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Is the imaging worth the risks?. . Outline. XRCTPediatric patients. Introduction. Xrays discovered by Roentgen in 1895Widespread use (including shoe fitting)Until reports of side effectsRadiation dose expressed as millisievert (mSv)Background radiation ~3mSv/yr Coast-to-coast round trip fligh
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1. Radiological Risks& Refeeding syndrome Kathy Lee
March 17, 2006
2. Is the imaging worth the risks?
3. Outline XR
CT
Pediatric patients
4. Introduction Xrays discovered by Roentgen in 1895
Widespread use (including shoe fitting)
Until reports of side effects
Radiation dose expressed as millisievert (mSv)
Background radiation ~3mSv/yr
Coast-to-coast round trip flight in a commercial airplane ~0.03 mSv
5. Commonly ordered XR
6. Radiation doses have been decreasing
better equipment
better training in its use
Shielding further helps to lower exposure
Distance cheap and effective
I / D2 = I / d2
3m for portable XR
trauma room is 3m
7. Pregnant patients Dr Martel’s presentation
Consider US/MRI
Shield uterus when possible
Scan if necessary
8. CT Dose burden concern to radiologists and to regulatory authorities
“high dose procedure”
Small individual risk of carcinogenesis from CT
Atomic bomb survivors
600% increase in all Ct exams mid-80s to mid-90s
UK National Radiological Protection Board (NRPB)
“increased lifetime risk of death from a malignancy induced by CT – abdomen on the order of 1 in 2000”
Image quality improves with increasing dose
Plain film will be overexposed if radiation dose increased
9. Plain film and CT doses
10. Spiral CTs higher dose than regular CT
Data set of higher and lower slice needed to recontruct highest/lowest slice
Larger volume of body is scanned than that selected
Image acquisition speed increased
Larger body volumes in little time
Responsibility of ordering MD, radiologist, manufacturer to lower radiation exposure to patients
Necessary study
Target suitable organs
Modify parameters for patient size
Avoid multiphase scans
Preset low dose protocols for children
11. Pediatric patients In USA, 2000, 11% of CT performed in children (2.7 million)
1 fatal cancer per 1000 pediatric CT exams
Evidence that CT techniques not often suitably modified
Smaller body volume
Smaller organs
Increase sensitivity to radiation – 10x
Girls more than boys
Longer lifetime for radiation effects to manifest
Increased radiosensitivity of certain tissues
Thyroid gland, breast, gonads
12. Is the anxiety justified? Small amount of radiation may actually be beneficial
Established in animal/plant models, but not in man
Epidemiological studies: lower level of cancer after low-level exposure
Below threshold of some 200 - 500mSv (66.7 – 166.7 yrs of background radiation), evidence of beneficial effects
Hormetic effect
Decreased chormosomal aberration
Immune response increased
Some truth of “therapeutic CT” Hormesis, then, is the term for generally-favorable biological responses to low exposures to toxins and other stressors. Hormesis, then, is the term for generally-favorable biological responses to low exposures to toxins and other stressors.
13. ALARA conference 2001 As Low As Reasonably Achieavable radiation dose strategies to reduce CT radiation dose in children
Judicious use of CT
Consider alternate modalities such as US or MRI
Adjust CT technique
Minimize use of multiple scans
Limit coverage to answer clinical questions
avoid routine scanning of pelvis as part of abdomen to reduce exposure to gonads
May seem obviousMay seem obvious
14. Consider breast shielding
Adjust individual settings based on indication
detection of large vs small abnormality
follow-up examination
Adjust individual settings based on body region scanned
lower tube current for chest and skeletal CT
less radiation needed than abdo/head
Adjust individual settings based on the size
Use new scanner technology that makes automatic regional adjustments in radiation dose during scanning
15. References http://www.radiologyinfo.org. Accessed March 12, 2006
Archer BR. 2005. Recent history of the shielding of medical X-ray imaging facilities. Health Phys. 88(6):579-596
Dawson P. 2004. Patient dose in multislice CT: why is it increasing and does it matter? Brit J Rad 77:S10-13.
Frush DP, Donnelly LF, Rosen NS. 2003. Computed tomography and radiation risks: What pediatric health care providers should know. Ped 112:951-957.
Slovis TL. 2002. CT and computed radiography: The pictures are great, but is the radiation dose greater than required? AJR 179:39-41.
