The photomultipliers tubes

" "

Their role is to convert light energy emitted by the crystal to an electrical signal that can be
exploited in electronic circuits [3, 5]. This is achieved by the combination of several elements,
placed in a vacuum to allow the flow of electrons. The first element, placed in contact with the
crystal is the photocathode, metal foil on which the light photons are able to extract electrons.
These electrons are attracted to the first dynode by the application of a high voltage between

it (positively charged) and the photocathode. The electrons acceleration allows them to extract
a much larger number of electrons from the dynode. Then there are several cascading dynodes,
on which the same phenomenon is repeated. The successive dynodes are submitted to
potentials higher and higher. From a dynode to another, we obtain a cascade of electrons more
intense (amplification phenomenon), which ultimately results in a measurable electric current.
This current is collected by the last element called anode and a real electrical signal is generated
(Figure 4).

Figure 4. PMTs disposition in a Gamma-camera. Generally a hexagonal shape of PTM is preferred then a circular because
it well cover the detection area. Additional very small PMT can also be used between principal PMT for best detection
area covering (CEM, Rennes, France).

The scintillator crystal

" "

The γ-camera crystals are generally composed of NaI(Tl). Features that make this crystal
desirable include high mass density and atomic number (Z), thereby effectively stopping γ
photons, and high efficiency of light output [3, 4]. The most important characteristics of the
crystal that must be ensured are: 1) high detection efficiency, 2) high energy resolution, 3). low
decay constant time and a light refraction index close to the glass one. Most current cameras
incorporate large (50 cm×60 cm) rectangular detectors. While expensive, the larger field of view
results in increased efficiency. In early designs, crystals were often 0.5 inches thick, which was
well-suited for high energy γ photons. In more recent implementations of the γ-camera,
crystals only 3/8-inch or 1/4-inch thick are used, which is more than adequate for stopping the
predominantly low-energy photons in common use today and which also results in superior
intrinsic spatial resolution.

The collimator

" "

The scintigraphic image corresponds to the projection of the distribution of radioactivity on
the crystal detector. Gamma rays cannot be focused using lenses as in the case of light. The use
of a special kind of collimator can permit just to one direction gamma rays to reach the crystal,
the most common being perpendicular to the crystal. A collimator is a wafer usually lead
wherein cylindrical or conical holes are drilled along a system axes determined. Gamma-ray
where the path does not borrow these directions is absorbed by the collimator before reaching
the crystal. The partition (wall) separating two adjacent holes i called "septa". The thickness of
lead is calculated to cause an attenuation of at least 95% of the energy of the photons passing
through the septa. The most commonly used collimator is the parallel holes. It retains the
dimensions of the image. For non-parallel collimators, the dimensions of the image depend on
the geometrical disposition and the divergence or convergence nature of the collimator. This
leads to a geometric distortion must be taken into account. The efficiency of a collimator is the
fraction of radiation passing through the collimator (without any interaction), reaching the
crystal and effectively participating in the image formation. The collimator resolution corresponds
to the accuracy of the image formed in the detector. Resolution improves with
increasing thickness of the septa at the expense of collimator efficiency. A good compromise
is to find the realization of a collimator performance depends on the intrinsic characteristics
of the detector and the use we want to make [2].

The Anger gamma camera

" "

