Anesthesia/Analgesia Flashcards
What is the definition of suffering
“an experience of unpleasantness and aversion associated with perception of harm or threat of harm in an individual”
What is a primal alert signal
Linked to animals need to maintain homeostasis
Designed to alert animals to threats to these needs being met and drive aversive and adaptive behaviors
What are the four most common clinical signs associated with illness
- Fever 2. Lethargy 3. Anorexia, 4. Cachexia
What can sleep deprivation lead to
Systemic hypertension, higher mortality
What are 8 palliative measures in ICU for suffering
1) Provide adequate opportunity for uninterrupted sleep
-Low lighting overnight when feasible
2) Clustering treatments to minimize patient awakenings
3) Addressing thirst, hunger, and pain
4) Small amount of oral liquids to maintain membrane moisture -
5) Serial monitoring for pain
6) Vigilance for nausea
7) Nebulized furosemide may provide symptomatic relief from dyspnea as may opioid administration
8) Get patients outside for portion of the day to express normal behaviors
Definition of pain
an unpleasant sensory and emotional experience associated with actual or potential tissue damage.
10 consequences of uncontrolled pain
- increased blood pressure and heart rate
- peripheral vasoconstriction
- increased metabolic rate and oxygen consumption
- decreased immune function
- Immobility
- decreased pulmonary function and atelectasis
- increased incidence of pneumonia
- Inappetence
- Restlessness
- Insomnia
What is the four goal of treating pain
- relieve patient suffering
- promote healing
- decrease length of hospitalization
- minimize long-term changes to the animal
What are physiological 4 parameters of pain
HR, RR, BP and pupil dilation
What is a measurable physiologic parameter and how does it relate to pain
Heart rate variability: variation in R-R interval obtained on ECG
Changes in parasympathetic and sympathetic nervous system tone have bigger impacts on high and low frequency components
Low HRV suggests dominance of once branch of ANS , typically the SNS if the evaluation made during noxious stimulation, stress, exercise
Correlated to chronic pain but not acute pain
What are endocrine markers of pain
epinephrine, NE, and cortisol
What are 10 altered behaviors of animals when in pain? Give an example of each
- Posture
-Hunched back, base-wide stance position, prayer position (neck and head extended forward with front of body lowered to the ground), head and/or tail tucked under the body, tension and rigidity of the painful area, frequent position changes, reluctance to assume normal body positions (e.g., will not lie down, sit or stand when they normally would) - Gait
-Stiff, lameness, reluctance to move - Abnormal movements
-Shaking, trembling
4.Interaction
Reducing willingness to interact with people
- Demeanor
Some animals become aggressive, some submissive
6.Attention to painful area
-Looking and staring, guarding, licking, chewing, and biting, self mutilation
- Palpation to painful area
Turn or flinch, withdrawal, or escaping effort to biting and aggression when applying pressure - Vocalization
-Altered vocalizatio patterns - Appetite
-hyporexia/anorexia - Grooming
-Excessive grooming or chewing
-In cats appropriate grooming decreased
What are two types of pain scales
Unidimensional and Multidimensional
What’s a unidimensional pain scale and what are its cons
Simple descriptive scale, numeric rating, scale, and visual analog scale
Poor interobserver agreement and sensitivity
Name 7 multidimensional scales and which ones are not validated?
1) 4AVetscale (validated for orthopedic pain)
2) Glasgow composite measure pian score (CMPS-C)
-validated for acute pain
3) Glasgow composite measure pain score short form
-validated for acute postop pain
4) university of melbourne pain scale
-acute pain
5) CSU pain scale
-not validated
6) UNESP-botucatu Multidimensional composite pain scale for cats
-validated
7) Glasgow composite measure pain score feline
-validated
What is an action unit in pain
unique changes in facial expression produced by facial muscle activity
Involuntary and cannot be properly suppressed, amplified or stimulated
What are three AU’s in cats
Bases of pinane moving away, dorsal movement of the nose, mouth, and cheek area, and eyes narrowing
In a study of 351 dogs and cats hospitalized in the ICU, ___% were prescribed analgesics, and in __% of those cases, drug administration deviated from prescribed orders (__% decreased dose and ___% increased dose).
In a study of 351 dogs and cats hospitalized in the ICU, 39% were prescribed analgesics, and in 36% of those cases, drug administration deviated from prescribed orders (62% decreased dose and 38% increased dose).
