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Chapter 56

TRAUMA
Ralph L. Slepian Jaideep K. Malhotra

A 31-Year-Old Man
sustained a multiple stab wounds to the left upper quadrant of his abdomen
and in the left hemithorax. Vital signs were as follows: blood pressure, 85/60
mm Hg; heart rate, 130 beats per minute; respiratory rate, 32 breaths per
minute; temperature, 34.5C (94.1F). Hematocrit was 27%. He was
emergently brought to the operating room for an exploratory laparotomy and
possible thoracotomy.

A. Medical Disease and Differential Diagnosis


1. How is trauma classified?
Trauma is usually separated into two distinct categories: penetrating and blunt
trauma. Both can cause havoc on the body's vascular, visceral, musculoskeletal, and
nervous systems.

2. What are the injuries associated with thoracic


trauma?
Penetrating injuries associated with thoracic trauma are typically associated
with stabbings and gunshot wounds, the latter being causing far more destruction as
a result of the much greater

amount of kinetic energy being transferred to the thoracic cavity from the impact
of the bullet. As a result, gunshot wounds to the thorax are diffuse and much more
likely to be fatal as compared to stabbings.

Blunt injuries to the chest are far more common than penetrating injuries. The
most common causes of blunt injuries are deceleration injuries (as a result of motor
vehicle accidents) and crush injuries. These can range from relatively minor injuries
such as rib fractures to more severe ones such as lung contusion, tracheobronchial
tears, flail chest, pneumothorax, hemothorax, injuries to the great vessels, and
traumatic ruptures of the esophagus and/or diaphragm.
3. What are the injuries associated with cardiac
trauma?
Penetrating cardiac injuries often lead to immediate cardiovascular collapse
and patients rarely survive to reach the operating room. Blunt cardiac trauma injuries
include cardiac contusion (most common), pericardial ruptures, rupture of a chamber,
valvular tears, coronary artery injuries, and ventricular aneurysms.

4. How is the initial assessment and management of


the trauma patient performed?
A systematic and organized approach to the assessment and management of the
trauma patient has been developed by the American College of Surgeons and is
taught as Advanced Trauma Life Support (ATLS). Initial evaluation and management
as stated by ATLS consists of five components:

The primary survey


Resuscitation
The secondary survey
Continued monitoring and reevaluation
Definitive care

5. What constitutes a primary survey and what is its


objective?
The assessment of the trauma patient consists of the primary and secondary survey.
The function of the primary survey is to identify and treat immediately life-threatening
injuries. The life-threatening injuries associated with chest trauma are:

Lost airway
Tension pneumothorax
Massive hemothorax

Open

6. What constitutes a secondary survey and what is


its objective?
The secondary survey is a more detailed examination aimed at identifying other
non- lifethreatening injuries and planning further laboratory and radiographic studies
and forming a workable differential diagnosis. Examples of chest injuries identified on
secondary survey are the following:

Simple pneumo/hemothorax
Rib fractures
Pulmonary contusion
Non-life-threatening blunt myocardial injury

7. What are the signs and symptoms of a


hemothorax? What is the definition of a massive
hemothorax?
The signs and symptoms of a hemothorax include diminished breath sounds
on the affected side, hemorrhagic shock, and mediastinal shift. A massive hemothorax
is defined as a rapid accumulation of greater than 1,500 mL of blood in the thoracic
cavity.

8. What are the indications for a thoracotomy to


treat a hemothorax?
Hemothorax, if severe enough, can lead to hemmorhagic shock. Therefore,
timely diagnosis and treatment is of utmost importance. After a chest tube is placed, if
drainage of blood is greater than 1,200 mL, or if drainage is greater than 200 mL per
hour for over 4 hours, then a thoracotomy is indicated. Alternatively, if the patient is
older than 60 years, then if drainage is greater than 100 mL per hour for over 4 hours,
a thoracotomy is also indicated. However, if the patient does not meet these criteria
but is still hemodynamically unstable or if ventilation is difficult, then emergent surgery
should be performed.

9. How are pneumothoraces categorized?


Pneumothoraces are categorized into three broad categories: open, closed,
and tension pneumothorax. Pneumothoraces, like hemothoraces, can cause severe
hypoxemia, impair venous return, and cause a severe mediastinal shift.

Open pneumothoraces are a result of penetrating wounds and allow


intrathoracic pressure to equalize with atmospheric pressure. The result is introduction
of outside air every time the patient takes a breath. Definitive treatment is to close the
wound and placement of a chest tube.

Closed pneumothoraces can result from both blunt and penetrating trauma to
the chest. It is defined as the presence of air in the pleural space. Diagnosis can be
made radiographically, but the patients' condition precludes obtaining a chest
radiograph in many trauma situations. In such cases, diagnosis can be made by
physical examination, that is, by percussion or by diminished or absent breath sounds.
Treatment is placement of a chest tube if the patient is unstable or if the pneumothorax
is greater than 10% of the pleural cavity.

Tension pneumothorax is the progressive build up of air within the pleural space
that cannot escape. Essentially, it is a one-way valve which is exacerbated by
positive pressure ventilation. This progressive build up of air can cause a mediastinal
shift, acute rise in airway pressures and obstruction of venous return. All of these
factors can result in a sudden and dramatic cardiovascular collapse.

10. What are the most commonly injured organs in


blunt abdominal trauma?
In blunt abdominal trauma, the most commonly injured organs are the spleen, liver,
kidneys, and bowel. Generally, blunt abdominal trauma leads to higher mortality rates
than penetrating trauma. The reason is multifactorial and includes greater difficulty in
diagnosis and frequent association with other injuries, such as head injury, chest
trauma, and fractures.

