Pain control is an essential component of post-operative recovery [Kavanagh BP et al. Anesthesiology 81: 737, 1994]. The most difficult to treat may be shoulder pain, which affects 80% of patients and may be due to diaphragmatic irritation (transmitted via the phrenic nerve).
There is some evidence that preemptive analgesia (in this case, before incision) reduces post-operative opioid requirements [Katz J et al. Anesthesiology 77: 439, 1992; Katz J et al. Pain 59: 395, 1994] although this is controversial even within the same group. [Kavanagh BP et al. Br J Anaesth 73: 184, 1993]
Intravenous and Oral Agents
Most commonly, IV opioids are used, although they may not be adequate. [Kavanagh BP et al. Anesthesiology 81: 737, 1994]
Low-dose (1 mg/kg) ketamine may be a reasonable adjuvant to opiates – at subanesthetic doses, the potential psychomimetic effects are unlikely.
Dexmedetomidine at 0.3-0.4 ucg/kg/hr may decrease opiate requirements as well as provide sedation (and some hypotension). Interestingly, dexmedetomidine for post-thoracotomy pain may also increase post-operative urine output compared to placebo. [Frumento RJ et al. J Clin Anesth 18: 422, 2006]
NSAIDs may reduce opiate consumption by up to 30% [Miller’s Anesthesia, 7th ed. 2009. p 1878] and are particularly good at addressing shoulder pain, but come with potential risks as well – decreased platelet function, GI tract ulceration, decreased renal function, and increased bronchial reactivity.
Acetaminophen, which is predominantly an antipyretic agent but does have some weak COX inhibition activity, may be a reasonable alternative. [Mac TB et al. J Cardiothorac Vasc Anesth 19: 475, 2005]
Intercostal nerve blocks (pre, intra, or post-operatively) are a reasonable adjuvant – 0.5% bupivacaine can provide 6-24 hours of relief at 2-3 mL per nerve (no more, as absorption at this site is significant) but does not cover shoulder (diaphragmatic) pain caused by chest tubes. Block should be placed as close as possible to the posterior axillary site, in order to provide coverage of the lateral cutaneous branch of the intercostal nerve.
Paravertebral catheters can be placed either percutaneously or under direct vision. Pain control is comparable to epidural analgesic techniques [Casati A et al. Eur J Anaesth 7: 1, 2006], however this technique is relatively new and its potential to reduce respiratory morbidity has not been well-studied.
Epidural opiates have been shown to be helpful, and morphine, which is relatively hydrophilic, can be given either at a lumbar (5-7 mg in 20 cc fluid) or thoracic entry site. Importantly, local anesthetics and opiates are highly synergistic [Wiebalck A et al. Anesth Analg 85; 124, 1997; Hansdottir V et al. Anesth Analg 83: 394, 1996] and should almost always be used in combination.
Subarachnoid morphine (10-12 ucg/kg) has also been used [Cohen E and Neustein SM. J Thorac Cardiovasc Anesth 7: 154, 1993]. Data on intrapleural analgesia are mixed. [Kavanagh BP et al. Anesthesiology 81: 737, 1994]
Other Analgesia Modalities
Cryoanalgesia can provide up to 6 months of pain relief, but because of its duration is not commonly used.
Almost always caused by intraoperative positioning. May not be obvious for several days. Brachial plexus is particularly vulnerable (usually stretch injury, sometimes crush). It is fixed at the transverse process of cervical vertebrae and also at the axillary fascia – most injuries are crush in origin (dependent arm), but some of them are stretch injuries (non-dependent arm). Lateral cervical flexion can also cause a stretch injury of the brachial plexus.
The suprascapular nerve can be injured when the arm is flexed at the shoulder across the chest. Intercostal nerves are also commonly injured. Recurrent laryngeal can be injured during node biopsy / mediastinoscopy. Phrenic is often injured during pericardiectomy, hiar dissection, division of diaphragm, or dissection of mediastinal tumors.
