Chapter 14:
Medications
_________TETANUS IMMUNIZATIONS
VITAMINS
Adults
________MULTIVITAMINS
1 TAB PO QD
________FOLIC
ACID 1MG PO QD
________VITAMIN
A 25, 000 UNITS PO QD
________ZINC
SULFATE 220 MG PO QD
________FERROUS
SULFATE 300 MG TID
________ASCORBIC
ACID 500 MG TID
Children
________POLY
VISOL W/IRON 1ML
________ASCORBIC
ACID 250 MG QD
________ZINC
SULFATE 55MG
ULCER PROPHYLAXIS
_________________
ANALGESIA
________________
________________
I.
Tetanus Immunization
For tetanus
prophylaxis, tetanus toxoid 0.5 ml should be provided unless
the patient has received tetanus immunization within the past
5 years.
II.
Vitamins
A.
There are no formal
rules governing vitamin and trace element supplementation in
burn patients. Most
recommendations are based on observations of burn wound
nutrient losses or low serum or tissue nutrient levels.
These losses are often difficult to evaluate clinically
in burn patients. In addition, metabolic changes as a result of the burn may
obscure other deficiencies.
B.
Vitamin A
Vitamin A stimulates and enhances
collagen accumulation in wounds and is required to generate an
adequate inflammatory response.[i],[ii]
C.
Thiamin
Thiamin is necessary for lysyl oxidase function in the formation of
collagen.2
D.
Riboflavin
Riboflavin is an element of the group of coenzymes flavin mononucleotide
(FMN) and flavin adenine dinucleotide (FAD) involved in
oxidation-reduction reactions of the electron transport chain
and in amino and fatty acid metabolism.
E.
Niacin
Niacin is an essential component of nicotinamide adenine dinucleotide (NAD)
and nicotinamide adenine dinucleotide phosphate (NADP), which
are electron transport carriers.
NAD and NADP are involved in scores of reactions of the
Krebs cycle, fatty acid metabolism, and glycolysis.
F.
Vitamin B6
Vitamin B6, or pyridoxine, is a coenzyme in amino acid
metabolism.
G.
Folic Acid
Folic acid is a substrate in reactions of DNA and RNA synthesis.
Inadequate vitamin B12
levels prevent folate utilization.
Thus folic acid and vitamin B12
deficiency produce the same physical signs (i.e.
hyperpigmentation, inflmammation, stomatitis, filiform
papillary atrophy, pallor of everted lower eyelids).
H.
Vitamin B12
Vitamin B12 deficiency
can result in loss of carnitine interfering with fatty acid
metabolism.
I.
Vitamin C
A free radical scavenger, and thus may benefit patients during fluid
resuscitation, since superoxide, hydroxyl, and
peroxide are elaborated as a result of the postburn
inflammatory response. These
substances may cause increase vascular permeability[iii],[iv],
and studies of high-dose vitamin C administration showed
reduced required fluid volume during resuscitation.[v]
Vitamin C may also improve vitamin E levels.[vi]
Vitamin C is an essential co-factor in the hydrolysis of
proline and lysine in collagen biosynthesis.
Thus, lack of vitamin C causes capillary fragility and
wound breakdown.
J.
Vitamin E
Vitamin E (a-tocopherol)
is a scavenger for lipid peroxyl radicals (LOO-).
K.
Copper
Copper is an essential component of superoxide dismutase, a free radical
scavenger. Copper
levels are related to ceruloplasmin, the copper plasma binding
protein. Ceruloplasmin
levels of fall, perhaps from leakage into the interstitium,
bringing copper along with it.[vii]
Copper levels are also decreased during the stress
response as a result of elevated hydrocortisone which promotes
biliary excretion of copper.[viii]
L.
Zinc
Zinc is needed for retinol binding protein (RBP) synthesis in the liver.
Reduced zinc levels cause decreased wound
epithelialization and collagen strength.
Zinc is also a component of the free radical scavenger
superoxide dismutase. The
hypermetabolism induced by the burn state causes excretion of
zinc at a rate five times normal.[ix],[x]
M.
Iron
Inflammation causes a decrease in intestinal iron absorption, a
decreases in iron release from parenchymal storage sites, and
an increase in ferritin.
These factors lead to low serum iron concentrations
after injury or infection. Low iron levels also impair the immune response.
N.
Selenium
Selenium is a component of the enzyme glutathione peroxidase, which has
a role in protecting against cellular oxidative damage.
Selenium also protects against silver, cadmium, and
mercury toxicity.[xi]
III.
Ulcer Prophylaxis
A.
Burn patients are prone to peptic ulceration
1.
The cause of stress ulceration is multifactorial,
and includes not only mucosal ischemia, but also increased
acid, bile reflux, and direct mucosal injury from intraluminal
tubes.
2.
Ulcers occur most frequently in septic patients and
those with large burns.[xii]
Ulcer perforation occurs in 12% of patients, but only
1/3 of these patients will feel pain or discomfort.
Since early fluid resuscitation, early antacid therapy,
and early enteral feeding have become standard in the
treatment of the burn patient, the incidence of clinical
gastroduodenal disease decreased to less than 2%.[xiii],[xiv]
B.
Prevention of stress
ulceration involves acid reduction and aggressive fluid
resuscitation to minimize mucosal ischemia.
1.
The early institution
of enteral feedings after a burn will provide acid buffering
and nutrition. Antacids,
histamine-2-receptor (H2) antagonists, and
sucralfate are considered equally effective in preventing
stress ulcer-related GI bleeding.[xv],[xvi]
2. Excellent prospective studies have shown the efficacy of
either H2-blockers or antacids in decreasing the
incidence of stress ulceration
II.
