SOGC CLINICAL PRACTICE GUIDELINES

No. 115, June 2002

HEMORRHAGIC SHOCK
This document has been reviewed by the Clinical Practice Obstetrics Committee and approved by
Executive and Council of the Society of Obstetricians and Gynaecologists of Canada.

PRINCIPAL AUTHOR
Marie-Jocelyne Martel, MD, FRCPC, Saskatoon SK

CLINICAL PRACTICE OBSTETRICS COMMITTEE

Catherine Jane MacKinnon, MD, FRCPC, Brantford ON (Chair)
Marc-Yvon Arsenault, MD, FRCPC, Montreal QC
Elias Bartellas, MD, FRCPC, St. John’s NF
Michael C. Klein, MD, CCFP, FCFP, Vancouver BC
Carolyn A. Lane, MD, CCFP, FCFP, Calgary AB
Marie-Jocelyne Martel, MD, FRCPC, Saskatoon SK
Ann E. Sprague, RN, BN, MEd, Ottawa ON
Ann Kathleen Wilson, BHSc, RM, London ON

Abstract 6. Isotonic crystalloid or colloid solutions can be used for vol-

Objective: To review the clinical aspects of hemorrhagic shock ume replacement in hemorrhagic shock (I-B). There is no
and provide recommendations for therapy. place for hypotonic dextrose solutions in the management
Options: Early recognition of hemorrhagic shock and prompt of hemorrhagic shock (I-E).
systematic intervention will help avoid poor outcomes. 7. Blood component transfusion is indicated when deficiencies
Outcomes: Establish guidelines to assist in early recognition of have been documented by clinical assessment or hematolog-
hemorrhagic shock and to conduct resuscitation in an orga- ical investigations (II-2B). They should be warmed and infused
nized and evidence-based manner. through filtered lines with normal saline, free of additives
Evidence: Medline references were sought using the MeSH term and drugs (II-3B).
“hemorrhagic shock.” All articles published in the disciplines of 8. Vasoactive agents are rarely indicated in the management of
obstetrics and gynaecology, surgery, trauma, critical care, anes- hemorrhagic shock and should be considered only when vol-
thesia, pharmacology, and hemotology between 1 January 1990 ume replacement is complete, hemorrhage is arrested, and
and 31 August 2000 were reviewed, as well as core textbooks hypotension continues. They should be administered in a
from these fields. Selected references from these articles and critical care setting with the assistance of a multidisciplinary
book chapters were also obtained and reviewed. The level of team. (III-B)
evidence has been determined using the criteria described by 9. Appropriate resuscitation requires ongoing evaluation of
the Canadian Task Force on the Periodic Health Examination. response to therapy, including clinical evaluation, and hema-
Recommendations: tological, biochemical, and metabolic assessments. (III-B)
1. Clinicians should be familiar with the clinical signs of hem- 10. In hemorrhagic shock, prompt recognition and arrest of the
orrhagic shock. (III-B) source of hemorrhage, while implementing resuscitative mea-
2. Clinicians should be familiar with the stages of hemorrhagic sures, is recommended. (III-B)
shock. (III-B) Validation: These guidelines have been reviewed by the Clinical
3. Clinicians should assess each woman’s risk for hemorrhagic Practice Obstetrics Committee and approved by Executive
shock and prepare for the procedure accordingly. (III-B) and Council of the Society of Obstetricians and Gynaecolo-
4. Resuscitation from hemorrhagic shock should include ade- gists of Canada.
quate oxygenation. (II-3A) Sponsors: The Society of Obstetricians and Gynaecologists of
5. Resuscitation from hemorrhagic shock should include Canada.
restoration of circulating volume by placement of two large-
bore IVs, and rapid infusion of a balanced crystalloid solu- J Obstet Gynaecol Can 2002;24(6):504-11.
tion. (I-A)

These guidelines reflect emerging clinical and scientific advances as of the date issued and are subject to change.The information should not be construed as
dictating an exclusive course of treatment or procedure to be followed. Local institutions can dictate amendments to these opinions.They should be well doc-
umented if modified at the local level. None of the contents may be reproduced in any form without prior written permission of SOGC.

FOR INFORMATION ON THE SELF-DIRECTED LEARNING EXERCISE SEE PAGE 521.

