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Co-existing Test 1 > Anesthesia and Musculoskeletal Diseases > Flashcards

Anesthesia and Musculoskeletal Diseases Flashcards

1
Q

What is Ehlers-Danlos Syndrome?

A
  • Joint hypermobility and lacity d/o
  • congenital
  • bleeding tendency
  • can have spontaneous rupture bowel, uterus, large arteries
    • increased risk during pregnancy
  • risk for pneumo
  • regional is not recommended d/t high incidence of hemtatome
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2
Q

Overview of scleroderma?

A
  • Inflammation and autoimmunity, vascular injury, fibrosis
  • generally affects females
  • pregnancy may accerlearte symptoms
  • unknown etiology, no treatment available
  • Can lead to CREST syndrome
  • Multi system effects
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3
Q

What is CREST syndrome?

A

afflict scleroderma patient

  • Calcinosis
  • Raynaud’s phenomenon
  • Esophageal hypomotility
  • Sclerodactyly (hand stiffness)
  • Tangelectasia (bunch of blood vessels inside body/skin lesion)
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4
Q

How does scleroderma affect skin and musculoskeletal system?

Anesthesia implications?

A
  • Skin- limited mobility; flexion contractures; thickened taut skin
    • dififcult IV placement
    • difficult regional
    • small oral aperture- difficult to open mouth
      • potential difficult airway- may need fiberoptic
  • Musculoskeletal: myopathy, proximal skeletal muscle weakeness
    • neck ROM issue, positioning issues
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5
Q

What are some CNS effects of scleroderma?

ENT effects?

Anesthesia implications?

A
  • Thickened connective tissue around nerve sheath leading to neuropathy, high incidence trigeminal neuralgia
    • may be on opioids for trigeminal neuralgia, may have upregulated opioid receptors
    • if there’s chronic wasting/weakness in muscles, may need avoid succiniylcholine if poor activity tolerance
    • document any existing neuropathies
  • ENT- dry eyes, oral/nasal tanglectasia, dry mouth
    • avoid OPA/NPA
    • Protect eyes!
    • fiberoptic intubation
    • patient will most likely have sore throat when waking up
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6
Q

CV effects scleroderm?

Pulmonary?

Anesthesia implications?

A
  • CV:
    • myocardial tissue replaced with fibrotic tissue,
    • conduction abnormalities
    • contracted vascular volume
      • from book- may produce hypotension during induction of anesthesia when anesthetic drugs with vasodilating properties exert their effects
    • high incidence of pulm hypotension,
      • avoid n2o, anything that increases pulmonary vascular resistance (avoid Hypercarbia, hypoxia)
    • vasopasm’s- raynauds
      • keep patient warm to prevent vasospasm’s
      • may see vasospasm on a-line
        • if you lose art line with no change ETCO2, probably art line issue
        • if lose art line and ETCO2 down- then bad news! probably cv collapse
  • Pulmonary:
    • fibrosis,
      • may have baseline o2 requirement
    • restrictive pattern,
    • decreased compliance
      • may need decreased TV and faster RR
    • careful with opioids!
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7
Q

What are some GI effects of scleroderma?

Renal effects?

Anesthesia implications?

A
  • GI:
    • dysphagia
      • increased risk aspiraiton
    • hypomotlity of lower esopagus and small intestine
    • lower esophageal tone decreased= regurg symptoms and increased risk aspiration
      • give prophylactics (antacid, PPI)
      • May need RSI
    • malabsorption
      • may need vit K if absorption issues
  • Renal
    • renal hypertension (ACE inhibitors effective)
      • assess renal preop, may need to change antibiotics
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8
Q

Broad overview lupus?

A
  • Multisystem inflammatory disease characterized by immune-mediated tissue damage
  • Mainly females (1:1000)
  • Presence of HTN and nephritis: poor prognosis
  • Onset of SLE may be drug induced (milder form)
    • hydralazine, procainamide, isoniazid, methyldopa
    • slow acetylators at risk
  • Physiologic stress may exacerbate the disease
    • sx, infection, pregnancy
      • poor fetal outcomes
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9
Q

Diagnosis of SLE?

