Exam 2 Musculoskeletal/nerves Spring 2024 Flashcards
What is scleroderma?
Inflammation and autoimmune disease that causes vascular injury and vascular obliteration. Chronic hardening and tightening of the skin and connective tissues.
Tissue fibrosis and organ sclerosis.
What are the 3 forms of scleroderma?
- Localized scleroderma- skin, face, distal limb
- Limited cutaneous systems sclerosis - CREST syndrome, has prominent skin manifestations
- Diffuse cutaneous system sclerosis- generalized skin involvement and cardiac complications.
The limited symptoms of scleroderma are referred to as CREST. What does CREST stand for?
S/S of Scleroderma
Skin:
MS:
Nervous System:
CV:
Skin: Taut skin
MS: Limited mobility/contractures, skeletal muscle myopathy
Nervous System: Nerve compression
CV: HTN, PAH, dysrhythmias, vasospasm in small arteries of fingers, CHF,CAD,
S/S of Scleroderma
Pulmonary:
Renal:
GI:
Pulmonary: Diffuse interstitial pulmonary fibrosis, decreased pulmonary compliance (stiff lungs)
Renal: Decreased renal blood flow and systemic HTN
GI: Xerostomia, poor dentition, fibrosis of GI tract (no Reglan, will not stimulate fibrotic GI tract), reflux
Scleroderma Treatment?
for reflux?
for Raynauds?
for PH?
- PPIs for reflux
- CCBs for Raynaud’s & vasospasms
- ACEIs for Renal protection (The only tx shown to alter the course of scleroderma is ACE inhibitors to treat scleroderma renal crisis)
(note: ACE-I cause angioedema & increased coughing)
- Prostacyclins or phosphodiesterase inhibitors, oxygen, anticoagulation, and diuretics for Pulmonary HTN
- Digoxin to Improve CO
- Immunosuppressive and steroid therapy targeted toward affected organ involvement: Skin, lung, cardiac, and muscle
SclerodermaAnesthesia Management and Considerations
Airway:
IV:
Pulmonary:
GI:
Eyes:
Other:
Airway: Mandibular motion, small mouth opening, neck ROM (do not manipulate neck while asleep), oral bleeding
CV: IV/arterial line access may be difficult, use US.
Pulmonary: Decreased pulmonary compliance and reserve, avoid increasing PVR (do not make them hypoxic)
GI: Aspiration
Eyes: tape eyes, ointment, gauze, goggles
Other: Regional anesthesia may be best for these patients, keep patient warm, VTE prophylaxis, Positioning with care, Pulse ox difficulties (ear probe)
What is Pseudohypertrophy Muscular Dystrophy/ Duchenne Muscular Dystrophy (DMD)
Mutation in the dystrophin gene (x-linked recessive) causes fatty infiltration leading to pseudohypertrophic muscles.
Common in 2-5 y/o boys
By age 8-10 Wheelchair bound
Usually live until ages 20-25 years (CHF, pneumonia)
large protein that plays a major role in stabilization of the muscle membrane and signaling between the cytoskeleton and extracellular matrix
Dystrophin
Initial symptoms of Duchenne Muscular Dystrophy
Initial symptoms: waddling gait, frequent falling, difficulty climbing stairs, tiptoes.
Duchenne Muscular DystrophyS/S
CNS:
MS:
CV:
Pulmonary:
GI:
CNS: Intellectual disability
MS: Kyphoscoliosis, skeletal muscle atrophy, serum CK 20-100x normal d/t increase muscle permeability
CV: Sinus tachycardia, cardiomyopathy, EKG abnormalities (tall R-wave in V1)
Pulmonary: OSA, weakened respiratory muscles, and cough
GI: Hypomotility, gastroparesis
Duchenne Muscular Dystrophy Anesthesia Management
Airway:
Pulmonary:
CV:
GI:
Airway: weak laryngeal reflexes and cough - consider increased secretions, possible ventilatory support
Up to 36 hours post-op
Pulmonary: weakened muscles, Will need Oral airways or nasal airways. Need to be woken up on CPAP or BIPAP
CV: Pre-op EKG and/or echo based on the severity
GI: Delayed gastric emptying, aspiration risk
Other anesthesia management for Duchenne Muscular DystrophyAnesthesia:
What drug do you want to avoid?
