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Orders in Burn Care

 

Chapter 8: Procedures, Tests, and Monitoring

 

PROCEDURES
_________INSERT NG TUBE
_________START PERIPHERAL IV
_________INSERT FOLEY CATHETER

TESTS
_________CBC
_________SERUM CHEMISTRIES
_________ABG
_________CARMOXYHEMOGLOBIN
_________URINALYSIS
_________TYPE AND SCREEN
_________TYPE AND CROSSMATCH
_________SICKLE CELL PREP
_________PREALBUMIN
_________URINE FOR PREGNANCY TEST
_________PT, PTT

MONITORING
_________PULSE OXIMETRY
_________VITALS SIGNS__________________________
_________CIRCULATION CHECKS OF INVOLVED EXTREMITIES__________________________
_________DAILY WEIGHTS

I.                   Proceudres

A.      Insert NG tube

Reasons for inserting an NG tube:

1.       To promptly initiate tube feedings

2.       Because of the risk of ileus during the immediate post-burn period in patients with burns greater than 20%TBSA, a nasogastric tube is necessary to evacuate gastric contents, thereby preventing emesis and aspiration.

B.      Start Peripheral IV

1.       Two large bore peripheral intravenous catheters should preferably be placed through nonburned viable tissue.

 

2.       If necessary, placement of intravenous catheters through burned skin is justified early postburn when the eschar is still sterile, since delays in resuscitation carry a high mortality.

 

3.       Priority of peripheral access sites:

a.    unburned tissue

b.    burned tissue

c.    central venous access

i.               subclavian vein- most desirable site due to lowest infection rate

ii.            internal jugular vein

iii.         femoral vein

 

C.      Insert Foley catheter

1.          Foley catheter should be placed in all patients undergoing resuscitation for severe burns and in patients with smaller burns with a history of difficulty voiding.

2.           A loose-fitting catheter should be placed to prevent urethral stricture.

3.          The catheter should remain in place throughout resuscitation.

               

II.               TESTS

A.    CBC on admission

1.       An elevated hematocrit is commonly seen in burn patients due to intravascular volume depletion.

2.       For patients who are being resuscitated, a CBC should be obtained every eight hours during the first 24 hours, and at least once daily thereafter.  A CBC should also be checked one hour after blood transfusion.

3.       Normal hemoglobin and hematocrit values (Table I):

 

 

 

 

 

 

 

 

 

Table I

Normal Hematological Values

 

Age                                    Hg (gm%)                            Hct (%)

                        <6 months

14.5-22.5

45-67

6mo- 2yrs

10.5-13.5

33-39

12-18yrs (male)

13-16

37-49

12-18yrs (female)

12-16

36-46

>18yrs (male)

13.5-17.5

41-53

>18yrs (female)

12-16

36-46

 

 

4.       White Blood Count

Granulocytosis peaks during the first postburn day and the white blood count (WBC) then falls in response to dilutional effects of resuscitation and margination of leukocytes.  At this point, the patient is then dependent on the bone marrow to respond with increased WBCs.  Following this, there either is a leukocytosis or a leukopenia.17,[i],[ii]

5.       Platelets

a.    During the resuscitative phase of burns, platelet levels fall due to both dilution and consumption.[iii]   This may be related to a serum effect, as labeled platelets from normal, unburned individuals have a reduced half-life if infused into a burned patient in the first postburn week.[iv] 

b.    There then follows either a thrombocytosis or a thrombocytopenia, which is considered an early indicator of sepsis.[v]  

c.    Thrombocytosis in patients with severe burns may actually obscure platelet destruction, which can be seen in patients with disseminated intravascular coagulation (DIC).

d.   Platelets should be transfused in the setting of either thrombocytopenia (<20,000 platelets/mm3) or active bleeding.  Platelets should be used sparingly, as repeated transfusions can produce platelet antibodies. 

 

B.    Serum chemistries

1.                A metabolic profile with the common electrolytes: Na, K, Cl, CO2 as well as BUN, creatinine, and serum glucose should be obtained on admission and daily for patients undergoing resuscitation.

