Sources of pain after thoracotomy include soft tissue, ribs, intercostal nerves, pleura, diaphragm, and pulmonary parenchyma. Afferents mediating this pain include intercostal nerves (4–8) and the vagal and phrenic nerves. No single modality ablates all sources of thoracotomy pain.
Ipsilateral shoulder pain is reported by 80% of thoracotomy patients who have functional epidurals. It is likely that the epidural unmasks shoulder pain by covering the dominant incisional pain. Shoulder pain is multifactorial. Postulated causes include referred pain (from the diaphragm, pericardium, pleura or bronchus), and pain from ligamentous injuries to the shoulder due to positioning or surgical mobilization of the scapula. Phrenic blockade reduces the incidences of shoulder pain by more than 50%,9 and shoulder blocks have variable efficacy. Systemic nonsteroidal anti-inflammatory drugs are the most consistently effective but carry risk of renal, gastrointestinal, or bleeding complications.
Chronic postthoracotomy pain syndrome (persistent pain along incision site for more than 2 months after thoracotomy, unrelated to recurrence or infection) is reported in over 50% of patients. The pain is neurolytic in nature and presumed to result from trauma to intercostal nerves. Entrapment by sutures, direct trauma, and crush injuries from retractors or instruments (including thoracoscopes) are among the postulated mechanisms. The severity is variable, with fewer than 10% of patients seeking treatment for postthoracotomy pain syndrome.
Thoracic Epidural Analgesia
TEA represents the current standard for acute postthoracotomy pain control. Small-bore multiport catheters inserted via 17-gauge needles into the midthoracic epidural space provide an avenue for intermittent bolus, continuous infusion, or patient-controlled delivery of analgesics. Most use a dilute solution of local anesthetic (e.g., bupivacaine, ropivacaine, or levobupivacaine) and opioid. The combination produces synergism of effect and permits reduced dosages. Fentanyl, meperidine, and hydromorphone are popular opioid choices because they possess intermediate lipophilicity. Highly lipophilic opioids (e.g., sufentanil) are absorbed quickly and produce greater systemic symptoms (i.e., sedation). Morphine is hydrophilic and thus spreads more broadly within the epidural space with risk of higher levels, pruritus, and delayed respiratory depression. The very dilute dose of bupivacaine, enabled by the synergistic effect of the opioid, has the advantage of producing very little motor blockade of respiratory muscles.
The most common side effect from TEA is hypotension from local anesthetic blockade of presynaptic sympathetic nerves. Sympatholysis results in dilation of venous capacitance vessels, venous pooling (especially in the splanchnic bed), and possibly reduced cardiac contractility. Treatment consists of intravascular volume expansion, vasopressors, and inotropes. Other complications of TEA are listed in Table 5-4.
Table 5-4. Complications of Thoracic Epidural Analgesia |Favorite Table|Download (.pdf)
Table 5-4. Complications of Thoracic Epidural Analgesia
- Postdural puncture headache
- Inadvertent subarachnoid (spinal) block
- Local anesthetic toxicity—seizures, heart block, cardiac arrest
- Epidural infection
- Nerve injury
- Epidural hematoma
- Nerve injury from needle on compression by epidural hematoma or abscess
- Horner syndrome
- Urinary retention
- Respiratory depression
- Failure to work
Evolving neurologic deficits in a patient who had a TEA should prompt urgent magnetic resonance imaging to rule out an epidural hematoma or abscess with spinal cord compression. Local anesthetic toxicity generally produces jitteriness progressing to seizures. Bupivacaine toxicity may manifest first with blockade of cardiac conduction. Treatment requires supportive care until the local anesthetic effects wear off. In extreme bupivacaine toxicity, this may require cardiopulmonary bypass. Central nervous system toxicity may not be evident during general anesthesia, highlighting the importance of a test dose preceding induction. Aspiration from the catheter before each injection serves to rule out migration of the catheter into blood vessels.
Contraindications to TEA include coagulopathy, infection at the insertion site, local anesthetic allergy (extremely rare), and patient refusal. Relative contraindications include sepsis, preexisting neurologic deficit, and tumor involvement at the site.
Perioperative outcome is improved by epidural analgesia. Meta-analyses indicate that epidural analgesia is associated with reduced pulmonary (infection, atelectasis)10 and cardiac (myocardial infarction)11 complications. Even when compared with equianalgesic systemic narcotic regimens, TEA confers superior “dynamic” analgesia while coughing. The cardiosympatholytic effect protects against myocardial ischemia and reduces postoperative supraventricular arrhythmias. The cardioprotective effects of TEA depend on how it is managed. Significant hypotension may counteract its beneficial anti-ischemic effects. Chronic postthoracotomy pain is reduced in patients with aggressive management of acute postoperative pain with TEA, lending support for a potential preemptive effect.
Pain Management Other Than Tea
Intravenous patient-controlled analgesia with opioids is used most commonly for video-assisted thoracic surgery (VATS) or sternotomy incisions, which, barring significant cardiopulmonary disease, do not warrant TEA. If TEA is used for sternotomy incisions, parenteral narcotics or parasternal blocks are often required to supplement the most cephalad portion. As mentioned previously, dynamic analgesia with patient-controlled analgesia is inferior to TEA. The need for adjuncts, including intercostal or paravertebral blocks, nonsteroidal anti-inflammatory drugs, or ketamine, is not uncommon. Paravertebral blocks rival TEA and only impose a unilateral sympathectomy but have a higher technical failure rate and last only 12–18 hours. Intercostal blocks are simple and familiar to surgeons. Rapid vascular uptake of local anesthetics after intercostal blockade limits duration to 4–8 hours and raises the risk of toxicity. To include the lateral cutaneous branch, intercostal blocks must be applied posterior to the posterior axillary line. A rule-of-thumb safe limit for intercostal blocks using bupivacaine with epinephrine is 2.5 mg/kg.
Cryotherapy to exposed intercostal nerves before chest closure produces a blockade lasting up to 6 months. Concern that it might cause chronic neuralgia has prevented its widespread acceptance.
Interpleural catheters delivering local anesthetics tend to be unreliable because the agents distribute within the chest by gravity and are lost to chest drainage. Transcutaneous electrical nerve stimulation, acupuncture, and hypnotherapy are used only occasionally as adjuncts in thoracic anesthesia. Lumbar intrathecal morphine (0.2–0.3 mg) provides 24 hours of good analgesia for patients in whom TEA is contraindicated. The high incidence of pruritus and concern over delayed respiratory depression from ascension within the spinal canal have limited its popularity.