pain management after craniotomy and spine surgery. as a neuroanesthesiologist it our duty to manage post operative pain. pain in these patient are under treated.
2. Introduction:
⢠In neurosurgical patients pain has often being
overlooked and traditionally has been a subject of
inconsistent research.
⢠No consensus regarding the standardization
of pain control.
⢠Pain after craniotomy is moderate to severe and
inadequately treated in approximately 50% of
patients.
Anesthesiology Clin; 25 (2007) 655â674; Perioperative Pain Management in the Neurosurgical Patient ; Jose Ortiz-Cardona, MD,
Audre´e A. Bendo, MD*
BioMed Research International; Pain following Craniotomy: Reassessment of the Available Options; Rudrashish Haldar,
Ashutosh Kaushal, Devendra Gupta, Shashi Srivastava, and Prabhat K. Singh; Volume 2015, Article ID 509164, 8 pages
3. Introduction:
⢠Various techniques and approaches, based on the
latest research and clinical trials.
⢠The greatest challenge in managing neurosurgical
patients is the need to assess neurologic function
while providing superior analgesia with minimal
side effects.
⢠To achieve this goal, a multimodal approach to
analgesia using various drugs and techniques is an
ideal choice.
Rahimi SY, Vender JR, Macomson SD, et al. Postoperative pain management after craniotomy:
evaluation and cost analysis. Neurosurgery 2006;59(4):852â7
4. What is pain?
Pain, as defined by the International Association for
the Study of Pain, is an unpleasant sensory and
emotional experience associated with actual or
potential tissue damage, or described in terms of
such damage or both.
It is an individual experience, with unique properties
varying from patient to patient.
5. Physiology of pain:
Myelinated A delta afferent
nerve fibers.
These are fast conducting, have
low threshold for activation.
Stimulus is sensed by
nociceptors free nerve endings
located in the skin, muscles,
joints, and mucosa, and in
visceral organs.
Unmyelinated, slow C
fibers.
Polymodal nociceptors
respond to
high-intensity
mechanical or chemical
stimuli, and cold-hot
stimuli.
6. Pain pathways:
Vasodilatation, plasma
extravasation ď activation
of nociceptors
Release on inflammatory mediators,
substance P, calcitonin - GRP
communicated with cell bodies of sympathetic
nervous system and ventral motor nuclei
Impluse generation
Primary afferent neuron to
dorsal horn of spinal cord
Synapses to form second
order neuron
Synapses at thalamus to
form 3rd order nerves
Relay in somatosensory
cortex
2nd order nerves transmit pain ,
temperature and light touch
Also transmit axonal br to reticular
formation, nucleus raphe magnus,
periaqueductal grey matter and
other area of brain stem.
7. Pain in neurosurgery:
⢠Pain experienced by patients after craniotomy
is of somatic origin, most likely involving the
scalp, pericranial muscles, and soft tissue, and
from manipulation of the dura mater.
⢠Correlation between the site of the surgical
wound and the pain.
⢠Subtemporal and suboccipital surgical routes
gives highest intensity of pain.
8. Innervations:
⢠The scalp receives its innervations from cervical plexus and
the trigeminal nerve.
⢠The anterior scalp: supraorbital and supratrochlear nerves,
divisions of the frontal nerve (ophthalmic division of
trigeminal nerve).
⢠The temporal scalp: zygomaticotemporal (maxillary division
of trigeminal nerve), temporomandibular, and
auriculotemporal nerves (mandibular division of trigeminal
nerve).
⢠The occipital scalp: cervical plexus ď greater auricular, and
the greater and lesser occipital nerves.
⢠The dura mater is innervated by nerves that accompany
the meningeal arteries.
10. Causes of inadequate pain control
Neurosurgical patients require frequent neurological
examinations.
But excessive sedation camouflages the new onset
neurological deficits and hamper the neurological
response monitoring.
Respiratory depression ď Hypercarbia ď â ICP.
Inadequate analgesia ď agitation, hypertension, shivering,
and vomiting ď which may increase the risk of
intracranial bleeding or other neurologic complications
11. Causes of inadequate pain control
2. Defective communication, altered mental
status or neurologic deficits.
3. Patients undergoing spine procedures, pain is
often a source of significant preoperative
distress.
ââchronic pain patientsââ require high doses of
narcotics to achieve satisfactory analgesia.
13. Classification of Headache Disorders
⢠International Classification of Headache
Disorders (ICHD-3) published by the
International Headache Society.
⢠They classified Postcraniotomy headache and
subdivided it into acute and persistent
varieties.
14. Classification of Headache Disorders
⢠Acute Headache Attributed to Craniotomy
Description. Headache is of less than 3
monthsâ duration caused by surgical craniotomy.