In above study What were reasons in above study for decreased dosing
sedation, hypothermia, hypotension, perceived absence of pain, and lack of access to controlled drugs.
In above study what were reasons for increased dosing
perceived pain, vocalizing, and anxiety.
What % PCV is necessary for adequate oxygen carrying capacity and oxygen delivery?
> 25%
During anesthesia PCV can decrease by how much %?
3-5%
What anesthetic protocols should be considered and administered for patient with renal insufficiency
Higher fluid rate may be required to maintain renal perfusion
Drugs excreted by kidney (ketamine in cats) may have delayed excretion
What anesthetic protocols should be considered and administered for patient with hepatic disease
Anesthetic protocols may be affected due to decreased glucose and albumin production, altered drug metabolism via cytochrome P-450 and decreased production of coagulation factors
What anesthetic protocols should be considered and administered for patient with cardiac disease
Avoid fluid overload
Monitor BP carefully because hypotension may come from decompensation
MOA for anticholinergic?
competitively inhibits acetylcholine or other cholinergic stimulants at postganglionic parasympathetic neuroeffector sites
Side effects of anticholinergics?
May make secretions more viscous
Increase anatomic dead space
Increase heart rate
Can increase myocardial work and oxygen consumption
Increase IOP, pupillary dilation
Glycopyrrolate does not cross blood–brain barrier or the placenta
Which U agonist has NMDA antagonist properties
Methadone
Pros and Cons of full u agonist
Complete reversal with naloxone
Analgesic- good for chronic and neuropathic pain
Minimal effect on CV performance
Give anticholinergic drug before starting CRI
Monitor for hyperthermia in cats
Cause respiratory depression
Cause bradycardia
Reduce reuptake of norepinephrine and serotonin, possible serotonin syndrome
morphine and meperidine cause histamine release => hypotension
GI effects
Pros and cons of partial u agonist
Slow onset, effects difficult to reverse
Good for moderate pain
Pros and cons of k agonist/u antagonist
Partial reversal of µ-agonist drugs
Minimal CV effects
Not good for severe pain
MOA of ketamine
binds N-methyl-D-aspartate (NMDA) receptors, reducing receptor activity and release of glutamate, an excitatory neurotransmitter
Pros and Cons of Ketamine
Cause salivation
Increase heart rate, CO via centrally mediated sympathetic response and endogenous catecholamine release, usually CV sparing
Increase ICP and intraoccular pressure
Analgesic
Renal elimination in cat
Cautious use in cats with HCM b/c increased cardiac contractility
Direct myocardial depressant effects in debilitated patients with decreased endogenous catecholamine response +. Hypotension and CV instability
Potential seizure as sole agent
doesn’t depress laryngeal protective reflexes and produces less ventilatory depression than opiods
Prevents response to nociceptive stimulie carried by p ain neurons
MOA of benzodiazepines
antagonism of serotonin
increased release of and/or facilitation of gamma-aminobutyric acid (GABA) activity
diminished release or turnover of acetylcholine in the CNS.
MOA of phenothiazines
block postsynaptic dopamine receptors in the CNS and may inhibit the release of dopamine and increase its turnover rate
alpha 1 receptor blockade
Pros and cons of phenothiazine
Vasodilatory
Long duration of action
Not analgesic
MOA of barbiturates
act directly on the CNS neurons in a manner similar to that of the inhibitory transmitter GABA
Pros and Cons of barbiturates
Cause cardiovascular depression
Cause respiratory depression
Provide rapid induction
Decrease ICP and intraoccular pressure
Effects may be potentiated by concurrent acidosis or hypoproteinemia
MOA of propofol
Potentiates the effects of gamma-aminobutyric acid (GABA; an inhibitory neurotransmitter) by decreasing the rate of dissociation of GABA from its receptors.
This prolonged binding results in an influx of chloride, causing hyperpolarization of the postsynaptic cell membrane.
Propofol may also have activity at the glycine and N-methyl-D-aspartate (NMDA) receptors, but this is unclear.