2.             Calcium

a.    Hypocalcemia can occur up to 7 weeks post burn.[vi],[vii],[viii] The normal  total serum calcium level is between 8.9-10.3 mg/dl.  The normal ionized calcium level is between 4.6-5.1 mg/dl.  Albumin adjustment is necessary, when measuring total serum calcium, for assessment of true calcium status.[ix]  

b.    The hallmark of hypocalcemia is increased neuronal membrane irritability and tetany.  Manifestations of this are laryngospasm, bronchospasm, respiratory arrest, abdominal cramping, urinary frequency, irritability, depression, dementia, hypotension, heart failures, and arrhythmias. 

c.    Calcium levels should be checked on admission and daily and also after each calcium supplementation.

3.          Phosphorus

a.      Burns induce a decrease in serum phosphorus levels, with the lowest levels reached between the second and fifth days.[x]  Normal levels are usually not reached again until the tenth postburn day despite aggressive phosphorus supplementation.[xi]

b.      Phosphate provides the primary energy bond in ATP.

c.       Depletion of phosphate causes cellular energy depletion.

d.      Possible causes of postburn hypophosphatemia include:

i.   fluid resuscitation

ii.   carbohydrate administration

iii.                     elevated catecholamines

iv.                      phosphate binding acids and/or sucralfate

v.    acid-base disturbances

vi.                      electrolyte imbalance

vii.                   carbonic anhydrase inhibition (from mafenide acetate)

e.       Clinical manifestations of hypophosphatemia include:

i.   CNS- lethargy, malaise, neuropathy, seizures, and coma

ii.      Cardiovascular- hypotension, and cardiac decompensation

iii.   Pulmonary- tachypnea, decreased vital capacity, and respiratory failure

iv.          Dysphagia

v.       Renal- glycosuria, calcuiuria, magnesuria, and renal tubular acidosis

vi.    Musculoskeletal- weakness, myalgia, arthralgia, and rhabdomyoloysis[xii]

        f.   Serum  phosphorus levels should be measured daily and phosphorus supplementation initiated for levels below 2.0 mg/dl.  Severe hypophosphatemia (i.e. below 1.0 mg/dl) should be corrected with intravenous phosphorus in the form of sodium or potassium phosphate at a dosage of 0.16 mm/kg phosphorus i.v..  Repeat phosphorus levels should be checked following the completion of supplementation.  Mild hypophosphatemia can be corrected with Neutra-phos 1 packet qid or Kphos 1-2 tabs tid.

 

   4.  Magnesium

1.    Hypomagnesemia in the burn patient is less commonly described and seems to occur only on postburn day 3.19 

2.    Magnesium is important for all reactions requiring ATP and in all reactions involving replication, transcription, and translation of nucleic acids.1

3.    Manifestations of hypomagnesimia (i.e. below 1.7 mg/dl) are similar to hypocalcemia, with increased neuronal irritability and tetany.[xiii]  Most symptomatic patients have serum magnesium levels less than 1.0 mg/dl.  Symptoms include weakness, lethargy, muscle spasms, paresthesias, and depression.  Severe hypomagnesemia may induce seizures, confusion, and coma.  Cardiovascular abnormalities include coronary artery spasm, cardiac failure, dysrhythmias, and hypotension. 

4.    Magnesium is commonly supplemented whenever the level falls below 2.0 mEq/L.  For patients unable to take oral medication, magnesium sulfate 2g iv is given.  Oral forms are magnesium gluconate 250-500 mg po qd or magnesium oxide 140-800 mg po qd or divided bid.  Magnesium levels should be checked once on admission and after every magnesium supplementation.

 

C.     Arterial Blood Gas (ABG) and Carboxyhemoglobin

1.    An ABG should be checked daily while the patient remains intubated and after a change in ventilator settings.      

 

 

Arterial Blood Gas Values

Normal Value

pH:  7.35-7.45

pCO2:  32-45mmHG

NaHCO3:  22-28mmHg/L

Compensation

Respiratory Alkalosis

up

down

normal until compensation

Kidneys will decrease NaHCO3.  This cannot be done quickly

Respiratory Acidosis

down

up

normal until compensation

Kidneys will increase NaHCO3.  This cannot be done quickly.

Metabolic Alkalosis

up

normal until compensation

up

Lungs will try to increase CO2.  This can be done quickly.

Metabolic Acidosis

down

normal until compensation

down

Lungs will try to decrease CO2.  This can be done quickly.

