16 Pain Management in the Neuro-Intensive Care Unit (ICU)

Amy Shah, David A. Wyler, and Andrew Ng

Abstract

Pain, an unpleasant sensory and emotional experience, presents unique challenges in the neuro-intensive care unit. A recent shift in strategy to address pain has evolved in the general ICU. Providers aim toward maintaining patient arousal while treating their patient’s pain. The ICU liberation collaborative focuses on analgosedation or treating pain first and utilizing numerous tools for continued assessment in distinguishing pain from agitation and delirium (PAD). The endpoint is earlier liberation from ICU and mechanical ventilation by reducing sedative medications and supporting early mobility. This chapter aims to highlight the challenges of managing pain in the neuro-ICU while practicing within the framework of the current ICU liberation movement. Tools for assessment, individualized therapy, patients with neurodegenerative diseases at risk for pain, and special cases that make management of pain in the neuro-ICU particularly difficult will be discussed in this chapter.

16 Pain Management in the Neuro-Intensive Care Unit (ICU)

16.1 Introduction

Pain, an unpleasant sensory and emotional experience, presents unique challenges to care providers in the neuro-intensive care unit (neuro-ICU). Over the last decade, convincing data has driven a paradigm shift in the general ICU toward maintaining patient arousal while treating pain. 1 The ICU liberation collaborative focuses on treating pain first and utilizing numerous tools for continued assessment in distinguishing pain from agitation and delirium (PAD). The endpoint is earlier liberation from ICU and mechanical ventilation by reducing sedative medications and supporting early mobility. 1 , 2 The Critical Care Medicine (CCM) collaborative created the ABCDEF bundle to accomplish this purpose which stands for:

  • Assess, Prevent, and Manage Pain

  • Both spontaneous awakening trials (SATs) and spontaneous breathing trials (SBTs)

  • Choice of Sedation

  • Delirium: Assess, Prevent, and Manage

  • Early Mobility and Exercise

  • Family Engagement and Empowerment 1 , 2 , 3

Several risks limit these strategies of caring for neurologically injured patients, and there is a paucity of data to validate the current trend in the neuro-ICU population. 4 , 5 Nonetheless, guidelines recommend whenever it is safe, treat pain judiciously and preserve the neurologic examination, the gold standard monitor for the central nervous system (CNS). 1 , 4

This chapter aims to highlight the challenges of managing pain in the neuro-ICU while practicing within the framework of the current ICU liberation movement. Individualized therapy will be discussed for postoperative patients, patients with neurodegenerative diseases at risk for pain, and special cases that make management of pain in the neuro-ICU particularly difficult. Although opioid therapy is the mainstay for pain management historically, these medications often over-sedate frail neurologically susceptible patients. 4 Thus, opioid-sparing therapies such regional anesthesia, adjunct pain medications, and various relaxation techniques are discussed in detail. This chapter intends to provide a quick guide for the A component (assess, prevent, and manage pain) of the ABCDEF bundle in the neuro-ICU.

16.2 Modern Strategy of Pain Management in ICU Liberation

  • Joint Commission on Accreditation of Healthcare Organization (JCAHO) mandated in 2002 “implementation of standards” in pain assessment, prevention, and treatment which was termed the “5th vital sign” in the ICU. 1 , 4

  • Studies supported reducing sedation and mobilizing patients improved ICU outcomes. 1 , 2 , 3 , 6

  • ABCDEF bundle implemented liberation strategy to address CCM Guideline 2012. 1 , 2

  • CCM guidelines excluded neurologically injured patients for safety reasons. 1

  • Addressing the A component (assess, prevent, and treat pain) of the ABCDEF bundle first was recommended since pain confounds delirium and agitation. 1 , 2

  • The use of different pain scales for continuous ongoing assessment was recommended. 1 , 6 , 7

  • Prevent/anticipate pain prior to surgery and painful procedures in ICU. 1

  • Opioid adjuncts reduce dose and ultimately neuro-confounding and neurotoxic effects. 3 , 5 , 6

16.3 Challenges of Pain Management in Neuro-ICU

1 , 4 , 5 , 7

  • Balance maintaining neurologic examination versus providing comfort.

  • Balance neurologic examination versus offering enough sedation for “neuro-specific” issues such as reducing cerebral blood volume (CBV), intracranial pressure (ICP), and cerebral metabolic rate for oxygen (CMRO2) and seizure control. 4 , 5 , 8

  • Severity of brain injury dictates, and ICP and other multimodality monitoring may be helpful. 4

  • Balance neurologic examination versus offering enough sedation to provide endotracheal tolerance, ventilator synchrony, and shivering control. 7

  • Early mobilization recommended only if neuro-specific issues are well controlled.