When do you want to extubate these patients?
What type of incidence are higher in these patients?
What type of anesthesia may be best?
Avoid succinylcholine can cause hyperkalemia and rhabdomyolysis. Use NDMR (Rocuronium).
Pharyngeal and respiratory muscle weakness, secure the airway. Make sure the patient is fully awake.
MH – increased incidence. Have Dantrolene ready. Use TIVA as an alternative
Regional Anesthesia may be best than GA.
What is Myasthenia Gravis?
A chronic autoimmune disorder involving the NMJ. There will be decreased functional post-synaptic AChreceptors.
Muscle weakness w/ rapid exhaustion of voluntary muscles. Partial recovery with rest.
ACh receptor-binding antibodies are linked to thymus abnormalities.
Myasthenia Gravis S/S
Eyes:
Oral:
Pulmonary:
Skeletal:
Heart:
Endocrine:
Ptosis (droopy eyelid), diplopia (double vision)
Dysarthria (slurred speech), dysphagia, and difficulty handling saliva
Isolated respiratory failure (rare)
Arm, leg, or trunk muscle weakness
Myocarditis
Autoimmune diseases associated
RA, SLE, pernicious anemia, hyperthyroidism
Myasthenic Crisis vs Cholinergic Crisis?
What is the effect of the Edrophonium/Tensilon Test in each condition?
Myasthenic crisis:
D/t drug resistance or insufficient drug therapy
S/S: severe muscle weakness and respiratory failure
Cholinergic crisis (SLUDGE):
D/t excessive anticholinesterase treatment
S/S: muscarinic side effects – profound muscle weakness, salivation, miosis, bradycardia, diarrhea, abdominal pain
Edrophonium/Tensilon Test:
1-2 mg IVPof edrophonium will improve the myasthenic crisis and makes the cholinergic crisis worse.
Myasthenia GravisTreatment
(first-line treatment): ?
surgical ?
Anticholinesterases:
The first line of treatment
Pyridostigmine last longer than neostigmine
Thymectomy:
Induces remission
Reduced use of immunosuppressives
Reduces ACh receptor antibody levels
Full benefit delayed (2-6 months)
MG treatment immunosuppression-wise?
Immunosuppression:
Corticosteroids, azathioprine, cyclosporine,mycophenolate
Indicated when skeletal muscle weakness is notadequately controlled by anticholinesterase drugs
Corticosteroids–most commonly usedand mostconsistently effective treatment
Immunotherapy :
Plasmapheresis: short-term clinical improvement
Removes antibodies from circulation . Repeated tx increases risk of infection, hypotension, and pulmonary embolism
Immunoglobulin: short term, No effect on circulating concentrations of ACh receptor antibodies
Myasthenia GravisAnesthesia Management
Weakened ________ effort
Marked sensitivity to ______
Resistance to ____________
Weakened pulmonary effort (Aspiration risk)
Marked sensitivity to nondepolarizing muscle relaxants (decrease amount). Use nerve stimulator and titrate to nerve stimulator
Resistance to succinylcholine (might need a higher dose for effect, but this can lead patients into MG Crisis, just avoid using Sux)
What is Osteoarthritis?
The most common joint disease in the ____?
OA is characterized by _________ inflammation.
Does stiffness fade throughout the day?
Degenerative process affecting articular cartilage, the most common joint disease in the elderly.
Characterized by minimal inflammation usually a result of chronic joint trauma (sports), biomechanical stresses, joint injury, abnormal joint loading, neuropathy, ligament injury, muscle atrophy, and obesity.
