8 Sedation and Pain Management in the Neurosurgical Intensive Care Unit Patient
Abstract
Pain is the fifth vital sign because if it is not recognized and treated it leads to disorders of the remaining vital signs and further tissue damage. Pain may be the result of ischemic tissue, dilated blood vessels, or tissue being compressed. Although tissue ischemia may be due to large forces the specific chemical nature of the action and response should be understood in order to effectively treat it. The treatment of pain is as detailed as the treatment of any disease; it cannot be left to the individual unfamiliar with the details of the nervous system for the type and duration of treatment or lack of treatment will affect the patient’s neurologic outcome.
Case Presentation
A 47-year-old woman was involved in a rollover motor vehicle accident, with resultant severe closed head injury, consisting of mild cerebral edema, right pneumothorax, pulmonary contusion, and multiple rib fractures. The patient’s pupils are 2 mm and reactive; she does not open her eyes, is intubated, and is unable to move any of her extremities, yielding a Glasgow Coma Scale (GCS) score of 3 T. The trauma team has placed a chest tube. The patient will remain on the ventilator while her GCS score is ≤ 8 and while the trauma team remains concerned about lung injuries. The vital signs demonstrate an increased heart rate and increased blood pressure anytime there is attempted movement of the patient; therefore, the patient is sedated and given pain medication.
See end of chapter for Case Management.
8.1 Introduction: What Is Pain?
Pain is “whatever the experiencing person says it is, existing whenever s/he says it does.” 1 It is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. 2 In biological terms, stimulus energy from any source is converted into nerve impulses and transferred from the site of transduction to the central nervous system (CNS) and brain, during which time the signal is modulated at multiple levels before being perceived at the highest centers of the brain.
Nociceptors are specific receptors that respond to tissue trauma or stimuli that may cause tissue trauma. 3 They are located in skin, connective tissue, muscle, tendon, muscle spindle, joint capsules, bone, and viscera, and around nerves and blood vessels. Thankfully, they are not located in the brain substance itself. The tissue changes from injury-released prostaglandins, substance P, bradykinins, cytokines, histamine, and serotonin. This is the first area where pain can be modulated. The impulses from the nociceptors responding to these substances or responding to simple mechanical deformation travel along slow-conducting unmyelinated C fibers or faster-conducting, small myelinated A delta fibers. Although both C fibers and large A delta fibers respond to pain, it is the ratio of response that determines the passage through the dorsal horns as pain; the response from C fibers must be greater than the response from A delta fibers. The impulses are mostly from the trunk and limbs, and therefore go to the dorsal horn of the spinal cord, usually activating N-methyl-D-aspartate (NMDA) receptors, the second site of pain modulation. NMDA receptor stimulation causes intraneuronal elevation of Ca2+, which stimulates nitric oxide synthase (NOS) and the production of nitric oxide (NO). 4 Substances known to block NMDA receptors include d-methadone, dextromethorphan, ketamine, naloxone, and amantadine. It is at the NMDA receptors that inherent spinal cord nociceptor modulators, such as γ-aminobutyric acid (GABA), serotonin, glutamate, substance P, norepinephrine, and endogenous opioids are released by spinal interneurons in laminae I, II, IV, and V of the dorsal horn, which are controlled by brain cortex centers, periaqueductal gray, or concurrent spinal cord input. The modified signal crosses in the spinal cord and ascends in multiple tracts, such as the spinoreticular, spinothalamic, spinomesencephalic, and spinohypothalamic, to the reticular formation, thalamus, mesencephalon, and hypothalamus, respectively, the third area of modulation. Sensations reaching the thalamus undergo complex modulation to determine if the sensation will be processed to reach the brain. From these intermediates, the signal passes to the frontal cortex, insular cortex, limbic structures, and sensory cortex to label the pain as good or bad, the fourth area of possible modulation.
A functioning brain is needed for the perception of pain. Each area through neurochemical release, such as GABA, norepinephrine, substance P, serotonin, and opioids, influences the pain. These same areas respond to memories, social influences, environmental influences, experiences, depression, and culture. Repeated stimuli at any location further change the characteristics of the pain and the threshold (► Table 8.1).