11. What is a Focused Abdominal Sonography for


Trauma (FAST) examination?
FAST is a rapid ultrasonography examination performed in the trauma resuscitation
room looking specifically for fluid (blood) in the peritoneum, pericardium, or thorax.
Currently, FAST is indicated for all hemodynamically unstable blunt trauma patients.
It may also have a role in some patients with penetrating trauma.

12. What is diagnostic peritoneal lavage (DPL)?


Peritoneal lavage is a procedure performed in the emergency room to help
determine whether a patient has internal bleeding that requires an exploratory
laparotomy. It is done by performing a mini-laparotomy under local anesthesia. A
catheter is then placed into the abdomen and is aspirated for gross blood. Aspiration
of 10 mL of blood is considered a positive finding. A grossly bloody aspirate is
indicative of solid or vascular injury. If less than 10 mL of blood is aspirated, then 1 L
of lactated Ringer's solution or normal saline (NS) is allowed to drain into the abdomen.
The lavage fluid is then allowed to return by gravity, and it is sent to the laboratory for
analysis. Criteria for a positive peritoneal lavage are an erythrocyte count of 100,000
per mm3, a white blood cell (WBC) count of 500 per mm3, the presence of bile or food
particles, and a fluid amylase concentration of 175 U per dL. WBC level itself should
not determine the need for laparotomy. The level of WBCs also does not rise initially,
but its rise requires several hours. Alkaline phosphatase and amylase are contained
in the small bowel and spill into the abdominal cavity after injury. These levels tend to
rise early in injury. Amylase in lavage fluid has been seen as a more accurate marker
than alkaline phosphatase. If the peritoneal lavage meets one or more of these
criteria, then the patient comes to the operating room for an exploratory laparotomy.

13. Why was diagnostic peritoneal lavage (DPL) not


performed for this patient?
Peritoneal lavage was not done for two reasons. First, it is felt that all
penetrating wounds to the abdomen need to be surgically explored. Second, this
patient was exhibiting signs of shock and obviously needed to be sent to the operating
room without delay.

Before computed tomography (CT) and ultrasonography (US) technologies,


DPL was the only mechanism to rapidly evaluate the abdomen for injury. CT now
allows for evaluation of all intraperitoneal organs and the retroperitoneum (an area
inaccessible to DPL). US has been used for detecting fluid in pouches and gutters and
is effective in determining injury to solid viscera. If patients are stable, US and CT
should be used unless other injuries take priority and the patient needs to go to the
operating room before any objective abdominal examination can be completed.

In penetrating trauma, DPL allows for rapid establishment of a hemoperitoneum


and for discovery of intraperitoneal injury.

14. Define shock


Shock is defined as the circumstance of insufficient oxygen delivery to sustain aerobic
metabolism in vital cells of essential organs. Shock of all forms appears to be
invariably related to inadequate tissue perfusion. The low-flow state in vital organs
seems to be the final common denominator in all forms of shock.

15. What are the four types of shock?


For a working classification of shock, the following classification offered by Blalock in
1934 is still useful and functional:

Hematogenic (hypovolemic, hemorrhagic) shockcharacterized by a loss of


circulatory blood volume.
Cardiogenic shockcharacterized by an inability of the myocardium to pump
blood.
Vasogenic (septic) shockcharacterized by an infection that causes a
decrease in peripheral vascular resistance.
Neurogenic shockcharacterized by an impairment of the central nervous
system- mediated control of vascular tone.

16. List the signs and symptoms of shock


Tachycardia, hypotension, cool extremities, pallor, oliguria, tachypnea, decreased
capillary refill, anxiety, restlessness, and loss of consciousness are signs and
symptoms of shock.

17. What is the pathophysiology of hypovolemic


shock?
a. Cardiovascular derangement
An acute decrease in circulating blood volume leads to an increase in
sympathetic activity with an outpouring of epinephrine and norepinephrine from
the adrenal gland. The -adrenergic response causes vasoconstriction, which
shunts blood from the skin, viscera, and muscle, thereby preserving the coronary
and cerebral circulation. With constriction of both precapillary and postcapillary
sphincters, a reduction occurs in hydrostatic pressure of the capillary bed, which
allows the osmotic pressure to draw fluid back into the vascular space from the
interstitial space. This process of hemodilution tends to expand the patient's blood
volume. In addition to the vasoconstriction and hemodilution, a tachycardic
response may be noted.

Myocardial-depressant factor is a peptide thought to be released from the


pancreas during low-flow states. This peptide is thought to be responsible for
some of the decreased cardiac performance seen in trauma patients.
Pancreatectomy and various myocardial-depressant factor antagonists
demonstrate protective myocardial effects during shock in animals.

b. Acid - base disturbance


Metabolic acidosis is almost always seen in association with a shock state.
As a result of decreased blood flow or a low rate of perfusion, oxygen delivery to
vital organs is reduced and consequently a mandatory change occurs from
aerobic to anaerobic metabolism. This shift will lead to the production of lactic acid
instead of carbon dioxide as the end product of metabolism. The increase in lactic
acid leads to a metabolic acidosis.

18. How would you classify hemorrhage?


Classification of hemorrhage based on blood loss is as follows:

Class I: Blood loss of up to 15% of the blood volume: normal pulse and blood
pressure
Class II: Blood loss of up to 30% of the blood volume: tachycardia, decreased
urine output, and anxiety
Class III: Blood loss of up to 40% of the blood volume: marked tachycardia,
hypotension, tachypnea, oliguria, and anxiety
Class IV: Blood loss of more than 40% of the blood volume: tachycardia and
hypotension, tachypnea, anuria, confusion, and lethargy

Crystalloid therapy can be used to treat blood losses of up to 30%. The lower limit of
human tolerance to acute normovolemic anemia has not been established; oxygen
delivery is believed to be adequate when a hemoglobin level is as low as 7 g per dL.

