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Orders in Burn Care

 

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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