The principle of radiation detection is based on the interaction of these radiations with the
matter. When a gamma photon enters in interaction with a detector material, it loses its energy
mainly in the form of ionizations or excitations. The excited atoms return to their ground state
through the emission of secondary low energy gamma photons. The incident gamma photon
can be partially or totally absorbed (photoelectric effect). In the first case, the energy loss is
accompanied by a deviation of the photon (Compton scattering). The photon loses "memory"
of its initial place of issue. So the photoelectric effect is the right phenomenon which must be
considered when we interest to the gamma-ray emission site.
In the gamma camera, the detection medium is historically a NaI scintillation crystal typically
doped with thallium. This crystal is able to emit light especially through a fluorescence process
after the excitation of its molecules by a charged particle (electron). The density of NaI is 3.67
g/cm3 and its atomic number 50. Its time of scintillation (fluorescence) is 230 nm and the
maximum light emission is at 4150 Angstroms wave length. Its refractive index is 1.85, and it
is relatively transparent to its own light; about 30% of emitted light is transmitted to the
detection chain [1]. The energy resolution can reach 7-8% at 1 MeV and the constant time of
their pulse is equal to ~10-7 sec. The detection efficiency of NaI is quite large, of the order of 40
photons/keV. Indeed, gamma-ray energy of 100 keV transferring all its energy in the crystal
results in the creation of approximately 4000 fluorescence light photons. These photons are
collected by the photocathode of a photomultiplier tube (Figure 1).
For the detection of the secondary light photons generated in the crystal by the interaction with
the incident gamma radiations, a photomultiplier tube (PMT) located behind the scintillator
is used (Figure 1). At the level of the PMT photocathode, each light photon is converted to
electrons. These electrons are then accelerated and multiplied by ten dynodes polarized by a
gradually increasing voltage, and finally collected by an anode placed at the other side of the
PMT where they give birth to an electrical impulse. This pulse has an amplitude proportional
to the energy of the detected gamma-ray.
The output signal is amplified by the PMT. Its amplitude is measured, digitized and stored.
Numerical analysis enables to obtain a spectrum (number of photons detected as a function of

their energy) characteristic of the detected gamma-rays. Detection time (acquisition) should
be sufficient to obtain good counting statistics. The theoretical gamma-rays spectrum reaching
the crystal is a line spectrum; the spectrum is continuous (Figure 2). The spectrum includes
the total energy peak corresponding to gamma directly emitted by the radioactive source
without any interaction before reaching the crystal and a background of lower energies due
to the partial absorption of gamma by Compton scattering. Compton scattering in the path of
the photon is changed making it impossible to locate its transmitter site. It is therefore necessary
to take into account only the events corresponding to the photoelectric interactions at the level
of the crystal with the total emission energy. This is achieved by the intermediate of a "window"
for selecting the double-threshold energy (pulse height analyzer).

Figure 2. Gamma-rays spectrum at the level of the crystal detector (ideal (top) and real (bottom) cases).
The width of the peak of total absorption depends essentially of the random statistical
fluctuations of the gain of the PMT. The width at half maximum ΔE relative to an average

energy E0 defines the energy resolution ΔE/E0. The energy resolution of PMT is about 10% at
140 keV (emission peak of technetium-99m). The pulses selected by the pulse analyzer
(maximum intensity) are directed to a time scaling circuit having a time integrator which then
delivers a count rate in counts per second (cps). This count rate can be correlated to the real
activity of the source after a number of corrections taking into account in particular the
geometric efficiency and the detection performance of the detection chain. For very high source
activity, the detector response is no longer linear so that a number of events are not taken into
account. The lapse of time in which these events are lost (not counted by the detector) is called
the dead time. In practice, it is usual, to work under conditions such that the detection dead
time correction is not necessary (medium activity source).
The Anger gamma scintillation camera (Figure 3) uses the information provided by the
amplitude of the electrical pulse not only to measure the energy of the detected radiation, but
also to locate in the space the emission site of this radiation.
The camera developed by Anger in 1953 has a crystal of sodium iodide (NaI) thallium
activated. It can take single crystal of large dimensions, up to 60x50 cm2 with a thickness
ranging from 1/4 inch to 1 inch [1]. These crystals are fragile and are highly sensitive to shocks
and moisture. The surface of the crystal is covered with a large number of PMTs (between 50
and 100). When scintillation occurs, the sum of the output signals of all the MPTs provides the
energy lost in the volume of the scintillator (Z coordinate). The large number of PMTs ensures
the collection of maximum light. Moreover, the amplitude of the output signal of PMT varies
with the distance between the centre of the photocathode and the place where the scintilaltion
is produced is in the crystal. The amplitude distribution of the output pulses of the PMT then
provides the location information (X and Y coordinates) by means of a computer listing. For
each photon interacting with the detector is thus obtained location coordinates (X and Y) and
a value of the energy given or lost in the crystal (Z coordinate). An amplitude analysis allows
selecting only the photon energy characteristic of the radionuclide used (eg. 140 keV for 99mTc)
having lost all their energy in the crystal (photoelectric peak).