Pain present with motion,relieved by rest. Morning stiffness fades throughout the day. (T-rex)
What joints will osteoarthritis affect?
Weight-bearing and distal interphalangeal joints.
Heberden nodes- Distal interphalangeal joints, first knuckle (pictured)
Protrusion of the nucleus pulposus (herniated disc) can lead to compression of nerve roots.
Degenerative disease – vertebral bodies and intervertebral disks. OA will affect the breakdown of the cartilage of the joints and discs in the neck and lower back. Middle to lower C-spine and L-spine.
Heberden nodes?
Heberden nodes- Distal interphalangeal joints, first knuckle (pictured)
OsteoarthritisTreatment
PT and exercise
Maintaining muscle function
Pain relief - heat, simple analgesics, anti-inflammatory drugs, transcutaneous nerve stimulator, acupuncture. OA patients are typically NOT on corticosteroids
Joint replacement surgery - necessary when pain is debilitating
OsteoarthritisAnesthesia Management
Airway
Be aware of limited ROM, and keep them comfortable.
Document the patient’s position on the OR table.
Don’t lean on the patient.
What is Rheumatoid Arthritis?
which joints affected?
IG present in how many pts
An autoimmune-mediated, systemic inflammatory disease that usually affects the proximal interphalangeal and metacarpophalangeal joints (2nd & 3rd knuckle).
2-3x higher in woman than men
Rheumatoid nodules at pressure points (elbows)
Rheumatoid factor (IG antibody present in 90% of patients with RA)
Characteristics of Rheumatoid Arthritis
Single or multiple joints
Painful synovial inflammation, swelling, and increased fluid
Morning stiffness like OA, but remains stiff throughout the entire day.
Symmetrical distribution of several joints.
Fusiform swelling - Joints become enlarged and the fingers crooked (pictured)
Synovitis of the temporomandibular joint (decrease mouth opening)
Affects nearly all joints (except the t-spine and lumbosacral spine)
Rheumatoid Arthritis S/S
Atlantoaxial subluxation:
Cricoarytenoid arthritis:
Osteoporosis
NM
Atlantoaxial subluxation instability (C1 and C2) (>3 mm separation): Odontoid process (dens) protrudes into the foramen magnum. The instability can place pressure on the transverse ligament and spinal cord. Instability can also impair vertebral artery blood flow.
Cricoarytenoid arthritis:
Acute – hoarseness, dyspnea, and stridor w/ tenderness over the larynx; swelling and redness of arytenoids
Chronic – asymptomatic or variable degrees of hoarseness, dyspnea, and upper airway obstruction
Osteoporosis: More common in women than men
NM: Weakened skeletal muscles (peripheral neuropathies)
Rheumatoid ArthritisS/S
CV:
Pulmonary:
Hematology:
Dryness:
CV: Pericarditis, accelerated coronary atherosclerosis
Pulmonary: Restrictive lung changes, decrease Vt
Hematology: anemia, neutropenia, elevated platelets
Dryness: Keratoconjunctivitis sicca (dry eyes) and xerostomia (dry mouth)
Rheumatoid ArthritisTreatment
NSAIDS
- Decrease joint swelling, relieve stiffness, provide analgesia
- COX-1 inhibitors, COX-2 inhibitors
Corticosteroids
- Decrease joint swelling, pain, and morning stiffness
DMARDs (Disease-modifying antirheumatic drugs)
- Halt or slow disease progression (might take 2-6 months to work)
Ex: Methotrexate (anti-inflammatory)
Tumor necrosis factor (TNF-alpha) inhibitors & interleukin (IL-1) inhibitors
- TNF-alpha inhibitors have faster onset than DMARDs
- IL-1 inhibitors: slower onset than TNF and less effective
Surgery
Intractable pain, impairment of joint function, joint stabilization
Total replacement
Rheumatoid Arthritis Anesthesia Management
Airway- Atlantoaxial subluxation: minimize movement of head and neck during DL; evaluate vertebral artery interference
- TMJ limitation : fiberoptic or video laryngoscopy
- Cricoarytenoid joints: hoarseness or stridor; or observation of erythema or edema of the vocal cords during DL
Severe rheumatoid lung disease-PFTs, ABGs, post-op vent may be needed
Protect eyes - Keratoconjunctivitis sicca (dry eyes)
Stress dose of corticosteriod
What is Systemic Lupus Erythematosus?
