-dependency or intensive care unit. The level of monitoring and care during transfer should be the same as that in the recovery room.

Although the recovery room nurse undertakes the direct care of the patient, the responsibility for the patient remains with the anaesthetist. Patients must only be discharged to the ward with the anaesthetist’s consent.

The remainder of this chapter is devoted to the diagnosis and management of common problems which occur in the postoperative period. Some of these occur most frequently in the immediate recovery period, while others may occur at any time during the patient’s convalescence from surgery. Some surgical procedures are associated with specific complications.

CENTRAL NERVOUS SYSTEM

Conscious Level

Many patients are unconscious on arrival in the recovery ward because of residual effects of anaesthetic drugs. The duration of impaired consciousness depends on:

The drugs used. Recovery of consciousness may be delayed if the following agents have been used:

volatile anaesthetics with a high blood/gas solubility coefficient

barbiturates, particularly if large total doses have been given

benzodiazepines

opioids with a long duration of action, including large doses of fentanyl.

The timing of drug use. Delayed recovery may occur if a long-acting i.v. anaesthetic or analgesic drug has been given towards the end of the procedure, or if the more soluble volatile agents have been continued until the end of surgery.

Pain. The presence of pain speeds recovery of consciousness. Recovery may be delayed after minor procedures or if potent analgesia has been provided by administration of opioids or by regional anaesthesia.

Undue prolongation of unconsciousness should not be attributed to these factors alone. Other causes should be considered, as their early recognition may prevent serious sequelae. These are:

hypoxaemia – in the presence of an adequate circulation, coma occurs only if profound hypoxaemia is present; agitation is a more common sign of hypoxia

hypercapnia – unconsciousness may occur if arterial carbon dioxide tension (PaCO₂) exceeds 9–10 kPa

hypotension

hypothermia.

Hypoglycaemia

This occurs most commonly in diabetic patients treated with oral hypoglycaemic agents or insulin and an inadequate intake of glucose. The perioperative management of the diabetic patient is discussed in Chapter 18.

Hyperglycaemia

Hyperglycaemia in known diabetics may occur as a result of inadequate provision of insulin or injudicious infusion of glucose. However, coma is unusual in acute hyperglycaemia. Undiagnosed diabetics with hyperglycaemia and ketosis may present for surgery because of abdominal pain, and prolonged postoperative coma may occur unless the metabolic defect is diagnosed and treated.

Cerebral Pathology

Consciousness may be impaired by functional or structural cerebral damage. Possible causes include:

episodes of cerebral ischaemia (e.g. carotid artery surgery, profound hypotension) or cerebral hypoxia during anaesthesia

intracranial haemorrhage, thrombosis or infarction – these may occur coincidentally or may have been associated with intraoperative hypertension, hypotension or arrhythmias

pre-existing cerebral lesions, e.g. tumour, trauma – anaesthetic techniques which increase intracranial pressure are likely to impair cerebral function

epilepsy – convulsions may have been masked by anaesthesia or neuromuscular blocking drugs

air embolism

intracranial spread of local anaesthetic solution after subarachnoid injection – introduction into the subarachnoid space may be accidental, e.g. during epidural block or, rarely, interscalene brachial plexus block; unconsciousness is almost always accompanied by apnoea.

Other Causes

Hypo-osmolar or TURP syndrome. This results most commonly from absorption of water from the bladder during transurethral resection of the prostate (TURP). The investigation and management of this condition are described on page 570.

Hypothyroidism.

Hepatic or renal failure.

Confusion and Agitation

These occur occasionally during emergence from an otherwise uncomplicated anaesthetic.

Various drugs are associated with postoperative confusion, including:

opioids

benzodiazepines

anticholinergics including atropine and cyclizine.

Atropine crosses the blood–brain barrier and may result in the central anticholinergic syndrome, characterized by restlessness and confusion, together with obvious antimuscarinic effects. Glycopyrronium does not cross the blood–brain barrier and is preferable to atropine for antagonism of the muscarinic effects of neostigmine in elderly patients; in addition to its lack of central effects, it produces less tachycardia and antagonizes the effects of neostigmine for a longer period.