16.4 Individualizing Therapy in NICU

16.4.1 Pharmacologic Interventions of Pain

(Table 16‑1)

Table 16.1 Properties of commonly used analgesics in critical care

Drug/Class

Mechanism of action

Dose

Advantages

Disadvantages

Metabolism

Notes

Acetaminophen

Exact mechanism unknown; antipyretic effect on hypothalamus; prostaglandin synthesis inhibition

IV: 1,000 mg every 6 hours

PO: 650–1,000 mg every 4–6 hours (≤4,000 mg/day)

Has analgesic and antipyretic properties

IV formulation rapid acting

No anti-inflammatory property

Hepatic

Available in IV formulation, may mask an infectious process

IV formulation is costly and may be restricted

Caution use with liver failure

Nonsteroidal anti-inflammatory drug*

Ketorolac

COX-1 and 2 inhibitor

IV: 15–30 mg every 6 hours up to 5 days

Potent analgesia, no respiratory depression

Good anti-inflammatory property

Risk of bleeding and renal dysfunction

Hepatic (with renal clearance)

Available in IV formulation,

use is limited to 5 days, avoid in renal failure

Infrequently used in neuro-ICU due to bleeding risk

Ibuprofen

COX-1 and 2 inhibitor

IV: 400–800 mg every 4–6 hours (<3,200 mg/day)

No respiratory depression

Risk of bleeding and renal dysfunction

Renal

Avoid in renal failure,

available in IV formulation

Naproxen Sodium

COX-1 and 2 inhibitor

PO: 500 mg every 12 hours

(Max 1,250 mg.day)

No respiratory depression

Used for arthritic pain, migraines, gout

Risk of bleeding and renal dysfunction

Hepatic

Not recommended with CrCl <30 mL/minute

Delayed-release not recommended for acute pain

Celecoxib

COX-2 inhibitor

200 mg twice a day

No respiratory depression, reduce risk gastric bleeding

Some risk of bleeding

Hepatic

Not commonly used in ICU setting

Opioids

Tramadol

Partially binding opioid µ receptor

Inhibits reuptake of norepinephrine and serotonin

Immediate release: 50–100 every 4–6 hours (max 400 mg/day)

Good for moderate to moderate-severe pain

CNS and respiratory depression

Increased risk of seizures Serotonin syndrome in patients on SSRI, SNRIs, TCAs, and neuroleptics

Hepatic

Titrating may improve tolerability

Active metabolite has 200-fold greater affinity for opioid receptor

Max dose for renal failure is 200 mg/day

Max dose for patients with cirrhosis 50 mg/12 hours

Toxicity may be due to mono-amine effect rather than opioid effect 28

Morphine

Opioid receptor agonist

IV: 2–5 mg every 2–4 hours

Initial continuous infusion: 1–2 mg/hour

PO: 10–30 mg every 3–4 hours

Easy titration

Risk of respiratory depression, active metabolites in renal failure

Hepatic (renal clearance)

Avoid in renal failure, pruritus related to histamine release

Fentanyl

Opioid receptor agonist

IV: 25–50 mcg every 5–15 minutes

Initial continuous infusion: 10–20 mcg/hour

Easy titration, available in several formulations; rapid onset

Risk of respiratory depression, chest wall rigidity at high doses

Hepatic

Short half-life, significant increase in context-sensitive half-life with prolonged infusion

Hydromorphone

Opioid receptor agonist

PO: 1–2 mg every 3–4 hours

IV: 0.5–1 mg every 3–4 hour

Initial continuous infusion: 0.2–0.3 mg/hour

Easy titration

Risk of respiratory depression

Hepatic

Shorter duration of action compared to morphine, may require frequent dosing in opioid tolerant, less pruritic than morphine

Remifentanil

Opioid receptor agonist

Loading dose: 1.5 mcg/kg

Continuous infusion: 0.5–15 mcg/kg/hour

Easy titration, ultra-rapid onset and elimination

Risk of respiratory depression, rebound hyperalgesia

Plasma esterases

Consider longer acting opioid before discontinuation

Oxycodone

Opioid receptor agonist

Initial PO: 5–10 mg every 3–4 hour

Intermediate duration of action

Respiratory depression

Hepatic

Available in combination with acetaminophen, caution with patients with simultaneous use of acetaminophen

Membrane channel stabilizers

Gabapentin

Analgesic mechanism is unknown: GABA analogue (no effect on GABA receptor)

100 mg three times a day can titrate up to 1,800 mg/day

Effective in neuropathic pain and partial seizures

Reduction in opioid requirement when used as part of multi-modal therapy

Sedation

Negligible (renal excretion)

Rapid discontinuation may precipitate seizure, gradual titration

Adjust dose for renal impairment based on CrCl

Pregabalin

Exact mechanism unknown: GABA analogue that binds to voltage gated calcium channel

50 mg three times a day, may increase to 100 mg three times a day

Effective in neuropathic pain, fibromyalgia and epilepsy

Reduction in opioid requirement when used as part of multi-modal therapy

Dose-dependent symptoms of dizziness and sedation Requires titration

Negligible (renal excretion)

Gradual titration

Adjust dose for renal failure based on CrCl

No effect on opiate receptor

Anesthetics

Ketamine

NMDA antagonist

Loading dose: 0.1–0.5 mg/kg

Infusion dose: 0.05–0.4 mg/kg/hour

Minimal respiratory depression, prevention in pain chronicization

Psychomimetic reactions

Hepatic

Minimal effect on ICP at subanesthetic dose, useful with opioid tolerant patients