A

Dx

  • Antinuclear antibodies (95% of pt with SLE) (aka ANA)
  • Rash
  • Thrombocytopenia
  • Serositis
  • Nephritis
  • Raynaud’s
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10
Q

What are some general effects in the body from inflammation and vasculities from SLE?

A
  • Vessel wall thickening, weakeneing, narrowing, scarring
    • CAD, stroke risk
  • HTN
  • Pulm HTN
  • Thromboembolism
  • Hypercoagulable state
  • femolytic anemia
  • frequent fevers
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11
Q

What are some skin, joint and muscle manifestations of SLE?

Anesthesia implications?

A
  • Skin
    • Butterfly rash with nasal erythema (50%)
    • oral and pharyngeal ulcers
      • avoid OPA/NPA
  • Joints/muscle
    • symmetrical arthritis (90%)
      • no spinal involvement
      • migratory and episodic
    • circoarytenoid arthritis
      • dififcult intubation
    • AVN
    • Myopathy
    • tendon ruptures
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12
Q

Airway effects of SLE? Pulmonary effects?

Consideration for anesthesia?

A
  • Laryngeal involvement in up to 1/3 patients
    • mucosal irritaiton
    • laryngeal erythema and edema common
    • circoarytenoid arthritis
    • recurrent laryngeal nerve palsy
  • Lungs
    • “lupus pneumonia”
      • diffuse pulmonary infiltrates, pleural effusion, dry cough, dyspnea, arterial hypoxemia
    • restrictive pattern
      • lower TV and higher RR may be needed for ventilation
    • Recurrent atelectasis (phrenic nerve neuropathy)
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13
Q

What effect does Lupus have on renal system? Hepatic effects?Anesthesia considerations?

A
  • Glomerulonephritis leading to nephrotic syndrome (protein in urine) and renal failure
    • check renal status, may need to alter abx other drugs
  • Liver
    • biliary cirrhosis
    • autoimmune hepatitis
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14
Q

What are some CNS effects of lupus?

A

1/3 have cognitive symptoms

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15
Q

Treatment for mild SLE? Severe?

A

Mild

  • NSAIDS for join symptoms and pleurisy
  • low dose corticosteroids such as prednison
  • antimalarial drugs (hydroxycholoroquine/quinacrine) and low dose corticosteroids for thrombocytopenia, hemolytic anemai, skin and arthritis symptoms
    • from John’s Hopkins: Anti-malarial medications help to control lupus in several ways by modulating the immune system without predisposing you to infection. Anti-malarials can protect against UV light and sometimes even improve skin lesions that do not respond to treatment with topical therapy

Severe

  • High dose coritocsteroids (need stress dose?)
    • chronic steroids- CAD accelerated
  • Immunosuppressive/chemo drugs
    • methotrexate, cyclophosphamide, azathioprine, mycophenolate
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16
Q

What is the current data on stress dose steroids in periop setting?

A
  • If patient already on steroids, continue at usual dose if possible
  • data supporting admin of stress dose limites, deicison to administer stress dose depends on procedure
  • small procedure (dental work, skin bx) no stress dose necessary
  • moderate proceudres give 25 mg hydrocortisone every 8 hours, then taper over 1-2 days
  • Major sx give 50 mg hydrocortisone every 8 hours, then taper over 2-3 days.
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17
Q

What are some considerations for neuraxial and regional nerve blocks in SLE?

A
  • Currently taking atnicaog or known caogulopathy
    • want to see PLT, coags before regional
  • presence of peripheral nerve lesion
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18
Q

Anesthetic considerations for SLE?

(non-med related?)

A
  • Interactions with drugs used in SLE treatment
  • degree of organ dysfunction
    • impaired renal
    • hepatic clearance of drugs
    • cardiopulmonary involvement
  • Strict asepsis with invasive procedures
    • reduce the already increased risk of infection
  • Maintain normothermia
    • may reduce risk of infection
    • lessening impact of raynaud’s if present
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19
Q

How can some of your anesthesia drugs be affected in SLE?

