Shock,

Hypovolemic

INTRODUCTION

Background: Hypovolemic shock refers to a medical or surgical condition in

which rapid fluid loss results in multiple organ failure due to inadequate
circulating volume and subsequent inadequate perfusion. Most often,
hypovolemic shock is secondary to rapid blood loss (hemorrhagic shock).

Acute external blood loss secondary to penetrating trauma and severe GI

bleeding disorders are 2 common causes of hemorrhagic shock. Hemorrhagic
shock can also result from significant acute internal blood loss into the thoracic
and abdominal cavities.

Two common causes of rapid internal blood loss are solid organ injury and
rupture of an abdominal aortic aneurysm. Hypovolemic shock can result from
significant fluid (other than blood) loss. Two examples of hypovolemic shock
secondary to fluid loss include refractory gastroenteritis and extensive burns.
The remainder of this article concentrates mainly on hypovolemic shock
secondary to blood loss and the controversies surrounding the treatment of this
condition. The reader is referred to other articles for discussions of the
pathophysiology and treatment for hypovolemic shock resulting from losses of
fluid other than blood.

The many life-threatening injuries experienced during the wars of the 1900s
have significantly affected the development of the principles of hemorrhagic
shock resuscitation. During World War I, W.B. Cannon recommended delaying
fluid resuscitation until the cause of the hemorrhagic shock was repaired
surgically. Crystalloids and blood were used extensively during World War II for
the treatment of patients in unstable conditions. Experience from the Korean
and Vietnam wars revealed that volume resuscitation and early surgical
intervention were paramount for surviving traumatic injuries resulting in
hemorrhagic shock. These and other principles helped in the development of
present guidelines for the treatment of traumatic hemorrhagic shock. However,
recent investigators have questioned these guidelines, and today,
controversies exist concerning the optimal treatment of hemorrhagic shock.

Pathophysiology: The human body responds to acute hemorrhage by

activating the following major physiologic systems: the hematologic,
cardiovascular, renal, and neuroendocrine systems.

The hematologic system responds to an acute severe blood loss by activating

the coagulation cascade and contracting the bleeding vessels (by means of
local thromboxane A2 release). In addition, platelets are activated (also by
means of local thromboxane A2 release) and form an immature clot on the
bleeding source. The damaged vessel exposes collagen, which subsequently
causes fibrin deposition and stabilization of the clot. Approximately 24 hours
are needed for complete clot fibrination and mature formation.

The cardiovascular system initially responds to hypovolemic shock by

increasing the heart rate, increasing myocardial contractility, and constricting
peripheral blood vessels. This response occurs secondary to an increased
release of norepinephrine and decreased baseline vagal tone (regulated by the
baroreceptors in the carotid arch, aortic arch, left atrium, and pulmonary
vessels). The cardiovascular system also responds by redistributing blood to
the brain, heart, and kidneys and away from skin, muscle, and GI tract.

The renal system responds to hemorrhagic shock by stimulating an increase in

renin secretion from the juxtaglomerular apparatus. Renin converts
angiotensinogen to angiotensin I, which subsequently is converted to
angiotensin II by the lungs and liver. Angiotensin II has 2 main effects, both of
which help to reverse hemorrhagic shock, vasoconstriction of arteriolar smooth
muscle, and stimulation of aldosterone secretion by the adrenal cortex.
Aldosterone is responsible for active sodium reabsorption and subsequent
water conservation.

The neuroendocrine system responds to hemorrhagic shock by causing an

increase in circulating antidiuretic hormone (ADH). ADH is released from the
posterior pituitary gland in response to a decrease in BP (as detected by
baroreceptors) and a decrease in the sodium concentration (as detected by
osmoreceptors). ADH indirectly leads to an increased reabsorption of water
and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle.