19. What is the initial treatment of hemorrhagic


shock?
The initial treatment of hemorrhagic shock is to attempt to stabilize
hemodynamics by administering fluids and blood products as required to maintain
tissue perfusion and oxygen delivery.
20. Would you choose crystalloid or colloid therapy
to treat hypovolemic shock?
Crystalloid solutions can sustain hemodynamics and deliver adequate
oxygenation in healthy patients who have lost as much as 30% of their total blood
volume. There continues to be some controversy about the use of crystalloid versus
colloid therapy.

Proponents of crystalloid therapy believe that both intravascular and interstitial


fluid losses occur in hypovolemic shock, and that these can be readily replaced with
crystalloids. Another benefit of crystalloids is the decrease in blood viscosity, which
may enhance perfusion. A particular advantage to lactated Ringer's solution is that
lactate is metabolized to bicarbonate, which may help to buffer the patient's acidosis.
Finally, in this age of medical economics, the cost of crystalloid is much less than that
of colloid. Because crystalloid leaves the intravascular space and enters the interstitial
space, large quantities are needed and some fear that these quantities may lead to
both pulmonary and peripheral edema, although studies have not confirmed this fear.

Proponents of colloid therapy believe that much less volume of fluid is needed
to counteract hypovolemic shock. Colloids maintain the oncotic pressure and hold the
interstitial fluids in the intravascular space, which is felt to possibly prevent pulmonary
edema. However, if leaky alveolar capillary membranes are seen within the lung,
colloids may worsen pulmonary edema.

21. Is there a place for dextran or hetastarch


(Hespan) in treating hypovolemic shock?
Dextran and hetastarch are synthetic polysaccharide solutions with varying
mean molecular weights. Dextran 40, dextran 70, and hetastarch have all been used
as volume expanders. Dextrans are relatively inexpensive, increase effective blood
volume, and decrease blood viscosity. However, their negative aspects are
considerable. They impair coagulation by coating platelets, and they impair typing and
cross-matching by coating red blood cells (RBCs). In addition, anaphylactic reactions
have been reported.

22. Is there a place for hypertonic saline (HTS) in the


treatment of hypovolemic shock?
HTS is now being used for resuscitation at some major centers. Its effects tend
to be of short duration, so it is not used alone. HTS is under investigation as a
resuscitative agent, particularly in the prehospital setting, because small volumes may
have beneficial cardiovascular effects. However, if one combines HTS and dextran,
the effective resuscitation will be prolonged. HTS is usually supplied as 7.5% NaCl,
often combined with a colloid, 6% dextran 70. The optimal dose is thought to be 4 mL
per kg.
The potential advantage is that the greater the sodium concentration, the less
total volume will be required for resuscitation. A serious potential danger exists in that
patients may become hypernatremic, which can lead to brain dehydration. In patients
with high intracranial pressure (ICP), this brain dehydration may have a potential
benefit in lowering ICP.

HTS solutions have been used successfully in hemorrhagic shock resuscitation


in animals and humans. This type of fluid resuscitation offers the advantage of
requiring smaller volumes for a similar effect (4 to 5 mL/kg), making it especially
attractive for use during prehospital resuscitation. HTS has been shown to elevate
mean arterial pressure and cardiac output and increase renal, mesenteric, total
splanchnic, and coronary blood flow. HTS causes a small and transient rise in
circulating volume by transcapillary refill. These beneficial effects after controlled
hemorrhage have been established. Its hypertonic nature and small volume usage are
particular advantages in traumatic brain injury. HTS promotes redistribution of fluid
into the vascular compartment and decreases ICP. HTS also seems to offer similar
advantages to improvement in microcirculatory flow of the spinal cord. Use of these
products during uncontrolled hemorrhage, however, has been strongly questioned.

B. Preoperative Evaluation and Preparation


1. What premedication would you order?
None. This is a critically ill patient who is coming to the operating room for
emergency surgery. Narcotics and sedatives would be contraindicated because they
could worsen his already tenuous hemodynamic state.

2. What preoperative tests would you order?


Because of the emergent nature of the trauma setting, preoperative tests and
imaging studies are frequently limited. If the patient is hemodynamically unstable, any
preoperative evaluation is often impossible. However, if the patient is stable, a portable
chest x-ray, arterial blood gas, complete blood count, and Focused Abdominal
Sonography for Trauma (FAST) can be obtained in a relatively short period of time in
the emergency department or operating room before surgery. Often these tests can
be obtained while the patient is being prepared for emergency surgery. This
information can be combined with other monitoring adjuncts such as oxygen
saturation, invasive blood pressure and electrocardiogram (ECG) to evaluate the
patient and formulate an appropriate management strategy.

C. Intraoperative Management
1. How would you monitor this patient?
Routine noninvasive monitor would include electrocardiogram (ECG), blood
pressure cuff, O2 monitor, pulse oximeter, end-tidal CO2, esophageal stethoscope,
temperature probe, and Foley catheter.
Invasive monitors for this patient would include an arterial line and a central
venous catheter. An arterial line is useful for blood sampling and direct blood pressure
monitoring. The central venous line is helpful for determining the patient's volume
status. A pulmonary artery catheter may be indicated if the patient shows signs of
heart failure.

