Pain Management Lecture Regional Anesthesia

Front 1

ALLODYNIA

Back 1

perception of an ordinarily non-noxious stimulus as pain

Front 2

ANALGESIA

Back 2

absence of pain perception

Front 3

ANESTHESIA

Back 3

absence of all sensation

Front 4

ANESTHESIA DOLOROSA

Back 4

pain in an area that lacks sensation with or without a stimulus

Front 5

DYSESTHESIA

Back 5

unpleasant or abnormal sensation with or without a stimulus

Front 6

HYPALGESIA (HYPOALGESIA)

Back 6

dimished response to noxious stimulation (pinprick)

Front 7

HYPERALGESIA

Back 7

inceased response to noxious stimulation

Front 8

HYPERESTHESIA

Back 8

increased response to mild stimulation

Front 9

HYPERPATHIA

Back 9

presence of hyperesthesia, allodynia, and hyperalgesia usually associated with overreaction, and persistance of the sensation after the stimulus

Front 10

HYPESTHESIA (HYPOESTHESIA)

Back 10

reduced cutaneous sensation (light touch, pressure, or temperature)

Front 11

NEURALGIA

Back 11

pain in the distribution of a nerve or a group of nerves

Front 12

PARESTHESIA

Back 12

abnormal sensation perceived without an apparent stimulus

Front 13

RADICULOPATHY

Back 13

functional abnormality of one or more nerve roots

Front 14

Neuropathic (burning, tingling, pins and needles sensation)

Back 14

caused by injury or acquired abnormalities of peripheral or central neural structures. (diabetes)

Front 15

Nocioception

Back 15

Describes the recognition and transmission of painful stimuli.
Stimuli generated from thermal, mechanical, or chemical tissue damage may activate nocioceptors, which are free afferent nerve endings of myelinated A-delta and unmyelinated C fibers.

Front 16

nocioceptors

Back 16

free afferent nerve endings of myelinated A-delta and unmyelinated C fibers.

Front 17

Nociceptors are

Back 17

receptors that transduce noxious stimuli.
free nerve endings that sense heat, mechanical, and chemical tissue damage.

Front 18

Mechanonociceptors

Back 18

Respond to pinch and pinprick.

Front 19

Silent nociceptors

Back 19

Respond to inflammation

Front 20

alogens

Back 20

pain producing substances

Front 21

Protopathic sensation

Back 21

noxious (pain) subserved by high-threshold receptors (very sensitive) conducted by smaller, lightly myelinated (Aδ) and unmyelinated (C) nerve fibers

Front 22

Epicritic sensation

Back 22

nonnoxious (not painful) light touch, pressure, proprioception, and temperature discrimination Characterized by low-threshold receptors Generally conducted by large myelinated nerve fibers

Front 23

Summary: Gate Theory

Back 23

The spinal cord and brain stem contain “gates,” which open or close.
Theorized: Large diameter fibers close gates while small diameter fibers open gates.
When there is no stimulation, the small and large fibers are silent; the gates are closed.

Front 24

A Beta fibers

Back 24

5-12 microns
Large, myelinated fibers.
Transmit impulses quickly.
Transmits sensations of touch, pressure and proprioception.
Carry sensations described as epicritic (non-noxious)

Front 25

A Delta fibers

Back 25

2-5 microns
Myelinated with lipid-like substance.
Transmit impulses fast.
Sense “sharp” and well-localized sensations. (needle poking your finger)
First pain or “Acute” pain
Carry sensations described as protopathic (noxious).
Warns you to react quickly.

Front 26

C Fibers

Back 26

0.4-1.2 microns (very small)
Unmyelinated
Transmit impulses slowly.
Sense dull, poorly localized sensations.
Second Pain or “Chronic” pain
Transmits protopathic sensations of pain, temperature, and touch.

Front 27

Non-painful stimulation

Back 27

Travels via large nerve fibers, A beta fibers; gates remain closed.

Front 28

Painful stimulation

Back 28

Travel via smaller diameter nerve fibers, A delta & C fibers; gates open and “painful sensation” is transmitted to the brain. (now you know you hurt)

Front 29

Acute pain

Back 29

Caused by noxious stimulation due to injury, a disease process, or abnormal function of muscle or viscera.
Associated with a neuroendocrine stress response (sympathetic nervous system stimulation) (kicked in the balls)
Self limited or resolves with treatment in a few days or weeks.
Two types: somatic ( either superficial or deep) or visceral

Front 30

ACUTE PAIN PATHWAY

Back 30

1) nociceptive stimulus (pinprick, acute burn, bee sting) ** skin
2) activation of nociceptors (activation of peripheral receptors, generation of action potentials, release of neurotransmitters from central terminals) ** dorsal root ganglion
3) activation of central pain pathways (dorsal horn to brainstem and thalamus)

Front 31

Acute pain: Superficial

Back 31

Due to nociceptive stimuli from skin, subcutaneous tissues, and mucous membranes.
Well localized
Described as sharp, pricking, throbbing or burning.

Front 32

Acute pain: Deep somatic

Back 32

Arises from muscles, tendons, joints, or bones.
Dull aching quality.
Less well-localized than superficial pain.