The pathophysiology of hypovolemic shock is much more involved than what

was just listed. To explore the pathophysiology in more detail, references for
further reading are provided in the bibliography. These intricate mechanisms
list above are effective in maintaining vital organ perfusion in severe blood loss.
Without fluid and blood resuscitation and/or correction of the underlying
pathology causing the hemorrhage, cardiac perfusion eventually diminishes,
and multiple organ failure soon follows.
 CLINICAL

History:

 In a patient with possible shock secondary to hypovolemia, the history is

vital in determining the possible causes and in directing the workup.
Hypovolemic shock secondary to external blood loss typically is obvious
and easily diagnosed. Internal bleeding may not be as obvious as
patients may complain only of weakness, lethargy, or a change in
mental status.

 Symptoms of shock, such as weakness, lightheadedness, and

confusion, should be assessed in all patients.

 In the patient with trauma, determine the mechanism of injury and any
information that may heighten suspicion of certain injuries (eg, steering
wheel damage or extensive passenger compartment intrusion in a motor
vehicle accident).

 If conscious, the patient may be able to indicate the location of pain.

 Vital signs, prior to arrival in the ED, should also be noted.

 Chest, abdominal, or back pain may indicate a vascular disorder.

 The classic sign of a thoracic aneurysm is a tearing pain radiating to the

back. Abdominal aortic aneurysms usually result in abdominal, back
pain, or flank pain.

 In patients with GI bleeding, inquiry about hematemesis, melena, alcohol

drinking history, excessive nonsteroidal anti-inflammatory drug use, and
coagulopathies (iatrogenic or otherwise) is very important.

o The chronology of vomiting and hematemesis should be

determined.

o The patient who presents with hematemesis after multiple

episodes of forceful vomiting is more likely to have Boerhaave
syndrome or a Mallory-Weiss tear, whereas a patient with a
history of hematemesis from the start is more likely to have peptic
ulcer disease or esophageal varices.

 If a gynecologic cause is being considered, gather information about the

following: last menstrual period, risk factors for ectopic pregnancy,
 vaginal bleeding (including amount and duration), vaginal passage of
products of conception, and pain. All women of childbearing age should
undergo a pregnancy test, regardless of whether they believe that they
are pregnant. A negative pregnancy test typically excludes ectopic
pregnancy as a diagnosis.

Physical: The physical examination should always begin with an assessment

of the airway, breathing, and circulation. Once these have been evaluated and
stabilized, the circulatory system should be evaluated for signs and symptoms
of shock.

Do not rely on systolic BP as the main indicator of shock; this practice results in
delayed diagnosis. Compensatory mechanisms prevent a significant decrease
in systolic BP until the patient has lost 30% of the blood volume. More attention
should be paid to the pulse, respiratory rate, and skin perfusion. Also, patients
taking beta-blockers may not present with tachycardia, regardless of the
degree of shock.

Classes of hemorrhage have been defined, based on the percentage of blood

volume loss. However, the distinction between these classes in the
hypovolemic patient often is less apparent. Treatment should be aggressive
and directed more by response to therapy than by initial classification.

 Class I hemorrhage (loss of 0-15%)

o In the absence of complications, only minimal tachycardia is

seen.

o Usually, no changes in BP, pulse pressure, or respiratory rate

occur.

o A delay in capillary refill of longer than 3 seconds corresponds to

a volume loss of approximately 10%.

 Class II hemorrhage (loss of 15-30%)

o Clinical symptoms include tachycardia (rate >100 beats per

minute), tachypnea, decrease in pulse pressure, cool clammy
skin, delayed capillary refill, and slight anxiety.

o The decrease in pulse pressure is a result of increased

catecholamine levels, which causes an increase in peripheral
vascular resistance and a subsequent increase in the diastolic
BP.
 Class III hemorrhage (loss of 30-40%)

o By this point, patients usually have marked tachypnea and

tachycardia, decreased systolic BP, oliguria, and significant
changes in mental status, such as confusion or agitation.

o In patients without other injuries or fluid losses, 30-40% is the

smallest amount of blood loss that consistently causes a
decrease in systolic BP.
o Most of these patients require blood transfusions, but the decision
to administer blood should be based on the initial response to
fluids.

 Class IV hemorrhage (loss of >40%)

o Symptoms include the following: marked tachycardia, decreased

systolic BP, narrowed pulse pressure (or immeasurable diastolic
pressure), markedly decreased (or no) urinary output, depressed
mental status (or loss of consciousness), and cold and pale skin.

o This amount of hemorrhage is immediately life threatening.

