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Issue 12 (2000) Article 12: Page 3 of 3   Go to page: 1 2 3
Anaesthesia For The Patient With Respiratory Disease (Continued)

Postoperative Care

The patient with underlying respiratory disease is at increased risk of postoperative pulmonary complications. This is particularly so in smokers, or after upper abdominal or thoracic surgery. The airway is vulnerable for up to 24 hours, and hypoventilation can occur for up to 3 days.

In the recovery room, the airway is kept patent, and adequate ventilation and oxygenation ensured before discharge to the ward. All neuromuscular paralysis must be reversed. If there are problems the patient will need to go to the HDU or ICU. Otherwise, the patient is kept warm and well hydrated, and fluid balance charts commenced.

Oxygen therapy

  • Following minor surgery hypoxia may occur for the first hour or two after surgery. Oxygen should therefore administered until the patient is fully awake and recovered from the anaesthetic.
  • After major surgery hypoxia can occur for up to for 3 days, particularly at night. This tendency is worse in patients who are receiving opioids by any route. This can put the patient with chest disease or ischaemic heart disease, at risk. Oxygen (2-4L/ min by nasal cannulae) should be given over this period to those at risk.
  • Some patients with very severe COPD depend on hypoxia to maintain ventilatory drive. It is difficult to diagnose but all affected patients will have had severe COPD for many years. This situation is very unusual, particularly in the developing world and hypoxia should always be treated immediately. If a patient like this presents, the inspired oxygen concentration shold be monitored and repeat arterial blood gas estimations carried out to guide the level of oxygen treatment tolerated by the patient (*BACK* Acute Oxygen Treatment, Update in Anaesthesia 2000;12:3).

Pain Relief

Effective analgesia reduces the incidence of postoperative respiratory complications. Opioids may be required for 48-72 hours after major surgery.

  • Intravenous opioid boluses can be titrated against pain in the recovery room, whilst observing for respiratory depression. This can be used as a guide to the dose of intramuscular opioid that may be given in relative safety on the ward. Continuous infusions of intravenous opioids demand very close supervision, as the risk of respiratory depression is significant.
  • The combination of opioids with rectal or oral drugs, such as paracetamol or non-steroidal anti- inflammatory agents (NSAIDs), gives particularly good analgesia whilst reducing opioid side effects.
  • If available, patient controlled analgesia (PCA) systems allow the patient to titrate opioid requirements to their pain. They give good quality analgesia and a fixed lockout period should prevent respiratory depression.

Epidural analgesia

The use of postoperative thoracic epidural analgesia for abdominal and thoracic surgical procedures results in good quality analgesia, with few respiratory complications. However, there is no clear evidence to demonstrate its superiority over other analgesic techniques, and it is not available everywhere.

The combination of low concentrations of local anaesthetic with low doses of opioids in an epidural infusion results in the best analgesia for the fewest side effects (i.e. opioid induced respiratory depression and local anaesthetic toxicity). For example give 50ml of 0.167% bupivacaine containing 5mg diamorphine given as an epidural infusion at a rate of 0-8ml/hr.

Whilst postoperative opioid analgesia is administered the patient must be observed in an area with sufficient medical and nursing skills, and staffing levels. Complications that may arise are then noted promptly and the appropriate help called. Regular observations are made of blood pressure, pulse, oxygenation (using a pulse oximeter), respiratory rate, conscious level and analgesia. Protocols may be used to guide nursing staff in the administration of analgesia, the observations required and when to call for help.

Physiotherapy

Teaching patients in the preoperative period to participate with techniques to mobilise secretions and increase lung volumes in the postoperative period, will reduce pulmonary complications. Methods employed are coughing, deep breathing, early mobilisation, and chest percussion and vibration together with postural drainage.

Steroid supplementation

The brittle asthmatic or severe COPD patient may benefit from a course of prednisolone (20-40mg daily) during the week before surgery. Seek the advice of the patient's chest physician.

Patients who have received a course of steroids in the 6 months before surgery, or who are on maintenance therapy of greater than 10mg of prednisolone a day, are presumed to have adreno-cortical suppression. Perioperative steroid supplementation will be required.

  • Intravenous hydrocortisone 100mg 8 hourly is given starting with the premedication. Over the next 5 days this is tapered to their normal daily dose, where 100mg intravenous hydrocortisone is equivalent to 25mg oral prednisolone.
  • Intravenous steroids must replace oral whilst these cannot be taken.