A
  • Most commonly used drugs in anesthesia are at least partly dependent on renal excretion for elimination
    • dose/frequency may need to be modified to prevent accumulation of drug
  • IV Agents
    • pharmacokinetics prop/etomidate- not sig affected by renal impairment
    • Benzos- undergo hepatic metabolism and conjugation prior to elimination in urine
    • Opioids- accumulation of morphine and meperidine metabolites prolong resp depression
  • Volatile agents- ideal due to lack of dependenc eon kidney for elimination
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20
Q

What is rhuematoid arthritis?

A
  • Chronic, systemic inflammatory disorder/auto-immune with articular and systemic involvement
    • characterized by exacerbations and remissions
    • affects about 1% of adults (females>males)
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21
Q

What is RA’s manifestations in joints/spine?

A

Symmetrical poly-arthritis in joints

  • Early disease- may need special protection/padding for joints
    • hand
    • wrists
    • feet
    • ankles
  • Later progression- may need special protection for joints
    • knees
    • elbows
    • shoulders
  • TMJ
  • Cerival spine (atlantoaxial instability and cord compression)
    • make sure patient goes into sniffing position on own or maintain head neutral. may need glidescope
    • tenderness on laryngeal palpation, hoarseness can be indication of cricoarytenoid arthritis
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22
Q

What are some extra-articular manifestations of rheumatoid arthritis?

A
  • Skin- special protection needed?
    • raynaud’s- keep warm
    • digital necrosis
  • eyes
    • scleritis
    • corneal ulceration- protect eyes
  • kidney- Look at BUN/Cr
    • interstitial fibrosis
    • glomerulonephritis
    • amyloid deposition
  • peripheral nervous system
    • compression syndromes
    • mononeuritis
  • Central nervous system
    • dural nodules
    • necrotizing vasculities
  • liver
    • hepatitis
  • blood
    • anemia- assess CBC
    • leukpenia
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23
Q

What are some cardiac manifestations of rheumatoid arthritis?

A
  • Dysrhythmia from rhumatoid nodules in the cardiac conduction system
  • cardaic valve fibrosis
  • pericarditis
  • myocarditis
  • coronary artery arteritis
  • dilation of aortic root- aortic regurg
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24
Q

What are some pulmonary manifestations of rheumatoid arthritis?

A
  • Pleural effusion and restirctive lung disease due to rheumatoid nodules in the lung tissue
    • decreased lung volume
      • look at PFTs
    • pulmonary fibrosis (Rare)
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25
Q

What are treatment options for rheumatoid arthritis?

A
  • Drugs to treat inflammation/pain
    • ASA
    • NSAIDS
      • chronic nsaid use might affect coagulation
    • corticosteroids (acute periods only)
  • DMARDS- alter immune response and slow disease progression. DO NOT GIVE DMARD WITH NSAID
    • methotrexate< check LFT/CBC
    • azathioprine
    • antimalrial drugs
    • minocyclin
    • TNF inhibitors/MAD
  • SX treatment
    • relieve pain and restore joint funciton
    • tendon release procedure, synovectomy, joint replacmenet
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26
Q

What are some considerations when evaluating/managing the airway of someone with RA?

A
  • Document preop ROM limits, baseline symptoms of pain, numbness, weakness
  • consider awake fiberoptic intubation
  • TMJ-
    • assess mouth opening
    • may be limids
    • TMJ with cervical spine immobility may limit DL visualization
  • Cricoarytenoid joints
    • fixation may present as voice changes or hoarseness
    • arthritis and inflammation can make glottic opening difficult to ID or stenotic
    • cricoarytenoid joint arthritis requiring decreased tube size
    • minimal edema may lead to airway obstruction postoperatively
  • Atlantoaxial instability
27
Q

What are some considerations for the c-spine in patient with RA?

A
  • Atlantoaxial subluxation (AAS)
    • distance between ant arch of atlas to odontoid process >3mm on radiologic imaging (during neck extension)
    • occurs in 25% severe RA patients
    • risk of cervical spinal cord/medulla compression by odontoid process and interference with vertebral artery blood flow
    • determine head positions AWAKE that can be tolerated
    • enquire about tingling of hands/feet, pain and assess ROM
    • AVOID EXCESSIVE MOVEMENT DURIGN LARYNGOSOCPY
28
Q

How does RA affect management of anesthesia?