⢠Diagnostic Criteria. They are as follows:
(A) Any headache fulfilling criteria (C) and (D).
(B) Surgical craniotomy which has been performed.
(C) Headache which is reported to have developed
within 7 days after one of the following:
15. Classification of Headache Disorders
(1) the craniotomy,
(2) regaining of consciousness following the craniotomy,
(3) discontinuation of medications that impair ability to
sense or report headache following the craniotomy.
(D) Either of the following:
(1) headache resolved within 3 months after the
craniotomy,
(2) headache not yet resolved but 3months have not yet
passed since the craniotomy.
(E) Not better accounted for by another ICHD-3 diagnosis.
16. Classification of Headache Disorders
Persistent Headache Attributed to Craniotomy
Description. Headache is of greater than 3
monthsâ duration caused by surgical
craniotomy.
17. Pain assessment
Pain History
â O â Onset
â P â Provoking / Palliating factors
â Q â Quality / Quantity
â R â Radiation
â S â Severity
â T â Timing
21. Methods to Treat Pain
⢠Non-Pharmacologic
⢠Pharmacologic
â Medications (po, iv, im, sc, pr, transdermal)
⢠Acetaminophen
⢠NSAIDs
⢠Opioids
⢠Gabapentin
⢠NMDA antagonists
⢠Alpha-2 agonists
â Procedures
⢠Regional Anesthesia
⢠LA infiltration at incision site
22. Methods to Treat Pain
Non pharmacological methods include:
1. Avoidance of trigger factors.
2. Behavioural approaches: relaxation techniques,
biofeedback,
3. Cognitive- behavioral therapy but require
specialist time or technical devices.
4. Acupuncture is controversial because of
methodologic difficulties. But studies
acknowledge their efficacy.
5. Radiofrequency or cryoablation,
6. Physiotherapy,
23. Multimodal Analgesia
B. Pharmacologic :
Using more than one drug for pain control
â Different drugs with different
mechanisms/sites of action along pain
pathway
â Each with a lower dose than if used alone
â Can provide additive or synergistic effects
â Provides better analgesia with less side
effects (mainly opiate related S/E)
24. Methods of analgesia for craniotomy:
B. Pharmacologic methods:
1. Opioids:
⢠stimulation of Ο and k receptors.
⢠Inhibition of voltage-gated calcium
channels and an increase in potassium influx.
Opioids inhibit the transmission from afferent first
neuron to the second neuron.
25. Pharmacologic methods: opioids
⢠Intermittent boluses cause oversedation (peak
opiate effect) followed by periods of
inadequate analgesia.
⢠Patient-controlled analgesia (PCA) with
morphine or fentanyl used effectively.
⢠Side effects
⢠nausea,
⢠vomiting,
⢠decreased gastrointestinal motility,
⢠pruritus,
⢠respiratory depression,
⢠oversedation.
26. Pharmacologic methods: opioids
As a consequence:
Additional pharmacologic intervention.
Increased length of hospital stay.
Hindrance to postoperative neurologic
examinations.
27. Pharmacologic methods: opioids
⢠Morphine: Intravenous (including PCA) or i.m.
routes.
Blunt the haemodynamic surges.
⢠Fentanyl: compared to morphine, it is more potent,
faster acting.
Transdermal route also.
Shorter duration of action so preferred in PCA .
⢠Tramadol: synthetic analgesic
Less potent.
28. 2. Nonsteroidal anti-inflammatory drugs
Mechanism of action:
⢠Reversible, nonselective inhibition of the
cyclooxygenase (COX) enzymes COX-1 and COX-
2.
⢠COX acts on arachidonic acid to synthesize
prostaglandins & thromboxane.
⢠Central and peripheral inhibition of
prostaglandin-mediated activation of sensory
pathways.
29. Nonsteroidal anti-inflammatory drugs
Drawbacks:
⢠Platelet dysfunction
⢠Increased bleeding times.
⢠Avoid in aneurysm repair, arteriovenous malformation
resection and hematoma evacuations.
⢠Asthma
⢠AKI
⢠Rash
30. Nonsteroidal anti-inflammatory drugs
⢠Paracetamol (acetaminophen):
N-acetyl-p-aminophenol
⢠Paracetamol alone is not sufficient to
provide adequate analgesia. *
⢠With opioids they are very effective.
* Verchere and colleagues
31. 3. Alpha-2 adrenergic agonists
Dexmedetomidine
⢠Potent and highly selective alpha-2 agonist
⢠Acts on presynaptic neurons in the spinal cord
dorsal horn.
⢠Provides sedation and analgesia without
respiratory depression.
Clinical applications:
⢠Awake craniotomy,
⢠Preoperative sedation
⢠Fiberoptic tracheal intubation.