Pros and Cons of Propofol
Rapidly acting with short duration of action
Causes respiratory depression
Causes peripheral vasodilation
Myocardial depressant
Can create arrhythmias
Not analgesic
Use with caution in patients with volume depletion or cardiovascular compromise; can cause significant depression
Increases ICP
Can cause Heinz body anemia in cats
MOA of etomidate
Acts at the GABA receptor in the CNS to increase chloride conductance, causing hyper-polarization of postsynaptic neurons and resulting in hypnosis and CNS depression
Pros and cons of etomidate
Maintains cardiovascular stability
Not used alone: otherwise retching and myoclonus
Suppresses adrenocortical function for 2–6 hr following single bolus dose
in cats repeated use => hemolysis due to propylene glycol
How are alpha 2 agonists metabolized
biotransformed by the liver, with inactive metabolites excreted in the urine
Pros and cons of alpha 2 agonist
Causes cardiovascular depression
Can cause vomiting
Provides good sedation and analgesia
diuresis
peripheral vasoconcstriction
bradycardia
muscle relaxation
Can be combined with butorphanol or ketamine
MOA of alfaxalone
neuroactive steroid, binds to and activates the GABA cell surface receptor, inducing postsynaptic cell membrane hyperpolarization by activating chloride ion transport and enhancing the inhibitory action of GABA in the CNS.
How is alfaxalone metabolized
undergoes phase I (cytochrome P450-dependent) and phase II (conjugation-dependent) metabolism in both species.27 Cats and dogs form the same 5 phase I metabolites. Phase II metabolites in cats are alfaxalone sulfate and alfaxalone glucuronide, with only alfaxalone glucuronide found in dogs. Alfaxalone metabolites are likely to be eliminated from dogs and cats by hepatic/fecal and renal routes, which is similar to other species studied.
MOA of Lidocaine in analgesia
reducing ectopic activity of damaged afferent neurons, action at different molecular sites, such as Na+, Ca2+, and K+ channels and N-methyl-D-aspartate (NMDA) receptors.
MOA of inhalants
Acts on GAB receptors and voltage-gated channels
Pros and cons of inhalants
Produces dose-dependent cardiovascular depression and peripheral vasodilation
Anesthesia depth can be adjusted rapidly
Potential for hypoxemia
Isoflurane and sevoflurane show rapid uptake and recovery
Nitrous oxide should be used with caution with closed gas spaces
Why is propoflo 28 not recommended in ill cats
Has benzyl alcohol as preservative which can be toxic when given in large doses
low capacity for glucuronic acid conjugation and therefore have limited ability to metabolize benzoic acid.
What drug should be avoided in splenic tumor/fracture patients and why?
acepromazine, thiopental, and propofol can result in splenomegaly.
What monitoring should you do during anesthesia?
Monitor ECG for changes in HR and rhythm
MAP > 60 mmHG to maintain renal perfusion
Perfusion parameters: CRT, MM, pulse quality
Depth
Oxygenation
Capnography
UOP
Temperature
Bloodwork (PCV/TP, BG in critical patietns)
What features do you look at in depth
eye position
pupil size
jaw tone
response to stimulus
heart rate
blood pressure
respiratory rate
Pulse ox will read less than 100% when PaO2 falls under ____
140 mmHg
Steps to trouble shoot intraoperative hypotension
First step decrease inhalant
Next fluid bolus
Inotropic/vasopressor support
Add second agent
What is the goal of pain control?
state in which the pain is bearable but some of the protective aspects of pain, such as inhibiting use of a fractured leg, still remain
Where do opioids react (central, peripheral, transduction)?
centrally
MOA of naloxone
bind to the same receptor as agonists but cause no effect and can competitively displace the agonist from the receptor and therefore reverse the agonist effect
Which opioids reach a maximal effect at upper end of dose rang
butorphanol and buprenorphine
How is remifentanil metabolized
tisseu plasma esterases
Duration of action of fentanyl?
30 min an up to 2 hours when Im or SC
Adverse effects of simbadol
hyperthermia, hypotension, bradycardia, or tachycardia
Side effects of naloxone
acute pain, excitement, emergence delirium, aggression, and hyperalgesia
What’s the benefit of using butorphanol as a reversal agent
that complete reversal of analgesia does not occur due to the κ-agonist effects of butorphanol. has sedative effects still
Why is buprenorphine not as easily reversed
difficult to displace form receptor
Draw arachidonic acid pathway
How do nsaids decrease pain
NSAIDs decrease the pain input to the CNS, which may aggravate central hypersensitivity.