 

 

Normal Carboxyhemoglobin Levels[xiv]

 

Nonsmokers

<2%

Smokers

5-9%

   

 

2.    A carboxyhemoglobin level should be checked if inhalation

      injury is suspected.

3.    With smoke inhalation there is an associated exposure to carbon monoxide.  Carbon monoxide has an affinity for the hemoglobin molecule that is 250 times that of oxygen.  With higher levels of carbon monoxide, the oxygen dissociation curve is shifted to the left, impairing oxygen delivery.  Patients may manifest no signs of peripheral cyanosis, but will instead appear cherry red.  Oxygen at an FIO2 of 1.0 should be administered, as it will decrease the half-life of carbon monoxide in blood from 250minutes to 40 minutes.

 

D.      Urinalysis

Urinalysis is used to check for the presence of hemoglobin and myoglobin in the urine.  If not detected and cleared from the renal tubules, these pigments will precipitate and cause renal failure.1  If myoglobin is present, urinalysis should be checked every 2 hrs for first 8hrs if initially elevated, and then every shift thereafter if the myoglobin level is decreasing and urine output is sufficient.

 

E.      Type and screen/type and cross match

                  1.    Type and screen patients expected to require excisional surgery. Blood losses can be approximately 0.75ml/cm2 of excised area.

2.   Anemia

a.     This is expected in patients with full-thickness burns involving greater than 10%TBSA, due to lysis of cells damaged by heat and, microvascular thrombosis.

b.     The decision to transfuse should depend on the clinical situation of the patient.  Optimally the hematocrit should be above 35.

3.   Patients with chronic anemia tolerate hemoglobin levels of 7 to 8 gm. per 100 ml. or less, as has been demonstrated in patients with chronic renal failure and in Jehovah's Witnesses. The cardiac output in such patients does not increase until the hemoglobin falls below approximately 7 gm. per 100 ml. Young healthy patients tolerate acute anemia to hemoglobin levels of 7 gm. per 100 ml. or less provided they have a normal intravascular volume and high arterial oxygen saturation.

4.   An equal number of units of FFP as units of packed red blood cells (RBCs) should be ordered. 

 

F.  Sickle cell prep

      1.             Pathophysiology

Sickle hemoglobin forms polymers when deoxygenated. In hemoglobin S, a substitution of T for A in the sixth codon of the (beta)-globin gene leads to the replacement of a glutamic acid residue by a valine residue. On deoxygenation, hemoglobin S polymers form, causing cell sickling and damage to the membrane. Some sickle cells adhere to endothelial cells, leading to vaso-occlusion,[xv] which can result in acute episodes of severe pain in the chest, back, abdomen, or extremities (crises). Multiple areas are often involved simultaneously, and symmetric involvement of the extremities is common. The episodes last for days or even weeks.

2.  Testing

Newborns should have routine blood testing for all major hemoglobinopathies, including sickle cell anemia, if not already done prior to admission.

3.  Distribution

In the US, sickle cell disease is found primarily in the African American population. Sickle cell disease also is found in white or Hispanic individuals who are originally from Central America, South America, and the Caribbean. The disease also occurs in individuals of Arab, East Indian, Greek, or Italian descent.

 

G.          Prealbumin

Should be checked on admission and weekly.  Studies have shown that the use of these this short-life proteins as an effective nutritional marker during short-term nutritional support.  A weekly rise in plasma prealbumin had a sensitivity of 88%, specificity of 70%, positive predictive value of 93%, and negative predictive value of 56% in detecting positive nitrogen balance. Prealbumin was found to be the most suitable plasma protein for use as a dynamic index of nutritional progress.[xvi],[xvii]

 

 

H. Pregnancy

                   1.  Tests

a.     A urine sample should be sent for qualitative pregnancy test in all females between the ages of 11 and 45. 

b.     Approximately 7 percent of women of reproductive age who are seen for treatment of burn injuries are pregnant[xviii],[xix],[xx]   One study tested all patients aged 12 to 44 years preoperatively and found that of 16,033 anesthetics administered, 1,849 (12.5%)  of patients ages 13 to 44 years were pregnant.  One patient conceived at the age of 12.[xxi] 

c.      The detection of the beta subunit of human chorionic gonadotropin (HCG) in urine or serum is the reference standard (or "gold standard") for diagnosing routine early pregnancy. The diagnostic reliability of both the serum and urine HCG tests are comparable. The sensitivity and specificity for the diagnosis of pregnancy for both tests are between 97% and 100%.[xxii]