32. Alpha-2 adrenergic agonists
Dexmedetomidine :
⢠Opioid-sparing effects: reducing morphine
requirements by 60% .
⢠They also have preemptive analgesic effect.
⢠Sedation to arousal immediately for
neurologic examinations.
⢠Side effect: Hypotension and bradycardia.
33. 4. N-methyl-D-aspartate (NMDA)
receptor antagonists
NMDA receptors are ligand-gated ion channels
⢠Permit calcium, sodium, and potassium
into the cell.
⢠Activated by glycine and glutamate.
Glutamate, sensitizes nociceptors, increasing the
magnitude and duration of neurogenic responses
to pain, even after the initial peripheral input has
stopped.
They are not actually analgesic but antinociceptive.
34. Methods of analgesia for craniotomy:
A. Regional analgesia:
1. Scalp block:
⢠Decrease the amount of rescue pain medication
requests.
⢠Increase the time between the end of surgery
and the first request for postoperative analgesics,
⢠Lower pain score values in the early
postoperative period .
⢠Lower pain scores lasting up to 48 hours a
⢠Preemptive analgesic effect.
35. Methods of analgesia for craniotomy:
2. Wound infiltration:
Preincision local anaesthetic injection:
â blunt the systemic responses to craniotomy
â minimize bleeding with skin incision.
visual analog scale (VAS) scores remains
comparable without LA inj.
Ayoub C, Girard F, Boudreault D, et al. A comparison between scalp nerve block and morphine
for transitional analgesia after remifentanil-based anesthesia in neurosurgery. Anesth
Analg 2006;103(5):1237â40.
36. Chronic pain after craniotomy
⢠Suboccipital craniotomy : M/C
⢠Causes: Dural traction
Cervical muscle
Destruction
Nerve entrapment
Cerebrospinal fluid leakage
Fibrin glue or drilling leading to Aseptic
meningitis.
⢠T/T: TENS, acupuncture, radiofrequency,
physiotherapy.
NSAIDs, paracetamol, or opioids, GABA
analogues, sumatriptan.
BioMed Research International; Pain following Craniotomy: Reassessment of the Available Options; Rudrashish Haldar,
Ashutosh Kaushal, Devendra Gupta, Shashi Srivastava, and Prabhat K. Singh; Volume 2015, Article ID 509164, 8 pages
37. Pain management in spine surgery
Considerations :
⢠a. Risk factors : Psychologic, social profile, and
preoperative pain severity .
⢠ââFailed back syndromeââ ď high baseline opiate
requirements
⢠Anxiety
⢠Frequent neurologic examinations .
⢠Patient cooperation and awareness
⢠Early ambulation
38. Pain management in spine surgery
1. Parenteral administration Opioids:
a. Fear of sedation
b. Respiratory depression,
c. Intolerance to the doses required for
adequate analgesia.
A multidrug approach is a better choice because of
higher Patient satisfaction and decreased doses
of opioids.
39. Nonsteroidal anti-inflammatory drugs
⢠NSAIDS as the sole medication is not sufficient to
provide adequate analgesia.
⢠Ketorolac, given IM or IV, is the most
investigated drug among the NSAIDS.
⢠It has good analgesic potency.
⢠Opioid-sparing effect.
Remy C, Marret E, Bonnet F. State of the art of paracetamol in acute
pain therapy.
Curr Opin Anaesthesiol 2006;19(5):562â5.
40. Nonsteroidal anti-inflammatory drugs
⢠High-dose (120â240 mg/d), but not low-dose,
ketorolac has been associated with nonunion
following spine fusion surgery .
⢠Low-dose ketorolac, is a safe and effective
adjuvant to an opioid-based regimen for acute
postoperative pain management after spine
surgery.
41. NSAIDs: Cyclooxygenase-2 inhibitors
Defective bone healing by NSAIDS.
COX-2â dependent PGE2 produced at the early stage
of bone healing is a prerequisite for efficient
skeletal repair.
⢠Paracetamol is safe option where NSAIDâs need to
be avoided in view of bleeding risks, asthma, or
renal derangements*.
⢠COX -2 inhibitors , given for shorter duration does
not affect bone healing.
* Journal of Craniovertebral Junction and Spine; Pain management following spinal surgeries: An appraisal of the
available options, Sukhminder Jit Singh Bajwa, Rudrashish Haldar1
42. NMDA receptor antagonist
Ketamine decreases postoperative pain by its
direct analgesic effects and preventing the
nociceptive sensitization in CNS.
Reduce or reverse opioid tolerance.
Dysphoria, sedation, diplopia, salivation, nausea,
and hallucination restricts its extensive use.
43. GABA Analogues: Gabapentin
⢠Anti-epileptic drug, also useful in:
â Neuropathic pain.
