4.7 Postoperative management: general considerations
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1 Introduction
The overall care plan for a trauma patient should cover the preoperative management, the surgical procedures, and postoperative care ( Table 4.7-1 ). All too often, it is following surgical intervention that vigilance is relaxed and complications may occur. These, at best, deprive the patient of the full benefit of the procedure and, at worst, may seriously reduce a patient′s quality of life.
Postoperative management is not limited to the time spent in hospital but must be continued at home and later at work and at leisure. To achieve this, three postoperative phases are recognized:
In the first phase, immediately after surgery, emphasis is on pain control, mobilization, prevention, and early recognition of complications.
In the second phase, after hospitalization, attention is centered upon integration into the social environment and mobilization.
The final phase concludes treatment and returns the patient to his/her preoperative capabilities including work, education, and leisure activities.
2 First phase—immediate postoperative phase
2.1 Postoperative pain management
The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” [1]. In addition to being an unpleasant experience for the patient, poorly controlled pain may have deleterious physiological consequences for the patient leading to increased morbidity [2].
With adequate analgesia the orthopedic patient will be able to mobilize and perform physical therapy better and recover more quickly.
The simplest and most common methods used to quantify pain are scales that measure the intensity of the pain. Among the most commonly used is the Visual Analog Scale (VAS), which consists of a straight line with the words “no pain at all” on one end and “worst pain imaginable” on the other ( Fig 4.7-1 ). Patients quantify the severity of their pain by placing a mark along the scale [3]. Measurement can be improved by using a standard 10 cm line and then quantifying the pain from 0 to 10 for later comparison. By quantifying pain on VAS, pain can be classified as mild (VAS 1–4), moderate (VAS 4–7), or severe (VAS 7–10). However, surgeons should be aware that pain scores can be affected by anxiety, with more anxious patients reporting higher pain scores [4] and a significant correlation between high anxiety and high reported pain. This emphasizes the close interaction of psychosocial factors and pain. The World Health Organization′s Analgesic Ladder can be adapted to suit the needs of the orthopedic patient ( Table 4.7-2 ).
2.1.1 Analgesics
Acetaminophen has no antiinflammatory effect; it is an effective analgesic and antipyretic. Doses are 10–15 mg/kg orally every 4–6 hours. For adults, these may be doses of 500–1,000 mg (depending on availability) every 4–6 hours. Rectal suppositories may be given in doses of 15–20 mg/kg every 4 hours and it is now available for intravenous administration. The total daily dose of acetaminophen for adults from all sources must not exceed 4 g to prevent liver toxicity.
Nonsteroidal antiinflammatory drugs (NSAIDs) given even as a single dose preoperatively can significantly decrease morphine requirements by up to 29% over 24 hours [5]. This translates into a lower incidence of opioid-induced adverse effects, such as pruritus, nausea and vomiting. Unlike opioids, which exert their effect predominantly on rest pain, NSAIDs have shown considerable efficacy in minimizing pain associated with movement, thereby facilitating postoperative physiotherapy and minimizing postoperative physiological impairment [6]. Reducing postoperative opioid requirements may also decrease the likelihood of sedation and opioid requirements may also decrease the likelihood of sedation and opioid-induced respiratory depression. In addition to single preoperative doses, NSAIDs may also be given at regular scheduled intervals as appropriate ( Table 4.7-3 ).
Some of the more common adverse effects of NSAIDs include gastric bleeding and ulceration, bleeding from the operative site, nephrotoxicity, bronchospastic hypersensitivity reactions, and the suppression of heterotopic bone formation. Nonsteroidal antiinflammatory drugs should be used with care in geriatric patients and avoided in patients with impaired renal function.
Of special interest is the effect of NSAIDs on bone healing. Although there is evidence from animal studies that NSAIDs inhibit bone healing via their antiinflammatory effect [9], there is increasing evidence that their short-term use in humans does not affect fracture healing [10].
COX-2 inhibitors are well known for their analgesic efficacy. Their lower potential to induce gastrointestinal bleeding and minimal effect on platelet function make them seem an attractive choice in the elderly orthopedic patient. However, their propensity for harm in patients at risk for cardiovascular disease precludes their use in this population [11].
Because of concerns about cardiovascular problems, many COX-2 inhibitors have been withdrawn.
Neuromodulating drugs, such as amitriptyline, gabapentin, and pregabalin have been explored for their coanalgesic effect in the setting of postoperative pain. Turan et al [12] found that in the setting of spine surgery, a single oral dose of 1,200 mg gabapentin preoperatively decreased not only early postoperative pain scores but also resulted in a large reduction in morphine requirements and a significant reduction in opioid-related adverse effects postoperatively. Anticonvulsant drugs exert their diverse pharmacological effects on both ascending and descending pain pathways through a variety of mechanisms, including sodium and calcium channel blocking [13]. The dose of gabapentin for chronic pain ranges from 900–1,800 mg/day. These drugs may also have a place in the management of phantom pain following amputation and in the setting of elective amputation may be started a few days before surgery.