2. How would you induce anesthesia?


Because all trauma patients are considered to have a full stomach, the best
way to protect the patient's airway is to perform an awake intubation. For an
uncooperative patient, one could do a rapid sequence induction. First, the patient
should be preoxygenated for 3 to 5 minutes, if hemodynamics will allow. Then, one
could give a defasciculation dose of a nondepolarizing muscle relaxant. Next,
ketamine, 1.0 to 2.5 mg per kg, might be given, followed by succinylcholine, 1.5 mg
per kg, while maintaining cricoid pressure. Ketamine was chosen in this case because
of its cardiovascular- stimulating effects and the patient's unstable hemodynamics. If
the patient was adequately resuscitated in the emergency room, then one could
possibly use a small dose of thiopental or midazolam/fentanyl for induction.

If the patient is comatose, in severe shock, or in full arrest on admission to the


resuscitation room, no drug other than oxygen and possibly a neuromuscular blocking
drug is required until the patient's blood pressure and heart rate sufficiently rebound
so anesthetics can be titrated. In awake traumatized patients who are thought to be
hypovolemic, etomidate is best tolerated.

3. What technique could you use if one-lung


ventilation was indicated?
If the patient does not already have a secure airway, the airway should be
secured in the manner described in the previous question. One-lung ventilation is
indicated in this situation if the patient is bleeding from one lung and protection of the
other lung is required, or to improve the surgical field (lower priority). Once the airway
is secured, there are several ways to obtain one-lung ventilation. The easiest and
safest technique would be to attach a bronchoscopy adapter to the endotracheal tube
(ETT) and to pass an embolectomy catheter (bronchial blocker) through the
bronchoscopy adapter and ETT. The bronchial blocker position can be confirmed by
fiber-optic bronchoscopy. The point at which the bronchial blocker enters the
bronchoscopy adapter can then be sealed with pliable bone wax (a pliable form of
sterile bees wax which is soft and kneadable).

Another method of obtaining one-lung ventilation would be to change the ETT


to a doublelumen tube through a Cook exchange catheter. The major risks of this
option are losing a previously secured airway and aspiration while attempting to
change the tube.

Other options would be to use a Univent tube while initially securing the airway
or using an Arndt endotracheal blocker if available.
4. What agents would you choose to maintain
anesthesia?
As the patient stabilizes and the hemodynamics improve, other anesthetic agents
can be carefully titrated to prevent hypotension, as follows:

Sedatives or amnestics should be added to the anesthetic as soon as tolerated.


Remember to start with small doses and to check the patient's reaction to the
drugs between doses.
Narcotics should be titrated to control the hemodynamic response to surgery.
Nitrous oxide must be carefully considered, because it has the capacity to
accumulate in closed airspaces.
Inhalational anesthetics may be used in low concentrations so the patient's
hemodynamics are not compromised.

5. What muscle relaxant would you choose?


Vecuronium, rocuronium, and cisatracurium are free of cardiovascular side
effects and have an intermediate duration of action. They are acceptable choices.

Pancuronium is a long-acting muscle relaxant with vagolytic properties that may


be deleterious to the patient.

Curare, metocurine, atracurium, and mivacurium all have the potential to cause
hypotension and therefore would not be chosen for this patient.

6. What can be done to decrease the incidence of


intraoperative awareness?
The incidence of intraoperative awareness is commonly cited as approximately 0.2%.
This is probably an overestimation. In other sources, the incidence of traumatic
intraoperative recall associated with pain is less that 0.03%. The American Society of
Anesthesiologists Closed Claims database states that claims associated to recall
during anesthesia constitute 1.5%. An increased relative risk of recall is seen in certain
types of surgery, including cardiac surgery, cesarean sections, and trauma surgery.
This most likely represents intentional light anesthesia associated with higher levels
of stimulation. Recently, the Bispectral Index (BIS) by Aspect Medical Systems
(Natick, MA) and the PSA 4000 by Physiometrix (Billerica, MA) have been used as
monitors of intraoperative awareness. It has been shown that patients with a BIS value
of 50 were able to respond to verbal commands less than 10% of the time. Although
this information may be potentially useful, the application of these monitors during a
trauma resuscitation may not be easily accomplished.
7. Five minutes after intubation, the peak airway
pressure increased from 20 to 40 cm H2O. What
were the possible causes?
Tension pneumothorax
Bronchospasm
Endobronchial intubation
Pulmonary edema
Secretions
Kink in the anesthesia circuit or endotracheal tube (ETT)

8. How would you make a diagnosis of tension


pneumothorax?
A tension pneumothorax can be defined by the absence of breath sounds on
the affected side. The chest movement may be asymmetric. Neck veins will be full,
and systemic hypotension can occur if the tension pneumothorax is severe. Any
patient who deteriorates under anesthesia and has wounds to the upper abdomen,
lower neck, or ribs should be assumed to have a tension pneumothorax until proven
otherwise.

9. What is the treatment of tension pneumothorax?


Immediate decompression of the chest is mandatory for tension pneumothorax
because a patient's hemodynamics will deteriorate. Diagnosis is made clinically not by
radiograph. An 18-gauge Angiocath is placed into the second intercostal space at the
midclavicular plane. After the air escapes, confirming your diagnosis, and the lung is
decompressed, a chest tube should be placed.

10. The patient's blood loss was continuing and the


hematocrit was 18%. What type of blood would you
give if the type and cross-match are not completed?
This patient should have blood transfused as soon as possible. Type O Rh-
negative packed cells are the universal donor. This should be started while type-
specific blood is being made available. Whenever the type-specific blood is ready, one
can switch to it. However, if the transfusion begins with type O Rh-negative whole
blood and more than 2 units has been infused, only type O Rh-negative blood should
continue to be used. Usually, by the time a patient reaches the operating room from
the emergency room, a partial cross-match can be done. This usually takes 5 to 10
minutes, after which time type-specific blood can be transfused.
11. What precautions should be taken if more than
2 units of type O Rh-negative un-cross-matched
whole blood is given?
The plasma from type O Rh-negative whole blood contains anti-A and anti-B
antibodies, which can cause hemolytic reactions with type A and type B blood cells if
given in significant quantities. Therefore, only type O Rh-negative blood should
continue to be transfused, although this will lead to minor hemolytic of the patient's
own red blood cells (RBCs). The patient should not receive his type-specific blood until
the blood bank determines that the transfused anti-A and anti-B antibody levels have
fallen sufficiently low to permit safe transfusion of type-specific blood. This usually
requires a 2-week waiting period.

