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Shock
• A condition that leads to inadequate
tissue perfusion that results in impaired
cellular metabolism.
Classification
• Hypovolemic shock
• Cardiogenic shock
• Neurogenic shock
• Anaphylactic shock
• Septic shock
• Endocrinal shock
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Hypovolemic shock
• d.t. diminished blood volume which may
occurs secondary to loss of:
- Blood as Internal or external hge.
- Plasma as in burns, acute pancreatitis &
peritonitis
- Sodium-containing fluids as in severe
vomiting, diarrhea.
C/P
• Early signs:
- Tachycadia (mild)
- Orthostatic hypotension
- Anxiety
- Sweating
- Pallor
• Late signs
- Depressed mental status
- ↓ blood pressure
- Tachycardia (marked)
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DANGEROUS
Irreversible shock
Multiple Organ Failure
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• Arresting the Volume loss
(Haemostasis)
• Fluid resuscitation
• Pulmonary support. (Oxygen mask)
• Monitoring
• Positioning
• Pain relief (analgesics)
• Inotropic agents (Dopamine,
Dobutamine)
Fluid resuscitation
• 1-2 Liters bolus of isotonic fluid .
• Normal saline (0.9% NaCl);
– Isotonic.
– High in chloride.
– Hyperchloremic acidosis.
• Lactated ringers;
– Lactate to buffer acidemia which occurs with
shock .
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Hypertonic Saline
• 7.5% Saline Solution.
• Pulls intracellular water out into intravascular
space.
• Much better blood volume expansion.
• Some evidence of favorable effects on
inflammatory response to injury.
Colloids
• Albumin or Dextran.
• Expand intravascular volume much more than
crystalloid.
• Theoretical advantage that the patient would
require less volume of fluid resuscitation.
• No clear evidence that they are better than
crystalloids.
• less available and more expensive.
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Transfusion
• Emergency: O(-) blood.
• Type Specific.
• Type and Cross-matched.
• Future of blood substitutes?
Guidelines
• Hb 7 g/dl is adequate in a young patient (No
Coronary Artery Dis., bleeding controlled)
• Hb 8 g/dl is adequate in a young patient who may
be at slight risk for further bleeding.
• Hb 9 g/dl is required if the risk of re-bleeding is
substantial.
• Hb 10 g/dl should be the goal if overt ischemia is
present or there is a significant risk of occult
ischemic disease (peripheral vascular disease, CAD)
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Monitoring
• Clinical parameters: pulse, bl pr, state of
filling of veins, capillary filling)
• Foley catheter
Q 1 hour (0.5-1ml/kg/hr)
• CVP (central venous pressure)
• PAWP (Pulmonary artery wedge pressure)
• ECG
• Temperature
• Ht & Hb
• Blood gases
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Positioning
Trunk supine Legs elevated
Cardiogenic Shock
There is inadequate flow to vital
organs
dt inadequate cardiac output
despite a normal blood volume
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• Commonest causes leading to sudden collapse
are:
- Acute Myocardial infarction (most common)
- Severe arrhythmias
- Massive pulmonary embolism
- Cardiac tamponade d t penetrating wounds of
the chest
- Myocarditis
- High spinal anaesthesia, can cause paralysis of
sympathetic supply of the heart
C/P
• Systolic &diastolic pressures fall
→ - compensatory peripheral vasoconstriction
& cold sweaty skin
- Inadequate tissue perfusion
- Increasing metabolic acidosis
• Cardiogenic shock is characterized by:
Congested neck veins & a high CVP
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Rx
• O2
• Treatment of the cause
• Mechanical:
Intraaortic balloon pulsating devise:
- Elevating diastolic bl pr = fill coronary a
- Reduction of myocardial work
Neurogenic Shock
• Paralysis of vasomotor fibers
• → peripheral pooling of bl & inadequate
venous return
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causes
• Vasovagal attack
- Simplest type
- Dt hearing bad news, watching unpleasant event,
painful stimuli
- Mechanism:
extensive vasodilatation in splanchnic area →sudden
fall of blood supply to vital organs
Extensive vagal stimuli to heart→bradycardia
• Sudden extreme vasodilatation occurs in pts suffering
from high transection of spinal cord
• Regional anesthesia.