JOGC 1 JUNE 2002
INTRODUCTION matory response may be associated with increased intraoperative
blood loss. Identification, isolation, and rapid control of bleed-
Hemorrhagic shock is a rare but serious complication, which ing encountered during the procedure will limit the total loss.
may occur in many obstetrical or gynaecological situations. The anatomy of the pelvis and landmarks of the vascular tree
Hemorrhage is a leading cause of maternal death in the deve- must be familiar to every pelvic surgeon.
loping world.1 Death and morbidity secondary to hemorrhage Patients with delayed postoperative hemorrhage may pre-
are becoming less common due to early recognition and inter- sent with bleeding from the wound or vagina or with evidence
vention and improved availability of medical resources.1 Ten rec- of a hemoperitoneum. Careful examination and resuscitation
ommendations for the management of hemorrhagic shock are with definitive and prompt control of blood loss is required,
listed in the following text and have been graded according to which may require a return to the operating theatre.
their level of evidence as determined by the criteria of the Cana-
dian Task Force on the Periodic Health Examination (Table 1).2 CLINICAL PRESENTATION AND
COMPLICATIONS OF HEMORRHAGIC SHOCK
HEMORRHAGIC SHOCK IN OBSTETRICS
Obstetrical hemorrhage is often acute, dramatic, and underesti- Hemorrhage occurs when there is excessive external or internal
mated.3 Postpartum hemorrhage is a significant cause of mater- blood loss.4 A defined volume is difficult to measure in most
nal death.3 Management of postpartum hemorrhage has been situations, and the loss evaluated visually is often underesti-
reviewed in detail in SOGC Clinical Practice Guidelines for the mated.4 Shock occurs when there is hypoperfusion of vital
Prevention and Management of Postpartum Hemorrhage.3 organs. Hypoperfusion may be due to malfunction of the
myocardium (cardiogenic shock), overwhelming infection lead-
HEMORRHAGIC SHOCK IN GYNAECOLOGY ing to redistribution of circulating volume into the extravas-
A surgical procedure is the most common antecedent of acute cular space (septic shock), or hypovolemia due to severe
gynaecological hemorrhage, although patients will occasionally dehydration or hemorrhage (hypovolemic shock).1 Signs and
present with acute hemorrhage from a ruptured ectopic preg- symptoms of hemorrhagic shock will vary depending on the
nancy or from a neoplasm.1 Risk identification is important in volume and rate of blood loss (Table 2).1
counselling patients prior to surgery and in preparation of the The key systems affected by hemorrhagic shock are the cen-
surgical team. Any process that distorts pelvic anatomy, such as tral nervous, cardiac, and renal systems.5 The central nervous
endometriosis, neoplasm, or adhesions, or that leads to an inflam- system is able to function despite hypoperfusion, until the mean

TABLE 1
QUALITY OF EVIDENCE ASSESSMENT2 CLASSIFICATION OF RECOMMENDATIONS
The quality of evidence reported in these guidelines has been Recommendations included in these guidelines have been
described using the Evaluation of Evidence criteria outlined in adapted from the ranking method described in the Classification
the Report of the Canadian Task Force on the Periodic of Recommendations found in the Report of the Canadian Task
Health Exam. Force on the Periodic Health Exam.
I: Evidence obtained from at least one properly random- A. There is good evidence to support the recommendation
ized controlled trial. that the condition be specifically considered in a periodic
II-1: Evidence from well-designed controlled trials without health examination.
randomization. B. There is fair evidence to support the recommendation
II-2: Evidence from well-designed cohort (prospective or that the condition be specifically considered in a periodic
retrospective) or case-control studies, preferably from health examination.
more than one centre or research group.
C. There is poor evidence regarding the inclusion or exclu-
II-3: Evidence obtained from comparisons between times or
sion of the condition in a periodic health examination,
places with or without the intervention. Dramatic
but recommendations may be made on other grounds.
results in uncontrolled experiments (such as the results
D. There is fair evidence to support the recommendation
of treatment with penicillin in the 1940s) could also be
that the condition not be considered in a periodic health
included in this category.
III: Opinions of respected authorities, based on clinical examination.
experience, descriptive studies, or reports of expert E. There is good evidence to support the recommendation
committees. that the condition be excluded from consideration in a
1 periodic health examination.

