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HEMORRHAGIC SHOCK

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									HEMORRHAGIC SHOCK

 Shock is a momentary pause
     in the act of dying
    CASE FOR DISCUSSION
27 y.o. construction worker fell from the 17
  feet ladder. He was brought to ER by
  paramedics. On arrival, his BP-105/55,
  HR-130, O2Sat-97(Face mask). He is
  agitated, blood in the mouth, right ankle
  open fx., head laceration.
             QUESTIONS
1.Differential diagnosis?
2.What are you going to do first?
3.Is patient in shock?
       WHAT IS SHOCK?
A medical condition, not a diagnosis.
Types: Hypovolemic (Hemorrhagic)
       Cardiogenic
       Distributive
       Obstructive
       TYPES OF SHOCK
More then 100 types of shock have been
described.
 -classified by the cause of the syndrome
 -two or more types are often combined
    hypovolemia may occur with septic
     shock
    hemorrhagic shock, combined with
     neurogenic shock
The 3 essential patterns of
    circulatory shock




       I     II    III
           SHOCK
REGARDLESS OF CLASSIFICATION
THE UNDERLYING DEFECT IS ALWAYS
INADEQUATE TISSUE PERFUSION!!!!!!
       SHOCK SYNDROM
Shock is a condition in which the CV system fails
to perfuse tissues adequately.
An impaired cardiac pump,circulatory system,
and/or volume can lead to compromised BF to
tissues.
Inadequate tissue perfusion can result in:
   -generalized cellular hypoxia(starvation)
   -widespread impairment of cellular
     metabolism
   -tissue damage>organ failure>death
   DIAGNOSIS OF SHOCK
MAP<60
Clinical s/s of hypoperfusion of vital organs
      ECG changes
      Mental disturbances
      Drop in UO
      Jaundice etc.
 CAUSES OF HYPOVOLEMIC
         SHOCK
Anything that causes rapid fluid loss
-Most commonly rapid blood loss.
-Also be caused by fluid loss.
  diarrhea,vomiting,water deprivation,
  third spacing ets.
  HEMORRHAGIC SHOCK
Caused by the loss of both circulating
blood volume and oxygen carrying
capacity.
    PATHOPHISIOLOGY OF
    HYPOVOLEMIC SHOCK
Impaired tissue perfusion is the result of
imbalance between cellular O2 supply
and cellular O2 demand.
     PATHOPHISIOLOGY
Acute hemorrhage results in activation of
following compensatory mechanisms:
 -Hematologic(coagulation)
 -Cardiovascular
 -Renal(increase renin production)
 -Neuroendocrine(ADH release)
COMPENSATORY MECHANISMS
Sympathetic Nervous System Response.
Acute hemorrhage results in a decreased
CO and BP, which is sensed by receptors
in the aortic arch and atrium.
 – Stimulated by baroreceptors
     Increasing HR
     Increasing contractility
     Vasoconstriction (SVR-Afterload)
     Increased preload
COMPENSATORY MECHANISMS
Mediated by renin-angiotensin system
     Decreasing renal perfusion
     Activation of renin-angiotensin system
     Angiotensin II is a very potent vasoconstrictor
   IN ADDITION
     Aldosteron released by adrenal cortex produces
     sodium and water retention
COMPENSATORY MECHANISMS
Mediated by antidiuretic hormone
    Osmoreceptors in hypothalamus stimulated
    ADH released by posterior pituitary gland
     – Vasopressor effect
     – Acts on renal tubules to retain water
COMPENSATORY MECHANISMS
Mediated by adrenal cortex
    Anterior pituitary releases adrenocorticotropic
    hormone (ACTH)
    ACTH stimulates adrenal cortex to release
    glucocorticoids
    Blood sugar increase to meet increased metabolic
    needs
     – In addition hyperglycemia is caused by glucagon and
       growth hormone- induced increase in gluconeogenesis
       and glycogenesis. Circulating catecholamines inhibit
       insulin release and activity, leading to increased plasma
       glucose.