However, packed red blood cells (PRBCs) have smaller volumes of plasma and
are virtually free of anti-A and anti-B antibodies. Therefore, whenever type-specific
blood is not yet available, type O Rh-negative un-cross-matched PRBCs should be
used in preference to type O Rh-negative whole blood. Once type-specific blood is
available, it can be used safely.

12. What are the complications associated with any


blood transfusion?
a. Transfusion reactions
Febrile reactions occur in approximately 1% of all transfusions. In an awake
patient, this is usually no more than an annoyance that requires decreasing the
infusion rate.

Allergic reactions to properly cross-matched blood will manifest as an increase


in temperature, pruritus, and urticaria. This may be difficult to diagnose in the
anesthetized patient. Treatment consists of administration of antihistamines
and discontinuation of the transfusion.

Hemolytic reactions occur when incompatible blood is administered. Caused


by activation of the complement system, they can be life threatening. In the
awake patient, fever, chills, dyspnea, substernal, and lumbar pain are seen in
addition to hypotension. Under general anesthesia, the only sign that is not
masked is hypotension. Also, if free hemoglobin can be documented in the
plasma or urine, this too would be indicative of a transfusion reaction.
Substances released by the hemolyzed cells can lead to disseminated
intravascular coagulation (DIC) and acute renal failure (ARF). Treatment
consists of immediate discontinuation of the transfusion. Hypotension should
be treated with hydration, vasopressors, and inotropic agents if needed. Urinary
output must be maintained by adequate hydration. Although its value is
uncertain, sodiumbicarbonate has been used to alkalinize the urine to improve
the solubility of the hemoglobin-degradation products. The risk of an ABO-
incompatible transfusion is 1:33,500 red blood cell (RBC) transfusions.
Mortality associated with this remains high, at approximately 40%

b. Transmission of disease
Transmission of disease can be a serious problem. Human immunodeficiency
virus (HIV), hepatitis B virus, hepatitis C virus, and cytomegalovirus can all be
transmitted by transfusion. Because the risk of disease transmission increases
with each unit of blood or its components given, they must be carefully
scrutinized before they are administered. The incidence of posttransfusion HIV
infection is 1:493,000 (1:200,000 to 1:2,000,000) per transfused unit of blood.
The risk of hepatitis B transmission is approximately 1 per 63,000 units. The
risk of hepatitis C transmission is 1:103,000 (1:30,000 to 1:150,000) per unit
transfused. Cytomegalovirus is the most common viral agent transmitted by
blood transfusion; however, it produces clinically important infections only in
immunodepressed patients. Malaria, syphilis, Lyme disease, Chagas' disease,
and other diseases may also be transmitted through transfusion of blood and
blood products. The aggregate infection risk is approximately 1 per 34,000. As
new nonhemoglobin solutions appear on the market, less blood will be
transfused and disease transmission will diminish.

c. Microembolization
Microembolization can occur from the transfusion of blood or its components.
Stored blood forms microaggregates that are too small to be removed by the
standard 170- micron blood filters. Smaller filters have been developed to
remove these particles. However, when using blood filters of the 20- to 40-
micron range, the rate of transfusion is dramatically decreased because of the
increased resistance of the filters. Some early reports suggested that these
microaggregates may lead to pulmonary dysfunction, but this has never been
proven.

13. What is considered a massive transfusion?


A massive transfusion is defined as the replacement of the patient's total blood
volume in a 24-hour period. This is usually between 8 and 10 units of packed red blood
cells (PRBCs). Many trauma cases far exceed this amount and may require other
blood components in addition to the RBCs.