• Neurological disorders
• The mere act of falling down to the ground as
the individual faints assists the venous return
& helps recovery
• c/p
- hypotension,
- Normal pulse or bradycardia
- Warm dry skin
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Rx
• Pt should lie flat, elevation of the legs to help
increase the venous return
• IV crystalloid solution as Ringer’s lactate
• Vasopressors may be given
Anaphylactic shock
• May follow administration of antibiotics esp
penicillins, anaesthetics, sera & dextran
• Antigen binds w Antibody
→histamine release in large amounts
• Patient develops:
- Bronchospasm
- Laryngeal spasm
- Respiratory distress
- Massive vasodilataIon → Hypotension
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Rx
• IV crystalloid infusion
• IV hydrocortisone
• Antihistaminics
• Endotracheal intubation may be needed
if laryngeal oedema & stridor are
developing
Septic shock
This is the most lethal type of
shock and is recognized as one of
the major killers in surgical
practice
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• When bacteraemia produces changes in
circulation such that tissue perfusion is
critically reduced,septic shock develops.
• this type of shock is the end result of
numerous complex interactions between:
- exogenous and endogenous mediators on one
side,
- and the host response to these mediators on
the other side.
Causes of rising incidences of
septicaemia & septic shock :
• Developping reservoirs of resistant and virulent
organisms
• Concentration of infected patients in critical care
units
• More extensive operations in elderly and poor-
risk patients
• Salvage of severely injured patients
• Growing population of patients who are
immunosuppressed by organ transplantation,and
by chemotherapy
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Aetiology
• Causative organisms:
- Gram-negative bacillli (the commonest)
- Staphylococci
- Candida
• Common sources of bacteria:
Peritonitis caused by perforated
viscus,gangrenous bowel,or leaking
anastomosis
Cholangitis or genitourinary infections
Infected central venous catheter that may be
used for monitoring or for nutrition
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Predisposing factors:
All conditions which suppress the immune
mechanism predispose to septic shock.these
include:
• old age,
• diabetes mellitus,
• corticosteroids,
• chemotherapy,
• malignancy,
• HIV/AIDS
Pathophysiology
• dead becteria
liberates:
• endotoxin (the lipopolysaccharide part of the
cell wall of G-ve bacilli)
triggers
• complex immunologic reactions
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• Endotoxin
Stimulates
• macrophages and kupffer cells of the liver
to release
• cytokines
cytokines
• these are large peptides whose normal function is
communication to mediate a useful inflammatory
response.in huge amounts,however,they have harmful
effect on the microcirculation,particularly on the
capillary endothelium.some of these mediators are:
• Tumour necrosis factor(TNF)
• Interleukines
• Platelet activation factor
• Prostaglandins(prostacyclin and thromboxane)
• Nitric acid which is one of the free oxygen radicals and
is also a strong vasodilator
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Staging of Septic Shock:
I. Compensated / Preshock / Hyperdynamic.
II.Decompensated / Organ hypoperfusion.
III. End organ failure / Irreversible.
Microcirculation
1- Septic shock
is initially caused by maldistribution of cardiac
output.under the effect of cytokines
vasodilatation of the arteries and arterio-
venous shunts are opened.the results are:
• Reduced peripheral resistance.Nitric acid
causes more reduction in the peripheral
resistance.
• Capillaries are bypassed and blood is shunted
in the oxygenated form from the arteriolar to
the venular side
• Oxygen delivery to the tissues is impaired
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2- DIC
Disseminated intravascular coagulation(DIC)is
the result of:
• Sluggish capillary circulation
• The action of platelet activation factor
3- Vascular endothelial damage
under the effect of cytokines is
the dominant harmful feature
of septic shock.
the result is leakage of protein-
rich fluid from the circulation
into the interstitial space
causing oedema
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Cellular Derangement :
• Oxygen delivery is reduced because of:
• Maldistribution of blood(main factor)
• Late pump failure
• Hypovolaemia
• When the delivery is reduced below a certain critical
level oxygen uptake by the cell is also impaired
• Oxygen uptake and utilization by the cells is also
directly suppressed by the toxins
(sequence of events that lead from hypoxia to cell death
are the same as hypovolaemic shock, but they proceed
at faster rate)
Acid-based imbalance:
• As in hypovolaemic shock,there is excess production of
lactic acid which produces metabolic acidosis.The body
tries to compensate by hyperventilation to wash out
CO2 and by renal conservation of bicarbonate to buffer
the acid.These measures temporarily restore pH.
Ultimately the kidneys are overwhelmed and fail
resulting in the production of frank metabolic acidosis.
• The usual changes in arterial blood gases(ABGs)are:
• Low pH(lactic acidosis)
• Low PO2<70mm hg(respiratory distress the failure)
• Low PCO2(hyperventilation)
• Low HCO3(depleted buffers)
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Treatment:
• Antibiotics.
• Resuscitation with crystalloids.