A
  • Anemia of chronic disease
  • effect of meds on PLT function
  • with lung DX
    • PFT/intraop ABG/post op vent support
  • may need corticosteroids
  • extubate with caution in those with cricoarytenoid arthritis
29
Q

What is the pathogenesis of osteoarthritis?

A
  • commonly referred to as degenerative joint disease (DJD)”wear and tear”
  • Hallmark is degerneration of articular cartilage
  • most commonly hip/knee
  • differ from RA in that there is minimal inflammatory reaction
  • typically in middle/lower cervical and lower lumbar
    • associated protrustion of nucleus pulposus resulting in nerve root compression
  • occurs in weight bearing joints or conditions that put undue stress on joint
    • obesity
    • joint deformity
30
Q

Anesthetic considerations for osteoarthritis?

A
  • positioning
    • support affected joints
    • position to minimize risk of injury
  • drugs used in treatment
    • corticosteroids not recommended
    • NSAIDS and ASA
      • potential bleeding issues
31
Q

What are anesthetic considerations specifically during reconstructive joint surgery?

A
  • Bone cement (polymethylmethacrylate or PMMA)
    • “cement” is a misnomer, not bonding two things together
  • Bone cement implantation syndrome (fat and marrow embolisms)
    • hypoxia (increased pulm shunt
    • hypotension
    • dysrhythmia
    • pulm hypertension
    • decreased CO
32
Q

What are anesthetic considerations with tourniquet use?

A
  • Provides a bloodless field that greatly facilitates surgery
  • inflation pressure usually aboug 100 mmHg over systolic blood pressure
    • prolonged inflation >2h, pain, nerve damage
    • be careful not to over administer opioids for touniquet pain!
      • better to admin esmolol to temporarily decrease BP
  • Deflation
    • hemodynamic changes
    • washout of accumulated metabolic wastes
      • can cause drop in BP
33
Q

What is pathophys of myasthenia gravis?

A

Autoimmune destruction of postsynaptic acetylcholine receptors at NMJ (up to 80% loss)

  • characterized by weakness and rapid exhaustion of skeletal muscle
    • particularly those innervated by cranial nerves (ocular, pharyngeal and laryngeal)
  • course marked by exacerbations & remissions
  • 1:7500 (women 20-30 and men >60 yo)
  • sx, infection, stress and pregnancy lead to exacerbations
  • association with thrmic hyperplasia and thymoma
34
Q

What are some clinical features of myasthetnia gravis?

A
  • Mild to severe weakness
    • Class I = mild
    • class IV= severe
  • ocular muscle most commonly affected
    • ptosis, dysphagia, and diplopia (most common initial complains)
  • Bulbar involvement/laryngeal and pharyngeal muscle weakness
    • difficulty clearing secretions
    • pulm aspiraiton
  • myocarditis possible
    • afib, heart block, CMP
  • Severe dx associated with asymmetrical proximal muscle weakeness (no atrophy though)
    • neck, shoulder, respiratory muscles affected
35
Q

Treatment for myasthenia gravis?

A
  • Usually oral anticholinesterase with or without steroid therapy
    • Cholinesterase inhbiitors (PO Pyridostigmine)
      • onset 30 min, peak 2 hours, DOA 3-6 HR
      • Higher dose can paradoxically enhance muscle weakeness= “cholinergic criss”
    • Corticosteroids- prednisone limits antibody production (second line therapy after failure of above)
  • Thymectomy- sx approach
    • can be cure for some pts
      • median sternotomy or mediastinoscopy
  • Plasmapheresis- removes antibodies during crisis (temporary)
    • depletes plasma esterase levels
    • prolonged effect of succ, mivacurium, ester linked LA etc
36
Q

Anesthetic considerations for mysthenia gravis?

A
  • Elective surgery only during remission
  • premedication/opioids minimized or avoided
    • prone to weakness
    • aminoglycoside antibiotics can enhance weakness
  • Induction
    • ​short acting agents (ie prop)
    • consider intubation without muscle paralysis
      • intubation with deep volatile agent may be sufficient<– synergistic effects with MR
      • topical lidocaine application to airway
      • if using NDMB, should use PNS at obicularis oculi (may overestimate block)
  • Aspiration risk- consier RSI
    • may need higher does succinylcholine (2mg/kg) to overcome resistance, but prolonged effect should be anticipated
    • if succinylcholine is used- do not use NDMR until muscle function has returned–> phase II block
37
Q

Anesthetic considerations for mainetnace and emergence with myasthetnia gravis?

