|
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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TE, et al. Plasma
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284-93.
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