Defined as PaO2 < 60 mm Hg, PaCO2 > 45 mm Hg, or > 24 hours post-operative mechanical ventilation, the incidence is somewhere between 2 and 18% [Miller’s Anesthesia, 7th ed. 2009. p 1876] and it is the leading cause of morbidity and mortality after major pulmonary resection. Risk factors include poor preoperative pulmonary function, advanced age, comorbid cardiac conditions, extent of resection, and inadequate OLV (leading to contralateral pneumonia). Thoracic epidural analgesia has been shown to be protective [Licker M et al. Ann Thorac Surg 81: 1830, 2006]. In order to avoid this complications, post-operative goals should include adequate analgesia, early extubation, ambulation, and chest physiotherapy.
Incidence s/p thoracotomy may be as high as 100%. Treatment should aim at restoration of FRC. Commonly recommended treatment modalities include bronchodilators, coughing, mobilization, improved analgesia, and incentive spirometry. However, two myths regarding atelectasis should be noted – first, its association with fever is not necessarily one of causation [Engoren M. Chest 107: 81, 1995], and second, a Cochrane database review found no evidence of any beneficial effects following incentive spirometry after upper abdominal surgery. [Guimaraes MM et al. Cochrane Database Systemic Review: CD006058, 2009]
Major concern after thoracic surgery, thus all these patients will have chest tubes. Most fearsome is a non-operative pneumothorax (ex. due to line placement), which can lead to bilateral lung compromise. During transport, chest tubes should never be clamped.
COPD patients are NOT at increased risk for sleep apnea hypoventilation syndrome (SAHS), but approximately 80% of them will desaturate to SpO2 < 50% overnight [Miller’s Anesthesia, 7th ed. 2009. p 1824] – the reason that they desaturate at night is that, like all individuals, they become tachypnic during REM stage sleep, however they are less able to tolerate this rapid breathing rate.
When Holter monitoring is applied, the true incidence of post-operative arrhythmias appears to be 30-50% (60-70% of these are atrial fibrillation) [Ratchie AJ et al. Ann Thorac Surg 50: 86, 1990]. Incidence is proportionate to age, extent of resection, blood loss, and malignancy (those with malignant disease may be seven times as likely as those with benign disease to have an arrhythmia [Beck-Nielsen J et al. Acta Med Scand 193: 425, 1973]). Patients with COPD are at particular risk for MFAT, and are also more likely to develop refractory atrial fibrillation. [Sekine Y et al. Chest 120: 1783, 2001]
Virtually all antiarrhythmics have been shown to reduce post-thoracotomy arrhythmias, however their respective side effect profiles preclude their widespread use. Of all the antiarrhythmics, diltiazem is probably the first that should be tried in the thoractomy population [Slinger P and Johnson MR. Thorac Surg Clin 15: 11, 2005]. Importantly, arrhythmias are largely thought to be a consequence of right heart dysfunction, and treating the arrhythmia does little to correct the underlying problem. In a small study of verapamil arrhythmia prophylaxis (25 total patients), RV pressure increases in response to decreased FiO2 (from 0.35 to 0.21) was predictive of post-operative arrhythmias. [Lindgren L et al. Br J Anaesth 66: 205, 1991]
Low Cardiac Output Syndrome
Must be differentiated from hypovolemia, however, be cautious with fluid administration as pulmonary edema is particularly risky in this population.
Right Heart Failure
There is at least some degree of right heart dysfunction after ALL pulmonary resections, likely proportional to the amount of vascular bed removed [Miller’s Anesthesia, 7th ed. 2009. p 1821]. Oftentimes right heart dysfunction in silent at rest, and manifests with exertion. In post-thoracotomy patients, the etiology is most likely a reduced compensatory response to increased demand, in which pulmonary vascular resistance is unable to compensate. [Thoracic Anesthesia, 3rd ed. 2003, p. 423]
Rare, but carries a 50% mortality rate. Caused by incomplete closure of the pericardium (or breakdown). Usually occurs within 24 hours of surgery. Presentation depends on the laterality of the defect – a right-sided defect (and cardiac herniation) will lead to impaired venous return (similar to SVC syndrome), whereas left-sided defects will lead to myocardial ischemia (edge of pericardium compressing the coronary arteries), arrhythmias, and ventricular outflow obstruction.