 

    2.     Risks

a.        Maternal and perinatal morbidity and mortality increase as the total body surface area burned increases, with the greatest risk occurring with a total body surface area burn of over 60 percent   Fetal risk has been shown to correspond with maternal well-being. Most fetuses survive when the mother survives and remain free of severe complications such as sepsis, hypotension, and hypoxia.43,44,45,[xxiii],[xxiv],[xxv],[xxvi],[xxvii],[xxviii]   

b.        A burn injury during pregnancy presents two important problems:  1) spontaneous uterine activity and 2)  intrauterine fetal demise. Severe burns and sepsis are associated with high levels of prostaglandins. Phospholipase A, an enzyme necessary for synthesis of arachidonic acid and eventually prostaglandins, is released from bacteria and/or the amnion, enhancing  spontaneous uterine activity leading to preterm labor.[xxix]   

c.        Carbon monoxide is frequently inhaled in a closed fire and freely crosses the placenta. Because fetal hemoglobin has a higher affinity for binding carbon monoxide, the effects may be more pronounced in the fetus than in the adult. Exposure to carbon monoxide in utero may affect cardiac development and may produce fetal cardiac edema.[xxx]

d.       Septicemia and pneumonia account for almost half of all deaths in burn patients and their fetuses.[xxxi]  The most common pathogens include Pseudomonas species, Staphylococcus aureus, Group D Enterococcus, and Candida albicans.[xxxii]

 

3.      Treatment

a.        Patients with minor burns (less than 10% TBSA) often do not require hospitalization, and there is rarely a threat to maternal or fetal well-being.

b.        Major burns[xxxiii] can be divided into three phases of recovery:  emergency, acute, and rehabilitative.[xxxiv]

c.        The Emergency phase encompasses the first 48 to 72 hours after a burn. Oxygenation and ventilatory support is essential in the pregnant patient because of the decreased pulmonary reserve of the mother and the inability of the fetus to tolerate prolonged hypoxia    Adequate urine output is considered to be 0.5 ml/kg/hr. Tetanus immunoglobulin is safe in this period and should be administered.[xxxv]  Radiographic studies should not be avoided when warranted, and with proper abdominal shielding should present minimal risk to the fetus.[xxxvi] Topical povidone-iodine solution, used in the cleansing of burn wounds, should be avoided because large amounts of iodine may be absorbed through the wound.[xxxvii]   Silver sulfadiazine (silvadene) can cause kernicterus in the fetus,[xxxviii] but is a problem confined mostly to the newborn period.

i.            The mother should be maintained in the left lateral decubitus position as much as possible after the second trimester to avoid supine hypotension and risk fetal compromise.

ii.            With acute volume depletion, compensatory mechanisms in the mother will maintain hemodynamic stability whilst decreasing uteroplacental perfusion. 

iii.            Due to a 35 to 40 percent increase in total blood volume during pregnancy, a higher volume loss is tolerated

iv.            The pulse rate increases approximately 15 percent in pregnancy, and blood pressure decreases in mid pregnancy. Although these signs may be early signs of shock in the nonpregnant woman, they are physiological in the pregnant patient.

v.            External fetal monitoring should also be undertaken. Fetal compromise is manifested by baseline tachycardia, loss of accelerations, and prolonged or late decelerations[xxxix]

4                    The Acute phase begins at the end of the emergency phase and lasts until all full-thickness wounds are covered with autografts.  Succinylcholine should be avoided because of the danger of hyperkalemia.  Instead, a nondepolarizing muscle relaxant such as curare or pancuronium is preferred.[xl]

5                    Adequate nutritional support is essential during this period.  When calculating caloric requirements, the developing fetus and the catabolic state should be considered. Once refeeding has started, an antacid should be given because of the increased risk of gastric ulceration.