COMPENSATORY MECHANISMS
In addition, the brain has remarkable
autoregulation that keeps cerebral BF
constant over a wide range of blood
pressures
The kidneys can tolerate a 90% decrease
in total BF for short period of time
With decreases in circulatory volume,
intestinal BF is reduced by splanchnic
vasoconstriction.
FAILURE OF COMPENSATORY
        RESPONSE
Decreased blood flow leads to cellular
hypoxia→ cells switch for anaerobic from
aerobic metabolism→ lactic acid
production→ cell swells (function ceases)
membrane becomes permeable→
electrolytes and fluids seep in and out of
cells→ Na+/K+ pump impaired,
mitochondria damage, cell death.
    STAGES OF SHOCK
Compensated shock
Decompensated shock
Irreversible shock
     STATES OF SHOCK
Compensated shock
– Decreased tissue perfusion, but the body’s
  compensatory responses overcome the
  decrease in intravascular volume
– CO and l BP are normal due to adrenal
  compensatory response
     STAGES OF SHOCK
Compensated Shock
– RR and TV increase (this is a result of
  metabolic acidosis, caused by tissue
  hypo perfusion and chemoreceptors
  activation)
– Acidosis is decreased by of hyperventilation
     STAGES OF SHOCK
Sympathetic stimulation
– Constriction of veins leading to ↑ BP and ↑ CO
  (increased preload)
– ↑ HR and ↑ contractility
– Arterial constriction leading to ↑ PVR
  (peripheral vasoconstriction-cool skin)
– Bronchodilatation (improved air exchange)
    STAGES OF SHOCK
Compensated shock
   Progression of shock to microcirculation produces
   a sequence of changes in capillary perfusion
  Oxygen delivery to the cells supplied by these
  capillaries decreased → anaerobic metabolism
                  ↓
      leaky capillary syndrome
                   ↓
  A-V shunts open in the skin, muscles, GI tract, to
  causing less flow to the arterials and less flow
  through capillaries
                   ↓
Blood is shunted to the heart, brain, and kidneys
         Stages of Shock
Compensated shock
– If the underlying cause of shock is untreated
  the compensatory mechanisms eventually
  collapse.
     STAGES OF SHOCK
Decompensated Shock
– Marked increase in HR
– BP and CO decrease
– Blood flow to critical organs drops
    ↓UO
    Altered mental status
    ECG changes
     STAGES OF SHOCK
Decompensated Shock
– As the shock continues, the precapillary
  sphincters relax with expansion of the
  vascular space and capillary engorgement
     STAGES OF SHOCK
Decompensated shock
– Hypotension and closing of the A-V shunts
  results in more BF through capillaries.
    More of capillary engorgement.
     STAGES OF SHOCK
Decompensated Shock
– Increased hypoxemia and acidosis lead to
  additional vasodilatation. The vascular bed
  expands greatly.
     STAGES OF SHOCK
Decompensated Shock
– The capillary and venule capacity may
  become great enough to reduce the volume of
  available blood for the great veins.
    Decreased venus return and a fall in CO
     STAGES OF SHOCK
Decompensated shock
– The viscera (lungs, kidneys, and GI mucosa)
  become congested due to stagnant blood
  flow.
     STAGES OF SHOCK
Decompensated shock
– The respiratory system attempts to
  compensate for the acidosis by increasing
  ventilation to blow off CO2
    Partially compensated metabolic acidosis
     STAGES OF SHOCK
Decompensated Shock
– Clotting mechanisms are also affected:
  hypercoagulability (DIC)
– This stage progresses to irreversible shock if
  fluid resuscitation is inadequate
     STAGES OF SHOCK
Irreversible shock
– Systolic and diastolic pressure drop.
– Pulse pressure narrows to the point of no
  detection.
     STAGES OF SHOCK
Irreversible shock
– S/S.