The scintillation Gamma-camera was used originally for planer projection imaging is mainly
composed by the following components:

Principles and Applications of Nuclear Medical Imaging: A Survey on Recent Developments

" "

1. Introduction
The main difference between nuclear imaging and other radiologic tests is that nuclear
imaging assesses how organs function, whereas other imaging methods assess anatomy, or
how the organs look. The advantage of assessing the function of an organ is that it helps
physicians make a diagnosis and plan present or future treatments for the part of the body
being evaluated. Fast improvements in engineering and computing technologies have made
it possible to acquire high-resolution multidimensional nuclear images of complex organs to
analyze structural and functional information of human physiology for computer-assisted
diagnosis, treatment evaluation, and intervention. Technological inventions and developments
have created new possibilities and breakthroughs in nuclear medical diagnostics. The
classic example is the discovery of Anger, fifty six years ago. The application and commercial
success of new nuclear imaging methods depends mainly on three primary factors:
sensitivity, specificity and cost effectiveness. The first two determine the added clinical value,
in comparison with existing medical imaging methods. Nowadays, much greater importance
is attached to cost effectiveness than in the past. This also holds true for diagnostic
equipment where, for example, one of the consequences is that price erosion will occur where
the functionality of an instrument is not open to further development. Cost effectiveness is
enhanced by more efficient data handling in the hospitals, which has become possible through
the digitization of diagnostic information. The inevitable integration of medical data also
offers other new possibilities, such as the use of pre-operatively acquired images during
surgical procedures.
This chapter presents the principles of nuclear imaging methods and some cases studies and
future trends of nuclear imaging. It discusses too the recent developments in image analysis
and the possible impact of some important current technological progression on nuclear

Rheumatologic Disorders

" "

Systemic Lupus Erythematosus
1.Admit to:
2.Diagnosis: Systemic Lupus Erythematosus
3.Condition:
4.Vital Signs: tid
5.Allergies:
6.Activity: Up as tolerated with bathroom privileges
7.Nursing:
8.Diet: No added salt, low psoralen diet.
9. Special Medications:
-Ibuprofen (Motrin) 400 mg PO qid (max 2.4 g/d) OR
-Indomethacin (Indocin) 25-50 mg tid-qid.
-Hydroxychloroquine (Plaquenil) 200-600 mg/d PO
-Prednisone 60-100 mg PO qd. Maintenance 10-20
mg PO qd or 20-40 mg PO qOD OR
-Methylprednisolone (pulse therapy) 500 mg IV over
30 min q12h for 3-5d, then prednisone 50 mg PO
qd.
-Betamethasone dipropionate (Diprolene) 0.05%
ointment applied bid.
10. Extras: CXR PA, LAT, ECG. Rheumatology consult.
11. Labs: CBC, platelets, SMA 7&12, INR/PTT, ESR,
complement CH-50, C3, C4, C-reactive protein, LE
prep, Coombs test, VDRL, rheumatoid factor, ANA,
DNA binding, lupus anticoagulant, anticardiolipin,
antinuclear cytoplasmic antibody. UA.
Acute Gout Attack
1.Admit to:
2.Diagnosis: Acute gout attack
3.Condition:
4.Vital Signs: tid
5.Activity: Bed rest with bedside commode
6.Nursing: Keep foot elevated; support sheets over
foot; guaiac stools.
7.Diet: Low purine diet.
8.Special Medications:
-Ibuprofen (Motrin) 800 mg, then 400-800 mg PO q4-
6h OR
-Diclofenac (Voltaren) 25-75 mg tid-qid with food OR
-Indomethacin (Indocin) 50 mg PO q6h for 2d, then
50 mg tid for 2 days, then 25 mg PO tid OR
-Ketorolac (Toradol) 30-60 mg IV/IM, then 15-30 mg
IV/IM q6h or 10 mg PO tid-qid OR
-Naproxen sodium (Anaprox, Anaprox-DS) 550 mg
PO bid OR
-Methylprednisolone (SoluMedrol) 125 mg IV x 1 dose
THEN
-Prednisone 60 mg PO qd for 5 days, followed by
tapering.
-Colchicine 2 tablets (0.5 mg or 0.6 mg), followed by 1
tablet q1h until relief, max dose of 9.6 mg/24h.
Maintenance colchicine: 0.5-0.6 mg PO qd-bid.
Hypouricemic Therapy:
-Probenecid (Benemid), 250 mg bid. Increase the
dosage to 500 mg bid after 1 week, then increase
by 500-mg increments every 4 weeks until the uric
acid level is below 6.5 mg/dL. Max dose 2 g/d.
Contraindicated during acute attack.
-Allopurinol (Zyloprim) 300 mg PO qd, may increase
by 100-300 mg q2weeks. Usually initiated after the
acute attack.
9. Symptomatic Medications:
-Famotidine (Pepcid) 20 mg IV/PO q12h.
-Meperidine (Demerol) 50-100 mg IM/IV q4-6h prn
pain OR
-Hydrocodone/acetaminophen (Vicodin), 1-2 tab q4-
6h PO prn pain.
-Docusate sodium (Colace) 100 mg PO qhs.
-Acetaminophen (Tylenol) 325-650 mg PO q4-6h prn
headache.
-Zolpidem (Ambien) 5-10 mg qhs prn insomnia.
10. Labs: CBC, SMA 7, uric acid. UA with micro.
Synovial fluid for light and polarizing micrography for
crystals; C&S, Gram stain, glucose, protein, cell count.
X-ray views of joint. 24-hour urine for uric acid.