Front 33

Acute pain: Visceral

Back 33

Due to a disease process or abnormal function of an internal organ or its covering.
Presents as aching, dull and diffuse.
Poorly localized.
Refer to M & M, Table 18-2 to review patterns of referred pain.

Front 34

CENTRAL DIAPHRAGM
(REFERRED PAIN)

Back 34

C4

Front 35

LUNGS (REFERRED PAIN)

Back 35

T2-T6

Front 36

HEART (REFERRED PAIN)

Back 36

T1-T4

Front 37

AORTA

Back 37

T1-L2

Front 38

ESOPHAGUS

Back 38

T3-T8

Front 39

PANCREAS AND SPLEEN

Back 39

T5-T10

Front 40

STOMACH, LIVER, AND GALLBLADDER

Back 40

T6-T9

Front 41

ADRENALS

Back 41

T8-L1

Front 42

SMALL INTESTINE

Back 42

T9-T11

Front 43

COLON

Back 43

T10-L1

Front 44

KIDNEY, OVARIES, AND TESTES

Back 44

T10-L1

Front 45

URETERS

Back 45

T10-L2

Front 46

UTERUS

Back 46

T11-L2

Front 47

BLADDER AND PROSTATE

Back 47

S2-S4

Front 48

URETHRA AND RECTUM

Back 48

S2-S4

Front 49

Chronic pain

Back 49

Neuropathic pain
Caused by an injury to the central nervous system that transmits pain.
Injury can be central or peripheral.
Described as burning, electrical and shooting.
Example: post-herpetic pain, diabetic neuropathy, or post surgical procedure

Front 50

Sympathetically Maintained Pain

Back 50

Complex Regional Pain Syndrome (CRPS)
Also called, Reflex Sympathetic Dystrophy
Nerve disorder that occurs at the site of injury, most often arms or legs.
Chronic condition characterized by severe burning pain, pathological changes in bone and skin, excessive sweating, tissue swelling and extreme sensitivity to touch.

Front 51

Effects of Surgical Trauma

Back 51

1) surgical trauma
2) Peripheral sensitization (primary and secondary hyperalgesia --> release of hydrogen ions, histamines, purines, leukotrienes, norepinephrine, K+ ions, cytokines, nerve growth factor, BK, PG's, 5-HT, neuropeptides
3) spinal wind up
4) central sensitization

Front 52

Perception & Response to Pain
Four distinct processes

Back 52

Transduction, transmission, interpretation, and modulation

Front 53

Transduction

Back 53

Nociceptors are stimulated in skin and muscle.
A noxious, painful or tissue-damaging stimuli affects a peripheral sensory nerve ending.
The nerve is depolarized.
Generates electrical impulse.

Front 54

Transmission

Back 54

The impulse is transmitted or carried throughout the nervous system.
The Spinothalamic Tract is the most important pathway for transmission

Front 55

Perception

Back 55

A subjective interpretation of pain by the patient.
How it feels to the patient.
Behavioral, psychological, and emotional factors are involved, which create an individualized perception of pain.

Front 56

Modulation

Back 56

Modulation can either inhibit (suppress) or facilitate (aggravate) pain.
It is a neural response.(you can’t control it)
Peptides, amino acids and other mediators are released.
Chemical messages are released.

Front 57

Endogenous mediators of inflammation

Back 57

Prostaglandins (PGE1 > PGE2)
Histamine
Bradykinin (peptide causes HR to slow down  a lot in the bowels) SNS you will have HR issues
Serotonin (found in brain and gut)
Acetylcholine
Lactic acid
Hydrogen ions
Potassium ions

Front 58

Pain Pathways

Back 58

Pain is conducted along three-neuron pathways from periphery to cortex (M&M, Figure 18-1).

First order neurons (FON) are located in the dorsal root.
Second order neurons (SON) are located in the dorsal horn.
Third order neurons (TON) are located in the inner chamber of the thalamus.

Front 59

First Order Neurons (FON)

Back 59

Located in the dorsal root ganglia.
Each neuron has a single axon which bifurcates, sending one end to the periphery and the other to the dorsal horn of the spinal cord.
Majority of FON send their axons into the spinal cord via the dorsal (sensory) spinal root.
Some unmyelinated fibers have been shown to enter the spinal cord via the ventral root.
This explains why patients still have pain after rhizotomy (transection of the dorsal nerve root).

Front 60

Second Order Neurons (SON)

Back 60

First order neurons synapse with second order neurons in the gray matter of the dorsal horn.
Spinal cord gray matter is divided into 10 lamina (Bror Rexed, 1952).
Lamina 1-6 make up the dorsal horn. These sites are where all afferent stimuli comes into the spinal cord.
Lamina 1-6 represent the principal site of modulation of pain by ascending and descending neural pathways.

Front 61

Rexed laminae

Back 61

The Rexed laminae comprise a system of ten layers of grey matter (I-X), identified in the early 1950s by Bror Rexed to label portions of the spinal cord.
Similar to Brodmann areas (defined based on its cytoarchitectonics, or organization of cells) Rexed laminae are defined by their cellular structure rather than by their location, but the location still remains reasonably consistent.