6                    Rehabilitative phase

a.    Once autografting has reduced the wound to less than 20 percent total body surface area, the threat to life decreases greatly.64  There are no prospective studies showing a benefit to heparinization in the pregnant burn patient who is not ambulatory.

b.    When there are extensive medical complications and/or a total body surface area burn of more than 50 percent, delivery is strongly encouraged for a fetus with an estimated gestational age >26 weeks due to the high maternal and perinatal morbidity and mortality rate.[xli]

 

I.                    PT, PTT

1.          Disorders of the coagulation cascade are followed by checking the prothrombin (PT) and partial thromboplastin (PTT) values on admission and after clotting factors have been administered.  Clotting factors are readily supplied via fresh frozen plasma (FFP). 

2.          The thrombotic and fibrinolytic mechanisms are activated following a burn from what is felt to be a dilution of clotting factors.[xlii]    Subsequently there is decrease in antithrombin III, protein C, and protein S levels and an increase in tissue plasminogen activator, which further increases thrombogenesis and fibrinolysis.  The frequency of coagulopathy in the burn patient is best reduced by adequate fluid resuscitation and early burn wound excision.

 

III.    MONITORING

                 A.    Vital signs and pulse oximetry

1.            Vital signs should be recorded hourly for patients who are hemodynamically unstable or in critical condition.  Otherwise vital signs should be recorded every 8 hours. The pulse oximeter is used to provide a real-time, noninvasive assessment of oxygenation.   Pulse oximetry should be used in all intubated patients and those on oxygen via nasal canula.  Hourly records of oxygen saturation are required with hypoxemia. 

2.      The pulse oximeter probe contains two electrodes, which emit light of specific wavelength through a cutaneous vascular bed, such as that of the digits or the ear lobe. A photodiode detector at the far side measures the intensity of transmitted light at each wavelength, from which oxygen saturation can be derived.[xliii]

3.      In most nonsmokers, COHb levels will be less than 2%. Heavy smokers have shown levels as high as 10% to 20%. Levels can be much higher still in significant carbon monoxide exposure. The pulse oximeter is unable to distinguish carboxyhemoglobin (COHb) and (MetHb) at the wavelengths used to determine the absorbances of hemoglobin and oxyhemoglobin.  Both COHb and MetHb will absorb light within the red to near-infrared range used by pulse oximetry.  Thus, the oximeter will read normal oxygen saturation levels even in the face of  carboxyhemoglobinemia and methemoglobinemia.

b.          Pulse rate

1.      Following a burn, tachycardia is inevitable,

due to accompanying hypovolemia and release of catecholamines as a result of tissue trauma and pain.

2.      A pulse rate lower than 120 beats/min

 usually indicates adequate volume. Whereas

 a pulse rate higher than 130 beats/min

 usually suggests inadequate resuscitation.

3.      Beware that in the elderly or those with

preexisting heart disease, the heart rate may not be able to increase in proportion to the stimulus.

C.          Blood pressure

1.      A minimal mean arterial pressure of

90mmHg should be maintained for adequate tissue perfusion.

2.      If the patient is hemodynamically unstable,

the extremities are burned or if frequent measurement of arterial blood gases are required, insertion of an arterial catheter may be necessary.

D.          Urine Output

1.          This is the single best monitor of fluid replacement.

2.          Acceptable values are 0.5ml/kg/hr in an adult and at least 1ml/kg/hr in a child.

          E.       Circulation checks of involved extremities

1.      Any patient with full thickness

circumferential burns requires immediate escharotomy, whether the burns are on the extremities, chest wall, or abdomen.

2.      Burn eschar is inelastic, and the edema that

forms may exceed venous and arteriolar pressure, impeding blood flow. Edema formation can be reduced by continuous elevation of the burned part.

3.  The clinical signs of compromised limb blood flow are the “five P’s:”

a.    Pain

b.    Pallor

c.    Paresthesias

d.   Pulselessness- the pulses are the last to go

e.    Perishing with Cold

F.    Escharotomy is performed on the ward 

1.    Conscious sedation is usually necessary.

2.    The eschar on a limb is incised in the mid-lateral lines, extending from the proximal to the distal extent of the burned area. Incisions should not be carried across joints, and should be deep enough into the superficial fascia to allow the wound edges to separate.  Bleeding is controlled with electrocautery. 

3.    Chest wall escharotomy incisions should be placed in the anterior axillary line bilaterally, extending from the clavicle to the costal margin. 

4.    If the anterior abdominal wall is involved, a costal incision should be used to connect the anterior axillary escharotomies. 