Typical Manifestation:
Multisystem chronic inflammation characterized by antinuclear antibody production.
- Common in young women & African Americans; ages 15 to 40
Typical manifestations (Usually will have 3 out 5 of the following):
1. Antinuclear antibodies
2. Malar rash (butterfly rash)
3. Thrombocytopenia
3. Serositis- inflammation of a serous membrane around the organ
5. Nephritis
Systemic Lupus Erythematosus S/S
Join/Spine:
CNS:
CV:
Pulmonary:
Renal:
Joint/Spine: Polyarthritis and dermatitis, symmetrical arthritis (most common sx), no spinal involvement, avascular necrosis of the femoral head or condyle
CNS: Cognitive dysfunction, psychological changes
CV: Pericarditis, coronary atherosclerosis, Raynaud’s
Pulmonary: Lupus pneumonia, restrictive lung disease, vanishing lung syndrome
Renal: Glomerulonephritis, decreased GFR, risk of renal failure
Systemic Lupus ErythematosusS/S
GI/Liver:
NM:
Hematology:
Skin:
GI/Liver: ABD pain, pancreatitis, elevated liver enzymes
NM: Skeletal muscle weakness
Hematology: Thromboembolism, thrombocytopenia, hemolytic anemia,
Skin: Butterfly-shaped malar rash, **Discoidlupuslesions, which are thick and disk-shaped. **
Systemic Lupus ErythematosusTreatment
NSAIDs or ASA - will treat arthritis and serositis
Anti-malarial (Hydroxychloroquine and quinacrine) - will treat arthritis and dermatological manifestations
Corticosteroids- The development and progression of coronary atherosclerosis is accelerated by treatment with corticosteroids.
Immunosuppressants better alternative than high-dose steroid(Methotrexate, azathioprine)
Systemic Lupus ErythematosusAnesthesia Management
Based upon manifestations and organ dysfunction
Airway: recurrent laryngeal nerve palsy (common), cricoarytenoid arthritis
Stress dose of corticosteroids
What is recurrent laryngeal nerve palsy?
How does lupus cause recurrent laryngeal nerve palsy?
A condition where the nerve that controls the muscles of the larynx (voice box) is damaged, which can lead to problems with speaking, breathing, and swallowing.
In lupus, the immune system attacks healthy tissues, including the nerves. This can lead to inflammation of the laryngeal nerve or blood vessels, which can cause them to become compressed or damaged.
What is Malignant Hyperthermia?
Hypermetabolic syndrome involving a genetic mutation to the Ryanodine receptor - RYR1 gene or Dihydropyridine receptor
Caused by exposure to inhaled VA and succinylcholine (50% mortality, investigate family history)
Uncontrolled elevation of sarcoplasmic calcium
Sustained activation of muscle contraction
Rhabdomyolysis
when do you first see MH in kids?
tonsillectomy
It is the sustained high levels of sarcoplasmic Ca2+that ….
rapidly drives skeletal muscle into a hypermetabolic state that may proceed to severe rhabdomyolysis.