Front 62

Rexed laminae II

Back 62

Laminae II is also called the “Substantia Gelatinosa.”
It contains many “interneurons” (also called relay neurons, association neurons, connector neurons or local circuit neurons) - a multipolar neuron which connects afferent neurons and efferent neurons in neural pathways. (stop cocks)
It plays a major role in processing and modulating nociceptive (noxious) input from the periphery.
Major site of action for opioids.

Front 63

Lamina III, IV & VI

Back 63

receive non-nociceptive sensory input. (touch pain pressure)

Front 64

Lamina VII

Back 64

also called the intermediolateral column, contains preganglionic sympathetic neurons.

Front 65

Lamina VIII & IX

Back 65

Anterior horn (motor).

Front 66

Lamina X

Back 66

Very small neuron surrounding the central canal. Involved in pain, temp and visceral sensations.

Front 67

Second Order Neurons (SON)

Back 67

SON are either nociceptive or wide dynamic range neurons (WDR).

Front 68

Nociceptive neurons

Back 68

respond only to noxious stimuli; primarily located in Lamina I.

Front 69

Wide dynamic range neurons (WDR):

Back 69

respond to noxious (protopathic signals) and non-noxious stimuli (epicritic signals: light touch, temp, and proprioception.); most abundant in Lamina V. (INTERESTING TO US) these cause spinal wind up.

Front 70

Wide Dynamic Range Neurons (WDRN)

Back 70

These neurons can cause “spinal wind up” or “ratchet up” stimulation associated with pain.
After repeated stimulation, WDRN can increase their firing rate without having an increase in intensity from the stimulation.
Increased response results from the same amount of stimulus.
Continuous spontaneous firing occurs even after the stimulus is stopped or removed
mastectomy patients having pain two years later is from spinal wind up. What use to cause pain, now causes 4x the amount of pain. Lamina V involved.

Front 71

PAIN PATHWAY

Back 71

1) pain signals in peripheral sensory nerve --> wind up
2) goes to the thalamus
3) periaqueductal grey matter --> descending inhibition down the spinal cord

Front 72

Spinothalamic Tract

Back 72

Major pain pathway.
Axons of the SON cross the midline to the contralateral side of the spinal cord before they form the Spinothalamic Tract.
Fibers leave the main pathway and enter the recticular formation, raphe magnus and periaqueductal grey matter (response to pain).
Spinothalamic tract is divided into lateral and medial tracts.

Front 73

Lateral Spinothalamic Tract

Back 73

Referred to as the “neospinothalamic tract”
“Neo” means “new.” evolved over time
Projects into the posterior lateral portion of the thalamus.
Lateral spinothalamic tract carries pain and temperature up to the brain.
Carries discriminative aspects of pain, such as location, intensity, and duration. Allows us to identify what pain sensations our patients are feeling.

Front 74

DORSAL HORN LAMINAE

Back 74

I- marginal
II and III- gelatinosa
IV, V, VI- nucleus proprius

Front 75

Medial Spinothalamic Tract

Back 75

Referred to a paleospinothalamic tract
“Paleo” means “older.”
Projects into the medial thalamus.
Mediates the autonomic and unpleasant emotional perceptions of pain. Remembers the pain.

Front 76

Alternative Pathways

Back 76

Some tracts mediate autonomic responses to pain.
Some tracts activate emotional behavior to pain.

Front 77

Ascending Sensory pathway
Also called, the dorsal lemniscal system.
Also called, the posterior column-medial lemniscus pathway .
Also called, the dorsal column-medial lemniscus (DCML) pathway.

Back 77

A sensory pathway responsible for transmitting fine touch, vibration and conscious proprioceptive information from the body to the cerebral cortex via the Cuneatus and Gracilis tracts (toSensory information ascends on the same side before crossing over in the brainstem to the contralateral thalamus.
SSEPs (Somatosensory Evoked Potentials) monitor the ascending sensory pathway.
Up and then it crosses over.
Make friends with these people.
Amplitude and latency everything but opioids effect these.
Some use N2O some don’t.
uch, pressure, vibration).

Front 78

DCML, touch, pressure and position

Back 78

. Spinothalamic, skin temp and pain and is a little more slower.

Front 79

Descending Tracts

Back 79

corticospinal, or pyramidal tracts, and the extrapyramidal tracts.
The pyramidal tracts descend directly without synaptic interruption, from the cerebral cortex to the spinal cord.

Front 80

Dorsolateral funiculus

Back 80

descending tract that modulates pain.
Action potentials in this tract activate the enkephalin-containing neurons of the substantia gelatinosa, which diminish the transmission of pain. (runner’s high)
Stimulation of several areas in the brain (periaqueductal gray, reticular formation, nucleus raphe magnus) activate descending inhibitory pathways. (brains attempt to control the stimulus that we are feeling)

Front 81

Descending Tracts

Back 81

These pathways modulate the incoming stimulus at the dorsal horn.
These areas in the dorsal horn contain high concentrations of endogenous opioid transmitters, including endorphins & enkephalins, which inhibit the incoming pain message.