Nephrologic Disorders

" "

Renal Failure
1.Admit to:
2.Diagnosis: Renal failure
3.Condition:
4.Vital Signs: q8h. Call physician if QRS complex
>0.14 sec; urine output <20 cc/hr; BP >160/90, <90/-
60; P >120, <50; R>25, <10; T >38.5 C.
5.Allergies: Avoid magnesium containing antacids, salt
substitutes, NSAIDS. Discontinue phosphate or
potassium supplements.
6.Activity: Bed rest.
7.Nursing: Daily weights, inputs and outputs, chart
urine output. If no urine output for 4h, in-and-out
catheterize. Guaiac stools.
8.Diet: Renal diet of high biologic value protein of 0.6-
0.8 g/kg, sodium 2 g, potassium 1 mEq/kg, and at
least 35 kcal/kg of nonprotein calories. In oliguric
patients, daily fluid intake should be restricted to less
than 1 L after volume has been normalized.
9.IV Fluids: D5W at TKO.
10. Special Medications:
-Consider fluid challenge (to rule out pre-renal azo-
temia if not fluid overloaded) with 500-1000 mL NS IV
over 30 min. In acute renal failure, in-and-out
catheterize and check postvoid residual to rule out
obstruction.
-Furosemide (Lasix) 80-320 mg IV bolus over 10-60
min, double the dose if no response after 2 hours to
total max 1000 mg/24h, or furosemide 1000 mg in
250 mL D5W at 20-40 mg/hr continuous IV infusion
OR
-Torsemide (Demadex) 20-40 mg IV bolus over 5-10
min, double the dose up to max 200 mg/day OR
-Bumetanide (Bumex) 1-2 mg IV bolus over 1-20 min;
double the dose if no response in 1-2 h to total max
10 mg/day.
-Metolazone (Zaroxolyn) 5-10 mg PO (max 20 mg/24h
30 min before a loop diuretic.
-Hyperkalemia is treated with sodium polystyrene
sulfonate (Kayexalate), 15-30 gm PO/NG/PR q4-6h.
-Hyperphosphatemia is controlled with calcium acetate
(PhosLo), 2-3 tabs with meals.
-Metabolic acidosis is treated with sodium bicarbonate
to maintain the serum pH >7.2 and the bicarbonate
level >20 mEq/L. 1-2 amps (50-100 mEq) IV push,
followed by infusion of 2-3 amps in 1000 mL of D5W
at 150 mL/hr.
-Adjust all medications to creatinine clearance, and
remove potassium phosphate and magnesium from
IV. Avoid NSAIDs and nephrotoxic drugs.
11. Extras: CXR, ECG, renal ultrasound, nephrology
and dietetics consults.
12. Labs: CBC, platelets, SMA 7&12, creatinine, BUN,
potassium, magnesium, phosphate, calcium, uric aci
osmolality, ESR, INR/PTT, ANA.
Urine specific gravity, UA with micro, urine C&S; 1st AM
spot urine electrolytes, eosinophils, creatinine, pH,
osmolality; Wright's stain, urine electrophoresis. 24h
urine protein, creatinine, sodium.
Nephrolithiasis
1.Admit to:
2.Diagnosis: Nephrolithiasis
3.Condition:
4.Vital Signs: q8h. Call physician if urine output <30
cc/hr; BP >160/90, <90/60; T >38.5 C.
5.Activity: Up ad lib.
6.Nursing: Strain urine, measure inputs and outputs.
Place Foley if no urine for 4 hours.
7.Diet: Regular, push oral fluids.