Acute injury is mostly transmitted as nociceptive pain. This differs in treatment from neuropathic pain associated with chronic repeated stimuli and caused by aberrant signal processing in the peripheral or central nervous system. After repeated stimulation, the pathophysiological abnormalities of neuropathic pain become unrelated to the provocative event. This type of pain occurs infrequently in the intensive care unit (ICU) but may be seen in patients with multiple strokes, multiple fractures, or cancer pain.
8.2 General Principles of Pain Management
Pain must be treated. Neglecting pain treatment results in undue suffering, anxiety expressed by the patient and the family, fear, anger, depression, slow recovery, decreased ability to participate in activities of daily living, weight loss, fever, increased heart and respiratory rates, increased blood pressure, chest pain, myocardial infarction (MI), atelectasis, constipation, and infection. 6 , 7 , 8
8.3 Assessment of Pain
The first step in pain management involves an appropriate assessment of the pain, most often recorded on a pain scale. Pain assessment in the awake cooperative patient requires obtaining a detailed history along with the examination. This allows the physician to adequately assess and address these issues. However, neurosurgical patients present a unique challenge when it comes to assessment of pain as a large number of our patient population are either intubated and sedated or just unable to accurately describe their pain due to a variety of reasons, such as altered mental status, increased agitation secondary to fearfulness or pain, and so forth.
The characteristics of the pain also play a role in the treatment, including but not limited to, its quality, location, intensity, duration, periodicity, exacerbating and relieving factors, present and past pain management, and associated signs and symptoms.
Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Therefore, assessment of pain requires an examination of the area of pain referral and any other diagnostic tests that will assist in determining the appropriate treatment.
Often only pain intensity is considered in the pain history; by itself, however, it may lead to unnecessary treatments. When there are difficulties in communication such as may occur in the very young, the very old, the mildly confused, and patients of different language, culture, or background, a pain assessment rating scale may be the only information available. Most widely used “pain scales” are based on 10 divisions. Because it is necessary to follow pain trends over time and with treatment, often between varying health care workers and health facilities, only a 10-division scale should be used until other scales become universal. 9 , 10
A numeric rating scale asks the patient or the health care worker to rate the pain on a scale of 0 to 10, with 0 being no pain at all and 10 being the worst possible pain the patient or health care worker could imagine. Often patients will state that they have a high pain threshold, much higher than others. However, it must be emphasized to patients that the worst possible pain that they could imagine is a 10, and the current pain is in relation to that level, not based on others’ perception. It may be appropriate at times to ask women who have had children by vaginal delivery, as ascertained in the history, to compare the current pain to the pain experienced during labor, which may have been a 10 (► Fig. 8.1).
The modified visual analog scale is a 10 cm line marked from 0 to 10, with 0 being no pain at all and 10 being the worst possible pain the patient could imagine. When teamed with the commonly used scales, such as the American Cancer Society Pain Scale, Facial Pain Scale, or Wong-Baker Faces Rating Scale for Children, all of which consist of multiple images of faces with varying expressions of pain, the modified Visual Analog Scale becomes the ultimate scale for the awake person (► Fig. 8.2).
Severely debilitated patients and those with severe head injuries are physically not able to use these scales to indicate their level of pain. In these cases, health care workers are responsible for acting in the best interest of the individual patient to relieve suffering without causing untoward side effects. A behavioral pain scale is useful when patients cannot communicate. One of the most widely accepted behavioral pain scales is the 10-point FLACC scale. The patient is assessed in five categories and given 0, 1, or 2 points depending on the behavior being demonstrated. The behaviors are facial expression, leg movement, general activity, crying, and ability to be consoled (► Table 8.2). The FLACC scale can also be used with children ages 6 months to 3 years.
8.4 Pain in the Neurosurgical Patient
Pain in the neurosurgery patient needs to be adequately controlled. In addition to the stressors in the ICU, neurosurgical patients can have physiological causes of pain, including postoperative pain, meningeal irritation due to subarachnoid hemorrhage (SAH) or meningitis, cranial nerve dysfunctions, invasive procedures, and neuropathy due to various conditions. Before the initiation of sedation, pain must be addressed adequately because it can cause significant anxiety, agitation, and deleterious neurological effects.