Inhibition of COX enzyme isoforms decreases inflammation
Which COX pathway responsible for basal prostaglandin production and normal homeostatic processes
Cox 1
Where are alpha 2 adrenergic agonists metabolized
biotransformed by the liver, with inactive metabolites excreted in the urine
Cons of atipamazole
abrupt hypotension and/or aggression
What can affect efficacy of fantanyl patch
Taken up by dermal blood flow
Hair, obesity and hypovolemic or hypothermic patients can alter
What are adverse effects of bupivicaine
arrhythmias, reduced CO diaphragmatic paralsyis
How does nocita work
multi-vesicular liposomes encapsulating bupivacaine
gradually released over several hours as the lipid bilayers break down
Adverse effects epidural
vasodilation and subsequent hypotension
vomiting, urinary retention, pruritus, and delayed hair growth at the clipped epidural site
Contraindications for epidural analgesia
include trauma over the pelvic region (with loss of appropriate landmarks), sepsis, coagulopathy, CNS disease, skin infection over the site of injection, hypovolemic shock, and severe obesity.
Complications of epidural catheter
catheter dislodgement, discharge from the site, fecal contamination, line or filter breakage, and localized dermatitis.
Why do you use lower dose if epidural goes into subarachinoid space
The lower dose is sufficient for an analgesic response because the roots of the spinal cord are more accessible within the subarachnoid space, where they are not protected by the dura
Why is lidocaine beneficial to ischemia re-perfusion injury
inhibiting Na+/Ca2+ exchange and Ca2+ accumulation during ischemia, scavenging hydroxyl radicals, decreasing the release of superoxide from granulocytes, and decreasing polymorphonuclear leukocyte activation, migration into ischemic tissues, and subsequent endothelial dysfunction
What % of human patients will experience ICUAW and can be u to 6 months
As much as 50% of muscle strength can be lost within 1 week of immobility
What are benefits of rehabilitation therapy in critically ill patients
- Decrease loss of muscle mass and strength
- Maintain functional ability
- Decrease pain and inflammation
- Improve healing time
- Reduce edema
- Improve ventilation and circulation
- Positive psychological benefits
- Prevent injury
- Decrease hospitalization time
- Guide post hospitalization home care
How does laser therapy work
photobiomodulation, involves the direct application of light energy (photons) to induce cellular responses in tissues
photons are absorbed by the cytochrome c complex in the mitochondria of target cells, which results in a biological cascade of events, including accelerated production of ATP, nitric oxide, and reactive oxygen species
reduces pain, inflamamtion, heals, improves muscle repair
Where are contraindicated areas of treatment for laser therapy
neoplastic lesions, near a pregnant uterus, gonads, or cornea, near the presence of active bleeding, the endocrine glands, and active epiphyses.
What’s Transcutaneous Electrical Nerve Stimulation
TENS is the application of high-frequency electrical current through electrodes placed on the skin.
TENS activates large cutaneous Aβ fibers, which is believed to stimulate inhibitory neurons in the spinal cord dorsal horn, interfering with transmission of C nerve fiber pain impulses to the brain (also known as the gate theory)
What is pulsed electromagnetic field therapy
a device that transmits a nonthermal electromagnetic field when applied over an area of tissue to reduce pain and inflammation
increase intracellular Ca2+, which leads to increased calcium binding to calmodulin. It is believed that this reaction leads to a variety of downstream pathways, including the production of nitric oxide
Contraindications to pulsed electromagnetic field therapy
not advisable to apply PEMF over tumor sites of hemangiosarcoma due to a potential increase in blood flow. Similarly, it should not be used with animals that have a pacemaker because of potential electrical interference.
What is cryotherapy
application of cold to tissues, results in vasoconstriction, which decreases local blood flow, inflammatory response, and edema, thereby reducing pain
Pain relieving effects are achieved by slowing of nerve conduction velocity, increasing pain threshold and pain tolerance
What is thermotherapy
Results in vasodilation, promotion of circulation of blood and lymphatics, edema reduction, release of muscular tension and spasm, pain reduction, and improved tissue elasticity
How does Prom help
diffusion of nutrients from synovial fluid to cartilage, improves circulation and flexibility, and reduces the tension of periarticular muscles.
In patients with femoral fractures, PROM is required to prevent quadriceps
What are three kinds of massage
1.Stroking 2. Effleurage 3. Petrissage
What is stroking massage
slow gliding movement over the body using the palm of the hand in the direction of fur growth, cranial to caudal and proximal to distal
What is effleurage massage
helps with fluid mobilization and lymphatic drainage; the palms of the whole hand are used for long strokes with light to moderate pressure distal to proximal and along the direction of muscle fibers towards the flow of lymphatic and drainage back to the heart.