8.IV Fluids: IV D5 ½ NS at 100-125 cc/hr (maintain
urine output of 80 mL/h).
9.Special Medications:
-Cefazolin (Ancef) 1-2 gm IV q8h
-Meperidine (Demerol) 75-100 mg and hydroxyzine
25 mg IM/IV q2-4h prn pain OR
-Butorphanol (Stadol) 0.5-2 mg IV q3-4h.
-Hydrocodone/acetaminophen (Vicodin), 1-2 tab q4-
6h PO prn pain OR
-Oxycodone/acetaminophen (Percocet) 1 tab q6h pr
pain OR
-Acetaminophen with codeine (Tylenol 3) 1-2 tabs P
q3-4h prn pain.
-Ketorolac (Toradol) 10 mg PO q4-6h prn pain, or 30
60 mg IV/IM then 15-30 mg IV/IM q6h (max 5
days).
-Zolpidem (Ambien) 10 mg PO qhs prn insomnia.
11. Extras: Intravenous pyelogram, KUB, CXR, ECG.
12. Labs: CBC, SMA 6 and 12, calcium, uric acid,
phosphorous, UA with micro, urine C&S, urine pH,
INR/PTT. Urine cystine (nitroprusside test), send
stones for X-ray crystallography. 24 hour urine
collection for uric acid, calcium, creatinine.
Hypercalcemia
1.Admit to:
2.Diagnosis: Hypercalcemia
3.Condition:
4.Vital Signs: q4h. Call physician if BP >160/90,
<90/60; P >120, <50; R>25, <10; T >38.5 C; or tetan
or any abnormal mental status.
5.Activity: Encourage ambulation; up in chair at other
times.
6.Nursing: Seizure precautions, measure inputs and
outputs.
7.Diet: Restrict dietary calcium to 400 mg/d, push PO
fluids.
8.Special Medications:
-1-2 L of 0.9% saline over 1-4 hours until no longer
hypotensive, then saline diuresis with 0.9% saline
infused at 125 cc/h AND
-Furosemide (Lasix) 20-80 mg IV q4-12h. Maintain
urine output of 200 mL/h; monitor serum sodium,
potassium, magnesium.
-Calcitonin (Calcimar) 4-8 IU/kg IM q12h or SQ q6-
12h.
-Etidronate (Didronel) 7.5 mg/kg/day in 250 mL of
normal saline IV infusion over 2 hours. May repeat
in 3 days.
-Pamidronate (Aredia) 60 mg in 500 mL of NS infuse
over 4 hours or 90 mg in 1 liter of NS infused over
24 hours x one dose.
9.Extras: CXR, ECG, mammogram.
10. Labs: Total and ionized calcium, parathyroid
hormone, SMA 7&12, phosphate, Mg, alkaline
phosphatase, prostate specific antigen and
carcinoembryonic antigen. 24h urine calcium, phos-
phate.
Hypocalcemia
1.Admit to:
2.Diagnosis: Hypocalcemia
3.Condition:
4.Vital Signs: q4h. Call physician if BP >160/90,
<90/60; P >120, <50; R>25, <10; T >38.5 C; or any
abnormal mental status.
5.Activity: Up ad lib
6.Nursing: I and O.
7.Diet: No added salt diet.
8.Special Medications:
Symptomatic Hypocalcemia:
-Calcium chloride, 10% (270 mg calcium/10 mL vial),
give 5-10 mL slowly over 10 min or dilute in 50-100
mL of D5W and infuse over 20 min, repeat q20-30
min if symptomatic, or hourly if asymptomatic.
Correct hyperphosphatemia before hypocalcemia
OR
-Calcium gluconate, 20 mL of 10% solution IV (2
vials)(90 mg elemental calcium/10 mL vial) infused
over 10-15 min, followed by infusion of 60 mL of
calcium gluconate in 500 cc of D5W (1 mg/mL) at
0.5-2.0 mg/kg/h.
Chronic Hypocalcemia:
-Calcium carbonate with vitamin D (Oscal-D) 1-2 tab
PO tid OR
-Calcium carbonate (Oscal) 1-2 tab PO tid OR
-Calcium citrate (Citracal) 1 tab PO q8h or Extra
strength Tums 1-2 tabs PO with meals.
-Vitamin D2 (Ergocalciferol) 1 tab PO qd.
-Calcitriol (Rocaltrol) 0.25 mcg PO qd, titrate up to
0.5-2.0 mcg qid.
-Docusate sodium (Colace) 1 tab PO bid.
9.Extras: CXR, ECG.
10. Labs: SMA 7&12, phosphate, Mg. 24h urine
calcium, potassium, phosphate, magnesium.
Hyperkalemia
1.Admit to:
2.Diagnosis: Hyperkalemia
3.Condition:
4.Vital Signs: q4h. Call physician if QRS complex
>0.14 sec or BP >160/90, <90/60; P >120, <50;
R>25, <10; T >38.5 C.
5.Activity: Bed rest; up in chair as tolerated.
6.Nursing: Inputs and outputs. Chart QRS complex
width q1h.
7.Diet: Regular, no salt substitutes.
8.IV Fluids: D5NS at 125 cc/h
9.Special Medications:
-Discontinue ACE inhibitors, angiotensin II receptor
blockers, beta-blockers, potassium sparing
diuretics.
-Calcium gluconate (10% solution) 10-30 mL IV over
2-5 min; second dose may be given in 5 min.
Contraindicated if digoxin toxicity is suspected.
Keep 10 mL vial of calcium gluconate at bedside
for emergent use.
-Sodium bicarbonate 1 amp (50 mEq) IV over 5 min
(give after calcium in separate IV).
-Regular insulin 10 units IV push with 1 ampule of
50% glucose IV push.
-Kayexalate 30-45 gm premixed in sorbitol solution
PO/NG/PR now and q3-4h prn.
-Furosemide 40-80 mg IV, repeat prn.
-Consider emergent dialysis if cardiac complications
or renal failure.
10. Extras: ECG.
11. Labs: CBC, platelets, SMA7, magnesium, calcium,
SMA-12. UA, urine specific gravity, urine sodium, pH,
24h urine potassium, creatinine.
Hypokalemia
1.Admit to:
2.Diagnosis: Hypokalemia
3.Condition:
4.Vital Signs: Vitals, urine output q4h. Call physician if
BP >160/90, <90/60; P>120, <50; R>25, <10; T
>38.5 C.
5.Activity: Bed rest; up in chair as tolerated.
6.Nursing: Inputs and outputs
7.Diet: Regular
8.Special Medications:
Acute Therapy:
-KCL 20-40 mEq in 100 cc saline infused IVPB over 2
hours; or add 40-80 mEq to 1 liter of IV fluid and
infuse over 4-8 hours.
-KCL elixir 40 mEq PO tid (in addition to IV); max total
dose 100-200 mEq/d (3 mEq/kg/d).
Chronic Therapy:
-Micro-K 10 mEq tabs 2-3 tabs PO tid after meals (40-
100 mEq/d) OR
-K-Dur 20 mEq tabs 1 PO bid-tid.
Hypokalemia with metabolic acidosis:
-Potassium citrate 15-30 mL in juice PO qid after
meals (1 mEq/mL).
-Potassium gluconate 15 mL in juice PO qid after
meals (20 mEq/15 mL).
9. Extras: ECG, dietetics consult.
10. Labs: CBC, magnesium, SMA 7&12. UA, urine Na,
Hypermagnesemia
1.Admit to:
2.Diagnosis: Hypermagnesemia
3.Condition:
4.Vital Signs: q6h. Call physician if QRS >0.14 sec.
5.Activity: Up ad lib
6.Nursing: Inputs and outputs, daily weights.
7.Diet: Regular
8.Special Medications:
-Saline diuresis 0.9% saline infused at 100-200 cc/h