Analgesia
A.
Adults and patients >40kg
1.
Acetaminophen
(Tylenol) (500mg 1-2 tabs po q6hr prn)
for mild pain. It
is
well tolerated, and rarely causes gastrointestinal side
effects as can be encountered with ibupofren and other NSAIDs.
2.
For
moderate pain, Vicodin (1-2 tabs po q4-6hrs prn) is used. This
Contains acetaminophen
500mg and hydrocodone 5mg. Acetominophen toxicity is not an
issue at this dose
3.
If the above is
inadequate, administer morphine (2-4mg iv q1-2hrs prn). All
patients requiring fluid resuscitation should be treated with
intravenous analgesia
B.
Children and patients<40kg
1.
Acetominophen
(Tylenol) (15mg/kg po q6h prn) for mild pain.
An acetominophen level should be checked the next day
one hour after a dose, then weekly (qMonday) thereafter.
2.
Lortab elixir (acetominophen
500mg/Hydrocodone 7.5mg per 15ml) for moderate pain. 0.6 mg
hydrocodone/kg/day po divided q6-8hrs (Max dose 1.25 mg/dose
if <2 yrs
if
2-12 yrs old, give 5mg/dose
if
>12 yrs old, give 10mg/dose
3.
Morphine (0.03 to 0.05
mg/kg iv q4h prn) if acetominophen is inadequate and for
procedures.
V. Sedation
A.
For mild anxiety, use
diphenhydramine (Benadryl)
B.
Intubated patients
should receive a Versed infusion
C.
Benzodiazepine
overdose
1.
When opioids are given
concurrently with benzodiazepines, cardiovascular and respiratory depression may result. Midazolam (VersedÒ)
has a rapid onset and a short half-life (3 hrs).
2.
Treatment for
overdosage includes the use of the specific benzpdiazepine
antagonist flumazenil (RomazoiconÒ)
and support of respiratory and cardiovascular function.
For benzodiazepine sedation reversal, give RomaziconÒ,
0.2 mg iv over 15 sec, then 0.2 mg q1 min prn up to 1mg total.
For overdose reversal, RomaziconÒ
0.2mg iv over 30 sec, then 0.3-0.5 mg q30 sec prn up to 3mg
total dose. RomaziconÒ
is contraindicated in mixed drug overdose or chronic
benzodiazepine use.[xvii]
Additional doses may be required after several hours
[i]
Demetriou AA, Levenson SM, Retture G, Seifter E.
Vitamin A and retinoic acid:
induced fibroblast differentiation in vitro.
Surgery 1985; 98:
931-34.
[ii]Goodson
WH, Hunt TK. Wound healing. In:
Kinney JM, Jeejeebhoy KN, Hill GL, Owen OE eds.
Nutrition and Metabolism in Patient Care.
Philadelphia:
WB Saunders, 1988: 635-42.
[iii]
Demling RH, Katz A, Lalonde C, Ryan P, Tin L-J.
The immediate effect of burn wound excition on
pulmonary function in sheep:
the role of prostanoids, oxygen radicals and
chemoattractants. Surgery
1987; 101: 44-5.
[iv]
Till GO, Guilds LS, Mahrougui M, Friedl HP, Trentz O, Ward
PA. Role of
xanthine oxidase in thermal injury of skin.
Am J Pathol 1989; 135: 195-202.
[v]
Matsuda T, Tanaka H, Shimazaki S, et al.
High dose vitamin C therapy for extensive deep
dermal burns. Burns
1992; 18:127-31.
[vi]
Machlin LJ, Langseth L. Vitamin-vitamin Interactions.
In: Bodwell
CE, Erdmand JW, eds.
Nutrient Interactions.
New York: Marcel
Dekker, Inc., 1988: 287-312.
[vii]
Brian JE, Caldwell FT, Wood RC.
Hypocupremia in a major burn.
J Trauma 1987; 27: 335-6.
[viii]
Hill CH, Starcher B, Matrone G.
Mercury and silver interrelationship with copper.
J Nutr 1977; 107:
1889-95.
[ix]
Ronaghy HA. The
role of zinc in human nutrition.
World Rev Nutr Diet 1987; 54:237-54.
[x]
Prasad AS. Zinc
in growth and development and spectrum of human zinc
deficiency. J
Am Coll Nutr 1988; 7:377-84.
[xi]
Levander OA, Cheng L. Micronutrient Interactions:
Vitamins Minerals and Hazardous Elements. New York: Academy
of Sciences, 1980: 335-72.
[xii]
Pruitt BA, Goodwin CW. Stress ulcer disease in the burned patient.
World J Surg 1981; 5: 209-22.
[xiii]
Jones WG, Minei JP, Barber AE, Fahey TJ, Shires GT III,
Shires GT. Splanchnic
vasoconstriction and bacterial translocation after thermal
injury. Am J
Physiol 1991; 261: H1190-H1196.
[xiv]
Jones WG, Minei JP, Barber AE, et. Al.
Additive effects of thermal injury and infection in
thesmall bowel. Surgery
1990; 108: 63-70.
[xv]
Shuman RB, Schuster SP, Zuckerman GR: Prophylactic therapy
for stress ulcer bleeding:
A reappraisal .
Ann Intern Med 1987; 106: 562-567.
[xvi]
Tryba M. Sucralfate
versus antacids or H2 andtagonists for stress
ulcer prophylaxis: A
meta-analysis on efficacy and pneumonia rate.
Crit Care Med 1991; 19: 942-9.
[xvii]
The 1999 Tarascon Pocket Pharmacopoeia.
Loma Linda, Ca: Tarascon Publishing. 1999. P. 66.
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