JOGC 2 JUNE 2002

 TABLE 2 sis.10 Multi-system injury can lead to coagulopathy, and meta-
CLINICAL FEATURES OF HEMORRHAGIC SHOCK1 bolic disturbances such as acidosis.1
System Early shock Late shock
RECOMMENDATION
CNS Altered mental status Obtunded
1. Clinicians should be familiar with the clinical signs of
hemorrhagic shock. (III-B)
Cardiac Tachycardia Cardiac failure
Orthostatic hypotension Arrhythmias PATHOPHYSIOLOGY OF HEMORRHAGIC SHOCK
Hypotension
Renal Oliguria Anuria
In hemorrhagic shock, an acute reduction in blood volume leads
to sympathetic compensation by peripheral vasoconstriction,
Respiratory Tachypnea Tachypnea tachycardia, and increased myocardial contractility, which in
Respiratory failure turn increases the myocardial demand for oxygen, to a level that
cannot be maintained.1 Simultaneously, tissue hypoperfusion
from precapillary vasoconstriction leads to anaerobic metabo-
Hepatic No change Liver failure
lism and acidosis.11 Tissue hypoxia, acidosis, and the release of
Gastrointestinal No change Mucosal bleeding various mediators lead to a systemic inflammatory response.5,11
Hematological Anemia Coagulopathy Reperfusion injury occurs when oxygen radicals released
Metabolic None Acidosis during the acute phase are systemically circulated as whole
body perfusion is restored.4,11,12 Humoral and cellular inflam-
Hypocalcemia
matory systems are also activated, and contribute to vascular
Hypomagnesemia and cellular injury.12,13 Transmigration of microorganisms and
endotoxins across weakened mucosal barriers contributes to
arterial pressure falls below 60–70 mmHg.1 With increasing sever- systemic inflammatory response syndrome (SIRS) and multi-
ity of hypovolemia, mild agitation and confusion progress to ple organ failure.4,10,11
lethargy and obtundation.1 The heart plays an important role in
the compensation for losses in early shock.3 Early hypovolemia is CLASSIFICATION OF HEMORRHAGIC SHOCK
associated with reflex tachycardia and increased stroke volume.4,6
With continued loss, hypoperfusion of the coronary arteries and A classification of hemorrhagic shock is outlined in Table 3. This
myocardium leads to cardiac dysfunction, ischemia, and failure:1 type of classification may aid in determining the volume required
symptoms of chest pain and dyspnea with signs of rales, tachyp- for initial replacement, and the listed signs of shock in deter-
nea, and murmurs or arrhythmias are indicative of this process. mining the severity of occult losses. The symptoms and seque-
The kidney will compensate for losses by activation of the renin- lae of hemorrhage are ultimately related to perfusion of tissues.
angiotensin-aldosterone system.4 Early, reversible renal injury is Loss of less than, or equal to, 15% of blood volume (compen-
associated with low urine sodium concentration and high urine sated shock) may not be associated with any change in blood
osmolality (>500 mOsm).1 Oliguria is a reliable sign that these pressure (BP), pulse, or capillary refill. Mild shock is usually eas-
compensatory mechanisms have been overwhelmed.1 ily compensated, especially in the younger, healthy woman of
All organ systems are ultimately affected in shock. Respira- reproductive age.14 Further losses lead to tachycardia, a cate-
tory, hepatic, and gastrointestinal systems can be affected early cholamine response characterized by increased sympathetic tone.
in the process since cardiac output is redirected to the most Resting BP is usually normal, but orthostatic changes in BP and
important organs: the heart, brain, and kidneys.6,7 Manifesta- pulse may be evident. Simple resuscitative measures will suc-
tions of lung injury include: dyspnea, tachypnea, pulmonary cessfully reverse these changes.1 Ongoing losses of blood volume
infiltrates, and edema leading to decreased tissue compliance may overtake the heart’s ability to compensate, and marked
and hypoxia. Symptoms of adult respiratory distress syndrome tachycardia is associated with a fall in BP, classified as moderate
(ARDS) include: intrapulmonary shunting, reduced pulmonary shock. With continued bleeding, hypoperfusion of tissues occurs,
compliance, and low arterial pO2 that often requires assisted leading to anaerobic metabolism and acidosis, classified as severe
mechanical ventilation.6,8 Moderate elevations of bilirubin and shock. The patient demonstrates marked tachycardia and tachyp-
alkaline phosphatase can be seen with ischemic hepatic injury.1 nea with respiratory failure, becomes oliguric, and then anuric.
Gastrointestinal ischemia manifests as bleeding of either frank Obtundation and loss of consciousness may also occur.1 Cellu-
blood or coffee ground hematemesis or hematochezia or with lar dysfunction, followed by cell death, leads to multiple organ
delayed abdominal pain secondary to gut ischemia.9 Erosion of failure, resulting in irreversible shock.1,15 The mortality rate at
the intestinal mucosa allows bacteremia and subsequent sep- this stage is in excess of 30%.1

JOGC 3 JUNE 2002

 TABLE 3
CLASSIFICATION OF HEMORRHAGIC SHOCK1,5,16
Compensated Mild Moderate Severe