    Bradicardia
    Dysrhythmias
    Hypotension
    Evidence of multiple organ failure
    Pale, cold and clammy skin
    Noticeably delayed capillary refill
      STAGES OF SHOCK
Irreversible shock
– Myocardial contractility
  decreases from
  ischemia secondary to
     A reduction of Hb
     A reduction in SO2
     A reduction in coronary
     perfusion
     Myocardial necrosis
      STAGES OF SHOCK
Irreversible shock
– DIC
– Pulmonary capillaries
  become permeable
  leading to pulmonary
  edema
     Absorption of O2↓
     Elimination of CO2↓
     ARDS
     STAGES OF SHOCK
Irreversible shock
– Multiple organ failure
    Usually hepatic failure occurs, followed by renal
    failure and heart failure
    GI bleeding and sepsis may result from GI
    mucosal necrosis
    Pancreatic necrosis may lead to further clotting
    disorders and severe pancreatitis
VARIATIONS IN RESPONSE TO
         SHOCK
Hemorrhagic shock is tolerated differently
depending on
– Pre-existing physiological state
– Age
  HEMORRHAGIC SHOCK IN
       CHILDREN
Pediatric patients have smaller blood
volumes and, therefore ,are at risk to lose
a proportionately greater percentage of
blood on an equivalent-volume basis.
  HEMORRHAGIC SHOCK IN
       CHILDREN
The kidneys of children younger then 2
years are not mature; they have blunted
ability to concentrate solute.
The body surface area is increased
relative to the weight, allowing for early
hypothermia, leading to coagulopathy.
  HEMORRHAGIC SHOCK IN
        ELDERLY
Elderly people may have both altered
physiology and may pre-existing medical
conditions that may severely impair their
ability to compensate for acute blood loss.
  HEMORRHAGIC SHOCK IN
        ELDERLY
Atherosclerosis and decreased elastin
cause arterial vessels to be less compliant
leading to blunted vascular compensation,
decreased cardiac arteriolar vasodilatation
and infarction.
  HEMORRHAGIC SHOCK IN
        ELDERLY
Older patients are less able to mount a
tachycardia in response to decreased
stroke volume because of:
– decreased beta-adrenergic receptors in the
  heart
– Decreased effective volume of pacing
  myocytes within the SA node
– These patients are treated with a variety of
  cardiac meds that may blunt the physiological
  response to shock
HEMORRHAGIC RESPONSE IN
       ELDERLY
Many older patients have significantly
decreased creatinine clearance in the
presence of near-normal serum creatinine.
Concentrating may be impaired by relative
insensitivity to ADH
          ASSESMENT OF
       HEMORRHAGIC SHOCK
S/S vary depending on severity of fluid loss:

 15%[750ml]- compensatory mechanism maintains
 CO

 15-30% [750-1500ml- Hypoxemia, decreased BP &
 UOP

 30-40% [1500-2000ml] -Impaired compensation &
 profound shock along with severe acidosis

 40-50% - refactory stage:
Clinical Classification of Shock
   EVALUATION/HISTORY
Obtaining a clear history of the type,
amount, and duration of bleeding is very
important. Many decisions are based on
knowing the amount of blood loss that has
occurred over a specific time period
   EVALUATION/HISTORY
For GI bleeding, knowing if the blood was
per rectum or per os is important. Because
it is hard to quantitate lower GI bleeding,
all episodes of bright red blood per rectum
should be considered major bleeding until
proven otherwise
Inquire about hematemesis, melena,
drinking history, NAID use, coagulopathies
   EVALUATION/HISTORY
Bleeding because of trauma is not always
identified easily. The pleural space, abdominal
cavity, mediastinum, and retroperitoneum are all
spaces that can hold enough blood to cause
death from exsanguination
Closed femoral fx fractures can cause major
bleeding into the tissues
Scalp lacerations are notorious for causing large
underestimated blood loss
   EVALUATION/HISTORY
If GYN cause is being considered, gather
information about the following
– Last menstrual period
– Risk factors for ectopic pregnancy
– Vaginal bleeding
– Vaginal passage of products of conception
– Pain
  EVALUATION/PHYSICAL
Differences exist between medical patients and
trauma patients
The very nature of shock dictates how difficult or
impossible is to find a pathognomonic
sign/symptom which is is invariably associated
with the presence of shock
Remember BP and HR are unreliable indicators
of rapid deterioration in trauma patients
Most important is the trend of the pulse and BP
    EVALUATION/PHYSICAL
     (MEDICAL PATIENTS)
The general appearance of a patient in
shock is very dramatic. The skin will have
a pale, ashen color, usually with
diaphoresis. The patients may appear
confused or agitated and may become
obtunded
   EVALUATION/PHYSICAL
    (MEDICAL PATIENT)
The pulse first becomes rapid and then
becomes dampened as the pulse pressure
diminishes. Systolic BP may be in the
normal range during compensated shock
    EVALUATION/PHYSICAL
     (MEDICAL PATIENT)
The conjunctivae are inspected for
paleness, a sign of chronic anemia. The
nose and pharynx are inspected for blood.
