princip-complications Flashcards
1
Q
malignant hyperthermia:
- what is it?
- what happens?
- incidence (adults and children)?
- most prevalant in what country (race)?
- what age and or gender is most affected?
A
- inherited skeletal muscle disorder triggered by anesthetics and depolarizing MRs
- trigger sustained skeletal muscle hypermetabolism or contracture characterized by fever, tachycardia, hypercarbia and rigidity
- 1: 15,000 in childern and 1:50,000 in adults
- can happen in any race but most prevalent in north america (french canadians)
- children and men
2
Q
what is the number for M-haus?
A
1-800-MHhyper
5
Q
- MH?
- what chromosome has the MH defect?
- what is the test for it?
A
- abnormalities of calcium release at ryanodine receptor (RYR1:a major calcium release channel of the sarcoplasmic reticulum) of skeletal muscle
- located on chromosone 19; 25% of families in north america the variant RYR1 gene.
- caffiene/halothane test on muscle plug
6
Q
- what happens on a cellular level with actin/myosin and calcium release in a normal cell?
- what happens in MH?
A
- depolarization releases calcium from sarcoplasmic reticulum, this activates the crossbridges between actin and myosin filaments, causing them to interdigitate which causes a contraction. muscle relaxation follows with re-uptake of calcium into sarcoplasmic reticulum
- with MH, there is a failure in reuptake of calcium by the sarcoplasmic reticulum d/t permeability. The excess calcium causes inablilty to relax muscle, sustained activation of actin and myosin filaments, this causes heat, enhanced glycolysis, uncoupling of oxidative phosphorylation.
7
Q
clinical features of MH:
- what skeletal muscle disorders predispose persons to MH
- what operations are associated with MH?
- what unexplained conditions are related to MH?
- can MH present after 1 exposure?
- does MH manifest immediately?
- how close of a family member with MH means high risk?
A
- duchenne’s m.d., central core disease, osteogenesis imperfecta
- orthopedic, opthalmic (ptosis, strabismus repair), head and neck procedures
- unexplained fevers, intolerance to caffiene, muscle cramps
- can happen on first exposure or on future exposure. 30% of patients have had 3 prior un-eventful surgeries receiving anesthesia.
- sometimes manifests post op
- relative with MH especially first degree relative
8
Q
how is MH manifested?
- most sensitive sign?
- earliest and most consistent sign?
- signs r/t head and neck?
- respiratory signs?
- cardiac signs?
- skin signs?
- urinary signs?
- muscle signs?
A
- increased ETCO2
- tachycardia
- trismus or masseter spasm after sux
- tachypnea
- arrhythmias (PVCs, bigeminy, VT)
- increased temp, cyanosis, skin mottling, profuse sweating
- myoglobinuria Tea colored urine (from myoglobinemia)
- muscle rigidity
9
Q
what are late signs (actually side effects) of MH?
A
- DIC
- pulmonary edema
- acute renal failure
- CNS signs (blindness, seizure, coma, paralysis)
10
Q
how long does it take for signs of MH to mainfest?
A
signs related to increased metablolic rate may take minutes to hours
11
Q
how is initial diagnosis made based on circumstancial data?
- metabolic signs?
- what happens to co2 absorber?
- what is a sudden severe response to sux?
- what is a facial sign seen, what can it mean?
A
- increased O2 consumption and CO2 production
- co2 absorber may become hot and exhausted
- sudden hyperkalemic responses after administration of sux to children with undiagnosed myopathy
- masseter spasm after sux (50% of children with masseter spasm have succeptibility to MH). aka “jaws of steel”
12
Q
lab findings with MH?(13 things)
A
- acidosis
- hypoxemia
- hypercapnia (on ABGs)
- hyperkalemia
- hypercalcemia
- elevated magnesium (hypermagnesemia)
- hyponatremia
- increased lactate (lactic acid)
- increased pyruvate
- increased ck
- increased lactate dehydrogenase
- increased aldolase
- increased myoglobin
13
Q
treatment of MH
physical action
A
- —-depends on early recognition; causal and symptomatic
- terminate anesthetic / inhaled anesthesia
- stop surgery
- 100% oxygen
- active cooling (surface with ice, ice water lavage to stomach and bladder, cool IV fluids); stop cooling when temp gets down to 38 degrees
- alkalanization with bicarb
- hydrate and diurese (osmotic and tubular diuretics)
14
Q
dantrolene:
- whats dantrolene made of?
- what does it do?
- why dantrolene?
- what is the dose/ interval?
- how is it supplied and reconstituted?
- what speeds up reconstitution?
- how long does it take to work?
A
- hydantoin (dilantin) derivative
- interferes with muscle contraction at the RYR1 receptor calcium channel
- it is the only reliable treatment for MH
- 2-3 mg/kg (up to 5 mg/kg) iv every 5 minutes to max of 10mg/kg.
- comes in 20 mg lyphilized powder to be dissolved in 60cc of sterile water.
- warm diluent to (40 degrees C) to speed reconstitution
- should respond in 45 minutes
15
Q
prognsis post MH
- how long in ICU?
- what was mortality before dantrolene, what is mortality with?
A
- 72 hours in aicu
- without dantrolene 70% mortality;
with dantrolene 5% mortality
16
Q
how to identify MH patients
- what is the test?
- what is the accuracy?
A
- halothane contracture test (a muscle chunk is exposed to halothane and caffiene to see if it contracts).
- 97-99% sensitivity
10-20% false positive
0% false negative though
17
Q
what does duchennes muscluar dystrophy do in regards to anesthesia?
A
highly related to anesthesia induced rhabdomyolysis due to stress on fragile muscle cells; they will have more sux induced hyperkalemia
70% of these patients have increased resting concentrations of creatnine kinase (although this is not a definitive diagnosis).