Overmedication results in the inability to perform a neurologic exam, which is the most important means of following a patient with neurologic disease or injuries. Overtreatment of pain and sedation leads to prolonged intubation, prolonged ICU stay, pneumonia, and deep venous thrombosis (► Table 8.1). 5
In a severe head injury or comatose patient who is intubated, only subtle changes may foretell drastic intracranial changes and problems, such as contusions blossoming or other small abnormalities leading to midline shift and herniation. If the patient is overmedicated, a treatable lesion will be missed. Frequently, in patients with severe head injury or severe neurologic deficits, an intracranial pressure (ICP) monitor is inserted; however, the ICP, although rising and falling with movement, suctioning, and pain, will change exponentially as the brain has reached the ability to compensate. A gradual change in neurologic exam precedes large changes in ICP. Therefore, there must be a fine line that is maintained between pain and sedation, and under- and overmedication in the neurologic patient. A key principle in the use of analgesics and sedatives in the neurosurgical ICU (NICU) is titration: after proving the analgesic or sedative is actually effective for the given patient, dosing of the analgesic or sedative of choice should be titrated gradually to avoid side effects of overdosing.
Some of the most commonly used medications in neurocritical care are outlined here.
8.4.1 Nonsteroidal Anti-inflammatory Drugs
Once a patient’s pain can be assessed using a pain scale, medication and other treatment can be quickly entertained. Pain that is rated as 4 or less can be managed with ice, acetaminophen, or nonsteroidal anti-inflammatory drugs (NSAIDs), with the last two inhibiting an isoform of the enzyme cyclo-oxygenase (COX 1–3) blocking prostaglandin synthesis. 11 The usual dose for acetaminophen (N-acetyl-p-aminophenol [APAP]) is 10 to 75 mg/kg/d in four to six divided doses. The maximum adult daily dose is 4,000 mg. It is now believed that an initial large dose of 50 mg/kg can be given, yielding relief comparable to that of some narcotics while maintaining a high safety profile. The side effects of acetaminophen are seen with elevated multiple doses, although they can occur with a single dose. They are acute hepatic necrosis, or liver toxicity nephrotoxicity and, with chronic use, thrombocytopenia. Those with impaired liver function or regular alcohol use should take no more than 2 g daily. Anyone who takes more than three alcoholic drinks a day should be advised to avoid acetaminophen.
Analgesics, including aspirin (acetylsalicylic acid [ASA]) and APAP, inhibit cyclo-oxygenase, preventing the production of prostaglandins. COX receptors are found throughout the body, and a specific group’s effect depends on which receptors are stimulated. COX-1 receptors are found in the CNS, kidneys, platelets, gastrointestinal (GI) system, skin, and other areas. COX-2 receptors are found in the brain and kidneys. COX-3 receptors are found in the CNS. Most NSAIDs are nonselective COX 1–3 receptor inhibitors. The location of the receptors in the CNS is the reason that APAP only lowers temperature and pain but does not inhibit platelet function or have any significant anti-inflammatory effect.
NSAIDs should be withheld for 4 to 10 days after mild bleeding and not given for at least 4 to 10 days after severe bleeding. NSAIDs inhibit platelet function only while at therapeutic dosage. They should be given with a stomach protectant and adequate hydration to help prevent side effects. The usual dose for ibuprofen is 50 mg/kg divided into 4 to 6 doses per day.
Ketorolac is another anti-inflammatory drug that can be given intravenously or orally. The usual dose for ketorolac is 30 to 60 mg per dose and can be given every 6 to 8 hours. Ketorolac can be given immediately after such neurosurgical procedures as lumbar diskectomy and lumbar spinal fusion when bleeding has been controlled. During these procedures, ketorolac 30 mg intravenous (IV) may be given initially, followed by 120 mg in 500 mL saline at 10 mL/h continuous drip until completed. This treatment modality, along with lidocaine patches or infusion, may greatly decrease or obviate the need for narcotics.
NSAIDs belong to multiple drug classes, with each class affecting individuals differently. Therefore, if one class of NSAID or even a drug in the same class does not work, consider treatment with another (► Table 8.3).