Where should
massage not be performed
areas of active infection or acute inflammation, near a tumor, over open wounds, in cases of deep vein thrombosis or coagulopathies, in patients with unstable fractures, over painful areas, in patients in shock, and animals adversely reactive to touch
What is neuromuscular electrical stimulation
low frequency, high pulse duration electrical stimulation to the muscles percutaneously through electrodes placed on the skin.
The current acts on motor nerves to achieve muscle contraction.
When is neuromuscular electrical stimulation contra-indicated
pacemaker patients or seizure disorders
Application is not recommended over areas of neoplasia, infection, impaired sensation or skin damage, thrombosis or thrombophlebitis, directly over the heart, carotid sinus, or trunk during pregnancy
Benefits of active movement
Active movement allows for natural joint motion and muscle contractions to maintain muscle strength and joint health
What are rehab options for pulmonary therapy
Positioning-alternating recumbency
Postural drainage
Pervussion
What is definition of pain
Unpleasant sensory and emotional experience associated with actual or potential tissue damage
What is nociception
Neural process of encoding noxious stimuli. Conscious perception of pain
What is physiologic pain
Noxious stimuli associated with the risk of injury
Proportional to stimulus intensity
Transient and characterized by a high stimulus threshold and narrow localization
Protective; Induces withdrawal reflexes and avoidance responses
What is pathologic pain
Persistent noxious stimuli perpetuated by
inflammation or nerve damage
Implies that tissue damage has already occurred
Exaggerated pain response (Hyperalgesia) either at the site of injury or surrounding areas (Extraterritorial pain)
What is adaptive pain
Transient normal response to tissue damage; confers tissue protection
Encompasses physiologic and pathologic pain
What is maladaptive pain
Alteration of spinal cord and brain function from prolonged stimulus
Decrease of peripheral threshold of nociceptor
Altered neuronal gene expression and increased spinal neuron responsiveness
Secondary to inadequate management of adaptive pain
What is allodynia
pain caused by a stimulus that doesn’t normally result in pain
what is analgesia
absence of pain in response to stimulation that would normally be painful
Causalgia
syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion, often combined with vasomotor and sudomotor dysfunction and later trophic changes
What is distress
acute anxiety or pain
Dysphoria
state of anxiety or restlessness, often accompanied by vocalization
Hyperalgesia
Increased response to a stimulus that is normally painful
What is paresthesia
abnromal sensation, whether spontaneous or evoked
What is the Pathway of Nociception
Perception/Transduction
-Nociceptors
Transmission
-sensorry nerve fibers
Modulation
-spinal cord and brain
Conduction and central integration
-pain perception
Draw pathway of nociception
What are the nociceptors in perception and transduction
Nociceptors in cutaneous tissue, muscles and viscera
What are the stimuli of nociceptors in perception and transduction
temperature, chemical ligands and mechanical shearing forces
How do nociceptors stimulate pain
Activation of nonselective ion channels gated = Na+/Ca+ ion influx
Voltage-gated Na+ channel activated, leading to large Na+ influx and further depolarization
What are chemical ligands that initiate nociception
Chemical ligands: pH, prostaglandins, leukotrienes, capsaicin, bradykinins, serotonin, anandamide, olvanil, resiniferatoxin
What are the three transmission-sensory nerve fibers
Aβ fibers
A δ fibers
C fibers
What do Aβ fibers do?