 In the patient with trauma, hemorrhage usually is the presumed cause of

shock. However, it must be distinguished from other causes of shock.
These include cardiac tamponade (muffled heart tones, distended neck
veins), tension pneumothorax (deviated trachea, unilaterally decreased
breath sounds), and spinal cord injury (warm skin, lack of expected
tachycardia, neurological deficits).
 The 4 areas in which life-threatening hemorrhage can occur are as
follows: chest, abdomen, thighs, and outside the body.

o The chest should be auscultated for decreased breath sounds,

because life-threatening hemorrhage can occur from myocardial,
vessel, or lung laceration.

o The abdomen should be examined for tenderness or distension,

which may indicate intraabdominal injury.

o The thighs should be checked for deformities or enlargement

(signs of femoral fracture and bleeding into the thigh).

o The patient's entire body should then be checked for other

external bleeding.

 In the patient without trauma, the majority of the hemorrhage is in the

abdomen. The abdomen should be examined for tenderness, distension,
 or bruits. Look for evidence of an aortic aneurysm, peptic ulcer disease,
or liver congestion. Also check for other signs of bruising or bleeding.

 In the pregnant patient, perform a sterile speculum examination.

However, with third-trimester bleeding, the examination should be
performed as a "double set-up" in the operating room. Check for
abdominal, uterine, or adnexal tenderness.

Causes: The causes of hemorrhagic shock are traumatic, vascular, GI, or

pregnancy related.

 Traumatic causes can result from penetrating and blunt trauma.

Common traumatic injuries that can result in hemorrhagic shock include
the following: myocardial laceration and rupture, major vessel laceration,
solid abdominal organ injury, pelvic and femoral fractures, and scalp
lacerations.

 Vascular disorders that can result in significant blood loss include

aneurysms, dissections, and arteriovenous malformations.

 GI disorders that can result in hemorrhagic shock include the following:

bleeding esophageal varices, bleeding peptic ulcers, Mallory-Weiss
tears, and aortointestinal fistulas.

 Pregnancy-related disorders include ruptured ectopic pregnancy,

placenta previa, and abruption of the placenta. Hypovolemic shock
secondary to an ectopic pregnancy is common. Hypovolemic shock
secondary to an ectopic pregnancy in a patient with a negative urine
pregnancy test is rare but has been reported.

DIFFERENTIALS

Abruptio Placentae
Aneurysm, Abdominal
Aneurysm, Thoracic
Fractures, Femur
Fractures, Pelvic
Gastritis and Peptic Ulcer Disease
Placenta Previa
Pregnancy, Ectopic
Pregnancy, Postpartum Hemorrhage
Pregnancy, Trauma
Shock, Hemorrhagic
Shock, Hypovolemic
Toxicity, Iron

Other Problems to be Considered:

Gastrointestinal bleeding
Penetrating trauma

WORKUP

Lab Studies:

 After the history is taken and the physical examination is performed,

further workup depends on the probable cause of the hypovolemia, as well
as on the stability of the patient's condition.

 Initial laboratory studies should include analysis of the CBC, electrolyte

levels (eg, Na, K, Cl, HCO3, BUN, creatinine, glucose levels), prothrombin
time, activated partial thromboplastin time, ABGs, urinalysis (in patients
with trauma), and a urine pregnancy test. Blood should be typed and
cross-matched.

Imaging Studies:

 Patients with marked hypotension and/or unstable conditions must first be

resuscitated adequately. This treatment takes precedence over imaging
studies and may include immediate interventions and immediately taking
the patient to the operating room.

 The workup for the patient with trauma and signs and symptoms of
hypovolemia is directed toward finding the source of blood loss.

 The atraumatic patient with hypovolemic shock requires ultrasonographic

examination in the ED if an abdominal aortic aneurysm is suspected. If GI
bleeding is suspected, a nasogastric tube should be placed, and gastric
lavage should be performed. An upright chest radiograph should be
obtained if a perforated ulcer or Boerhaave syndrome is a possibility.
Endoscopy can be performed (usually after the patient has been admitted)
to further delineate the source of bleeding.