5.    If an escharotomy does not restore blood flow, fasciotomy may be required in the operating room.   Fasciotomies may be necessary following high-voltage electric injuries and limb trauma.

 

                    G.            Daily Weights

Weight should be measured daily, as changes in weight from   admission allow an assessment of fluid balance[xliv] and nutrition.[xlv] 

 

 

 



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[iii] Bartlett RH, Fong SW, Marrujo G, Hardeman T, Anderson W.  Coagulation and platelet changes after thermal injury in man.  Burns 1981; 7:370-7.

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[viii] Szyfelbein SK, Drop LJ, Martyn JA.  Persistent ionized hypocalcemia in patients during resuscitation and recovery periods of body burn.  Crit Care Med 1981;9: 454-458.

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[xi] From the US Army Institute of Surgical Research, Fort Sam Houston, Texas, USA.

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[xviii]Akhtar MA, Mulawkar PM, Kulkarni HR. Burns in pregnancy: Effect in maternal and fetal outcomes. Burns 1994;20:351-355.

[xix] Amy BW, McManus WF, Goodwin CW et al. Thermal injury in the pregnant patient. Surg Gynecol Obstet 1985;161:209-212.

[xx] Gang RK, Bajec J, Tahboub M. Management of thermal injury in pregnancy-An analysis of 16 patients. Burns 1992;18:317-320.

[xxi] Kempen PM. Norton P. Vu H. A risk index for pregnancy during anesthesia. Journal of Clinical Anesthesia. 9(3):194-9, 1997 May.  

[xxii]O'Connor RE, Bibro CM, Pegg PJ, Bouzoukis JK. The comparative sensitivity and specificity of serum and urine HCG determinations in the ED. Am J Emerg Med. 1993;11:434-436.

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[xxv] Rayburn W, Smith B, Feller I et al. Major burns during pregnancy: Effects on fetal well-being. Obstet Gynecol 1984;63:3:392-395.

[xxvi] Rode H, Millar AJW, Cywes S et al. Thermal injury in pregnancy-The neglected tragedy. S Afr Med J 1990;77:346-348.

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[xxx] Fechter LD, Thakur M, Miller B et al. Effects of prenatal carbon monoxide exposure in cardiac development. Toxicol Appl Pharmacol 1980;56:370-375.

[xxxi] Feller I, Archambeault C. Nursing the burned patient. Ann Arbor: National Institute for Burn Medicine, 1973.

[xxxii] Smith BK, Rayburn WF, Feller I. Burns and pregnancy. Clin Perinatol 1983;10:383-398.

[xxxiii] Reiss G. Thermal Injuries. In: Lopez-Viego MA, ed. The Parkland Trauma Handbook. St. Louis: Mosby, 1994, pp. 389-412.

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[xxxvi] Bocka J, Courtney J, Pearlman M et al. Trauma is pregnancy. Ann Emerg Med 1988;178:829-834.

[xxxvii] Pietsch J, Meaklins JL. Complications of povidine-iodine absorption in topically treated burn patients. Lancet 1976;1:280-282.

[xxxviii] Briggs GB, Freeman RK, Yaffe SJ. Drugs in Pregnancy and Lactation, 3rd Ed. Baltimore: Williams & Wilkins, 1990, pp. 581-583.

[xxxix] Shere DM, Schnenkier JF. Accidental injury during pregnancy. Obstet Gynecol Surv 1989;44:330.

[xl] . Gronert GA, Theye RA. Pathophysiology of hyperkalemia induced by succinylcholine. Anesthesiology 1975;43:88-99.

[xli] Smith BK, Rayburn WF, Feller I. Burns and pregnancy. Clin Perinatol 1983;10:383-398.

[xlii] Bartlett RH, Fong SW, Marrujo G, Hardeman T, Anderson W.  Coagulation and platelet changes after thermal injury in man.  Burns 1981; 7:370-7.

[xliii] Sinex JE. Pulse oximetry: principles and limitations.  Am J Emerg Med - 1999 Jan; 17(1): 59-67.

[xliv] Gump FE, Kinney JM:  Energy balance and weight loss in burned patients, Arch Surg 103:442-448, 1971.

[xlv] Morath MA, Miller SF, Finley RK, Jones LM:  Interpretation of nutritional parameters in burn patients, J Burn Care Rehabil 4:361-366, 1983.

 

 


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