N-methyl-D-aspartate antagonists receptor antagonists, such as ketamine, magnesium and dextromethorphan, potentiate opioid analgesia through their modulation of pain pathways. Their use results in decreased morphine consumption and significantly decreased postoperative pain [14].
Opioid analgesics are a cornerstone of treatment for moderate to severe postoperative pain. Opioids exert their analgesic effects in the central nervous system at the µ-, κ-, and δ-receptors. All pure opioid analgesics cause a dose-dependent sedation and respiratory depression that is similar at equianalgesic doses. This phenomenon is exacerbated by the concomitant use of benzodiazepines, sedating antiemetics, and antihistamines.
Codeine is a weak opioid frequently used in conjunction with acetaminophen for the treatment of mild to moderate pain. Codeine is a prodrug that undergoes hepatic O-de-methylation to morphine, which is primarily responsible for its analgesic effect. Approximately 7–10% of Caucasians lack the enzyme cytochrome CYP2D6 that is necessary to convert codeine to morphine, and it is likely that this sizable segment of the population will not obtain pain relief from this drug. Conversely, in some populations up to 30% of patients have duplicate copies of the gene resulting in much higher and potentially dangerous serum morphine levels [15]. For this reason, codeine should not be used as a first-line analgesic unless the patient has a favorable history with this drug ( Table 4.7-4 ).
Oxycodone and hydrocodone are oral opioid analgesics used in the treatment of moderate to severe pain. Unlike codeine, neither drug undergoes extensive metabolism prior to exerting their analgesic effect. Both oxycodone and hydrocodone are commonly used in conjunction with acetaminophen for the treatment of pain. Oxycodone, like morphine, is commonly used as a sustained-release preparation for around-the-clock dosing.
Morphine is the drug to which other opioids are compared. It penetrates the blood-brain barrier poorly, so that peak analgesic effects do not occur for 15–30 minutes after intravenous injection. It is hepatically conjugated and renally excreted as morphine-6-glucuronide. Because this metabolite can accumulate in renal failure and cause respiratory depression, morphine should be avoided in patients with renal insufficiency.
Meperidine is a synthetic opioid with 1/10 the potency of morphine. Its onset is significantly faster than morphine and it exerts a potent effect on the κ-receptor, which makes it useful in low doses to treat shivering. Its major drawback, however, is its hepatic metabolism to normeperidine, which can induce seizures. For this reason, many institutions discourage its use and limit its dosage to 10 mg/kg daily. Normeperidine is renally excreted, making meperidine an unsuitable choice for patients with a history of either epileptic seizures or renal failure.
Hydromorphone is 6–7 times as potent as morphine and is indicated for moderate to severe pain. It has a slightly faster onset than morphine and like morphine undergoes glucuronidation in the liver. Unlike morphine and meperidine, however, it is relatively devoid of toxic metabolites that depend on renal excretion making it a more appropriate drug in patients with renal insufficiency.
Fentanyl is a synthetic opioid analgesic with approximately 100 times the potency of morphine. It is also indicated in the treatment of moderate to severe pain. The onset of action is less than 30 seconds with a peak effect of 2–3 minutes when given intravenously. It has a relatively short duration of action. Like hydromophone, its lack of toxic metabolites makes it a suitable drug for patients with renal failure. However, its short duration of action makes it difficult to maintain a steady state of analgesia in patients using fentanyl as a patient-controlled analgesia (PCA).
Fear of causing addiction has traditionally been one of the major reasons that physicians avoid prescribing opioid analgesics and by 2015, overdoses attributed to opioid analgesics outnumbered deaths from trauma in the US [16].
The incidence of addiction when prescribing opioids appropriately for the treatment of pain is remarkably low, likely far lower than the incidence of untoward cardiopulmonary adverse effects when pain is not adequately treated. However, surgeons should also be aware of the natural recovery period following trauma and prolonged, outpatient prescription of opioids (more than 3–4 weeks) during the recovery period should be discouraged and is rarely required to treat pain from acute trauma.
Another common reason for under prescribing opioid analgesics is the fear of inducing respiratory depression. This risk can be minimized by using PCA to deliver opioids, instead of larger intramuscular or intravenous injections. When PCA is compared with intramuscular administration of opioids, PCA is found to provide better analgesia with fewer pulmonary and cognitive complications [17]. Smaller, more frequent PCA doses will result in more consistent blood levels with fewer and smaller peaks and troughs in drug levels. Other keys to avoiding oversedation in these patients are to minimize the use of unnecessary sedating medications. Benzodiazepines or sedatives should not be used unnecessarily and, even then, only in smaller doses. Opioid consumption is greatest during the first 24 hours and patients require closer monitoring during this time. In many institutions, patients will routinely be administered oxygen by nasal prongs once therapy with PCA is started.