Blood Loss (mL) ≤1000 1000 –1500 1500 –2000 >2000

Heart rate (bpm) <100 >100 >120 >140

Blood pressure Normal Orthostatic change Marked fall Profound fall

Capillary refill Normal May be delayed Usually delayed Always delayed

Respiration Normal Mild increase Moderate tachypnea Marked tachypnea:

respiratory collapse

Urinary output (mL/h) >30 20 –30 5–20 Anuria

Mental status Normal or agitated Agitated Confused Lethargic, obtunded

RECOMMENDATION atic approach to vascular areas, will be useful in the prompt con-
2. Clinicians should be familiar with the stages of hemor- trol of hemorrhage. As soon as the first signs of excessive blood
rhagic shock. (III-B) loss and shock are evident, assistance from other members of the
health care team, which may include an anesthetist, a second
RISK FACTORS gynaecologist, a general surgeon, a vascular surgeon, a critical
care specialist, a hematologist, and experienced nursing staff,
Evaluation of all patients presenting for obstetrical care or should be considered when appropriate and if available. Labo-
surgery should include a complete medical history. A personal ratory and blood bank services should be informed and available
or family history of coagulopathy, or personal use of anticoag- for support. Since cell death due to hypoxic injury is the final
ulants, should be documented. A complete physical examina- common pathway in shock, all efforts should be directed at
tion may reveal extensive bruising or petechiae. Investigations restoring tissue oxygenation as soon as possible. A useful
to assess coagulation status should be obtained in these situa- mnemonic to achieve this goal is ORDER: Oxygenate, Restore
tions and consultation from other disciplines considered. circulating volume, Drug therapy, Evaluate response to therapy,
All proposed procedures should be reviewed with the Remedy underlying cause.1,14 Outcome is dependent on early
patient. The risk of complications including hemorrhage recognition and on immediate aggressive therapy, which relies
should be outlined and the discussion documented in the on two basic principles: replace losses and arrest bleeding.
chart.17 Certain clinical conditions and their surgical manage-
ment are associated with an increased risk of hemorrhage, such OXYGENATION
as ectopic pregnancy, myomectomy, abruptio placenta, pla- The initial step in any patient resuscitation is to secure an airway
centa previa, and malignant disease.17 In some situations, it and provide adequate oxygenation.16 In most surgical situations,
may be appropriate to counsel women about autologous blood an airway will already be in place, managed by the anesthetist. If
transfusion or hemodilution techniques.17,18 Jehovah’s Wit- regional anesthesia has been used, supplemental oxygen should
nesses may require special consideration.19 be applied.4 Consideration should be given to endotracheal intu-
bation, if the patient is becoming disoriented or is tiring, and in
RECOMMENDATION an obtunded patient should be instituted immediately.1 After
3. Clinicians should assess each woman’s risk for hemor- extensive fluid resuscitation, edema of the trachea may make intu-
rhagic shock and prepare for the procedure accordingly. bation difficult. Positive ventilatory pressures may be required in
(III-B) those patients with decreased pulmonary compliance.

MANAGEMENT RECOMMENDATION
4. Resuscitation from hemorrhagic shock should include
Early resuscitation includes control of bleeding and restoration adequate oxygenation. (II-3A)
of circulating blood volume for oxygenation of tissues.16 Tech-
niques to minimize blood loss should be applied whenever pos- RESTORE CIRCULATING VOLUME
sible. Exposure of the bleeding site, experienced assistance, and Intravascular replacement of blood volume lost may be accom-
sound knowledge of pelvic anatomy, as well as a calm, system- plished using crystalloid, colloid, or blood products. Initial

JOGC 4 JUNE 2002

therapy should consist of 1–2L of intravenous (IV) crystal- COLLOID SOLUTIONS
loid.1,16 Intravenous access should be of large calibre (14–16 Colloid solutions contain molecules designed to stay within the
gauge) and in multiple sites to facilitate rapid volume infu- intravascular compartment.1,6,11,20-23 These products include
sion.5,16 A central line may be considered, but it does not albumin, hydroxyethyl starch, dextrans, and gelatins. They are
appear to provide any advantage over peripheral lines for rapid more expensive and less available than crystalloids.22,24 Each of
infusion of volume.5,16 The time and skill required to establish these oncotic replacement products carries the risk of reac-
a central line, and the risk of complications such as pneumo- tion.1,20,23 Some will bind calcium or affect circulating
thorax, should also be considered.1,5 Central venous pressure immunoglobulins.6,7,20,26 There is no convincing evidence that
measurements may be helpful for safe resuscitation, if there has colloid solutions offer any advantage over crystalloid solutions
been injury to the cardiovascular system or vascular injury in in the replacement of volume in hemorrhagic shock.1,4,5-7,
the lung, as the amount of fluid required to restore tissue per- 20-22,24,27,28 A recent review of the use of albumin in the treat-