A
  • Maintenance
    • deep anesthesia with volatile agent can provide sufficient relaxation for many surgical procedures
  • Emergence
    • at great risk for postop respiratory failure
    • advise patient may awaken with ETT in place
    • careful evaluation of vent function prior to extubation
    • close observation in recovery
38
Q

What is myasthenic syndrome?

A
  • Referred to as Lambert-Eaton myasthenic syndrome (LEMS)
  • presents with proximal muscle weakeness
  • develops in association wiht a neoplasm, but also seen with other ocult malignancies or idiopathic autoimmune
    • usually small cell carcinoma of lung
  • Disorder results form presynaptic side defect of NM transmsission
    • IgG antibodies form agianst presynaptic voltage gate calcium channel
      • decreased release of ACh
    • If tumor present, these antibodies are directed at the tumor but cross-react with calcium channels
      • when tumor resolves, symptoms resolve
39
Q

What are some clinical features of myasthenic syndrome?

Where is weakness typically noted?

How are hemodynamics potentially affected?

A
  • Proximal muscle weakness (most central muscles)
    • typically begin with lower extremities, spreads ot upper limbs, bulbar, respriatory muscles
    • change in gait, ability to stand, climb stairs
    • exercise improves strength
  • Autonomic dysfunction very common
    • hemodynamic instability
    • dry mouth
    • urinary hesitancy
40
Q

What are anesthesia considerations for mysthenic syndrome?

A
  • May be undiagnosed. suspect in bronc, mediastinosocpy, thoracoscopy for suspected lung Ca
  • unlike myasthenia gravis, LEMS pts are very sensitive to both depolarizing and nondepolarizing NM blocker
    • AChe drugs not helpful in these disease and may not effectively reverse clinical effects of NDMR
  • Volatile agnets alone often sufficient to provide muscle relaxation for both inbuation and surgical procedures
  • NMBAs should only be givne in small increments and with careful NM monitoring
41
Q

What are manifestation, affected gender, co-existing patho conditions, and response to muscle relaxants in myasthenic syndromes vs myasthenia gravis

A

MYASTHENIC SYNDROME

  • Manifestations- proximal limb weakenss (legs more than arms), exercise improves strength, muscle pain common, reflexes absent/decreased
  • Gender- affects male more htan femlas
  • Co-exist condition: small cell lung Ca
  • Response to muscle relaxants
    • ​sensitive to sucicnylcholine AND non depolarizing MR
    • Poor response anticholinesterases

MYASTHENIA GRAVIS

  • Manifestations- extraocular, bulbar and facial muscle weakness; exercise causes fatigue; muscle pain unommon
  • Gender: affects females more often than males
  • Co-existing patho conditon- thymoma
  • Reponse to MR-
    • ​resistant to succinylcholine (need more! up to 2mg/kg)
    • sensitive to nondepolarizing MR
    • Good response to anticholinesterases
42
Q

What is pathophys behind muscular dystophy?

A
  • A range of congenital muscular disorders characterized by progressive weakness and degeneration of muscle
    • affected individuals produce abnormal dystrophin
      • protein found on sarcolemma of muscle fibers
      • increased permeability of skeletal muscle precedes symptoms
  • Painless degeneraiton
  • atrophy of skeletal muscle
  • Classified according to inheritane
    • x-linked: Duchenne’s (psudohypertrophic) and Becker
      • most common
    • autosomal recessive: limb-girdle, congenital
    • autosomal dominant: facioscapulohumeral, oculopharyngeal
43
Q

What is the most common and severe form of MD?

gender affected?

characterized by?

Prognosis?

A
  • Duchenne’s (pseudohypertrophic)
  • ALmost exclusively male
    • incidence 1-3 per 10,000 live male births
    • presents between 2-5 yo
  • Characterized by symmetric proximal muscle weakness manifesting in gait disturbance
    • pelvic girdle
    • psudohypertrophic- fatty infiltration
  • Kyphoscoliosis results form progressiv eweakness and contractures
    • muscle weakness pronoucnced in proximal extremities
    • wheelchair by age 8-10
    • fatal by 20 yo
44
Q

What are some cardiac dysfunctions associated with muscular dystrophy?