 A pregnancy test should be performed in all female patients of

childbearing age. If the patient is pregnant and in shock, surgical
consultation and the consideration of bedside pelvic ultrasonography
should be immediately performed in the ED. Hypovolemic shock
 secondary to an ectopic pregnancy is common. Hypovolemic shock
secondary to an ectopic pregnancy in a patient with a negative pregnancy
test, although rare, has been reported.

 If thoracic dissection is suspected because of the mechanism and initial

chest radiographic findings, the workup may include transesophageal
echocardiography, aortography, or CT scanning of the chest.

 If a traumatic abdominal injury is suspected, a FAST (Focused Abdominal

Sonography for Trauma) ultrasound exam may be performed in the stable
or unstable patient. Computed Tomography (CT) scanning typically is
performed in the stable patient.

 If long-bone fractures are suspected, radiographs should be obtained.

TREATMENT

Prehospital Care: The treatment of patients with hypovolemic shock often

begins at an accident scene or at home. The prehospital care team should work
to prevent further injury, transport the patient to the hospital as rapidly as
possible, and initiate appropriate treatment in the field. Direct pressure should be
applied to external bleeding vessels to prevent further blood loss.

 Prevention of further injury applies mostly to the patient with trauma. The
cervical spine must be immobilized, and the patient must be extricated, if
applicable, and moved to a stretcher. Splinting of fractures can minimize
further neurovascular injury and blood loss.

 Although in selected cases stabilization may be beneficial, rapid transport

of sick patients to the hospital remains the most important aspect of
prehospital care. Definitive care of the hypovolemic patient usually
requires hospital, and sometimes surgical, intervention. Any delay in
definitive care, eg, such as delayed transport, is potentially harmful.

 Most prehospital interventions involve immobilizing the patient (if trauma is

involved), securing an adequate airway, ensuring ventilation, and
maximizing circulation.
o In the setting of hypovolemic shock, positive-pressure ventilation
may diminish venous return, diminish cardiac outcome, and worsen
the shock state. While oxygenation and ventilation are necessary,
excessive positive-pressure ventilation can be detrimental for a
patient suffering hypovolemic shock.
o Appropriate treatment usually can be initiated without delaying
transport. Some procedures, such as starting intravenous (IV) lines
 or splinting of extremities, can be performed while a patient is being
extricated. However, procedures in the field that prolong
transportation should be delayed. Benefits to giving IV fluids prior to
departure from the scene are not clear; however, IV lines and fluid
resuscitation should be started and continued once the patient is en
route to definitive care.

 In recent years, there has been considerable debate regarding the use of
military antishock trousers (MAST). MAST were introduced in the 1960s
and, based mostly on anecdotal reports of success, their use became
standard therapy in the prehospital treatment of hypovolemic shock in the
late 1970s. By the 1980s, the American College of Surgeons Committee
on Trauma included their use in the standard of care for all patients with
trauma and signs or symptoms of shock. Since that time, studies have
failed to show improved outcome with the use of MAST. The American
College of Surgeons Committee on Trauma no longer recommends the
use of MAST.

Emergency Department Care: Three goals exist in the emergency department

treatment of the patient with hypovolemic shock as follows: (1) maximize oxygen
delivery - completed by ensuring adequacy of ventilation, increasing oxygen
saturation of the blood, and restoring blood flow, (2) control further blood loss,
and (3) fluid resuscitation. Also, the patient's disposition should be rapidly and
appropriately determined.