fusion may be difficult to estimate. These patients are at risk ment of hypovolemia suggests that its use may increase the risk
for pulmonary edema and lung injury, if excessive fluid replace- of death.29 Crystalloids and colloids may be used together.22
ment is given.6,7 In monitoring patients with multiple organ
failure, central venous pressure measurements may also be use- RECOMMENDATION
ful in resuscitation and monitoring.16 Normal central venous 6. Isotonic crystalloid or colloid solutions can be used for
pressure is 5 mmHg (range 0–8 mmHg).14 Elevated pressures volume replacement in hemorrhagic shock (I-B). There
are seen in fluid overload, right ventricular failure, pulmonary is no place for hypotonic dextrose solutions in the man-
embolus, cardiac tamponade, and severe tricuspid regurgita- agement of hemorrhagic shock (I-E).
tion. Low values are seen with shock from hypovolemia, sep-
sis, and anaphylaxis.14 TRANSFUSION
Many blood products are available to restore circulating vol-
RECOMMENDATION ume, and replace coagulation factors and oxygen-carrying
5. Resuscitation from hemorrhagic shock should include capacity (Table 4). Component therapy allows specific replace-
restoration of circulating volume by placement of two ment to address specific needs. Hypovolemia is best corrected
large-bore IVs, and rapid infusion of a balanced crystal- with crystalloid solution. In hemorrhagic shock, packed red
loid solution. (I-A) blood cells (PRBC) are most commonly used to restore intravas-
cular volume and oxygen-carrying capacity. The oxygen-
CRYSTALLOID SOLUTIONS carrying capacity of most healthy individuals will not be com-
Crystalloid solutions are electrolyte solutions administered intra- promised until the hemoglobin concentration falls below
venously. Advantages of crystalloid solutions include availabil- 60–70 g/L.1,7,20,30,31 There is no recommended “threshold
ity, safety, and low cost.5,6 The main disadvantage of using hemoglobin.”7,30 Blood losses greater than 20–25% or cases of
crystalloid solutions is their rapid movement from the intravas- documented or suspected coagulopathy may require replace-
cular to the extravascular space, leading to three or more times ment of coagulation factors; coagulation studies are recom-
requirement for replacement,1,4,20,21 and resulting in tissue mended after transfusion of 5 to 10 units of PRBCs.14
edema.22 Ringer’s lactate is preferred over normal saline to avoid Platelet transfusions are indicated in situations of signifi-
hyperchloremic acidosis associated with prolonged use of sodi- cant thrombocytopenia (platelet count less than 20,000 to
um solutions.1,23,24 Hypertonic salt solutions are not generally 50,000 per mm3) and continued hemorrhage.31 Coagulation
recommended because of the risk of electrolyte distur- factor concentrates are available for identified deficiencies, and
bances.1,6,20,25 There is no role for hypotonic dextrose solutions fresh frozen plasma can be administered in acute situations
in the management of hypovolemic shock.21 where the partial thromboplastin time and prothrombin time

TABLE 4
INDICATIONS FOR BLOOD COMPONENT THERAPY14,20,30-35
Component Indication Usual starting dose