Conducts nonnoxious stimuli (Touch, vibration, pressure, rapid movement)
Large myelinated fibers activated by low-intensity stimuli
What are A δ fibers
Responsible for sensation of physiologic pain, fast pain or ‘first pain’
-Sharp, localized, transient
Small receptive fields and high-threshold
Thermal and mechanical input
Small myelinated fibers, rapidly conducting
What are C fibers
Responsible for slow pathologic pain (Poorly localized, dull/aching or burning sensation)
Polymodal (Activated by thermal, mechanical and chemical stimuli)
Most of the cutaneous nociceptic innervation
-Also found extensively in the muscles and viscera
Large receptive field, slow conduction (Non-myelinated)
Where do sensory fibers synapse for modulcaton
dorsal horn of spinal cord
What molecules inhibits transmission of nociceptive stimuli
GABA, glycine, endogenous opioid peptides (Encephalin and endorphins) inhibits transmission of nociceptive stimuli
What are three principal pathways of modulation
- local interneurons (excitatory and inhibitory)
- neurons of segmental spinal reflexes
- Neurons that projects to supraspinal structures
-wide dynamic range (WDR) neurons, nociceptive specific neurons
What is the principal excitatory synaptic neurotransmitter (spinal cord and brain)? what are the receptors
glutamate and tachykinin
What is glutamate’s receptor
NMDA, ampa, kainite
Intense stimulation required to overcome Mg2+-mediated receptor blockade- Pain remains after stimulus has disappeared
Where is tachykinin released, and what does it mediate
c fibers, mediates pathologic pain
What three area is Central Integration
- Brain stem (Medulla) and midbrain (Periaqueductal grey matter)
- Hypothalamus
- Cortex
What three actions does brain stem and midbrain do in central integration
Cardiorespiratory center alert responses
Motor and emotional responses
Alertness mechanisms (Fight-or-flight response)
What does hypothalamus do in central integration
Control of the autonomous nervous system response
Hormone release for stress control
What does cortex in central integration
Pain perception (Quality, location, intensity and duration)
Generation of complex emotional response
What causes peripheral sensitization
- Tissue inflammation
- Allodynia
- Hyperalesia
How does tissue inflammation cause peripheral sensitization
Release of chemical ligands (H+, K+, ATP, proteases, COX-2, serotonin, histamine, chemokins and cytokines)
Lowers threshold of activation for A-δ and C-fiber
Recruits silent nociceptors
How does central sensitization “wind up”occur
NMDA receptor dishinibition and glial cell activation
How does nmda receptor dishinibition occur
Caused by repeated depolarization of the dorsal horn neurons
NMDA stimulation leads to intracellular Ca2+ mobilization → Increased glutamate responsiveness
↑ Dorsal horn neuron excitability
↓ Spinal cord neuron inhibition
How does glial cell activation occur
Proinflammatory mediator production after nerve trauma
Role in reduction of opioid efficacy
Three reasons to control pain
- sympathetic tone increase
- Counterregulatory hormone and RAAS activation
- Behavioral changes
What does sympathetic tone increase do in pain
Proinflammatory mediator production after nerve trauma
Role in reduction of opioid efficacy
What doe counter regulatory hormone and RAAS activation do in pain control
Cortisol, glucagon, ADH, growth hormone and IL-1 secretion, inhibition of insulin release
Catabolic state
-Hyperglycemia, proteolysis, lipolysis, sodium and water retention, decreased GFR, Immunosuppression, decreased wound healing
Which analgesics medications inhibit perception?
Anesthetics
Opiods
alpha 2 agonists
benzodiazepines
Phenothiozines
Which analgesics medications inhibit modulation?
Local anesthetics
opioids
alpha 2 agonists
tricyclic antidepressants
cholinesterase inhibitors
NMDA antagonsits
NSAIDS
Anticonvulsants
Which analgesics medications inhibit transmission
Local anesthetics
alpha 2 agonists
Which analgesics medications inhibit transduction
local anesthetics
opiods
NSAIDS
Corticosteroids
When to use local blocks?
Enhance analgesia, lead to less use of systemic agents, decrease pain and wind up pain when used preemptively
What are 6 types of loco-regional anesthesia
- Topical or surface
- Infiltrative
- Regional
- Neuraxial
- Intraarticular
- IV regional
What is an epidural? vs spinal?
Administration of drugs into epidural (extra-dural) space.
Spinal = subarachnoid space
What is the site of action for epidural
the nerve roots as they leave the spinal cord and travel out from the intervertebral foramina
Describe how to perform an epidural
- Patient placed in sternal recumbence
- Clip an area a tthe lumbosacral junction.
- Aseptically prepare the skin
- After washing hands and while donning sterile gloves palpate the wings of the ilium with your thumb and middle finger. Using index finger palpate the spinous process of 7th lumbar vertebra
- Slide the index finger caudally down spinous process until LS space is palpable between L7 and S1
- Keeping index finger in place insert a 20-22 gauage, 1.5 to 2.0 inch spinal needle perpendicular to the skin on midline
- Advance needle to through ligamentum flavum usually a “pop” can be felt
- remove stylet and confirm placement with hanging drop “fill hub of needle with saline and fluid in needle should rop into epidural space”
- observe needle for blood
- slowly inject local anesthetic of choice , should be no resistance
- remove needle
What are three layers for epidural
Skin -Fascia- ligamentum flavum
What are contraindications for epidural
- Infection at the site (wounds/contamination)
- Coagulopathy
- Hypotension/hypovolemia
- Trauma in the region of injection
- CNS disease/increased ICP