Anesthesia considerations?

A
  • Degeneration of cardiac muscle- may see cardiopulmonary depresison with volatile anesthetics
    • ECG abnormalities
      • atrial arrhythmias
      • prolonged PR interval
    • Decreased myocardial contractility and CMP
    • Mitral regurg secondary to papillary muscle dysfunction
45
Q

What are some pulmonary issues associated with muscular dystrophy?

A
  • Chonic weakness of inspiratory muscles
    • decreased ability to cough and clear secretions
  • Frequent pulmonary infections
    • ​anticipate post op pulmonary dysfunction
  • kyphoscoliosis and muscle degernation lead ot severe restrictive disease pattern
  • sleep apnea is common
  • pulmonary hypertension with disease progression
46
Q

Preop Anesthetia considerations with muscular dystrophy?

A
  • Muscle weakness, cardiac and pulm involvement
  • preop sedation/opioids best avoided
    • resp muscle and laryngela reflex weakness
    • gastric hypomotility
  • aspiration prophylaxis
    • antacid with H2 blocker or PPI
    • Prokinetic like reglan to reduce volume
    • antisialogogue like glyco if secretions are an issue
  • Positioning can be complicated by kyphoscoliosis and flexion contractures
47
Q

Anesthesia considerations during induction for muscular dystophy?

A
  • Succinylcholine contraindicated
    • risk of inducing severe hyperkalemia, rhabdomyolysis, v fib and cardiac arrest
    • malignant hyperthemia risk
48
Q

Anesthesia considerations during maintenance for muscular dystophy?

A
  • Marked cardiopulmonary depression may be seen with voltaile anesthetics
  • normal to prolonged resposne to NDMR
  • Anticipate post op pulm dysfunction
  • Regional anesthesia may be preferable
49
Q

What is marfan syndrome?

A
  • Multi system disorder of the connective itssue caused by mutations in extracellular matrix protein fibrillin 1
  • classic marfan’s syndrome occurs in about 4-6 our of 100,000 people
  • involve cv, skeletal and ocular systems
  • classic manifestations include proximal aortic aneurysm, dislocation of ocular lengs and long-bone overgrowth
    • need to see recent echo, cardiac workup
50
Q

CV manifestations of marfan’s syndrome?

A
  • Aortic aneurysm and dissection remain most life-threatening manifestations (increased risk in pregnancy)
  • Cardiac valve prolapse/dysfunction/regurg
    • mitral valve
    • aortic valve- incompetence often related to dilation of ascending aorta
    • arrhythmia- BBB
    • aortic and atrioventricular valves prone to calcification
51
Q

Pulmonary manifestations of marfan’s syndrome?

A
  • High incidence pneumothorax
  • spinal/sternal deformities can lead to restrictive lung disease
52
Q

Ocular manifestations of marfan’s syndrome?

A
  • Dislocation of ocular lengs
  • Retinal detachment
53
Q

What is standard treatment for marfan’s?

A
  • Beta blockers is standard of care
    • reduce workload of heart
    • delay/prevention aortic aneurysm and dissection
  • Surgical procedures
    • elective aoritc repair
      • may electively repair aortic root when >4.5 cm
    • spinal fusion for scoliosis
      • may be prone and that increases risk of ocular dislocation
54
Q

Marfan syndrome anesthesia consideration for airway?

A
  • Preop assessment should concentrate on cardiac abnormalities
  • airway evaluation and management
    • high arched palate with crowded teeth
      • visualization of the laryngx during direct larngosocpy rarely difficult
    • TMJ dislocation
      • tendency for join laxity
      • avoid extreme movement of mandible
    • Tracheomalacia
      • floppy tracheal cartilage leading to tracheal collapse
  • Beta blockade- should b econtinued perioperativley
  • Continuous monitor for pneumothorax!
55
Q

What is critical to maintain during anesthesia for marfan’s syndrome?

A

hemodynamic stability!