Packed RBC Replacement of oxygen-carrying capacity 2– 4 Units IV

Platelets Thrombocytopenia or thrombasthenia with bleeding 6–10 Units IV

Fresh frozen plasma Documented coagulopathy 2– 6 Units IV

Cryoprecipitate Coagulopathy with low fibrinogen 10 –20 Units IV

JOGC 5 JUNE 2002

are elevated. There is no indication for prophylactic adminis- mine, the dopamine receptors in the cerebral, renal, and
tration of platelets, plasma, or specific components in resusci- mesenteric circulation are stimulated, resulting in vasodilata-
tation of hemorrhagic shock.20,30-33 Immediate complications tion and increased urinary output. At moderate doses
of blood transfusions are increased when large volumes of (2–10 µg/kg/min), alpha- and beta1-adrenergic receptors are
blood product are infused.30 All blood products should be also stimulated, increasing myocardial contractility and cardiac
cross-matched and administered through filtered lines with output, resulting in an increase in myocardial oxygen con-
normal saline, free of additives or drugs.16 Acid-base and elec- sumption. At higher doses (>10 µg/kg/min), the alpha-adren-
trolyte disturbances can be evident with large volume transfu- ergic receptors are stimulated, leading to vasoconstriction
sions. 16 Blood products should be warmed to prevent and increases in blood pressure.1,7
hypothermia.1,30,32 Dobutamine is a beta1- and beta2-adrenergic stimulator.
Beta2 stimulation leads to systemic vasodilatation and reduced
RECOMMENDATION afterload.7 Dobutamine is associated with less pulmonary con-
7. Blood component transfusion is indicated when defi- gestion and less tachycardia than dopamine.7
ciencies have been documented by clinical assessment or Phenylephrine, norepinephrine, and epinephrine are used
hematological investigations (II-2B). They should be in situations of refractory shock. Their principal effect is to
warmed and infused through filtered lines with normal increase blood pressure by increasing systemic vascular resistance.
saline, free of additives and drugs (II-3B). They also produce some degree of coronary vasoconstriction,
which may exacerbate myocardial ischemia (Table 5).7
DRUG THERAPY
VASOACTIVE AGENTS RECOMMENDATION
After adequate volume replacement has been achieved, vaso- 8. Vasoactive agents are rarely indicated in the management
active agents, which include inotropes and vasopressors, may of hemorrhagic shock and should be considered only
be considered but are not often required in hemorrhagic shock.1 when volume replacement is complete, hemorrhage is
When required, inotropic agents are administered first, followed arrested, and hypotension continues. They should be
by vasopressors in refractory cases. There is a risk that these administered in a critical care setting with the assistance
agents may cause a further limitation of perfusion and oxy- of a multidisciplinary team. (III-B)
genation of distal organs.7,14 Ideally, these drugs should be
administered in a critical care setting with the assistance of a OTHER DRUG THERAPY
multidisciplinary team. Broad coverage antibiotic therapy should be instituted in cases
Dopamine can stimulate the function of alpha- and beta1- of hemorrhagic shock, as there is a significant risk of sepsis.1
adrenergic receptors.7 At low doses of 1–3 µg/kg/min dopa- Ischemic injury to the gut makes it vulnerable to transmucosal

TABLE 5
PHARMACOLOGICAL SUPPORT OF THE CARDIOVASCULAR SYSTEM1,7
Agent Usual dose range Effect
Inotropic agents
Dopamine 1–3 µg/kg/min Increased renal output
Vasodilation
2–10 µg/kg/min Increased heart rate
Increased cardiac output
>10 µg/kg/min Peripheral vasoconstriction
Increased heart rate and contractility
Dobutamine 2 –10 µg/kg/min Increased heart rate and contractility
Decreased afterload
Vasopressor agents
Phenylephrine 1–5 µg/kg/min Peripheral vasoconstriction
Norepinephrine 1– 4 µg/min Peripheral vasoconstriction
Epinephrine 1– 8 µg/min Peripheral vasoconstriction