to replace urine loss AND
-Calcium chloride, 1-3 gm added to saline (10%
solution; 1 gm per 10 mL amp) to run at 1 gm/hr
AND
-Furosemide (Lasix) 20-40 mg IV q4-6h as needed.
-Magnesium of >9.0  mEq/L requires stat
hemodialysis because of risk of respiratory failure.
9. Extras: ECG
10. Labs: Magnesium, calcium, SMA 7&12, creatinine.
24 hour urine magnesium, creatinine.
Hypomagnesemia
1.Admit to:
2.Diagnosis: Hypomagnesemia
3.Condition:
4.Vital Signs: q6h
5.Activity: Up ad lib
6.Diet: Regular
7.Special Medications:
-Magnesium sulfate 4-6 gm in 500 mL D5W IV at 1
gm/hr. Hold if no patellar reflex. (Estimation of Mg
deficit = 0.2 x kg weight x desired increase in Mg
concentration; give deficit over 2-3d) OR
-Magnesium sulfate (severe hypomagnesemia <1.0)
1-2 gm (2-4 mL of 50% solution) IV over 15 min,
OR
-Magnesium chloride (Slow-Mag) 65-130 mg (1-2
tabs) PO tid-qid (64 mg or 5.3 mEq/tab) OR
-Milk of magnesia 5 mL PO qd-qid.
8. Extras: ECG
9. Labs: Magnesium, calcium, SMA 7&12. Urine Mg,
electrolytes, 24h urine magnesium, creatinine.
Hypernatremia
1.Admit to:
2.Diagnosis: Hypernatremia
3.Condition:
4.Vital Signs: q2-8h. Call physician if BP >160/90, <7-
0/50; P >140, <50; R>25, <10; T >38.5 C.
5.Activity: Bed rest; up in chair as tolerated.
6.Nursing: Inputs and outputs, daily weights.
7.Diet: No added salt. Push oral fluids.
8.Special Medications:
Hypernatremia with Hypovolemia:
If volume depleted, give 1-2 L NS IV over 1-3 hours
until not orthostatic, then give D5W IV to replace
half of body water deficit over first 24hours
(correct sodium at 1 mEq/L/h), then remaining
deficit over next 1-2 days.
Body water deficit (L) =  0.6(weight kg)([Na serum]-
140)
             140
Hypernatremia with ECF Volume Excess:
-Furosemide 40-80 mg IV or PO qd-bid.
-Salt poor albumin (25%) 50-100 mL bid-tid x 48-72
h.
Hypernatremia with Diabetes Insipidus:
-D5W to correct body water deficit (see above).
-Pitressin 5-10 U IM/IV q6h or desmopressin
(DDAVP) 4 mcg IV/SQ q12h; keep urine specific
gravity >1.010.
9. Extras: CXR, ECG.
10. Labs: SMA 7&12, serum osmolality, liver panel,
ADH, plasma renin activity. UA, urine specific gravity.
Urine osmolality, Na, 24h urine K, creatinine.
Hyponatremia
1.Admit to:
2.Diagnosis: Hyponatremia
3.Condition:
4.Vital Signs: q4h. Call physician if BP >160/90, <7-
0/50; P >140, <50; R>25, <10; T >38.5 C.
5.Activity: Up in chair as tolerated.
6.Nursing: Inputs and outputs, daily weights.
7.Diet: Regular diet.
8.Special Medications:
Hyponatremia with Hypervolemia and Edema (low
osmolality <280 mOsm/L, UNa <10 mmol/L:
nephrosis, heart failure, cirrhosis):
-Water restrict to 0.5-1.0 L/d.
-Furosemide 40-80 mg IV or PO qd-bid.
Hyponatremia with Normal Volume Status (low
osmolality <280 mOsm/L, UNa <10 mmol: water
intoxication; UNa >20: SIADH, diuretic-induced):