Front 82

EFFERENT MODULATING PATHWAYS

Back 82

raphespinal, reticulospinal,

Front 83

A posterior left-sided rhizotomy is performed on your patient:

Back 83

Sensations carried in the spinothalamic tract (i.e., pain and temperature) would be lost on the opposite side from the dermatomes at, and below, the level of the rhizotomy.

Front 84

If the right dorsal lemniscal tract is severed, which senses are lost?

Back 84

Touch, pressure and vibratory senses would be lost from the right (same side of the body).

Front 85

If the spinothalamic tract is severed at C2 on the right, what will happen?

Back 85

Loss of pain and temperature transmission on the left side of the body at and below the level of the lesion.

Front 86

If the left lateral spinothalamic tract is severed at C3, which sensations are lost?

Back 86

Pain and Temp sensations on the right side of the body, at and below, C3.

Front 87

Intergration : Sympathetic and Motor systems

Back 87

Somatic and visceral afferents are connected to the skeletal motor and sympathetic systems in the spinal cord.
Afferent dorsal horn neurons synapse with anterior horn motor neurons.
Responsible for reflex muscle activity associated with pain.
Synapses between afferent nociceptive neurons and sympathetic neurons result in reflex sympathetically mediated vasoconstriction, smooth muscle spasm, and the release of catecholamines.

Front 88

Third Order Neurons (TON)

Back 88

Second order neurons synapse with third order neurons in the thalamus
Sends fibers to the somatosensory areas of the cortex.
Somatosensory areas are responsible for evoked potentials, the electrical signals generated by the nervous system in response to sensory stimuli.

Front 89

Chemical mediators of pain

Back 89

There are over 15 different amino acids, peptides and chemicals that act as neurotransmitters in the pain process.
Most neurons contain more than one neurotransmitter that is released at the same time. Anyting that effects pain by either inhibiting or stimulating it. Ex bradykinin, histamine, etc…

Front 90

Excitatory pain-modulating neurotransmitters

Back 90

Glutamate
Aspartate
Vasoactive intestinal polypeptide
Cholecystokinin
Gastric-releasing peptide
Angiotensin
Substance P

Front 91

The most important excitatory peptides

Back 91

Substance P (pain) and calcitonin gene related peptide (CGRP). (CGRP is a powerful arteriolar vasodilator.)

Front 92

most important excitatory amino acid.

Back 92

Glutamate is the most important excitatory amino acid. Transmits pain impulses. Binds to receptors and causes changes in sodium ion channels. (can either increase or decrease the rate of transmission)

Front 93

Inhibitory pain-modulating neurotransmitters

Back 93

Chemical mediators of pain (also called alogens)
Enkephalins
Endorphins
Substance P
Somatostatin

Front 94

Substance P

Back 94

11-amino acid peptide.
Synthesized and released by FON, both peripherally and in the dorsal horn.
Facilitates ascending transmission in pain pathways.
Sensitizes nociceptors. (this is not good)
Causes a release of histamine from mast cells.
Causes a release of serotonin (5-HT hydroxytryptamine) from platelets.
Potent vasodilator.
Chemoattractant for leukocytes.
Just keeping your patient light does a whole lot of stuff as shown by this side

Front 95

Modulation of Pain

Back 95

Occurs peripherally at the nociceptor, in the spinal cord, or in supraspinal structures.
Modulation can either inhibit (suppress) or facilitate (aggravate) pain.
Supraspinal structures fancy word for brain. Specifically the limbic the thalamus and the hypothalamus

Front 96

Peripheral Modulation

Back 96

Nociceptors become oversensitized after repeated stimulation.
Sensitization: enhanced response to noxious stimuli.
Newly-acquired responsiveness to a wider range of stimuli, including non-noxious stimuli.

Front 97

Two types of peripheral modulation

Back 97

Primary hyperalgesia
Primary happens when it is damaged and at the site.

Secondary hyperalgesia

Front 98

Primary Hyperalgesia

Back 98

Hyperalgesia: increased response to noxious stimulation.
Nociceptor sensitization usually occurs from injury or heat.
Results in a decrease in threshold and an increase in the frequency response to the same stimulus intensity. (repeated stimulus that now it hurts worse)
Spontaneous firing occurs even after the cessation of the stimulus.

Front 99

Primary Hyperalgesia

Back 99

Primary hyperalgesia is mediated by the release of alogens from damaged tissues, which contribute to inflammation and associated sensitivity and pain.
Histamine is released from mast cells and platelets.
Bradykinin is released from tissues and causes increased vascular permeability, promotes vasodilation, induces leukocytes, activates nocioceptors, and are potentiated by prostaglandins.
Prostaglandins are produced following tissue damage.

Front 100

Secondary Hyperalgesia

Back 100

Neurogenic inflammation.
Triple response: Redness, edema, and sensitization to noxious stimuli.
Occurs due to the release of prostaglandins and CGRP (calcitonin gene related peptide) from collateral axons of the afferent neuron.
Initially injured.

Front 101

Prostaglandins

Back 101

Potent vasodilators.
Intensify the effects of histamine, serotonin and bradykinins. (synergistically)
Cause increased permeability of blood vessels.
Lead to formation of substance P.

Front 102

How are prostaglandins formed?