All the factors listed above as causes of prolonged coma may also result in confusion and agitation. Pain may also contribute, although it is seldom responsible alone. Emergence delirium is associated particularly with the use of ketamine and may occur after the administration of etomidate. Septicaemia may result in confusion, as may distension of the stomach or bladder.

A lightly sedated, conscious patient with inadequate antagonism of neuromuscular blocking drugs may appear to the inexperienced observer to be agitated and confused. Movements are uncoordinated. The condition is distressing to the patient and is an indication of a poor anaesthetic technique. It should never be allowed to develop.

Pain

This subject is discussed fully in Chapter 41. The effects of pain should be differentiated from those of hypercapnia and hypovolaemia (Table 40.2).

TABLE 40.2

Common Problems in the Recovery Room: Symptoms and Signs

RESPIRATORY SYSTEM

Hypoventilation

Common causes of hypoventilation in the immediate postoperative period are listed in Table 40.3. Hypoventilation results in an increase in PaCO₂ (Fig. 40.2) and a decrease in alveolar oxygen tension (PAO₂), and thus hypoxaemia, which may be corrected by increasing the inspired concentration of oxygen. The risk factors for developing hypoventilation include:

TABLE 40.3

Causes of Postoperative Hypoventilation

Factors Affecting Airway	Factors Affecting Ventilatory Drive	Peripheral Factors
Upper airway obstruction	Respiratory depressant drugs	Muscle weakness
Tongue	Preoperative CNS pathology	Residual neuromuscular block
Laryngospasm	Intra- or postoperative cerebrovascular accident	Preoperative neuromuscular disease
Oedema	Hypothermia	Electrolyte abnormalities
Foreign body	Recent hyperventilation (PaCO₂ low)	Pain
Tumour		Abdominal distension
Bronchospasm		Obesity
		Tight dressings
		Pneumo-/haemothorax

CNS, central nervous system; PaCO₂, arterial carbon dioxide tension.

FIGURE 40.2 Gas exchange during hypoventilation. Note the relatively rapid increase in alveolar partial pressure of carbon dioxide (PCO₂) compared with the slow decrease in arterial oxygen saturation. PO₂, partial pressure of oxygen.

old age

obesity

prolonged surgical operations

opioids

upper abdominal or thoracic surgery.

Airway Obstruction

Airway obstruction caused by the tongue, by indrawing of the pharyngeal muscles or by blood or secretions in the pharynx may be ameliorated by placing the patient in the lateral or recovery position (see Fig. 21.7). This position should be used for all unconscious patients who have undergone oral or ear, nose and throat surgery, and for patients at risk of gastric aspiration.

Partial obstruction of the airway is characterized by noisy ventilation. As the obstruction increases, tracheal tug and indrawing of the supraclavicular area occur during inspiration. Total obstruction is signalled by absent sounds of breathing and paradoxical movement of the chest wall and abdomen.

In many patients, a clear airway is maintained only by displacing the mandible anteriorly and extending the head. In some, it is necessary also to insert an oropharyngeal airway, although this may stimulate coughing, gagging and laryngospasm during recovery of consciousness. A nasopharyngeal airway is often tolerated better, but there is a risk of causing haemorrhage from the nasopharyngeal mucosa. Occasionally, insertion of a laryngeal mask airway is necessary to maintain the airway until consciousness has returned fully; very occasionally, tracheal intubation is required.

Blood, oral secretions or regurgitated gastric fluid which have accumulated in the pharynx should be aspirated and the patient placed in the recovery position to allow any further fluid to drain anteriorly.

Foreign bodies, such as dentures (particularly partial dentures) or throat packs, may cause airway obstruction. It may be difficult to maintain a patent airway in an unconscious patient with an oral, pharyngeal or laryngeal tumour.

Obstruction of the upper airway occurs intermittently after recovery from anaesthesia. Obstructive sleep apnoea is common in the postoperative period and may result in decreases of arterial oxyhaemoglobin saturation (SaO₂) to less than 75%. Episodes occur with the greatest frequency in the first 4 h after anaesthesia and are more common and severe in patients who receive opioids for postoperative analgesia than in those in whom analgesia is provided by a regional technique. However, the use of regional techniques does not reduce the risk to zero.