JOGC 6 JUNE 2002

erosions and may lead to bacteremia.10 The gastric mucosa is tion and ligation of the uterine or internal iliac arteries are useful
susceptible to stress ulceration, which can be reduced by the use techniques to control hemorrhage in the pelvis.17 The ureter is
of antacids or H2 blockers.1 especially vulnerable during the placement of hemostatic sutures
Stroma-free hemoglobin (diaspirin cross-linked hemo- in the pelvis. If hemorrhage continues, coagulation should be eval-
globin) is a new product currently under evaluation, which can uated and any identified deficiencies should be corrected. Adjunc-
replace the oxygen-carrying capacity of PRBCs. Its affinity for tive measures such as radiologic embolization and packing of the
nitric oxide contributes to peripheral vasoconstriction. Poten- pelvis should be considered in refractory cases.17
tial advantages include a longer shelf life and universal com- Careful documentation of events and the interventions per-
patibility.35 There is no clear clinical advantage over PRBCs. formed should be completed in a timely fashion. Communi-
Risks include extravasation, possible coagulopathy, and the risks cation with the patient, her partner, and her family should be
associated with human blood components, as well as docu- prompt, frequent, and clear.
mented toxicities.15,20,35-37
RECOMMENDATION
EVALUATION OF RESPONSE TO THERAPY 10. In hemorrhagic shock, prompt recognition and arrest
Once oxygenation and circulating volume have been restored, of the source of hemorrhage, while implementing resus-
re-evaluation of the clinical situation is in order. Vital signs, citative measures, is recommended. (III-B)
mental status, urinary output, and capillary refill should be
assessed regularly throughout resuscitation.14,16 Initiation of CONCLUSION
central monitoring may be indicated at this time, if the response
to initial resuscitation has been less than expected or if blood Hemorrhagic shock may occur in many obstetrical or gynaeco-
loss is ongoing.7 Blood should be drawn to assess hematologi- logical conditions. Prompt recognition of blood losses and imple-
cal, coagulation, electrolyte, and metabolic status. Electrolyte mentation of resuscitative measures in a calm and systematic
and metabolic disorders as well as coagulation deficiencies fashion are imperative. A multidisciplinary approach to the multi-
should be corrected. Arterial blood gases should be obtained to system effects of shock is essential to optimize the outcome.
determine adequacy of oxygenation. Management of alterations
to oxygenation, ventilation, pH, fluid, and electrolyte balance REFERENCES
should now be made based on laboratory measurements.16 Blood
components may also be used to replace identified deficiencies. 1. Smith HO. Shock in the gynecologic patient. In: Rock JA,Thomson JD,
editors.Te Linde’s operative gynecology. 8th ed. Lippincott-Raven; 1997.
p. 245-61.
RECOMMENDATION 2. Woolf SH, Battista RN,Angerson GM, Logan AG, Eel W. Canadian Task
9. Appropriate resuscitation requires ongoing evaluation of Force on the Periodic Health Exam. Ottawa: Canada Communication
Group; 1994. p. xxxvii.
response to therapy, including clinical evaluation, and 3. SOGC Clinical Practice Guidelines. Prevention and management of post-
hematological, biochemical, and metabolic assessments. partum hemorrhage. J Soc Obstet Gynaecol Can 2000;22(4):271-81.
(III-B) 4. Barber A, Shires GT. Shock. In: Schwartz SI, editor. Principles of surgery.
7th ed. McGraw-Hill. 1999. p.101-22.
5. Falk JL, O’Brien JF, Kerr R. Fluid resuscitation in traumatic hemorrhagic
REMEDY THE UNDERLYING CAUSE shock. Crit Care Clin 1992;8(2):323-40.
Most cases of unresponsive shock in gynaecologic patients are due 6. Shires GT, Barber AE, Illner HP. Current status of resuscitation:
to ongoing losses of blood volume. While initial stabilization is solutions including hypertonic saline. Adv Surg 1995;28:133-70.
7. Domsky MF,Wilson RF. Hemodynamic resuscitation. Crit Care Clin
taking place, attention should be directed to the prompt arrest of 1993;10(4):715-26.
bleeding. Aggressive restoration of normal blood pressure without 8. Croce MA, Fabian TC, Davis KA, Gavin TJ. Early and late acute respira-
arrest of hemorrhage will enhance further losses of blood volume tory distress syndrome: two distinct clinical entities. J Trauma
1999;46(3):361-8.
by increasing flow and impeding coagulation at the site of 9. Ludwig KA, Quebbeman EJ, Bergstein JM,Wallace JR,Wittmann DH,
injury.11,15,25,27,38-40 Mild to moderate hypotension allows clot for- Aprahamian C. Shock-associated right colon ischemia and necrosis.
mation and slows bleeding from the injured vessel.39 The source J Trauma 1995;39(6):1171-4.
10. Kale IT, Kuzu MA, Berkem H, Berkem R, Acar N.The presence of
of blood loss should be identified and arrested as soon as possi-
hemorrhagic shock increases the rate of bacterial translocation in
ble.14 Occult retroperitoneal hemorrhage should be suspected in blunt abdominal trauma. J Trauma 1998;44(1):171-4.
patients who have a deteriorating hemodynamic status more than 11. Marzi I. Hemorrhagic shock: update in pathophysiology and therapy.
12 hours post surgery.17 In these cases, identification of the exact Acta Anaesthesiol Scand Suppl 1997;111:42-4.
12. Heckbert SR,Vedder NB, Hoffman W,Winn RK, Hudson LD,
site of bleeding can be very difficult. Hemorrhage during or fol- Jurkovich GJ, et al. Outcome after hemorrhagic shock in trauma
lowing an operative procedure should be addressed surgically, with patients. J Trauma 1998;45(3):545-9.
immediate exploration, isolation, and ligation of bleeding vessels. 13. Seekamp A, Jochum M, Ziegler M, van Griensven M, Martin M, Regel G.
Cytokines and adhesion molecules in elective and accidental trauma-
In most cases, hemostasis can be achieved in this manner. Isola- related ischemia/reperfusion. J Trauma 1998;44(5):874-82.