Back 102

Tissue damage.
Phospholipase A2 enzyme, which is present in cell membranes, is stimulated by tissue damage.
Activation of phospholipase A2 causes release of arachidonic acid from the phospholipid cell membrane.
Two reaction pathways are catalyzed by the enzymes cyclooxygenase and lipoxygenase.

Front 103

Cyclooxygenase

Back 103

converts arachidonic acid to prostaglandins and prostacyclins , which potentiates the edema from bradykinin.
ASA, NSAID, and COX inhibitors inhibit cyclooxygenase.

Front 104

Lipoxygenase pathway

Back 104

converts arachidonic acid to leukotrienes, which cause increased vascular permeability and release of leukocytes.

Front 105

Central Modulation

Back 105

Exaggerated pain sensation (real but way more than we think is appropriate)
Facilitation: Central sensitization
Inhibition: Segmental and Supraspinal (these can occur to decrease it)

Front 106

Wind-up and sensitization of second order neurons:

Back 106

WDR neurons increase their frequency of discharge with the same stimuli and exhibit prolonged discharge even after stimulus has stopped.

Front 107

Receptor field expansion

Back 107

adjacent neurons become responsive to stimuli.

Front 108

Facilitation of Central Sensitization

Back 108

Wind-up and sensitization of second order neurons: WDR neurons increase their frequency of discharge with the same stimuli and exhibit prolonged discharge even after stimulus has stopped.
Receptor field expansion: adjacent neurons become responsive to stimuli.
Hyperexcitability of flexion reflexes. Spindles contracted and they can’t relax or straighten out.

When someone loses a limb and they still feel it.

Front 109

Causes of Facilitation

Back 109

Neurochemical mediators (i.e., prostaglandins, CGRP, glutamate, kinins, and aspartate) cause membrane changes and changes in intracellular calcium levels.
Glutamate and aspartate play an important role in spinal wind-up via activation of N-methyl-D-aspartate (NMDA) and non-NMDA receptors.
Results in increases in calcium concentration in spinal neurons, which eventually results in a release of prostaglandins.

Front 110

Inhibition

Back 110

Transmission of nociceptive input in the spinal cord can be inhibited by activity in the cord itself, as well as by descending activity from the supraspinal centers.

Front 111

Segmental inhibition

Back 111

A fibers serving epicritic sensation inhibit WDR neurons and spinothalamic tract activity (i.e., the Gate theory.) gates are shut no message gets to the brain and you don’t hurt.
Glycine and gamma aminobutyric acid (GABA) are amino acids that function as inhibitory neurotransmitters.
Inhibition of Glycine and GABA causes facilitation of WDR neurons.

Front 112

Supraspinal Inhibition

Back 112

Several supraspinal structures send fibers down the spinal cord to inhibit pain in the dorsal horn.
Impulses arising in the periventricular and periaquaductal grey are transmitted through the nucleus raphe magnus to the substantia gelatinosa (lamina II) by way of the descending dorsolateral funiculus.
Limbic, hypothalamus, and thalamus, mu, kappa, and delta but primary is Mu1 in the brain. Doesn’t take away the pain but alters the patient’s response to the pain. (opioids , knee is smashed up, they just don’t care about it)

Front 113

Supraspinal Inhibition

Back 113

Enkephalins (may be considered the gate in the gate theory), endorphins, dynorphins, GABA, norepinephrine, oxytocin (bond with their babies, and also causes the uterine contractions and to let down the milk) and relaxin are inhibitory neurotransmitters
These molecules bind to opioid receptors and decrease the release of substance P, resulting in decreased pain.

Front 114

Neural Blockade

Back 114

Local anesthetics (LA) play a major role by manipulating the sympathetic system and its pathways.
Neuraxial administration of LA-opioid mixtures ensures better preservation of pulmonary function, earlier ambulation, earlier physical therapy and lowers the risk for postoperative venous thrombosis.
Pre-emptive analgesia ensures a smoother transition following surgery or manipulation.

Front 115

Chronic Pain Management (CPM

Back 115

Diagnostic & therapeuticneural blockade
Neural blockade with local anesthetics are useful in delineating pain mechanisms.
Facilitates evaluation of the sympathetic nervous system.
Pain relief following diagnostic neural blockade is favorable, indicating relief will be successful.

Front 116

Chronic Pain Management (CPM)
Therapeutic adjuncts

Back 116

include psychological interventions, physical therapy, acupuncture and electrical stimulation
TENS or transcutaneous electrical nerve stimulation
SCS or spinal cord stimulation
Intracerebral stimulation

Front 117

Somatic Blocks for CPM

Back 117

Trigeminal nerve blocks
Facial nerve blocks
Glossophayngeal blocks
Occipital nerve blocks
Phrenic nerve blocks
Suprascapular nerve blocks
Cervical paravertebral nerve blocks (would be useful in the OR)

Front 118

Sympathetic nerve blocks for CPM

Back 118

Cervicothoracic (Stellate) block
Thoracic sympathetic chain block
Celiac plexus block
Splanchic nerve block
Lumbar sympathetic nerve block
Hypogastric plexus block
Ganglion impar block

Front 119

Additional methods of neural blockade for CPM

Back 119

Differential neural blockade
Radiofrequency ablation
Cryoneurolysis
Alcohol & phenol neurolytic blocks

Front 120

What effects are attributed to Mu-1 receptors?