16. Refeeding Syndrome
17. Outline Pathogenesis
Clinical manifestation
Prevention and management
18. Introduction Potentially lethal condition
Severe lyte and fluid shifts
Associated with metabolic abN in malnourished patients undergoing refeeding orally, enterally or parenterally
19. Patients at risk incl:
>10% weight loss over mos - hunger strikers
not fed for 7-10d - chronic EtOH
prolonged IVF repletion - anorexia nervosa
malnourished elderly Pt - post-op Pt
oncology Pt undergoing chemoTx
More common in those fed enterally, elderly
20. Pathogenesis During starvation:
Overall catabolism of adipose tissue and muscle, loss of lean body mass
Insulin decr, glucagon incr
Glc synthesis via lipidand protein breakdown products
Adipose tissue release FA, glycerol
Muscle release aa
KB and FFA replace glc as major energy source
21. During refeeding:
Shift from fat to CHO metabolism
Incr protein synthesis
glc load incr insulin release
Incr cellular uptake of glc, PO4, K, Mg, water
22. Clinical manifestation Disturbance of body-fluid distribution
CHO / high protein– decr water/Na excretion
Protein – incr Na excretion
Resulting hyper/hypo-natremia, dehydration/fluid overload
AbN glc and lipid metabolism
Hyperglycemia can lead to ketoacidosis/metabolic acidosis ? hyperosmolar nonketotic coma
Glc converted to fat ? hypertriglyceridemia, fatty liver, abN LFT, higher respiratory quotient ? incr CO2 production / incr PaCO2
Level of hyperTG further decr in critically ill Pt
23. Thiamine deficiency
Cofactor for enzymatic activity
CHO refeeding incr cellular thiamine utlization
Wernicke’s encephalopathy (ocular disturbance, confusion, ataxia, coma)
Korsakov’s syndrome (short-term memory loss, confabulation)
24. Hypophosphatemia
Predominant feature, major intracell anion
80% in bony skeleton, 20% in soft tissues
Rich source in protein-rich food, cereals, nuts
Absorb 70%, Excrete renal (90%)
Kidney recycle, homeostasis
Buffer, part of PL, nucleic acid, enzymatic phosphorylation, ATP, chemotaxis
Clinical manifestations:
Neurologic (fits, weakness, parethesia, acute encephalopathy)
Muscular (weakness, myalgia, rhabdomyolysis, decreased cardiac contractility, cardiomyopathy)
Hematologic (dysfunction of platelets and leukocytes, thrombocytopenia, hemolysis)
Respiratory (impaired respiratory muscle function sometimes resulting in respiratory failure or ventilator dependency)
Bone (osteomalacia)
Renal (acute tubular necrosis)
25. Hypokalemia
Intracell, maintaines cell-membrane action potential
Homeostasis regulated by kidney
Clinical manifestations:
Neurologic (paralysis, paresthesia)
Musculoskeletal (rhabdomyolysis, respiratory depression, weakness)
Cardiac (arrhythmias, hypotension, digoxin toxicity, cardiac arrest)
GI (constipation, paralytic ileus)
Renal (Decreased urinary concentrating ability)
Metabolic (metabolic alkalosis, glc intolerance)
26. Hypomagesemia
Intracell, found in bone and muscle
Largely absorbed in upper sm intestine
Absorb 30%, Excrete kidneys
Clinical manifestations:
lyte (hypo -K, hypo- Ca)
Neurologic (tetany, paresthesiae, seizures, ataxia, tremor, weakness)
Cardiac (arrhythmias, e.g., torsade de pointes, hypertension)
Gastrointestinal (anorexia, abdominal pain)
27. Prevention and Management Monitor lytes (Na, K, PO4, Mg
Correct electrolyte disorders before refeeding
Restore circulatory volume
Correct vitamins (thiamine) / trace elements
Cal repletion slowly at 20kcal/kg, 1.5g/kg protein
28. Repletion of PO4 not necessary unless <0.30mmol/L or Sx
PO PO4 ? diarrhea
IV Na or K PO4 15-30mmol
Stop refeeding
Monitor urine output
Repletion of Mg not necessary unless <0.5mmol/l or Sx
PO Mg ? GI upset, poorly absorbed
IV MgSO4 4g
Can treat refractory hypo-K
29. References Crook MA, Hally V, Panteli JV. 2001. The importance of the refeeding syndrome. Nutrition 17:632-637.
Marinella MA. 2005. Refeeding syndrom eand hypophosphatemia. J Intensive Care Med 20:155-159.