JOGC 7 JUNE 2002

14. ACOG Educational Bulletin. Hemorrhagic shock. Number 235. April 39. Bickell WH. Are victims of injury sometimes victimized by attempts at
1997 (replaces no. 82, December 1984). American College of Obstetri- fluid resuscitation? [editorial; comment]. Ann Emerg Med
cians and Gynecologists. Int J Gynaecol Obstet 1997;57(2):219-26. 1993;22(2):225-6.
15. Shoemaker WC, Peitzman AB, Bellamy R, Bellomo R, Bruttig SP, 40. Dries DJ. Hypotensive resuscitation. Shock 1996;6(5):311-6.
Capone A, et al. Resuscitation from severe hemorrhage. Crit Care
Med 1996;24(2 Suppl):S12-23.
16. The American College of Surgeons. Shock. In:The American College
of Surgeons, editor. Advanced trauma life support. 1990. p. 59-73.
17. Thompson JD, Rock WA. Control of pelvic hemorrhage. In: Rock JA,
Thomson JD, editors.Te Linde’s operative gynecology. 8th ed.
Lippincott-Raven Publishers; 1997. p.197-232.
18. Rebarber A, Lonser R, Jackson S, Copel JA, Sipes S.The safety of intra-
operative autologous blood collection and autotransfusion during
Cesarean section. Am J Obstet Gynecol 1998;179:715-20.
19. Culkin Mann M,Votto J, Kambe J, McNamee J. Management of the
severely anemic patient who refuses transfusion: lessons learned during
the care of a Jehovah’s Witness. Ann Intern Med 1992;117:1042-8.
20. Gould SA, Sehgal LR, Sehgal HL, Moss GS. Hypovolemic shock. Crit
Care Clin 1993;9(2):239-59.
21. Lucas CE. Update on trauma care in Canada. 4. Resuscitation through
the three phases of hemorrhagic shock after trauma. Can J Surg
1990;33(6):451-6.
22. Davies MJ. Crystalloid or colloid: does it matter? J Clin Anesth
1989;1(6):464-71.
23. Dubick MA,Wade CE. A review of the efficacy and safety of 7.5%
NaCl/6% dextran 70 in experimental animals and in humans. J Trauma
1994;36(3):323-30.
24. Vassar MJ, Perry CA, Holcroft JW. Prehospital resuscitation of hypo-
tensive trauma patients with 7.5% NaCl versus 7.5% NaCl with added
dextran: a controlled trial. J Trauma 1993;34(5):622-32.
25. Deakin CD. Early fluid resuscitation in haemorrhagic shock. Eur J Emerg
Med 1994;1(2):83-5.
26. Sillett HK,Whicher JT,Trejdosiewicz LK. Effects of resuscitation fluids
on nonadaptive immune responses.Transfusion 1997;37(9):953-9.
27. Napolitano LM. Resuscitation following trauma and hemorrhagic shock:
is hydroxyethyl starch safe? [editorial; comment]. Crit Care Med
1995;23(5):795-7.
28. Poole GV, Meredith JW, Pennell T, Mills SA. Comparison of colloids
and crystalloids in resuscitation from hemorrhagic shock. Surg Gynecol
Obstet 1982;154:577-86.
29. Bunn F, Lefebvre C, Li-Wan-Po A, Li L, Roberts I, Schierhout G. Human
albumin solution for resuscitation and volume expansion in critically ill
patients. Cochrane Database Syst Rev 2000;2:CD001208.
30. Guidelines for red blood cell and plasma transfusion for adults and
children. Can Med Assoc J 1997;156(11):S1-S54.
31. Schwartz SI. Hemostasis, surgical bleeding and transfusion. In: Schwartz
SI, editor. Principles of surgery. 7th ed. McGraw-Hill; 1999. p. 77-100.
32. Hocker P, Hartmann T. Management of massive transfusion.
Acta Anaesthesiol Scand Suppl 1997;111:205-7.
33. Harrigan C, Lucas CE, Ledgerwood AM.The effect of hemorrhagic
shock on the clotting cascade in injured patients. J Trauma
1989;29(10):1416-21.
34. Martin DJ, Lucas CE, Ledgerwood AM, Hoschner J, McGonigal MD,
Grabow D. Fresh frozen plasma supplement to massive red blood cell
transfusion. Ann Surg 1985;202(4):505-11.
35. ACOG technical bulletin. Blood component therapy. Number 199 –
November 1994 (replaces no. 78, July 1984). Committee on Technical
Bulletins of the American College of Obstetricians and Gynecologists.
Int J Gynaecol Obstet 1995;48(2):233-8.
36. Ogden JE, Parry ES.The development of hemoglobin solutions as red
cell substitutes. Int Anesthesiol Clin 1995;33(1):115-29.
37. Rabinovici R, Neville LF, Rudolph AS, Feuerstein G. Hemoglobin-based
oxygen-carrying resuscitation fluids [editorial; comment]. Crit Care
Med 1995;23(5):801-4.
38. Assalia A, Schein M. Resuscitation for haemorrhagic shock. Br J Surg
1993;80(2):213.

JOGC 8 JUNE 2002