Back 120

Supraspinal analgesia, decreased heart rate, euphoria, and itching.

Front 121

What effects are attributed to Mu-2 receptors?

Back 121

Spinal analgesia, respiratory depression, and addiction.

Front 122

Adjuvant agents

Back 122

Adjuvant agents include antidepressents, anticonvulsants, neuroleptics, corticosteroids, adrenergic agonists, and botulinum toxin.
Alternative methods of treatment include psychological interventions, physical therapy, acupuncture or acupressure, electrical stimulation and Child Life therapy.

Front 123

TRIGEMINAL NERVE BLOCK

Back 123

INDICATIONS: trigeminal neuralgia and intractable cancer pain in the face
PERFORMED ON: gasserian ganglion itself, one of the major divisions (opthalmic, maxillary, or madibular) or one of the smaller branches
ANATOMY: rootlets of CNV arise from the brain stem and join one another to form a crescent-shaped sensory (gasserian) ganglion in Meckel's cave. Most is invested with a dural sleeve. The three subdivisions of the trigeminal nerve arise from the ganglia and exit the cranium separately.

Front 124

GASSERIAN GANGLION BLOCK COMPLICATIONS

Back 124

Horner's syndrome, and motor block of the muscles of mastication. The potential for serious hemorrhage is greatest for blockade for the maxillary nerve. The facial nerve may inadvertently be blocked.

Front 125

FACIAL NERVE BLOCK
(SOMATIC)

Back 125

INDICATIONS: relieve spastic contraction of the facial muscles and to treat herpes zoster affecting this nerve.
ANATOMY: the facial nerve exits the cranium through the stylomastoid foramen, where it can be blocked. A small sensory component supplies special sensation (taste) to the anterior two-thirds of the tongue and general sensation to the tympanic membrane, the external auditory meatus, soft palate, and part of the pharynx.
COMPLICATIONS: if the needle is inserted too deeply past the level of the styloid bone, the glossopharyngeal and vagal nerves may also be blocked.

Front 126

GLOSSOPHARYNGEAL BLOCK
(SOMATIC)

Back 126

INDICATIONS: used for patients with pain due to malignant growths at the base of the tongue, the epiglottis, and palatine tonsils. Also used to distinguish glossopharyngeal neuralgia from trigeminal and geniculate neuralgia.
ANATOMY; exits from the cranium via the jugular foramen medial to the styloid process and courses anteromedially to supply the posterior third of the tongue, pharyngeal muscles, and mucosa. The vagus and spinal accessory nerves also exit the cranium via the jugular foramen and descend alongside the glossopharyngeal nerve.
COMPLICATIONS: dysphagia and vagal blockade resulting in ipsilateral vocal cord paralysis and tachycardia. Block of the accessory nerve and hypoglossal nerves causes ipsilateral paralysis of the trapezius muscle and the tongue, respectively.

Front 127

OCCIPITAL NERVE BLOCK
(SOMATIC)

Back 127

INDICATIONS: patients with occipital H/A and neuralgias
ANATOMY: greater occipital nerve is derived from the dorsal primary rami of the C2 and C3 spinal nerves, whereas the lesser occipital nerve arises from the ventral rami of the same roots.

Front 128

PHRENIC NERVE BLOCK
(SOMATIC)

Back 128

INDICATIONS: may provide relief for pain arising from the central portion of the diaphragm. It can also be useful in patients with refractory hiccups (singultation).
ANATOMY: arises from C3-C5 nerve roots at the lateral border of the anterior scalenus muscle.
COMPLICATIONS: pulmonary compromise may occur in patients with preexisting lung disease or injury. Simultaneous bilateral phrenic nerve block should never be performed.

Front 129

SUPRASCAPULAR NERVE BLOCK (SOMATIC)

Back 129

INDICATIONS: useful for painful conditions arising from the shoulder (most commonly arthritis and bursitis)
ANATOMY; major sensory nerve of the shoulder joint. It arises from the brachial plexus (C4-C6) and passes over the upper border of the scapula in the suprascapular notch to enter the suprascapular fossa.
COMPLICATIONS: pneumothorax if the needle is advanced too far anteriorly. Paralysis of the surpraspinatus and infraspinatus muscles can be troublesome.

Front 130

CERVICAL PARAVERTEBRAL NERVE BLOCK (SOMATIC)

Back 130

INDICATIONS: diagnostic with pain coming from the cervical spine or the shoulder
ANATOMY: cervical spinal nerves lie in the sulcus of the transverse process of their respective vertebral levels. Cervical spinal nerves exit above their respective vertebral levels (unlike the rest which exit inferior to their respective levels)
COMPLICATIONS: unintentional intrathecal, subdural, or epidural anesthesia at this level rapidly causes respiratory paralysis and hypotension. Horner's syndrome, as well as blockade of the recurrent laryngeal and phrenic nerves.