Prophylaxis of venous thromboembolism

Prophylactic measures should begin before surgery in those at risk and continued until early mobilisation reduces the risk of postoperative deep vein thrombosis and pulmonary embolism. Regular subcutaneous heparin and anti-embolism stockings are commonly used.

Nutrition

Patients with severe respiratory disease are often malnourished and weak. This is associated with increased risk of postoperative infection, an increase in length of hospital stay and increased mortality. Therefore, early resumption of normal oral intake of food is important. If this is delayed postoperatively (more than 5 days) enteral feeding will be required. [Top]

Postoperative Respiratory Problems

Breathlessness usually indicates respiratory difficulty and hypoxia, but can be due to pain, anxiety, sepsis, acidosis and anaemia due to bleeding. Initial treatment is to ensure a patent airway and give a high percentage of humidified oxygen by facemask. This is guided by pulse oximetry to maintain a peripheral saturation adequate for the patient (usually > 92%). The cause is then sought by history, examination and chest X-ray, and treated.

Stridor

The postoperative airway may be compromised because of the residual effects of anaesthesia (in particular opioid or midazolam sedation), by vomit, or by surgical complications. After thyroid/parathyroid surgery recurrent laryngeal nerve palsy may cause vocal cord palsy, and cervical haematoma cause airway compression. The airway must be re-established using standard techniques. Laryngeal surgery may cause airway oedema. This may respond to nebulised adrenaline 2.5-5mg and intravenous dexamethasone 4-8mg.

Atelectasis and pneumonia

Wound splinting, pain, dehydration, and immobility lead to collapse and atelectasis of basal lung segments in the hours after surgery, which will be clearly seen on chest X-ray. A poor cough may lead to retention of secretions. The mainstays of treatment are good analgesia, humidified oxygen, careful fluid balance, physiotherapy and early mobilisation. Suctioning through a minitracheostomy can remove secretions.

Infection and pneumonia may intervene. The patient usually becomes febrile with purulent sputum (often not coughed up effectively) and a neutrophil leucocytosis. Consolidation is seen on the chest X-ray. (Widespread bronchopneumonia is much more common than lobar pneumonia).

Supplemental oxygen is given by facemask to maintain adequate peripheral saturations. Sputum and venous blood specimens are sent for microscopy, culture and sensitivity testing. Regular physiotherapy is required, and supplemental intravenous fluids to replace losses due to fever. Appropriate antibiotic therapy will depend on microbiological results and local prevalences of organisms, but cefotaxime or cefuroxime, and gentamicin are often used.

Bronchospasm

This may be a due to an exacerbation of pre-existing asthma, perioperative pulmonary aspiration of blood or vomit, or a reaction to a drug. Pulmonary oedema or pulmonary embolus may mimic bronchospasm, and if suspected are treated (see below).

The patient will be dyspnoeic, tachypnoeic and using their accessory muscles. Speaking is difficult, and an expiratory wheeze is audible on auscultation. A quiet chest is ominous as it may represent very little airflow taking place. A chest X-ray is useful to exclude pneumothorax, but may show collapsed areas following pulmonary aspiration. Arterial blood gas hypercarbia indicates fatigue, and imminent respiratory collapse.

Treatment is high flow oxygen by mask, nebulised salbutamol 2.5-5mg (initially every 15 minutes, unless severe tachycardia occurs), nebulised ipratropium bromide (Atrovent) 250-500mcg 6 hourly, and intravenous hydrocortisone 200mg. For patients not usually taking oral theophyllines, consider addition of intravenous aminophylline (5mg/kg over 15 minutes, followed by an infusion at 0.5mg/kg/hr). Nebulised adrenaline 2.5mg may be used when salbutamol is not available. Intramuscular adrenaline 0.5mg may be used with extremely severe bronchospasm, and may be repeated. Respiratory failure can occur rapidly, so equipment for sedation, re-intubation and assisted mechanical ventilation should be prepared. This will enable tracheal suction if aspiration is suspected.

Pulmonary oedema

Intraoperative fluid overload, ARDS and failure of the left ventricle (typically in patients with ischaemic heart disease), may all result in pulmonary oedema. ARDS is discussed below.