None of the drugs in this group should be given if there is a known sensitivity to an NSAID. Salicylates should not be given to children with viral infections. In general, the nonselective COX inhibitor NSAIDs have similar side effects, such as dyspepsia; ulcers; GI perforation and bleeding (antiplatelet activity lasts for 2–3 days while therapeutic); kidney and liver dysfunction; hypersensitivity reaction, such as urticaria-angioedema; respiratory, attention, and memory deficits; headache; and tinnitus. Rofecoxib, a COX-2 inhibitor, was recently shown to have cardiac side effects, such as MI and stroke, and has been voluntarily removed from the market. Celecoxib, another COX-2 inhibitor, has not been removed from the market. Celecoxib side effects are thought to be less problematic than those of other NSAIDs.
There is no significant difference between the GI effects of nonselective COX NSAIDs and a proton pump inhibitor and selective COX-2 NSAIDs. ASA inhibits platelet function irreversibly, whereas NSAIDs inhibit platelet function only while at therapeutic dosage.
8.4.2 Other Pain Treatment
There are numerous ways to administer effective pain treatment, and in the neurologic patient these routes must be tried unless there is a contraindication. Initially, local pain should be treated with ice. Icing works by stimulating large A delta fibers in the peripheral nervous system, increasing output above C fibers, and inhibiting pain transmission. Longer-lasting pain, such as that caused by muscle spasm, may be treated with ice, heat, or both, depending on the response. If there is severe extremity or axial pain epidural at the approximate dermatome or caudal, anesthetics and analgesics may be delivered. The elevated pain from the disruption or destruction of large muscle areas may be treated appropriately with the local continuous infusion of long- or short-acting lidocaine derivatives. When the pain is of less severity, or to augment delivery of other pain medication, topical solutions can be used. Although used for chronic and neuropathic pain, they can be used for acute pain. Compounds such as a 5% lidocaine patch can significantly reduce pain and improve the quality of life. Lidocaine is believed to block sodium channels in the damaged nerve endings. It can be applied to the newly traumatized or operated tissue. The 5% lidocaine patch should not be applied directly to the open tissue or freshly sutured tissue. In those cases, it can be applied on both sides of the wound for 12 continuous hours per day (► Table 8.4).
8.4.3 Nonopioid Pain Treatment
For pain greater than 4 on a 0 to 10 pain scale, acetaminophen and NSAIDs, as well as other nonconventional, nonnarcotic complementary drugs, can be used (► Table 8.5). Each may be used with narcotics, potentiating the effects of a smaller narcotic dosage, resulting in less sedation and other deleterious side effects. The nonconventional medications can be beneficial, especially if the history can provide clues as to environmental, physiological, or psychological factors influencing the current pain. The nonconventional medications include antiepileptic drugs (AEDs), tricyclic antidepressants (TCAs), GABA, norepinephrine, α- and β-blockers, capsaicin, serotonin, benzodiazepines, caffeine, and barbiturates. These nonconventional medications are particularly beneficial in neuropathic and chronic pain.
Nonconventional pain medications work in multiple areas and by a variety of mechanisms, as listed here (► Table 8.6).
TCAs inhibit neuronal discharge, decrease sensitivity of adrenergic receptors, block reuptake of norepinephrine and serotonin, and bind to histaminergic, cholinergic, and adrenergic receptors.
Selective serotonin reuptake inhibitors (SSRIs) potentiate serotonin and norepinephrine pathways, inhibit cytochrome P-450, and assist in treating patients with depression and anxiety. Side effects include tremor, fever, diarrhea, delirium, and increased muscle tone.
AEDs suppress abnormal neuronal discharges by blocking sodium channels, whereas others increase the inhibiting GABA transmission.
Benzodiazepines potentiate inhibitory GABA transmission while also having antianxiety and antispasticity properties.
Alpha-adrenergic blockers decrease hyperarousal symptoms by activating autoinhibitory presynaptic receptors of the locus cerulus.
Common potentiating adjuvant nonnarcotic pain medications are listed in ► Table 8.5. The medication should be carefully chosen and reflect the clinical situation associated with the drug’s major use. For example, if depression exacerbates the pain, consider the addition of amitriptyline.
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