  • Prevent sudden increase in myocardial contractility
    • this produces an increase in aortic wall tension
  • Avoid excessiv eendogenous catecholamine production
    • control pain/anxiety
    • hemodynamic stable inudction should be performed
  • Treat hypertensive episodes immediately
  • volatile anesthesia can decrease force of cardaic ejection
    • decrease risk of aortic dissection
56
Q

What is ankylosing spondylitis?

A
  • Chronic, progressive inflammatory disease involving joints of spine and adjacent soft tissues
  • associated with HLA B27 in most cases
  • male to feamle ratio 4:1
  • important anesthesia implications both articular and non-articular
57
Q

What is standard treatment for anklyosing spondylitis patients?

A
  • Relieve pain, reduce inflmmation, maintain good posture and function
  • traditional treatments include NSAIDS, education, exercise, and PT
    • exercise/PT maintain joint mobility and flexibility
  • early dx is essential
  • surgery considered in patients with sever,e advanced dx associated with refractory pain or disability
58
Q

Airway manifestations of ankylosing spondylitis?

A

Difficult intubation associated when AS invovles cervical spine

  • increased difficulty when TMJ involved
  • limited mouth opening d/t TMJ involvement
  • sig risk of neuro injury with any excessive neck extension
  • progressive kyphosis and spine flexion may limit intubation
  • risk of occult cervical fracture with minimal trauma
  • cricoarytenoid arthritis
    • cords susceptible to trauma
59
Q

Cardiac involvement/anesthesia concerns for ankylosing spondylitis?

A
  • Aortic regurgitation (avoid sudden increases in SVR/keep H R>90 bpm, low normal BP)
  • Conduction abrnomalities- BBB
  • Cardiomegaly
60
Q

Pulmonary abnormalities in ankylosign spondylitis?

A
  • Pulmonary fibrosis
  • apical cavity lesions
  • pleural thickening (similar ot TB)
  • decreased compliance of chest wall
  • Decreased VC
61
Q

Anesthetic management for ankylosing spondylitis?

A
  • Anesthetic management influence by severity of dx
    • upper airway involvement
    • presence of restrictive lung disease
    • degree of cardiac involvement
    • may be using neuro monitoring during corrective spinal sx
  • Awake fiberoptic tracheal intubaiton if spinal deformity is extensive
  • spinal and epidural anesthesia is technically difficult
    • may result in an increased risk of complications
    • consider paramedian approach
62
Q

What is achondroplasia?

A
  • Most common cause of dwarfism
  • caused by premature ossification of bones combined with normal periosteal bone formation
    • results in characteristic appearance of short limbs and a relatively normal cranium
  • often present to OR for sub-occipital creaniectomy for foramen magnum stenosis, laminectomy, VP shunt
    • consider need for VAE monitoring (sitting crani)
      • may need right atrial catheter
    • evoked potential monitoring (limits anesthetic options)
      • ensures good cerebral circulation
63
Q

Anesthetic considerations for achondroplasia?

A
  • Normal response to anesthetic agents and NMB
  • C-section required
    • cephalopelvic disproportion
    • kyphoscoliosis and narrow epidural space, spinal canal increase tehcnical difficulty
    • no evidence based dosing guidlines- epidural may be better so you can titrate local anesthetic slowly
  • Difficult intravenous and central line access
    • short neck
    • excess skin and SQ tissue
  • Cardiac/pulmonary
    • pulm HTN leading to cor pulmonale is most common disturbance
    • restrictive bent defects may occur and lead to pulm htn
    • central sleep apnea (related to brainstem compression by foramen magnum) and upper airway obstruction
64
Q

Challenges with airway management for patient with achondroplasia ?

A
  • Facial features lead to dififcult mask management
    • large protruding forehead, short maxilla with long mandible, flat nose and large tongue
  • larynx may be small and intubation occasionally difficult
    • difficult to exposre glottis
    • range of tube sizes and dififcult airway cart avilable
    • weight rather than age is best guide for predicting porper size
  • Foramen magnum stenosis, fusion of atlantooccipital joint with odontoid, atlantoaxial instabilty, buling disc, cervical kyphosis common
    • avoid hyperextension during intubation

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