Airway obstruction may result from haemorrhage after surgery to the neck, including thyroid, carotid and spinal surgery; the wound should be opened urgently and the haematoma drained. This may not relieve the obstruction if venous engorgement or tissue oedema are marked. Occasionally, tracheal collapse occurs after thyroidectomy in patients who have developed chondromalacia of the cartilaginous rings of the trachea caused by pressure from a large goitre. Inspiratory stridor may be present or there may be total obstruction during inspiration; the trachea must be reintubated immediately.

Laryngeal Spasm

This complication is relatively common after general anaesthesia. In particular, children undergoing oropharyngeal surgery are more at risk. It may be partial or complete and is caused usually by direct stimulation of the cords by secretions or blood, or of the epiglottis by an oropharyngeal airway or laryngeal mask. It may follow extubation of the trachea in the semiconscious patient. It may be difficult to differentiate this condition from airway obstruction caused by the pharyngeal wall; if airway obstruction persists despite implementation of the measures described above, laryngoscopy should be undertaken.

Any obvious foreign material causing laryngospasm should be removed by aspiration, and oxygen 100% administered. If obstruction is complete, positive-pressure ventilation by mask may force some oxygen through the cords to maintain arterial oxygenation until the spasm has subsided; there is a significant risk of inflating the stomach with oxygen during this procedure. If attempts to oxygenate the lungs fail, a small dose of succinylcholine should be administered, and the lungs ventilated with oxygen when the spasm is relieved. When satisfactory oxygenation has been achieved, it may be advisable to intubate the trachea to reduce the risk of regurgitation of gastric contents, as the stomach may have been inflated with oxygen. Appropriate methods to avoid awareness should be instituted. When the effects of succinylcholine have terminated, oxygen 100% is administered and the trachea is extubated when the patient regains consciousness.

Rarely, laryngeal obstruction occurs after thyroid surgery if both recurrent laryngeal nerves have been traumatized.

Laryngeal Oedema

This occurs occasionally after tracheal intubation and may result in severe obstruction, particularly in a child. Treatment depends on the severity of the obstruction; immediate reintubation may be required if obstruction is complete, but partial obstruction may subside if the patient is treated with heated humidified gases. Dexamethasone may hasten resolution of the oedema.

Bronchospasm

This may result from stimulation of the airway by inhaled material. It is commoner in asthmatic or bronchitic patients and in smokers. It may result directly from intrinsic asthma or may be part of an anaphylactic reaction. Several drugs used in anaesthetic practice may precipitate bronchospasm either by a direct effect on bronchial muscle or by releasing histamine; these include barbiturates, morphine, mivacurium and atracurium. Treatment comprises the removal of any predisposing factor and the administration of oxygen and bronchodilators.

Ventilatory Drive

There are several possible causes of reduced ventilatory drive during recovery from anaesthesia (see Table 40.3). The presence of intracranial pathology, e.g. tumour, trauma or haemorrhage, may affect ventilatory drive in the postoperative period. Ventilation is reduced in the presence of hypothermia, although it is usually appropriate for the metabolic needs of the body. Hypoventilation occurs in the hypocapnic patient, e.g. after a period of hyperventilation until PaCO₂ is restored to normal, and in the presence of primary metabolic alkalosis.

The most important cause of reduced ventilatory drive during recovery is the effect of drugs administered by the anaesthetist in the perioperative period. All the volatile and i.v. anaesthetic agents – with the exception of ketamine – depress the respiratory centre; significant concentrations of these drugs remain in the brainstem during the early postoperative period.

All opioid analgesics depress ventilation. With most opioids, the effect is dose-dependent, although the agonist-antagonist agents are claimed to have a ceiling effect. In the majority of patients, opioids do not produce apnoea, but result in decreased ventilatory drive and an increase in PaCO₂, which plateaus at an elevated value. The elderly are particularly sensitive to drug-induced ventilatory depression. The treatment of postoperative pain begins in the recovery area, often by administration of i.v. opioids by the medical or nursing staff, and ventilation must be monitored carefully after each dose.