 Maximizing oxygen delivery

o The patient's airway should be assessed immediately upon arrival

and stabilized if necessary. The depth and rate of respirations, as
well as breath sounds, should be assessed. If pathology (eg,
pneumothorax, hemothorax, flail chest) that interferes with
breathing is found, it should be addressed immediately. High-flow
supplemental oxygen should be administered to all patients, and
ventilatory support should be given, if needed. Excessive positive-
pressure ventilation can be detrimental for a patient suffering
hypovolemic shock and should be avoided.
o Two large bore IV lines should be started. The Poiseuille law states
that flow is inversely related to the length of the IV catheter and
directly related to its radius to the fourth power. Thus, a short large-
caliber IV catheter is ideal; the caliber is much more significant than
the length. IV access may be obtained by means of percutaneous
access in the antecubital veins, cutdown of saphenous or arm
veins, or access in the central veins by using the Seldinger
technique. If central lines are obtained, a large-bore single-lumen
catheter should be used. In children younger than 6 years,
intraosseous access also may be used. The most important factor
 in determining the route of access is the practitioner's skill and
experience.
o Placement of an arterial line should be considered for patients with
severe hemorrhage. For these patients, the arterial line will provide
continuous blood pressure monitoring and also ease arterial blood
gas testing.
o Once IV access is obtained, initial fluid resuscitation is performed
with an isotonic crystalloid, such as lactated Ringer solution or
normal saline. An initial bolus of 1-2 L is given in an adult (20 mL/kg
in a pediatric patient), and the patient's response is assessed.
o If vital signs return to normal, the patient may be monitored to
ensure stability, and blood should be sent for typed and cross-
matched. If vital signs transiently improve, crystalloid infusion
should continue and type-specific blood obtained. If little or no
improvement is seen, crystalloid infusion should continue, and type
O blood should be given (type O Rh-negative blood should be
given to female patients of childbearing age to prevent sensitization
and future complications).
o If a patient is moribund and markedly hypotensive (class IV shock),
both crystalloid and type O blood should be started initially. These
guidelines for crystalloid and blood infusion are not rules; therapy
should be based on the condition of the patient.
o The position of the patient can be used to improve circulation; one
example is raising the hypotensive patient's legs while fluid is being
given. Another example of useful positioning is rolling a
hypotensive gravid patient with trauma onto her left side, which
displaces the fetus from the inferior vena cava and increases
circulation. The Trendelenburg position is no longer recommended
for hypotensive patients, as the patient is predisposed to aspiration.
In addition, the Trendelenburg position does not improve
cardiopulmonary performance and may worsen gas exchange.
o Autotransfusion may be a possibility in some patients with trauma.
Several devices that allow for the sterile collection, anticoagulation,
filtration, and retransfusion of blood are available. In the trauma
setting, this blood almost always is from a hemothorax collected by
means of tube thoracostomy.

 Controlling further blood loss

o Control of further hemorrhage depends on the source of bleeding

and often requires surgical intervention. In the patient with trauma,
external bleeding should be controlled with direct pressure; internal
bleeding requires surgical intervention. Long-bone fractures should
be treated with traction to decrease blood loss.
o In the patient whose pulse is lost in the ED or just prior to arrival, an
emergency thoracotomy with cross-clamping of the aorta may be
 indicated to preserve blood flow to the brain. This procedure is
palliative at best and requires immediate transfer to the operating
room.
o In the patient with GI bleeding, intravenous vasopressin and H2
blockers have been used. Vasopressin commonly is associated
with adverse reactions, such as hypertension, arrhythmias,
gangrene, and myocardial or splanchnic ischemia. Therefore, it
should be considered secondary to more definitive measures. H2
blockers are relatively safe but have no proven benefit.
o Somatostatin and octreotide infusions have been shown to reduce
gastrointestinal bleeding from varices and peptic ulcer disease.
These agents possess the advantages of vasopressin without the
significant side effects.
o In patients with variceal bleeding, use of a Sengstaken-Blakemore
tube can be considered. These devices have a gastric balloon and
an esophageal balloon. The gastric one is inflated first, and then
the esophageal one is inflated if bleeding continues. The use of this
tube has been associated with severe adverse reactions, such as
esophageal rupture, asphyxiation, aspiration and mucosal
ulceration. For this reason, its use should be considered only as a
temporary measure in extreme circumstances.
o Virtually all causes of acute gynecological bleeding that cause
hypovolemia (eg, ectopic pregnancy, placenta previa, abruptio
placenta, ruptured cyst, miscarriage) require surgical intervention.

o Early consultation and definitive care are the keys. The goal in the
ED is to stabilize the hypovolemic patient, determine the cause of
bleeding, and provide definitive care as quickly as possible. If
transfer to another hospital is necessary, resources should be
mobilized early.
o In patients with trauma, if the emergency medical services
personnel indicate potential serious injury, the surgeon (or trauma
team) should be notified prior to the patient's arrival. In a 55-year-
old patient with abdominal pain, for example, emergency
ultrasonography of the abdomen may be necessary to identify an
abdominal aortic aneurysm before the vascular surgeon is notified.
Every patient should be individually evaluated, because delaying
definitive care can increase morbidity and mortality.