The patient is dyspneoic, cyanosed, clammy, sweaty and tachycardic. Pink frothy sputum indicates severe pulmonary oedema. The jugular venous pressure is raised and there are coarse bibasal inspiratory crepitations on auscultation, or a "cardiac" wheeze. Chest X-ray shows bilateral, midzone, fluffy infiltrates and upper lobe blood diversion. The patient is sat up, and intravenous fluids stopped. Give high flow oxygen by facemask, intravenous diuretics (e.g. frusemide 50mg - consider a urinary catheter), and, if systolic blood pressure > 90mmHg, 2 puffs of sublingual GTN (glyceryl trinitrate). Intravenous diamorphine 2.5-5mg (or 5 -10mg of morphine) can also reduce preload, but observe for sedative side effects. If the above fail, application of CPAP (Continuous Positive Airways Pressure) 5-10cm H2O, by tight fitting facemask, is often helpful. An ECG may show signs of perioperative myocardial ischaemia, and a new murmur may indicate acute cardiac valvular dysfunction.

Pneumothorax

This may occur as a complication of surgery, central line placement or follow positive pressure ventilation in a patient with asthma or COPD. The patient will be breathless and often complains of pain over the affected lung. There is diminished air entry and hyper-resonance on percussion, and if severe, tracheal deviation away from the pneumothorax, raised jugular venous pressure and cardiovascular collapse; these are signs of tension pneumothorax and require immediate life-saving treatment.

In stable patients the chest X-ray will confirm the diagnosis. There is no time to do this if tension pneumothorax is suspected. Immediate insertion of a large 14-guage intravenous cannula into the pleural cavity at the second intercostal space, mid-clavicular line will be followed by a whoosh of air as the pneumothorax is decompressed.

Small pneumothoraces (<20% of the lung field), without patient compromise, may be observed untilresolution. Larger pneumothoraces will require placement of an intercostal chest drain attached to an under water seal.

Pulmonary embolus

This is rare in the recovery room. Embolus can be due to thrombus, air, fat or tumour. Massive embolus will result in cardiorespiratory arrest. A small embolus results in dyspnoea, pleuritic chest pain, haemoptysis and tachycardia. There may be signs of DVT (Deep Vein Thrombosis), and a pleural rub. Arterial blood gases typically show hypoxia, and hypocarbia of hyperventilation. A chest X-ray is more helpful in excluding other diagnoses (e.g. pneumothorax), but may show a wedge shaped pulmonary infarct. The commonest ECG finding is a sinus tachycardia, but right ventricular stain or an S1-Q3-T3 pattern (S wave in lead 1, Q wave in lead 3, and T wave in lead 3) may be seen.

Treatment is 100% humidified oxygen by facemask, and analgesia with intravenous morphine (5-10mg). Consideration is given to anticoagulation with intravenous heparin. This involves discussion with the surgical team as it may be contraindicated postoperatively. An alternative, to prevent recurrence of pulmonary embolus, is an inferior vena caval filter. If a V/Q (Ventilation/Perfusion) scan is available this will confirm the diagnosis.

ARDS (Acute Respiratory Distress Syndrome)

ARDS develops after a variety of major insults including shock, sepsis, pancreatitis, massive blood transfusion and multitrauma. Oxygenation is poor (and not the result of cardiac failure) and the X-ray shows widespread pulmonary infiltrates of alveolar oedema. Onset is generally within 24 hours of the insult. The patient may require mechanical ventilation on the ICU, with application of PEEP (Positive End Expiratory Pressure) and high inspired oxygen concentrations. Steroids are not useful in the early stages. [Top]

Further Reading

  1. Smetana GW. Preoperative Pulmonary Evaluation. New England Journal of Medicine 1999;340(12):937-944.
  2. Nicholls A, I Wilson. Perioperative Medicine. Oxford University Press. 2000.
  3. Hirshman CA. Perioperative management of the asthmatic patient. Canadian Journal of Anaesthesia 1991;38(4):R26-32.
  4. Wong DH, Weber EC, Schell MJ et al. Factors Associated with Postoperative Pulmonary Complications in Patients with Severe Chronic Obstructive Pulmonary Disease. Anesthesia and Analgesia 1995;80:276-284.
  5. Nunn JF, Milledge JS, Chen D et al. Respiratory criteria of fitness for surgery and anaesthesia. Anaesthesia 1988;43:543-551.
  6. Rees PJ, Dudley F. ABC of oxygen. Oxygen therapy in chronic lung disease. British Medical Journal 1998;317:871-4. [Top]


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