Guia Shock Hemorragico Canada 2002
Guia Shock Hemorragico Canada 2002
Guia Shock Hemorragico Canada 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
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 procedu re 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 SaGe.
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 otten 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 ofPostpartum 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 I
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-I: Evidence from well-designed controlled trials without health examination.
randomization. B. There is fair evidence to support the recommendation
11-2: 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.
e. There is poor evidence regarding the inclusion or exclu-
11-3: 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
periodic health examination.
JOGC 2002
TABLE 2 sis. 10 Multi-system injury can lead to coagulopathy, and meta-
CLINICAL FEATURES OF HEMORRHAGIC SHOCKI bolic disturbances such as acidosis. I
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. I Simultaneously, tissue hypo perfusion
from precapillaty vasoconstriction leads to anaerobic metabo-
Hepatic No change Liver failure
lism and acidosis. II Tissue hypoxia, acidosis, and the release of
Gastrointestinal No change Mucosal bleeding various mediators lead to a systemic inflammatory response. 5,1I
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 fulls below 60-70 mrnHg. I With increasing sever- systemic inflammatory response syndrome (SIRS) and multi-
ity of hypovolemia, mild agitation and confusion progress to ple organ failure. 4,lo,11
lethargy and obtundation. 1The 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: I 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 ofless 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. I 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 oflung injury include: dyspnea, tachypnea, pulmonary cessfully reverse these changes. I 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 p02 that often requires assisted leading to anaerobic metabolism and acidosis, classified as severe
mechanical ventilation. 6,s Moderate elevations of bilirubin and shock The patient demonstrates marked tachycardia and tachyp-
alkaline phosphatase can be seen with ischemic hepatic injury. I 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. I 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 l ,15 The mortality rate at
the intestinal mucosa allows bacteremia and subsequent sep- this stage is in excess of 30%.1
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 secute 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
TABLE 4
INDICATIONS FOR BLOOD COMPONENT THERAPy14,20,30-35
TABLE 5
PHARMACOLOGICAL SUPPORT OF THE CARDIOVASCULAR SYSTEW·7
Agent Usual dose range Effect
Inotropic agents
Dopamine 1-3 IJg/kg/min Increased renal output
Vasodilation
Vasopressor agents
Phenylephrine 1-5 IJg/kg/min Peripheral vasoconstriction