 Whether crystalloids or colloids are best for resuscitation continues to be a

matter for discussion and research. Many fluids have been studied for use
in resuscitation; these include isotonic sodium chloride solution, lactated
Ringer solution, hypertonic saline, albumin, purified protein fraction, fresh
frozen plasma, hetastarch, pentastarch, and dextran 70.

o Proponents of colloid resuscitation argue that the increased oncotic

 pressure produced with these substances decreases pulmonary
edema. However, the pulmonary vasculature allows considerable
flow of material, including proteins, between the intravascular space
and interstitium. Maintenance of the pulmonary hydrostatic
pressure at less than 15 mm Hg appears to be a more important
factor in preventing pulmonary edema.
o Another argument is that less colloid is needed to increase the
intravascular volume. Studies have shown this to be true. However,
they still have not demonstrated any difference in outcome with
colloids compared with crystalloids.
o Synthetic colloid solutions, such as hetastarch, pentastarch, and
dextran 70, have some advantages compared with natural colloids
such as purified protein fraction, fresh frozen plasma, and albumin.
They have the same volume-expanding properties, but because of
their structures and high molecular weights, they remain mostly in
the intravascular space, reducing the occurrence of interstitial
edema. Although theoretic advantages exist, studies have failed to
show a difference in ventilatory parameters, pulmonary function test
results, days using a ventilator, total hospital days, or survival.
o The combination of hypertonic saline and dextran also has been
studied because of previous evidence that it may improve cardiac
contractility and circulation. Studies in the US and Japan have
failed to show any difference when this combination was compared
with isotonic sodium chloride solution or lactated Ringer solution.
Thus, despite the many available resuscitation fluids, current
recommendations still advocate the use of normal saline or lactated
Ringer solution. In the US, one reason for the predominant use of
crystalloids over the other resuscitative fluids is cost.

 Another area of interest regarding resuscitation is whether the goal should

be to restore normal circulating volume and BP prior to definitive control of
bleeding.

o During World War I, Cannon observed and characterized patients

in clinical shock. He later suggested a model of permissive
hypotension in the treatment of torso wounds, with the intent of
minimizing further bleeding.
o Findings from early studies showed that animals that were bled had
increased survival if they received fluid resuscitation. However, in
these studies, bleeding was well controlled with ligation after the
animals were bled.
o During the Korean and Vietnam wars, much more aggressive fluid
resuscitation, as well as rapid access to definitive care, was
emphasized. It was noted that patients who were aggressively
resuscitated tended to have better outcomes, and in the 1970s,
these principles were widely adopted in civilian patients.
 o Since then, many studies have been conducted to determine if
these principles are valid in patients with uncontrolled hemorrhage.
Most of these studies revealed increased survival in the permissive
hypotension or delayed treatment arms. The theory is that
increased pressure causes more bleeding and disrupts initial clots,
whereas extreme hypotension may increase the risk of cerebral
perfusion.
o The questions that have not been answered adequately are as
follows: Which mechanisms and injury patterns are more amenable
to the restoration of circulating blood volume? What BP is adequate
but not excessive?
o Although some data indicate that a systolic BP of 80-90 mm Hg
may be adequate in penetrating truncal trauma without head injury,
further studies are needed.

o Current recommendations are for aggressive fluid resuscitation with

lactated Ringer solution or normal saline in all patients with signs
and symptoms of shock, regardless of underlying cause.

MEDICATION

The goals of pharmacotherapy are to reduce morbidity and prevent

complications.

Drug Category: Antisecretory agents -- These agents have vasoconstrictive

properties and can reduce blood flow to protal systems.