The rigidity that is frequently seen during a fulminant MH episode is the result of…
The inability of the Ca2+pumps and transporters to reduce the unbound sarcoplasmic Ca2+below the contractile threshold (10–6M)
Malignant HyperthermiaNon-triggering Agents
Malignant HyperthermiaS/S
Early Sign:Elevated end-tidal CO2
Tachypnea and/or tachycardia
Generalized muscle rigidity
Mixed metabolic and respiratory acidosis
MASSETER SPASM – muscle for mastication Masseter spasm if succinylcholine has been used
- also caused by etomidate
Malignant HyperthermiaTreatment
D/C all triggering gas/drugs
Hyperventilate with 100% O2 at 10 L/min
Change breathing circuit and soda lime
Dantrolene (Have someone else do this, hard to mix)
20 mgj vial + 3 G mannitol (Mix with 60 mL sterile water)
Initial dose 2.5 mg/kg
Max upper limit 10 mg/kg
Treat arrhythmias
ICE, cool them down
Monitor urine output
Malignant HyperthermiaPost-Op
Transfer to ICU 24-48 hours
Report to MH registry
MH testing for pt and family members:
**Muscle biopsy contracture testing
Diagnosis relies on the caffeine–halothane contracture test,measuring contraction forces upon exposure of muscle to caffeine or halothane
What type of anesthesia would be used if you know the patient has a history of MH?
Use TIVA and go slow.
Where is the cervical plexus located?
It is located in the posterior triangle of the neck, halfway up the sternocleidomastoid muscle, and within the prevertebral layer of cervical fascia.
- The plexus is formed by the anterior rami (divisions) of cervical spinal nerves C1-C4.
What is the Stellate Ganglion?
- a collection of sympathetic nerves found anterior to the neck of the first rib.
Stellate ganglion block indication - refractory angina
- scleroderma
- it is star-shaped (“stellate” meaning star-shaped)
- When blocking the stellate ganglion: we have horner’s syndrome
- Downside: carotid artery and phrenic nerve are running along the stellate ganglion. So it can be dangerous
What is Horner’s Syndrome?
- Partial ptosis (drooping or falling of the upper eyelid)
- Miosis (constricted pupil)
- Facial anhidrosis (absence of sweating) due to a disruption in the sympathetic nerve supply: Anhidrosis, only on the side where it is blocked
- Phrenic Nerve Blockade - Horner’s syndrome results from paralysis of the ipsilateral sympathetic cervical chain (stellate ganglion)
- caused by blockade of stellate
- associated with blockade of phrenic, which gives breathing issues
What and where is the brachial plexus?
- The brachial plexus is a network of nerve fibers that supplies the skin and musculature of the upper limb.
- It begins in the root of the neck, passes through the axilla, and runs through the entire upper extremity.
- The plexus is formed by the anterior rami (divisions) of cervical spinal nerves C5, C6, C7 and C8, & T1.
Axillary nerves
Spinal roots: C5 and C6.
Sensory functions: Gives rise to the upper lateral cutaneous nerve of arm, which innervates the skin over the lower deltoid (‘regimental badge area’).
Motor functions: Innervates the teres minor and deltoid muscles.
Musculocutaneous nerves
Nerve roots – C5-C7.
Motor functions – muscles in the anterior compartment of the arm (coracobrachialis, biceps brachii and the brachialis).
Sensory functions – gives rise to the lateral cutaneous nerve of forearm, which innervates the lateral aspect of the forearm.
Ulnar Nerve
Spinal roots: C8-T1.
Motor functions:
Two muscles of the anterior forearm – flexor carpi ulnaris and medial half of flexor digitorum profundus
Intrinsic muscles of the hand (apart from the thenar muscles and two lateral lumbricals)
Sensory functions: Medial one and half fingers and the associated palm area.
Radial nerve
Nerve roots – C5-T1.
Sensory – Innervates most of the skin of the posterior forearm, the lateral aspect of the dorsum of the hand, and the dorsal surface of the lateral three and a half digits.
Motor – Innervates the triceps brachii and the extensor muscles in the forearm.
Lumbar Plexus :
The anterior rami of the L1-L4 spinal roots divide into several cords. These cords then combine together to form the six major peripheral nerves of the lumbar plexus. These nerves then descend down the posterior abdominal wall to reach the lower limb, where they innervate their target structures.
A useful memory aid for the branches of the lumbar plexus is: I, I Get Leftovers On Fridays. This stands for the Iliohypogastric, Ilioinguinal, Genitofemoral, Lateral cutaneous nerve of the thigh, Obturator and Femoral.