The chest is auscultated and percussed to
evaluate for hemothorax.
The abdominal examination searches for
signs of abdominal bleeding (distention,
pain with palpation, and dullness to
percussion)
    EVALUATION/PHYSICAL
     (MEDICAL PATIENT)
The flanks are inspected for ecchymosis, a sign
of retroperitoneal bleeding.
Ruptured aortic aneurisms can present with
shock, palpable pulsatile mass in the abdomen,
scrotal enlargement from retroperitoneal blood
tracking, diminished femoral pulses.
Rectum is inspected for internal or external
hemorrhoidal bleeding.
Patients with vaginal bleeding undergo full pelvic
examination, including pregnancy test to rule out
ectopic pregnancies
    EVALUATION/PHYSICAL
      (TRAUMA PATIENT)
Primary survey is a quick exam to identify life
threatening problems
– Airway (ask the patients name. If answers clearly the
  airway is patent)
– Oral pharynx is inspected for blood/foreign bodies
– Neck inspected for hematomas/ tracheal deviation
– Lungs inspected for pneumo/hemothorax
– Radial and femoral pulses
– Quick inspection to rule out any external sources of
  bleeding
– Gross neurological examination (AVPU- alert,
  response to voice, response to pain, unresponsive)
    EVALUATION/PHYSICAL
      (TRAUMA PATIENT)
The secondary survey is a head to toe
careful examination to identify all injuries.
         DON’T FORGET
In the patient with trauma, hemorrhage is
usually the presumed cause of shock.
However it must be distinguished from
other causes of shock
– Cardiac tamponade (muffled heart tones,
  distended neck veins)
– Tension pneumothorax (deviated trachea,
  decreased breath sounds)
– Spinal cord injury (warm skin, lack of
  expected tachycardia, neurological deficits
EVALUATION/LAB STUDIES
Generally, lab values are not helpful in
acute hemorrhage because values do not
change from normal until redistribution of
interstitial fluid into the blood plasma
occurs after 8-12 hours. Many of the
derangements that occur are a result of
replacing a large amount of blood with
fluids.
EVALUATION/LAB STUDIES
Hb and hct unchanged from baseline
immediately after acute blood loss. During the
course of resuscitation, the hct may fall
secondary to crystalloid infusion and re-
equilibration of extracellular fluid in the
intravascular space.
No absolute threshold hct/Hb level that should
prompt transfusion exists. (Physician’s
judgment/patient’s comorbidity)
EVALUATION/LAB STUDIES
Arterial blood gas is the most important lab value
in the patient with severe shock
– Acidosis is the best indicator of ongoing O2
  imbalance at the tissue level.
– A pH < 7.25 may begin to interfere with
  catecholamine action and cause hypotension
  unresponsive to inotropes.
– Metabolic acidosis must be treated aggressively.
– Life threatening acidemia (pH < 7.2) initially may be
  buffered by the administration of sodium bicarbonate
  (be aware that no survival benefit to this practice has
  been documented).
EVALUATION/LAB STUDIES
Coagulation studies produce normal results in
the early course
Electrolyte studies are not helpful in the acute
setting. After massive resuscitation:
– Na and chloride may increase with administration with
  large amounts of isotonic sodium chloride.
  Hyperchloremia may cause a non-ion gap acidosis
  and worsen an existing acidosis.
– Ca levels may fall w/ large volume blood transfusion
– K levels may rise with large volume blood transfusion
EVALUATION/LAB STUDIES
A blood specimen for type and cross
should be obtained on arrival.
For patients who are actively bleeding 4 U
of PRBC and 4 U of FFP should be
prepared. Platelets may be obtained
depending on physicians judgment.