Spinal (intrathecal or epidural) opioids, particularly lipid-insoluble agents such as morphine, may produce ventilatory depression some hours after administration. Patients who have received subarachnoid or epidural opioids should be cared for in areas where protocols and training programmes for surgical ward nurses have been implemented.

Reduced ventilatory drive is easy to diagnose if the ventilatory rate or tidal volume is clearly reduced. However, lesser degrees of hypoventilation may be difficult to detect, and the signs of moderate hypercapnia, e.g. hypertension and tachycardia, may be masked by the residual effects of anaesthetic agents, or misdiagnosed as pain-induced (see Table 40.2).

Mild hypoventilation is acceptable provided that oxygenation remains adequate; this may easily be achieved by a modest increase in the inspired fractional concentration of oxygen (FiO₂; see below). If ventilatory drive is reduced excessively by opioids, resulting in an increasing PaCO₂ or delayed recovery of consciousness, naloxone in increments of 1.5–3 μg kg⁻¹ should be administered every 2–3 min until improvement occurs. Administration of excessive doses of naloxone reverses the analgesia induced by systemic (but not to the same extent by spinal) opioids; large doses may cause severe hypertension and have been associated with cardiac arrest on rare occasions. The effects of i.v. naloxone last only for 20–30 min; in order to prevent recurrence of reduced ventilation after long-acting opioids, an additional dose (50% of the effective i.v. dose) may be administered intramuscularly or an i.v. infusion commenced.

Peripheral Factors

The commonest peripheral factor associated with hypoventilation is residual neuromuscular blockade. This may be exaggerated by disease of the neuromuscular junction, e.g. myasthenia gravis, or by electrolyte disturbances. Inadequate reversal of neuromuscular blockade is usually associated with uncoordinated, jerky movements, although these may occur occasionally during recovery of consciousness in patients with normal neuromuscular function. Measurement of tidal volume is not a reliable guide to adequacy of reversal of neuromuscular blockade; a normal tidal volume may be achieved with only 20% return of diaphragmatic power, but the ability to cough remains severely impaired. Traditional clinical signs of adequacy of reversal of neuromuscular blockade (such as if the patient is able to lift the head from the trolley for 5 s or maintain a good hand grip) correlate poorly with objective signs of neuromuscular function. Some more objective means of assessment are listed in Table 40.4, but these require the cooperation of the patient. In the unconscious or uncooperative patient, nerve stimulation (see Ch 6) provides the best means of assessing neuromuscular function, although there are differences among the non-depolarizing relaxants in the relationship between their actions in the forearm and diaphragm.

TABLE 40.4

Clinical Assessment of the Adequacy of Antagonism of Neuromuscular Block

Subjective

Grip strength

Adequate cough

Objective

Ability to sustain head lift for at least 5 s

Ability to produce vital capacity of at least 10 mL kg⁻¹

If residual non-depolarizing blockade is confirmed, further doses of neostigmine may be administered (with glycopyrronium) up to a total of 5 mg; in higher doses, neostigmine can worsen neuromuscular function. Patients who have received rocuronium or vecuronium can be given sugammadex (2 mg kg⁻¹ if there are signs of reversal of neuromuscular blockade; or 4 mg kg^− 1 if there are no twitches present using train-of-four stimulation). If the block persists, artificial ventilation must be maintained while the cause is sought.

Factors responsible most commonly for difficulty in antagonism of neuromuscular block include overdosage with muscle relaxant, too short an interval between administration of the drug and the antagonist, hypokalaemia, respiratory or metabolic acidosis, administration of aminoglycoside antibiotics, local anaesthetic agents, diseases affecting neuromuscular transmission and muscle disease.

Delayed elimination of all of the non-depolarizing muscle relaxants (except atracurium and cisatracurium) has been reported, and causes prolonged neuromuscular block. Delayed elimination occurs most frequently in the presence of renal or hepatic insufficiency, or in dehydrated patients with low urine output. Muscle paralysis may recur 30–60 min after administration of neostigmine if elimination of the relaxant is inadequate, even if antagonism appears to be satisfactory initially. A similar phenomenon may occur if acidosis develops, or when patients who have been hypothermic are rewarmed.