⢠Blocks voltage-gated Ca channels in CNS
⢠Additive effect with NSAIDs
⢠Reduces opioid consumption by 16-67%
⢠Reduces opioid related side effects
⢠Drowsiness if dose increased too fast
⢠Dose: 300 â 3600 mg/day
Tremont-Lukats IW. Anticonvulsants for neuropathic pain syndromes: mechanisms of
action and place in therapy. Drugs 2000;60(5):1029â52.
44. Steroids
⢠Steroids are anti-inflammatory drugs:
⢠Inhibit phospholipase A2,
⢠Decrease in the expression of substance P at
the dorsal root ganglion.
45. Steroids
Intraoperative IV injection of 40-mg dexamethasone
⢠Reduces postoperative radicular leg pain
⢠Reduces narcotic use.
⢠Oral and intravenous steroid administration as
well as Intraoperative irrigation.
46. Neuraxial administration
Neuraxial administration: Intrathecal
Opioids Intrathecal (IT)
⢠Preservative-free morphine.
⢠Fentanyl
⢠Side effects as with iv route.
⢠Prolonged continuous infusion of drug through
an IT catheter is not recommended because of
the risk of cauda equina syndrome.
47. Neuraxial administration
Local anesthetics:
⢠Local anesthetics is mostly in combination with
opioids or other adjuvants.
⢠Doses 0.6 mg/kg/h of morphine with
bupivacaine .
⢠But they may show prolonged sensory and
motor block which is not desirable.
48. Neuraxial administration: epidural
⢠Epidural opioids have a better safety margin
⢠Low incidence of dose-dependent respiratory
depression and urinary retention.
The controversy: More invasive procedure is
superior to the standard IV or IM route after
spine surgery.
49. Neuraxial administration: epidural
Opioid and local anesthetic:
Ropivacaine, more favoured.
Different techniques like
A. Single and double catheters,
B. Intermittent boluses,
C. Patient-controlled epidural analgesia,
D. Continuous infusion of medication.
Epidural catheter can be placed intraoperatively can
be done by the surgical team under direct vision .
52. Neuraxial administration: epidural
Other agents:
Alpha-2 agonists can be combined with opioids,
local anesthetic, or both to potentiate their
action.
They produce minimal respiratory depression when
compared with opioids.
Duration of action is prolonged.
53. Newer possibilities:
⢠Transcutaneous electrical nerve stimulation
It is an efficient and opioid sparing method.
TENS applied before surgery and postoperatively
reduces opioid requirement.
⢠Extended release formulations
Multivesicular liposomes containing bupivacaine.
Single dose produces analgesia for several days.
55. Summary
Pain management in neurosurgical patients has been
inconsistently recognized and inadequately treated.
An increased awareness of pain management along with
advances has led to improved practice and
perioperative care of patients.
The greatest challenge to managing neurosurgical
patients is the need to assess neurologic function while
providing superior analgesia with minimal side effects.
To achieve this goal, a multimodal approach to analgesia
using various drugs and techniques should be
preferred.
Hinweis der Redaktion
improved awareness and advances in the practice of
pain management have resulted in the implementation of diverse techniques
to achieve adequate analgesia in this undertreated group of patients.
[4,10]
Depressed respiration can give rise
to hypercarbia which increases cerebral blood volume and
consequently raise the intracranial pressures (ICP).
Exact quantification of pain in postcraniotomy patients is problematic as the patients should be capable of perceiving and expressing pain which might not be always possible following neurosurgical procedures
helps in estimating the neurophysiological and psychological domains of pain. It allows to identify the location and quality of pain
aids in evaluating the eff ect
of pain on general activity, mood, ambulation, relationships,
sleep, and work enjoyment.
, but are supported by some evidence, which is mostly old.
An ongoing large German study may provide valuable evidence in the near future.Â
(brainstem, hypothalamus, limbic system, substantia gelatinosa of the spinal cord)
(gastrointestinal tract, peripheral histamine receptors)
They also activate the descending inhibitory pathways that go from the midbrain, rostral ventromedial medulla, ending in the dorsal horn
of the spinal cord.
COX-1 is expressed constitutively in the brain and spinal cord.
When nalbuphine or tramadol
were added to this regimen, VAS levels of less than 30 mm were achieved
and maintained in the immediate postoperative period
of patients with aneurysmal subarachnoid hemorrhage,
These agents do not possess intrinsic analgesic properties, but rather carry out their antinociceptive effects by
inhibiting central sensitization to painful stimuli.
sharp
aching, pressurising, or throbbing.
given 1 hour before the induction of anesthesia and every 12 hours after surgery for the first 5 postoperative days, resulted in a significant reduction in postoperative pain and opioid use following spine fusion surgery.