EVALUATION/IMAGING STUDIES
Chest X-ray (useful to dx. Hemothorax/pneumothorax)
Abdominal x-rays are not helpful
CT scan (sensitive and specific for dx. Intrathoracic, intra-
abdominal, and retroperitoneal bleeding).
Ultrasound is rapidly replacing CT scan as the diagnostic
test of choice for ID of hemorrhage in major body cavities.
EGD is the test of choice for upper GI bleeding
Colonoscopy is used to diagnose acute lower GI bleeding.
Angiography is one of the best tests to localize a bleeding
source.
Diagnostic peritoneal lavage.
           TREATMENT
Medical care of hemorrhagic shock
consists of resuscitation. The resuscitation
should occur before, or concurrently with
any diagnostic studies.
The standard care consists of rapid
assessment and expeditious transport to
an appropriate center for evaluation and
definitive care.
            TREATMENT
Central venous access is considered an adjunct
to large bore (16 or 14 gauge) peripheral IV lines
(flow through a catheter is inversely proportional
to the length and directly proportional to the
diameter).
If significant intra-abdominal bleeding from a
venous injury is suspected, volume lines should
be avoided in the femoral veins.
In general, access above and below the site of
the injury is a good practice.
           TREATMENT
Crystalloid is the first fluid of choice for
resuscitation. Fluid administration should
continue until the patient’s hemodynamics
becomes stabilized.
Because crystalloids leak from the
vascular space, 3 liters of fluid need to rise
the intravascular volume by one liter.
           TREATMENT
Alternatively, colloids restore volume in 1:1
ratio.
Current colloids include human albumin,
hydroxy-ethyl starch products, and
hypertonic saline-dextran combinations.
Hydroxy-ethyl starch product in large
volumes has been associated with
coagulopathy.
           TREATMENT
PRBC’s should be transfused if the patient
remains unstable after 2-3 liters of
crystalloid resuscitation.
– Blood n crystalloid infusions should be
  delivered through the fluid warmer.
– Patients who require large amounts of
  transfusion inevitably will become
  coagulopathic (consider platelets and FFP)
          TREATMENT
Intravenous access and fluid resuscitation
are standard.However it has become
controversial.
  For many years,agressive fluid
administration has been advocated.Recent
studies of urban patients with penetrating
trauma have shown that mortality
increases with these interventions.
          TREATMENT
Reversal of hypotension prior to the
achievement of hemostasis may increase
hemorrhage,disloge clots and dilute
existing clotting factors. Findings from
animal studies support these postulates.
           TREATMENT
These provocative results raise possibility
that moderate hypotension may be
physiologically protective and should be
permitted.
           TREATMENT
These findings should not yet be clinically
extrapolated.Permissive hypotension in
humans remains speculative.
                 TREATMENT
Surgical care (just in general)
– Life threatening bleeding within the abdominal or thoracic cavity
  is an indication for operation
– Retroperitoneal bleeding is difficult to control operatively and
  generally is treated nonoperatively
– Severe upper GI bleeds should be managed first be EGD
– Severe vaginal bleeding should prompt early involvement of
  GYN
      Ectopic pregnancies are treated with immediate surgery
      Abruptio placenta is a true emergency and should prompt c-section
– Consultation with a hematologist is essential when coagulopathy
  fails to be corrected with standard measures. (He may offer
  gamma-globulin infusion, plasmapheresis, or large-volume
  clotting factor repletion).
        COMPLICATION OF
      HEMORRHAGIC SHOCK
Patients often are unable to mount bone marrow
response in the acute setting. Using erythropoieten is
useful. This strategy has been successful in decreasing
RBC transfusions in multicenter trials in Canada
Acute tubular necrosis
Acute lung injury
Transfusion related acute lung injury
Infections (nosocomial and related to operative sites or
indwelling catheters).
Multiple organ dysfunction
The cascade of systemic inflammatory response
syndrome (SIRS) progressing to organ failure will
complicate 30-70% of patients with hemorrhagic shock
Death
PROGNOSIS OF HEMORRHAGIC
         SHOCK
Related to the ability to be resuscitated
from shock as well as the underlying
illness or injury, not the presentation of
hemorrhagic shock.

								
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