Front 131

THORACIC PARAVERTEBRAL NERVE BLOCK (SOMATIC)

Back 131

INDICATIONS: anesthetizes both the dorsal and ventral rami of spinal nerves. Useful in patients with pain originating from the thoracic spine, thoracic cage, or abdominal wall, including compression fractures, proximal rib fractures, and acute herpes zoster. Must be used for blockade of upper thoracic segments, because the scapula interferes with the intercostal technique at these levels.
ANATOMY: each thoracic root exits from the spinal canal just inferior to the transverse process of its corresponding spinal segment.
COMPLICATIONS: most common is pneumothorax, sympathetic blockade and hypotension may be obtained if multiple segments are blocked or a large volume is injected at one level. CXR is mandatory afterward to r/o pneumothorax.

Front 132

LUMBAR PARAVERTEBRAL SOMATIC NERVE BLOCK

Back 132

INDICATIONS: useful in evaluating pain due to disorders involving the lumbar spine or spinal nerves.
ANATOMY: lumbar spinal nerves enter the psoas compartment as soon as they exit through the intervertebral foramina beneath the transverse process. This compartment is formed by the psoas fascia anteriorly, the quadratus lumborum fascia posteriorly, and the vertebral bodies medially.
COMPLICATIONS: unintentional subarachnoid, subdural, or epidural anesthesia

Front 133

LUMBAR MEDIAL BRANCH AND FACET BLOCKS (SOMATIC)

Back 133

INDICATIONS: may establish the contribution of lumbar facet (zygapophyseal) joint disease in back pain. Corticosteroids are commonly injected with the local anesthetic when the intraarticular technique is chosen.
ANATOMY: each facet joint is innervated by the medial branches of the posterior primarry division of the spinal nerves above and below the joint. Every joint is supplied by two or more adjacent spinal nerves. Each medial branch crosses the upper border of the lower transverse process running a groove between the root of the transverse process and the superior articular process.
COMPLICATIONS: injection into a dural sleeve results in a subarachnoid block, whereas injection near the spinal nerve root results in sensory and motor blockade at that level. Large injections can cause rupture of the joint capsule.

Front 134

TRANS-SACRAL NERVE BLOCK (SOMATIC)

Back 134

INDICATIONS: useful in diagnosis and treatment of pelvic and perineal pain. Blockade of the S1 spinal root can help define its role in back pain.
ANATOMY: five paired sacral spinal nerves and one pair of coccygeal nerves descend in the sacral canal, forming the cauda equina. Each then travels through its respective intervertebral foramen. The S5 and coccygeal nerves exit through the sacral hiatus.
COMPLICATIONS: nerve damage and intravascular injection

Front 135

PUDENDAL NERVE BLOCK (SOMATIC)

Back 135

INDICATIONS: perineal pain
ANATOMY: arises from the S2-S4 and courses between the sacrospinous and the sacrotuberous ligaments to reach the perineum.
COMPLICATIONS: unintentional blockade and intravascular injection are common complications

Front 136

SYMPATHETIC BLOCKS

Back 136

subarachnoid, epidural, and paravertebral. These block both somatic and sympathetic fibers.
INDICATIONS: reflex sympathetic dystrophy, visceral pain, acute herpetic neuralgia, postherpetic pain, and peripheral vascular disease.
CHARACTERIZED by unaltered somatic sensation but loss of sympathetic tone as evidenced by increased cutaneous blood flow and temp. Other tests include loss of the skin conductance (sympathogalvanic) and sweat response (ninhydrin, cobalt blue, or starch tests) following a painful stimulus.

Front 137

CERVICOTHORACIC (STELLATE) BLOCK
(SYMPATHETIC BLOCK)

Back 137

INDICATIONS: head, neck, arm, and upper chest pain. Blocks the upper thoracic as well as all cervical ganglia. Injection of large volumes >10 ml often blocks down to T5 ganglia.
ANATOMY: sympathetic innervation of the head, neck, and most of the arm is derived from four cervical ganglia. The largest is the stellate ganglion which usually represents a fusion of the lower cervical and first thoracic ganglia. The sympathetic supply to the arm in some persons may originate from T2-T3 (kuntzs nerves) that join the brachial plexus high in the axilla, these nerves may be missed by a stellate block but not by an axillary block. The stellate (where u inject) lies posterior to the origin of the vertebral artery from the subclavian artery, anterior to the longus colli muscle and the first rib, anterolateral to the prevertebral fascia, and medial to the scalene muscles.
COMPLICATIONS: hematoma, pneumothorax, epidural anesthesia, brachial plexus block, hoarseness due to blockade of the recurrent laryngeal nerve, and rarely, osteitis or mediastinitis following esophageal puncture.

Front 138

HORNERS SYNDROME

Back 138

ipsilateral ptosis, meiosis, enophthalmos, nasal congestion, and anhidrosis of the neck and face.

Front 139

THORACIC SYMPATHETIC CHAIN BLOCK

Back 139

INDICATIONS: usually not used b/c the sig risk of pneumothorax
-the thoracic sympathetic ganglia lie just lateral to the vertebral bodies and anterior to the spinal nerve roots.

Front 140

CELIAC PLEXUS BLOCK (SYMPATHETIC)

Back 140

INDICATIONS: pain arising from the abdominal viscera, particularly abdominal malignant growths. Usually blocks the lumbar sympathetic chain.
ANATOMY: vary, generally clustered at the level of L1, posterior to the vena cava on the right, just lateral to the aorta on the left, and posterior to the pancreas.
COMPLICATIONS: most common is postural hypotension, which is largely due to blockade of the lumbar sympathetic chain.