• Operative drainage of infected collections.
• Inotropes.
Individual systems and organs:
In septic shock multiple organ
failure(MOF)proceeds faster than in
hypovolaemic shock
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The heart
If septic shock is inadequately treated heart
failure takes place because of:
• Direct effect of some cytokines,e.g.TNF and
leukotrienes on the heart
• Reduced coronary flow when the blood
pressure becomes very low
• Increased oxygen demands of the cardiac
muscle because of over-work
Lungs:
adult respiratory distress
syndrome(ARDS)
the generalized capillary endothelial damage →alveolar &
interstitial oedema.the results are:
• Reduced compliance,and alveoli that are filled with fluid
.both affect ventilation
• Opening of arterio-venular shunts that divert blood away
from the capillaries impairs perfusion
• Interstitial oedma widens in the space between blood in
the capillaries and air in the alveoli,the so-called thickened
alveolo-capillary membrane.this,in addition,impairs gas
diffusion
• The three components of
respiration,viz,ventillation,perfusion,and diffusion are thus
impaired;and ultimately lead to respiratory failure
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• Brain:if bl pr drops below 60 mmHg,
compensatory mechanisms are overwhelmed
with resultant cerebral ischaemia
• Kidneys:lead to renal failure
• Liver:under the effect of ischaemia and the
chemical mediators cholestasis and
hyperbilirubinaemia may develop,the so-called
”ICU jaundice”
• Gastrointestinal tract:ischaemia of the gut
mucosa produces:
- Gastro –duodenal stress ulceration
- Gut barrier failure.the result is translocation of
bacteria and endotoxin from the colon lumen to
the blood stream and further deterioration of
condition
N.B.
• Septic shock is considered to b part of a
syndrome called:
System inflammatory response syndrome SIRS
Other members of the syndrome r:
Major trauma
Major burns
Acute Pancreatitis
Neglected hypovolaemia
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C/P
Early:
Hyperdynamic (warm)septic shock.diagnosis is difficult and a
high index of suspicion is required to detect cases at this
early stage. the patient has:
• Restlessness and confusion
• Fever above 38 ͦC and chills
• Mild reduction in blood pressure
• Tachypnoea
• Tachycardia
• Patient is flushed with warm dry extremities
• Oliguria
• The cardia output is elevated
Later
Hypodynamic(cold)septic shock.if the previous
stage is not treated efficiently,the patient will
develop a picture similar to that of hypovolaemic
shock with reduced cardiac output
• Systolic blood pressure<90mmHg
• tachycardia and tachypnoea
• cold clammy skin
• oliguria
• Multiple organ failure starts at this stage:
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Dx
• polymorphonuclear leucotycosis with
abundance of immature forms
• finding high lactate level in blood
• looking for a source of sepsis
• repeated blood culture at the peak of fever or
culture from the septic ficus will guide
antibiotic treatment,but at a later stage
Rx
Treatment should be started as soon as possible
and should be carried out in an intensive care
unit(ICU).
Treatment has two main components:
• support of body systems,
• and fighting
• In addition: monitoring
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Support different systems
• Cardiovascular support:
- Fluid replacement: Ringer’s Lactate. any
deficiency in red blood cell:transfusion of
packed red blood cells
- Medications(inotropes and vasopressors).if
the patient remains hypotensive despite
adequate fluid replacement
• Respiratory support.oxygen administration
• Renal support.Adequate volume
replacement and dopamine administration
improve renal blood flow.haemodialysis is
required is case of acute renal failure,until
the kidneys recover
Fighting infection
• Eradication of sepsis,e.g.,drainage of a huge abscess or
peritonitis,or resection of gangrenous bowel
• Antibiotics.aggressive treatment with multiple and
braod-spectrum antibiotics is started immediately
without waiting for the results of culture and
sensitivity.the antibiotic choice is based on the possible
suspected organisms which in most cases are gram-
negative bacilli.A combination of
cephalosporin,aminoglycoside and metronidazole can
cover the usual organisms.when the results of culture
are available one may change the antibiotic regimen
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Monitoring
• Same as Hypovolemic shock
Prognosis
• Mortality ranges from 25 to 90%.Death is
usually the result of failure to unstitue therapy
soon enough
Endocrinal shock
This may occur in patients with Addison’s
disease or those receiving continuous
cortisone therapy if they are subjected to
any stressful situation,e.g.,infection or
surgery.the patient develops severe shock
due to failue of release of corticosteroids
necessary to cope with the stress from the
suppressed adrenal cortex.the result will
be a state pf peripheral circulatory
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