14. What are the complications associated with a


massive transfusion?
Complications of a massive transfusion include dilutional coagulopathy,
disseminated intravascular coagulation (DIC), fibrinolysis, citrate toxicity,
hyperkalemia, hypokalemia, acid-base imbalance, impaired hemoglobin function, and
hypothermia.
Dilutional coagulopathy usually becomes a problem during massive
transfusions. Both platelets and coagulation factors are markedly decreased
and must be replaced. They should be administered after laboratory
documentation of the deficiency. It is no longer accepted practice to give fresh
frozen plasma (FFP) routinely after 5 units of packed red blood cell (PRBC),
and it is not proper to give platelets after 10 units of PRBC. At present, dilutional
coagulopathies appear to be rare, even with the transfusion of one blood
volume. Approximately 40% of the coagulation factors remain after one blood
volume replacement, and this should be sufficient to allow normal coagulation.
Platelets can be reduced to 30% to 40% of normal after one blood volume
transfusion. This decrease will usually represent a platelet count less than
100,000 per L and may lead to a prolonged bleeding time.
DIC and fibrinolysis may occur after massive transfusions. An important
triggering event of DIC and fibrinolysis is shock, with its accompanying tissue
ischemia, acidemia, and waste product accumulation. Therefore, early and
prompt treatment of hypoperfusion is mandatory.
Citrate toxicity is frequently discussed, but it is rarely a problem. However, in
the pediatric population, citrate toxicity is much more of a problem and should
be considered in any child who does not respond to rapid volume
administration of blood products. Citrate is added to stored blood to bind
calcium and therefore prevent clotting. The citrate anticoagulant stays with the
plasma, and obviously FFP would contain much more citrate that PRBCs.
Citrate binds calcium and decreases the patient's ionized calcium level.
Hypocalcemia may present as a prolongation of the QT interval with little effect
of cardiac performance. In some cases, ventricular performance may be
compromised. However, cardiac performance may also be decreased by
acidemia, hyperkalemia, and hypothermia, which all accompany the shock
state. Therefore, the routine administration of supplemental calcium is not
indicated. A point worth noting is that citrate is metabolized to bicarbonate, and
it can contribute to posttransfusion metabolic alkalosis.
Hyperkalemia can be a rare occurrence in the massively transfused patient.
Plasma potassium levels of stored whole blood range between 12 and 32 mEq
per L. The potassium level increases approximately 1 mEq/L/day in stored
blood. A unit of whole blood would contain between 4 and 8 mEq of potassium,
which is hardly enough to cause hyperkalemia. A unit of PRBC contains
insignificant amounts of potassium because most plasma is removed.
However, in the shock state with hypoperfusion and acidemia, hyperkalemia
may become evident.
Hypokalemia is also a possibility after a massive transfusion. Citrate is
metabolized to bicarbonate, resulting in a metabolic alkalosis that can cause
hypokalemia. In addition, the transfused RBCs take up potassium, which can
also result in hypokalemia.
Acid-base imbalance is a problem after massive transfusion. Banked blood with
a pH level of 6.8 is acidotic and may worsen the acidosis that accompanies
shock. However, this acidosis is easily reversible with the restoration of normal
perfusion. No need is seen to give supplemental bicarbonate based on an
arbitrary number of units transfused. However, if a metabolic acidosis persists,
then sodium bicarbonate is warranted. As stated, citrate from stored blood and
lactate from lactated Ringer's solution are metabolized to bicarbonate, and this
can cause a metabolic alkalosis.
Impaired hemoglobin function is a theoretic possibility after massive
transfusion. The 2,3-diphosphoglycerate (2,3-DPG) level is decreased in
banked blood. This will shift the oxygen-hemoglobin dissociation curve to the
left, and oxygen will be held more tightly by the hemoglobin molecule. However,
no studies have documented any adverse effects from this.
Hypothermia is an obvious consequence of infusing cold banked blood.
Therefore, is recommended that the blood be reconstituted with warm normal
saline (NS). In addition, all fluids should pass through a warming device to help
prevent hypothermia.

15. Can the shift of the oxygen-hemoglobin


dissociation curve be quantitated?
Yes, the shift of the oxygen-hemoglobin dissociation curve is quantified by
means of the P50 values (i.e., the partial pressure of oxygen at which hemoglobin is
50% saturated with oxygen). A leftward shift of the curve indicates a low P 50 value.
The normal P50 value of blood is 27 mm Hg and the normal level of 2,3-
diphosphoglycerate (2,3-DPG) is 4.8 mmol per mL of erythrocytes.

16. How is hypothermia defined?


Hypothermia is defined as a core body temperature of less than 35C (95F).
A trauma patient brought to the emergency room may already be hypothermic.
Prolonged exposure to a cold operating room, evaporative heat loss from the
respiratory tract, infusions of cold fluids, and loss of heat production secondary to
shock cause decreased core temperature in most patients.

All skin surfaces not in the surgical field should be covered to reduce convective
and radiant heat loss. Humidification of inspired gases reduces evaporative heat loss
from the lung. All intravenous fluids should be warmed.

Warming the operating room may also lessen heat loss, as will the use of
warming blankets.

17. What are the adverse effects of hypothermia?


Shivering-induced increase in O2 consumption by as much as 400%
A leftward shift in the oxygen-hemoglobin dissociation curve
Decreased coagulation of blood
Increased epinephrine and norepinephrine levels, causing vasoconstriction
As hypothermia becomes severe, possible decreases in both heart rate and blood
pressure
Cardiac irritability, leading to ventricular fibrillation

18. What is the treatment of hypothermia?


The normal response to hypothermia is shivering, which is blocked by general
anesthesia. Therefore, it is of utmost importance to prevent and treat hypothermia.
Recommendations include the following:

Increase the temperature of the operating room.

Use a warming blanket.

Preheat intravenous fluids.

Pass all fluids through a warming device.

Use low-flow anesthesia.

Use a heat moisture exchanger in the anesthesia circuit.

19. What are the effects of blood transfusion on the


immune system?
Blood transfusion will result in immunologic changes that can be harmful in
some patients and helpful in others. This immunomodulation occurs from immune
suppression. The blood components crucial to these changes are thought to be the
white blood cells (WBCs) or plasma.

An example of a beneficial effect is the increased survival of the renal allograft


in patients who had received a prior transfusion. In patients who have cancer, a
possible harmful effect of immunosuppression is the increased cancer recurrence rate
seen in patients who have had prior transfusion. Finally, a number of clinical studies
have demonstrated that perioperative transfusion is associated with an increased
incidence of infection and sepsis.