Iliohypogastric nerve:
The iliohypogastric nerve is the first major branch of the lumbar plexus. It runs to the iliac crest, across the quadratus lumborum muscle of the posterior abdominal wall. It then perforates the transversus abdominis, and divides into its terminal branches.
Roots: L1 (with contributions from T12).
Motor Functions: Innervates the internal oblique and transversus abdominis.
Sensory Functions: Innervates the posterolateral gluteal skin in the pubic region. (Tip: an easy way to remember that the IlioHypogastric comes before the IlioInguinal is that Hcomes before I in the alphabet!)
Ilioinguinal nerve:
The ilioinguinal nerve follows the same anatomical course as the larger iliohypogastric nerve. After innervating the muscles of the anterior abdominal wall, it passes through the superficial inguinal ring to innervate the skin of the genitalia and middle thigh.
Roots: L1.
Motor Functions: Innervates the internal oblique and transversus abdominis.
Sensory Functions: Innervates the skin on the superior antero-medial thigh. In males, it also supplies the skin over the root of the penis and anterior scrotum. In females, it supplies the skin over mons pubis and labia majora.
Lateral Femoral Cutaneous Nerve
This nerve has a purely sensory function. It enters the thigh at the lateral aspect of the inguinal ligament, where it provides cutaneous innervation to the skin there.
Roots: L2, L3
Motor Functions: None.
Sensory Functions: Innervates the anterior and lateral thigh down to the level of the knee.
Obturator nerve
Roots: L2, L3, L4.
Motor Functions: Innervates the muscles of the medial thigh – the obturator externus, adductor longus, adductor brevis, adductor magnus and gracilis.
Sensory Functions: Innervates the skin over the medial thigh.
Femoral nerve
Roots: L2, L3, L4.
Motor Functions: Innervates the muscles of the anterior thigh – the illiacus, pectineus, sartorius and quadriceps femoris.
Sensory Functions: Innervates the skin on the anterior thigh and the medial leg.
Sacral plexus nerve
The sacral plexus is a network of nerve fibers that supplies the skin and muscles of the pelvis and lower limb. It is located on the surface of the posterior pelvic wall, anterior to the piriformis muscle.
The plexus is formed by the anterior rami (divisions) of the sacral spinal nerves S1, S2, S3 and S4. It also receives contributions from the lumbar spinal nerves L4 and L5.
Sciatic nerve:
The sciatic nerve is a major nerve of the lower limb. It is a thick flat band, approximately 2cm wide – the largest nerve in the body.
Nerve roots: L4-S3.
Motor functions:
Innervates the muscles of the posterior thigh (biceps femoris, semimembranosus and semitendinosus) and the hamstring portion of the adductor magnus (remaining portion of which is supplied by the obturator nerve).
Indirectly innervates (via its terminal branches) all the muscles of the leg and foot.
Sensory functions: No direct sensory functions. Indirectly innervates (via its terminal branches) the skin of the lateral leg, heel, and both the dorsal and plantar surfaces of the foot
Median Nerve
Nerve roots: C6 – T1 (also contains fibers from C5 in some individuals).
Motor functions: Innervates the flexor and pronator muscles in the anterior compartment of the forearm (except the flexor carpi ulnaris and part of the flexor digitorum profundus, innervated by the ulnar nerve). Also supplies innervation to the thenar muscles and lateral two lumbricals in the hand.
Sensory functions: Gives rise to the palmar cutaneous branch, which innervates the lateral aspect of the palm, and the digital cutaneous branch, which innervates the lateral three and a half fingers on the anterior (palmar) surface of the hand.
What is C5-7 (Interscalene) ?
Part of brachial plexus
Covers shoulder
On US image on right: shows how close we are to important things
Downside: sits around carotid and vertebral artery, stellate ganglion, phrenic nerve
When you deposit local anesthetic here… you can block everything else as well