Prolonged neuromuscular block after succinylcholine or mivacurium occurs in the presence of atypical plasma cholinesterase or a low concentration of normal plasma cholinesterase. Paralysis after succinylcholine may persist for up to 8 h, although in most instances recovery occurs within 20–120 min. Neostigmine should not be administered if prolonged neuromuscular block occurs after administration of succinylcholine.

Artificial ventilation of the lungs must be maintained or resumed in any patient who has inadequate neuromuscular function. Anaesthesia should be provided to prevent awareness.

Hypoventilation may be caused also by restriction of diaphragmatic movement resulting from abdominal distension, obesity, tight dressings or abdominal binders. Pain, particularly from thoracic or upper abdominal wounds, may cause reduced ventilation.

The presence of air or fluid in the pleural cavity may result in hypoventilation. Pneumothorax may occur during intermittent positive-pressure ventilation (IPPV). It is an occasional complication in healthy patients, but is a particular risk in those with chronic obstructive airways disease, especially if bullae are present, and after chest trauma. It may complicate brachial plexus nerve block, central venous cannulation or surgery involving the kidney or neck. Haemothorax may result from chest trauma or central venous cannulation. Hydrothorax may be caused by pleural effusions or inadvertent infusion of fluids through a misplaced central venous catheter. These rapidly remediable causes of hypoventilation are often overlooked.

Treatment

This consists primarily of treatment of the cause. Mild or moderate hypoventilation resulting from residual effects of anaesthetic drugs may respond to a bolus dose or infusion of doxapram. Artificial ventilation should be started if severe hypercapnia is present or PaCO₂ continues to increase, or if the clinical condition of the patient is deteriorating.

Hypoxaemia

A functional classification of causes of hypoxaemia in the early recovery period is shown in Table 40.5. An inspired oxygen concentration of less than 21% should never occur, although PaO₂ is decreased when air is breathed at high altitudes.

TABLE 40.5

Functional Classification of the Causes of Hypoxaemia in the Postoperative Period

Reduced inspired oxygen concentration

Ventilation–perfusion abnormalities

Shunting

Hypoventilation

Diffusion deficits

Diffusion hypoxia after nitrous oxide anaesthesia

Ventilation–Perfusion Abnormalities

These are the commonest cause of hypoxaemia in the recovery room. Cardiac output and pulmonary arterial pressure may be reduced after general or regional anaesthesia, causing impaired perfusion of some areas of the lungs. Functional residual capacity (FRC) is reduced during and immediately after anaesthesia. Patients who are elderly, obese or those undergoing thoracic or upper abdominal surgery are particularly at risk. The closing capacity may encroach on the tidal breathing range, resulting in reduced ventilation of some lung units, particularly those in dependent alveoli. Thus, the scatter of ventilation/perfusion () ratios is increased. Areas of lung with increased ratios constitute physiological dead space. Areas of lung with low ratios increase venous admixture which results in hypoxaemia unless the inspired oxygen concentration is increased.

Shunt

Physiological shunt may be increased in the immediate postoperative period if small airways closure has been extreme. Shunting may be present also in patients with pulmonary oedema of any aetiology, or if there is consolidation in the lung. Shunt may be increased in the later postoperative period as a result of retention of secretions and underventilation of the lung bases because of pain; these changes lead to alveolar consolidation and collapse.

Hypoventilation

This has been discussed in detail above. Moderate hypoventilation, with some elevation of PaCO₂, leads to a modest reduction in PaO₂ (Fig. 40.2). Obstructive sleep apnoea may produce profound transient but repeated decreases in arterial oxygenation. SaO₂ may decrease to less than 75%, corresponding to a PaO₂ of less than 5 kPa (40 mmHg). These repeated episodes of hypoxaemia cause temporary, and possibly permanent, defects in cognitive function in elderly patients and may contribute to perioperative myocardial infarction. Obstructive sleep apnoea is exacerbated by opioid analgesics, and patients who are known to suffer from this condition should be monitored carefully in the postoperative period, preferably in a high-dependency unit. Patients who normally use a continuous positive airways pressure (CPAP) mask to reduce obstructive sleep apnoeic episodes should use the mask at night throughout the postoperative period.