20. What are the guidelines for transfusion of blood


products?
The New York Presbyterian Hospital Guidelines for blood product usage are as
follows:

a. Red blood cell transfusion criteria


Hemoglobin (Hb) level less than 8 g per dL and mean red cell volume within
normal limit (81 to 100 fL, 70 to 125 fL for patients aged 14 years)
Hb level less than 8 g per dL and high risk/acute bleed
Hb level less than 11 g per dL and clinically symptomatic
Hb level less than 11 g per dL and bleed more than 1 U per 24 hours
Any Hb level and high risk1 and acute bleed
Any Hb level and symptomatic2 and acute bleed
Any Hb level and bleed more than 2 U per 24 hours, or more than 15% of
blood volume per 24 hours

b. Platelet transfusion criteria


Platelet count less than 20,000 per L without thrombotic thrombocytopenic
purpura (TTP), idiopathic thrombocytopenic purpura, posttransfusion
purpura, or hemolytic-uremic syndrome

Platelet count less than 50,000 per L with minor bleed, preoperative for a
minor procedure or prematurity

Platelet count less than 90,000 per L with bleed requiring RBC transfusion
or preoperative for a major procedure

Massive RBC transfusion (>8 U/24 hours)

Bleeding time longer than 10 minutes

Open heart surgery transfusion of more than mean number of RBC units (6
units/case)

c. Fresh frozen plasma transfusion criteria


Massive transfusion more than 8 units of RBC per 24 hours (>1 blood
volume infants/children)

Abnormal coagulation test results prothrombin time more than 15 seconds


or partial thromboplastin time more than 45 seconds during prior 24 hours
or known congenital coagulation factor disorder and bleeding or prophylaxis
for major procedures
Clinical evidence of abnormal bleeding from venipuncture sites or
generalized oozing

Patients with diagnosis of thrombotic thrombocytopenic purpura (TTP)

Open heart surgery transfusion of more than mean number of RBC units (6
units/case)

d. Cryoprecipitate transfusion criteria

Massive transfusion more than 8 units of RBCs per 24 hours


Open heart surgery transfusion of more than mean number of RBC units (6
units/case)
Bleeding or invasive procedure with hypofibrinogemia or disseminated
intravascular coagulation (DIC)
Deficient factor VIII of von Willebrand factor or abnormal fibrinogen and
presurgical or bleed

21. If a patient were a member of the Jehovah's


Witness religious sect, would you give a blood
transfusion?
Jehovah's Witnesses are best known for refusing the transfusion of blood and
blood products. This belief is based on the Bible (Acts 15:28-29). In the awake and
otherwise competent adult, courts have ruled that physicians cannot be held liable if
they comply with a patient's directive and withhold life-saving blood administration
after specific and detailed informed consent of the consequences of such an omission
of treatment. The issue becomes clouded when patients are incompetent,
unconscious (most Jehovah's Witnesses carry cards informing medical personnel of
their religious beliefs), or minors. They believe all hope of eternal life is forfeited if they
accept a transfusion. Therefore, a blood transfusion is considered a physical violation.
The right of a Jehovah's Witness to refuse a blood transfusion is absolute. The courts
have upheld their rights to refuse a blood transfusion. Most witnesses take adequate
legal steps to relieve the liability of the medical personnel. Most carry a medical alert
card that states their wishes and they usually have made arrangements for proxy or
surrogate decision makers. In addition, an open and honest avenue of communication
must exist between the patient, surgeon, and anesthesiologist.

They will refuse transfusion of whole blood, packed red blood cells (PRBCs),
white blood cells (WBCs), plasma, and platelets. However, they will allow the use
of cardiopulmonary bypass, dialysis, or similar equipment, as well as intraoperative
blood salvage where the extracorporeal circulation is uninterrupted. Their religious
understanding does not absolutely prohibit albumin, immune globulins, or hemophiliac
preparations; those products must be decided on an individual basis. They accept all
nonblood replacements, including nonblood colloids, crystalloids, dextrans, or oxygen-
carrying blood substitutes.

An anesthesiologist may refuse to care for any patient when a procedure is elective.
In an emergency situation, legal and ethical requirements apply. Conversely, any
competent adult also has the right to refuse any therapy, and to treat such a patient
against that person's will is to commit battery.

22. If a child is a Jehovah's Witness and suffered


from hemorrhagic shock, what would you do?
Care of minors presents the greatest concern and often leads to legal action
against the parents under child-neglect status. Such actions are questioned by
Jehovah's Witnesses who do seek good medical care for their children, while claiming
that consideration be given to their families' religious beliefs. Doctors can appeal to
the court for permission to transfuse blood to children of this sect who are underage.
In an unforeseeable emergency, generally, blood may be given without consulting a
court.

23. Are there artificial blood substitutes available?


Three types of artificial blood are being investigated: hemoglobin solutions,
liposomeencapsulated hemoglobin, and perfluorocarbons.

a. Hemoglobin solutions
Hemoglobin can now be prepared from outdated human blood. Intravascular
free hemoglobin has a high affinity for oxygen and is quickly excreted.
Hemoglobin can now be modified and dissolved in an isotonic medium that will
decrease renal filtration, prolong intravascular life, and restore a normal P 50 of
oxygen. Hemoglobin solutions can restore circulating blood volume and provide
adequate tissue oxygenation in animal models. Detrimental effects include
renal toxicity and increased systemic and pulmonary vascular pressures.

b. Liposome-encapsulated hemoglobin
Hemoglobin can be membrane encapsulated for modification. It is then possible
to add 2,3-diphosphoglycerate (2,3-DPG), or inositol hexaphosphate to the
membrane, thereby adjusting the P50 to mcats the RBCs. In theory, the
encapsulated hemoglobin will have a longer intravascular duration and greater
oxygen-carrying capacity. The membrane is being further modified to try to
decrease the deposition in the reticuloendothelial

system, thereby further increasing the intravascular duration.

c.Perfluorocarbons
Perfluorocarbons are synthetic substances that have a capacity for dissolved
oxygen. It is unlikely these will be useful because a high PaO 2 is needed to
allow the

perfluorocarbon to carry even small amounts of dissolved oxygen. Initial studies


of stromafree hemoglobin have shown potential harm in renal function, and
stromafree hemoglobin is not approved for clinical use.