Dexmedetomidine

Central α2-receptor agonist

Loading dose: 1 mcg/kg over 10 minutes

Infusion dose:

0.2–0.7 mcg/kg/hour

Easy titration, no respiratory depression, mild analgesic property, minimal effect on ICP

Hypotension, bradycardia at high doses

Hepatic

Useful with mechanical ventilation weaning process, cooperative sedation

Loading dose not commonly used due to rapid decrease in BP

Extended use up to 5–7 days feasible in appropriate patient selection

Lidocaine 30

Sodium channel blocker

Loading dose: 1–2 mg/kg

Infusion dose: 1–2 mg/kg/hour optimal dose

Effective in treatment of acute pain

Anti-inflammatory properties

Reduction in opioid requirement when used as part of multi-modal therapy

Cardiac toxicity at high dose

Seizures

Prolonged time to reach steady state without bolus

Hepatic

Avoid in chronic liver failure

Therapeutic plasma level 2.5–3. 5µg/mL

CNS toxicity can occur at levels of >5 µg/mL.

CNS toxicity signs: numbness of tongue, metallic taste, light headedness, tinnitus, drowsiness, muscle twitching, unconsciousness, coma, and death

Note: *NSAIDs are contraindicated for perioperative pain in the setting of coronary artery bypass graft surgery.

Abbreviations: BP, blood pressure; CNS, central nervous system; GABA, gamma aminobutyric acid; ICP, intracranial pressure; ICU, intensive care unit; IV, intravenous; NMDA, N-methyl-D-aspartate; NSAIDs, nonsteroidal anti-inflammatory drugs; SNRIs, serotonin–norepinephrine reuptake inhibitor; SSRI, selective serotonin reuptake inhibitor; TCAs, tricyclic antidepressants.

Specific comorbidities that require special considerations for pain management (Table 16‑2)

Table 16.2 Pain management in specific patient populations

Pathophysiology

Notes

Elderly

Decreased GFR, drug doses adjusted based on creatinine clearance

Decreased respiratory center sensitivity, opioids started at lower dose

Decreased receptors in CNS (5HT, AcH, and Dop); therefore, side effects of buprenorphine, tramadol, and tapentadol are potentiated

End-stage renal disease

Decreased GFR and increased volume of distribution, renal dosing

Chronic liver disease

Decreased hepatic blood flow and drug metabolism, doses should be decreased

Cardiac disease

Caution drugs that may cause bradycardia or hypotension (e.g., high doses of opioids, dexmedetomidine) or hypertension or arrhythmias (e.g., ketamine)

Pulmonary disease

Obese patients have obstructive sleep apnea and decreased FRC Supplemental oxygenation or CPAP use may be helpful

Minimize opioid use and maximize adjuncts

Dementia

Avoid drugs that potentiate cognitive impairment (e.g., opioids, membrane channel stabilizers)

Avoid polypharmacy

PCA less suitable

Opioid tolerant

Exhibit opioid-induced hyperalgesia; therefore, higher doses of opioids required

Respiratory depression less common

Variable opioid cross-tolerance

Ketamine helpful in opioid tolerance

Maximize use of adjuvants

Substance use disorder

Methadone maintenance therapy should continue with addition of opioids to manage acute pain

Should discontinue the use of buprenorphine; intravenous opioids which exhibit high μ-receptor affinity should be used to manage pain

Maximize use of adjunct agents

PCA to maintain a more stable plasma concentration compared to intermittent intravenous boluses

Alcoholism

Acute ingestion has depressive effect on CNS and increases sensitivity to sedatives

Alcohol increases endogenous opioid levels

Chronic alcohol ingestion causes chronic liver disease which decreases drug metabolism

Postoperative spine

NSAIDs may inhibit bone healing

Membrane channel stabilizers help with neuropathic pain

Treat muscle spasms with muscle relaxants (e.g., diazepam, cyclobenzaprine, tizanidine, baclofen)

Craniotomy

Frequent neurologic assessments; thus, easily titratable drugs preferred

Avoid drugs that sedate and decrease respiratory function

Opioids decrease ICP in adequately ventilated patients

Dexmedetomidine and subanesthetic ketamine have minimal effect on ICP

Scalp blocks reduce opioid requirements

Abbreviations: CNS, central nervous system; CPAP, continuous positive airway pressure; FRC, functional residual capacity; GFR, glomerular filtration rate; ICP, intracranial pressure; NSAIDs, nonsteroidal anti-inflammatory drugs; PCA, patient-controlled analgesia.

Nonopioid Analgesics (Primarily for Mild Pain)

5

  • Acetaminophen 10 , 11

    • Useful in patients unable to receive oral medications

    • Intravenous (IV) dose may reduce opioid requirements 11

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) 12

    • Avoid in neurosurgical population for platelet inhibition

    • May lead to kidney injury with chronic use and risk aseptic meningitis

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Feb 6, 2021 | Posted by in NEUROLOGY | Comments Off on 16 Pain Management in the Neuro-Intensive Care Unit (ICU)

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