-Water restrict to 0.5-1.5 L/d.
-Conivaptan (Vaprisol) 20 mg IV over 30 minutes
once, followed by a continuous infusion of 20 mg
over 24 hours. If the response is insufficient,
increase dose to 40 mg/24 hours; max 4 days.
Hyponatremia with Hypovolemia (low osmolality <280
mOsm/L) UNa <10 mmol/L: vomiting, diarrhea, third
space/respiratory/skin loss; UNa >20 mmol/L:
diuretics, renal injury, RTA, adrenal insufficiency,
partial obstruction, salt wasting:
-If volume depleted, give 0.5-2 L of 0.9% saline over
1-2 hours until no longer hypotensive, then 0.9%
saline at 125 mL/h or 100-500 mL 3% hypertonic
saline over 4h.
Severe Symptomatic Hyponatremia:
If volume depleted, give 1-2 L of 0.9% saline (154
mEq/L) over 1-2 hours until no longer orthostatic.
Determine volume of 3% hypertonic saline (513
mEq/L) to be infused:
 Na (mEq) deficit = 0.6 x (wt kg)x(desired [Na] - actual
[Na])
  =     Sodium to be infused
     Volume of solution (L)
(mEq)     
      Number of hrs           (mEq/L in solution) x Num-
ber of hrs
-Correct half of sodium deficit intravenously over 24
hours until serum sodium is 120 mEq/L; increase
sodium by 12-20 mEq/L over 24 hours (1
mEq/L/h).
-Alternative Method: 3% saline 100-300 mL over 4-6h,
repeated as needed.
9. Extras: CXR, ECG, head/chest CT scan.
10. Labs: SMA 7&12, osmolality, triglyceride, liver panel.
UA, urine specific gravity. Urine osmolality, Na.
Hyperphosphatemia
1.Admit to:
2.Diagnosis: Hyperphosphatemia
3.Condition:
4.Vital Signs: qid
5.Activity: Up ad lib
6.Nursing: Inputs and outputs
7.Diet: Low phosphorus diet.
8.Special Medications:
Moderate Hyperphosphatemia:
-Restrict dietary phosphate to 0.7-1.0 gm/d.
-Calcium acetate (PhosLo) 1-3 tabs PO tid with meals
OR
-Aluminum hydroxide (Amphojel) 5-10 mL or 1-2
tablets PO before meals tid.
Severe Hyperphosphatemia:
-Volume expansion with 0.9% saline 1-2 L over 1-2h.
-Acetazolamide (Diamox) 500 mg PO or IV q6h.
-Consider dialysis.
9. Extras: CXR PA and LAT, ECG.
10. Labs: Phosphate, SMA 7&12, magnesium, calcium.
UA, parathyroid hormone.
Hypophosphatemia
1.Admit to:
2.Diagnosis: Hypophosphatemia
3.Condition:
4.Vital Signs: qid
5.Activity: Up ad lib
6.Nursing: Inputs and outputs.
7.Diet: Regular diet.
8.Special Medications:
Mild to Moderate Hypophosphatemia (1.0-2.2 mg/dL):
-Sodium or potassium phosphate 0.25 mMoles/kg in
150-250 mL of NS or D5W at 10 mMoles/h.
-Neutral phosphate (Nutra-Phos), 2 tab PO bid (250
mg elemental phosphorus/tab) OR
-Phospho-Soda 5 mL (129 mg phosphorus) PO bid-
tid.
Severe Hypophosphatemia (<1.0 mg/dL):
-Na or K phosphate 0.5 mMoles/kg in 250 mL D5W or
NS, IV infusion at 10 mMoles/hr OR
-Add potassium phosphate to IV solution in place of
maintenance KCL; max IV dose 7.5 mg
phosphorus/kg/6h.
9. Extras: CXR PA and LAT, ECG.
10. Labs: Phosphate, SMA 7&12, Mg, calcium, UA.