Human studies have been disappointing because of unacceptable side effects,


such as renal failure, platelet dysfunction, and vasoconstriction. No product has
been approved for use in trauma patients, although phase III trials are under
way in centers throughout the United States using hemoglobin-based oxygen
carriers. Currently, artificial blood substitute use is not indicated.

D. Postoperative Management
1. What is acute respiratory distress syndrome
(ARDS)?
ARDS is an acute respiratory failure seen in patients with healthy lungs after
being exposed to shock, trauma, sepsis, aspiration, transfusion, burns, or toxic
inhalation. Initially, when this lung injury was thought to be related to the shock state
and its resuscitation, names such as shock lung and traumatic wet lung were
applied to acute respiratory insufficiently following injury. It is now recognized that
many types of lung insults will result in damage to the alveolar capillary membrane,
resulting in leakage of proteinaceous fluid from the intravascular space into the
interstitium and subsequently into the alveolar spaces. This injury with its resulting
interstitial and alveolar edema produces a clinical picture ranging from mild to severe
pulmonary dysfunction that can actually be fatal.

Acute lung injury (ALI) is characterized by impaired oxygenation, defined as a


ratio of PaO2/FIO2 of 300 or less; bilateral pulmonary infiltrates on the frontal chest
radiograph; and a pulmonary artery occlusion of 18 mm Hg or more. ARDS is defined
as ALI with a PaO2/FIO2 ratio of 200 or less. ARDS is characterized by the following:

Hypoxemiais relatively unresponsive to increasing inspired oxygen


concentration

Decreased pulmonary complianceclinically appears as stiff lungs


Initially normal chest radiograph progressing to diffuse infiltrates or even to
areas of complete consolidation

Decrease in resting lung volumes, specifically functional residual capacity

2. How is acute respiratory distress syndrome


(ARDS) treated?
The treatment of ARDS is primarily supportive. Currently, mechanical ventilation is the
mainstay of supportive therapy for ARDS. The principal goal of mechanical ventilation
is to minimize the deleterious effects on gas exchange. Unfortunately, mechanical
ventilation has also been associated with further lung injury. Excessive alveolar
volumes (volutrauma), high mean and peak airway pressures (barotrauma), and
shearing forces caused by frequent collapse and opening of alveolar units are
responsible for this further lung injury. Positive end-expiratory pressure (PEEP) is
used to increase oxygenation at a fixed FIO2.

Investigators have looked at lung protection in patients with ARDS. Strategies were
used to prevent ventilator-associated lung injury. Amato et al. used a strategy to limit
peak inspiratory pressures by using low tidal volumes (< 6 mL/kg) and the institution
of PEEP. Their strategy was associated with a lower 28-day mortality (38% vs. 71%),
higher weaning rate (66% vs. 29%), and lower barotrauma rate (7% vs. 42%).

The National Heart, Lung, and Blood Institute ARDS network reported improved
survival in patients using a low tidal volume strategy (6 mL/kg vs. 12 mL/kg). These
investigators found a decrease in mortality of approximately 25% in the intervention
group compared with the control group.

3. In the recovery room, you are called to see this


patient because of oliguria. How would you evaluate
and treat this patient?
Oliguria is a decrease in urinary output to less than 0.5 mL/kg/hour. Acute renal
failure (ARF) is a syndrome characterized by a rapid (hours to weeks) decline in
glomerular filtration rate and retention of nitrogenous waste products such as blood
urea nitrogen (BUN) and creatinine. The kidney is remarkable in its ability to recover
from almost complete loss of function. Most ARF is reversible. ARF is associated with
major in- hospital morbidity and mortality. The diagnosis of ARF usually hinges on
serial analysis of BUN and serum creatinine.

Renal failure can be divided into three categories.


a. Prerenal
Prerenal failure is the most common cause of ARF and is an appropriate
physiologic response to renal hypoperfusion. It is usually caused by a low
cardiac output due to hypovolemia or cardiac failure. It can be evaluated by
checking the patient's heart rate, blood pressure, central venous pressure,
pulmonary capillary wedge pressure, and cardiac output. If hypovolemia is the
cause, then treatment would consist of a fluid bolus. If the patient is in cardiac
failure, then inotropic support and diuretics could be administered. Severe renal
hypoperfusion may cause ischemic acute tubular necrosis (ATN). Therefore,
prerenal azotemia and ischemic ATN are part of a spectrum of manifestations
of renal hypoperfusion.

b. Renal
Intrinsic renal failure is generally due to toxic injury or ischemia. Ischemic
injury is caused by a decrease in perfusion pressure that can lead to renal
cellular dysfunction. Substances that affect renal tubular function in addition to
renal blood flow can cause toxic injury. Ischemic ATN, unlike prerenal
azotemia, is associated with injury to renal parenchyma and does not resolve
immediately on restoration of renal perfusion. In its more extreme form, renal
hypoperfusion may result in bilateral renal cortical necrosis and irreversible
renal failure. Urinalysis may show cells and/or casts that are indicative of ARF.
Intrinsic renal failure can be minor and short lived, or it can progress to chronic
renal failure, depending on the severity of the insult. In the absence of
congestive heart failure, use of diuretics should generally be avoided as they
can exacerbate ATN. In particular, loop diuretics increase oxygen and
adenosine triphosphate (ATP) consumption at the level of the tubules.

c. Postrenal
Urinary tract obstruction accounts for less than 5% of cases of ARF.
Urinary tract obstruction must be sought and corrected to treat possible causes
of postrenal oliguria. This usually requires irrigation and/or changing of the
Foley catheter. Consider the possibility of and intraoperative mishap causing
postrenal obstruction.