Front 141

SPLANCHNIC NERVE BLOCK (SYMPATHETIC)

Back 141

INDICATIONS: less likely to block the lumbar sympathetic chain and req < anesthetic volume.
ANATOMY: 3 groups of splanchnic nerves (greater, lesser, and least) arise from the lower seven thoracic sympathetic ganglia on each side and descend alongside the vertebral bodies to communicate with the celiac ganglia.
COMPLICATIONS: hypotension and possible injuries to the azygos vein on the right or the hemiazygos vein and the thoracic duct on the left.

Front 142

LUMBAR SYMPATHETIC BLOCK

Back 142

INDICATIONS: painful conditions involving the pelvis or the lower extremities, and possibly in some patients with peripheral vascular disease.
ANATOMY: lumbar sympathetic chain contains 3-5 ganglia and is a continuation of the thoracic chain; it also supplies sympathetic fibers to the pelvic plexus and ganglia. Anterior to the psoas muscle and fascia, posterior to the vena cava on the right but is just lateral to the aorta on the left
COMPLICATIONS: somatic nerve block of the lumbar plexus

Front 143

HYPOGASTRIC PLEXUS BLOCK (SYMPATHETIC)

Back 143

INDICATIONS: pain that originates from the pelvis and that is unresponsive to lumbar or caudal epidural blocks. Cancer of the cervix, uterus, bladder, prostate, or rectum, also some women with chronic nonmalignant pelvic pain.
ANATOMY: postgagnlionic fibers derived from the lumbar sympathetic chain, but also visceral sensory fibers from the cervix, uterus, bladder, prostate, and rectum. Superior L5 and inferior S2-S4 (preganglionic parasympathetic fibers)
COMPLICATIONS: transient bowel and bladder dysfunction

Front 144

GANGLION IMPAR BLOCK (SYMPATHETIC)

Back 144

INDICATIONS: patients with visceral or sympathetically maintained pain in the perineal area
ANATOMY: (ganglion of Walther) most caudal part of the sympathetic trunks. the two lowest pelvic sympathetic ganglia often fuse forming one ganglion in the midline just anterior to the coccyx.
COMPLICATIONS: transient bowel or bladder dysfunction

Front 145

DIFFERENTIAL BLOCKADE

Back 145

-Preganglionic sympathetic (B) fibers most sensitive
--> pain (C and A delta) --> somatosensory (A beta) fibers --> motor fibers (A alpha)

Front 146

ALCOHOL BLOCKS

Back 146

INDICATIONS: severe intractable cancer pain, can be associated with morbidity, and are not permanent (temporary destruction of nerve fibers or ganglia can be accomplished)
-ethyl alcohol causes extraction of membrane phospholipids and precipitation of lipoproteins in axons and schwann cells
-causes severe pain on injection
-hypobaric
-preferred for celiac plexus blocks

Front 147

PHENOL BLOCKS

Back 147

painless, preferred for lumbar sympathetic blockade, hyperbaric

Front 148

ANTIDEPRESSANTS

Back 148

-analgesic effect that occurs at a dose lower than needed for their antidepressant action
-both actions are due to blockade of presynaptic reuptake of serotonin, norepi, or both
-older are more effective analgesics
-potentiate opioids
-differ in their S/E (antimuscarinic effects, such as dry mouth (xerostomia), impaired visual accommodation, urinary retention, and constipation; antihistaminic effects (H1 and H2), such as sedation and increased gastric pH, alpha adrenergic blockade resulting in orthostatic hypotension; and a quinidine like effect
-extensive first pass metab and are highly protein bound
-many have active metabolites

Front 149

ANTICONVULSANTS

Back 149

-useful in neuropathic pain, (trigeminal neuralgia and diabetic neuropathy)
-block Na gated channels
-gabapentin, phenytoin, carbamazepine, valproic acid, clonazepam
-highly protein bound and have relatively long half lives
-carbamazepine slow and unpredictable absorption so levels need to be monitored

Front 150

NEUROLEPTICS

Back 150

-useful in neuropathic pain and marked agitation or psychotic symptoms
-most common agents are fluphenazine, haloperidol, chlorpromazine, and perphenazine
-can produce undesirable extrapyramidal side effects, such as mask like faces, a festinating gait, cogwheel rigidty, and bradykinesia
-long term side effects include akathisia (extreme restlessness) and tardive dyskinesia (involuntary choreoathetoid movements of the tongue, lipsmacking, truncal instability)

Front 151

SIGNS OF EXCESS GLUCOCORTICOID ACTIVITY

Back 151

-hypertension, hyperglycemia, increased susceptibility to infection, peptic ulcers, osteoporosis, aseptic necrosis of the femoral head, proximal myopathy, cataracts, and rarely psychosis
(can also develop features of cushings syndrome)

Front 152

SIGNS OF EXCESS MINERALCORTICOID ACTIVITY

Back 152

-sodium retention and hypokalemia and can precipitate CHF