Somatostatin (Zecnil) -- Naturally occurring

tetradecapeptide isolated from the hypothalamus and
pancreatic and enteric epithelial cells. Diminishes
blood flow to portal system because of
Drug Name
vasoconstriction. Has similar effects as vasopressin
but does not cause coronary vasoconstriction.
Rapidly cleared from the circulation, with an initial
half-life of 1-3 min.
250 mcg IV bolus, followed by a 250-500 mcg/h
Adult Dose
continuous infusion; maintain for 2-5 d if successful
Pediatric Dose Not established
Contraindications Documented hypersensitivity
Epinephrine, demeclocycline, and thyroid hormone
Interactions
supplementation may decrease effects
Pregnancy C - Safety for use during pregnancy has not been
 established.
May exacerbate or cause gall bladder disease; alters
Precautions balance in counterregulatory hormones and may
cause hypothyroidism and cardiac conduction defects
Octreotide (Sandostatin) -- Synthetic octapeptide.
Compared to somatostatin, has similar
pharmacological actions with greater potency and
longer duration of action.
Drug Name
Used as adjunct to nonoperative management of
secreting cutaneous fistulas of the stomach,
duodenum, small intestine (jejunum and ileum), or
pancreas.
25-50 mcg/h IV continuous infusion; may be followed
Adult Dose
by initial IV boluses of 50 mcg; treat for up to 5 d
Pediatric Dose 1-10 mcg/kg IV q12h; dilute in 50-100 mL NS or D5W
Contraindications Documented hypersensitivity
May reduce effects of cyclosporine; patients on
insulin, oral hypoglycemics, beta-blockers and
Interactions
calcium channel blockers may need dosage
adjustments
Pregnancy B - Usually safe but benefits must outweigh the risks.
Side effects primarily related to altered GI motility and
include nausea, abdominal pain, diarrhea, and
increased prevalence of gallstones and biliary sludge;
because of alteration in counter-regulatory hormones,
(insulin, glucagon and GH) hypo- or hyperglycemia
Precautions may be seen; bradycardia, cardiac conduction
abnormalities, and arrhythmias have been reported;
because of inhibition of TSH secretion,
hypothyroidism may also occur; exercise caution in
patients with renal impairment; cholelithiasis may
occur
FOLLOW-UP

Complications:

 Neurologic sequelae

 Death
Prognosis:

 The prognosis is dependent on the degree of volume loss.

Patient Education:

 For excellent patient education resources, visit eMedicine's Shock Center.

Also, see eMedicine's patient education article Shock.

MISCELLANEOUS

Medical/Legal Pitfalls:

 A common error in the management of hypovolemic shock is failure to

recognize it early.

o This error leads to delay in diagnosing the cause and in

resuscitating the patient.

o This error often is caused by a reliance on BP or initial hematocrit

level, rather than signs of decreased peripheral perfusion, to make
the diagnosis.

o Injuries in patients with trauma can be missed, especially if the

examining physician focuses on more obvious injuries. This error
can be avoided by completing a full physical examination,
continuously and closely monitoring the patient's status, and
performing serial examinations.

o Elderly individuals have less tolerance for hypovolemia compared

with the rest of the general population. Aggressive therapy should
be instituted early to prevent potential complications, such as
myocardial infarction and stroke.

o In patients who require extensive volume resuscitation, care should

be taken to prevent hypothermia, because this can contribute to
arrhythmia or coagulopathy. Hypothermia can be prevented by
warming the intravenous fluids prior to their administration.

o Patients taking beta-blockers or calcium-channel blockers and

those with pacemakers may not have a tachycardic response to
hypovolemia; this lack of response may lead to a delay in the
diagnosis of shock. To minimize this potential delay, history taking
 should always include questioning about medications. The
examiner should also rely on signs of decreased peripheral
perfusion other than tachycardia.

o Coagulopathies can occur in patients receiving large amounts of

volume resuscitation. This is due to dilution of platelets and clotting
factors but is rare within the first hour of resuscitation. Baseline
coagulation studies should be drawn and should guide the
administration of platelets and fresh frozen plasma.