Approach to hypovolemic and septic shock. reference: Nelson text book of pediatrics, 19th edition

1. 11 September 2014
APPROACH TO HYPOVOLEMIC
AND SEPTIC SHOCK
Prepared by: Dr. Ahmed M. Bahamid
pediatric resident at Alsabeen hospital

2. OBJECTIVES
 Definition of shock
 Pathophysiology, common types and
etiologies of shock
 Clinical manifestations and diagnosis
 Management of child with septic and
Hypovolemic shock

3. DEFINITION
 Shock is an acute syndrome characterized
by the body’s inability to deliver adequate
oxygen to meet the metabolic demands of
vital organs and tissues.

4. EPIDEMIOLOGY
 Shock occurs in 2% of all hospitalized
patients in USA.
 Death usually occur due to complications
rather than during hypotensive phase
 The presence of MODS in patients with
shock substantially increases the probability
of death

5.  Mortality in septic shock as low as 3% in
previously healthy children & 6-9% in
children with chronic illness
 Early effects of O2 deprivation on the cell are
REVERSIBLE
 Early intervention reduces mortality
 Often masked in pediatrics . Why?

6. PATHOPHYSIOLOGY
 An initial insult triggers shock, leading to
inadequate O2 delivery to organs and tissues
 Compensatory mechanisms attempts to
maintain BP

7. COMPENSATORY MECHANISMS
 Increase HR, stroke volume, & vascular
smooth muscle tone. Regulated through
sympathetic NS & neurohormonal
responses.
 Increased RR with greater CO2 elimination is
a compensatory response to the metabolic
acidosis & increased CO2 production from
poor tissue perfusion

8. COMPENSATORY MECHANISMS
 Renal excretion of H ions & retention of
bicarbonate also increase in an effort to
maintain normal body pH.
 Maintenance of intravascular volume is
facilitated via sodium regulation through the
renin-angiotensin-aldosterone & atrial natriuretic
factor axes, cortisol & catecholamine synthesis
& release, and ADH secretion.

9.  Despite these compensatory mechanisms,
the underlying shock and host response lead
to vascular endothelial cell injury and
significant leakage of intravascular fluids into
interstitial extracellular space.

10. Initial insult
Triggers shock
Decreased
perfusion
Compensatory
mechanisms
Compensated
shock
Decompensated shock
Tissue damage
Multisystem organ
failure
Death

11. In adequate O2 at tissue level
Anaerobic metabolism with resultant
progressive LACTIC ACIDOSIS
Inadequa
te
perfusion
persist
Adverse VASCULAR, INFLAMMATORY, METABOLIC,
CELLULAR, ENDOCRINE, AND SYSTEMIC responses
Physiological
instability

12. STAGES OF SHOCK
 Pathophysiology of shock passes into 3
progressive stages; (INTERVENE EARLY)
1)- compensated shock
2)- decompensated shock
3)- irreversible sock

13. Why is it important to identify the stage of
shock?

14. COMPENSATED SHOCK
 Compensatory mechanisms attempts to
maintain BP
 NORMAL BLOOD PRESSURE
 Unexplained tachycardia
 Mild tachypnea
 Delayed capillary refill
 Orthostatic changes in pressure or pulse
 irritability

15. DECOMPENSATED SHOCK
 It is a state of inadequate end-organ
perfusion
 Compensatory mechanisms fails and
HYPOTENSION occurs.
 Increased tachycardia, increased tachypnea
 Altered mental state, low urine output,
 Poor peripheral pulses.
 Capillary refill markedly delayed
 Cool extremities

16. IRREVERSIBLE SHOCK
 It occurs as a consequence of
decompensated shock not managed properly
and at right time.
 Permanent cellular damage & MODS.
 Recovery does not occur even with adequate
restoration of circulatory volume
 Death occurs due to refractory acidosis,
myocardial and brain ischemia.

17. Pathophysiology of shock
Extracorporeal fluid loss
Hypovolemic shock may be due to direct blood loss through hemorrhage or
abnormal loss of body fluids (diarrhea, vomiting, burns, diabetes mellitus or
insipidus, nephrosis)
Lowering plasma oncotic pressure
Hypovolemic shock may also result from hypoproteinemia (liver injury, or as a
progressive complication of increased capillary permeability)
Abnormal vasodilation
Distributive shock (neurogenic, anaphylaxis, or septic shock) occur when there is
loss of vascular tone- venous, arterial or both (sympathetic blockade, local
substance affecting permeability, acidosis, drug effects, spinal cord transection)
Increased vascular permeability
Sepsis may change vascular permeability in the absence of any change in
capillary hydrostatic pressure (endotoxins from sepsis, and excess histamine
release in anaphylaxis)
Cardiac dysfunction
Peripheral hypoprfusion may result from any condition that affects the heart’s
ability to pump blood efficiently (ischemia, acidosis, drugs, constrictive

18.  In septic shock it is important to distinguish
between the inciting infection and the host
inflammatory response.
 Normally host immunity prevents the
development of sepsis via activation of the
reticular endothelial systems.
 This host immune response produces an
inflammatory cascade of toxic mediators,
including hormones, cytokines, and enzymes
 If this inflammatory cascade is uncontrolled,
derangement of the microcirculatory system leads
to subsequent organ and cellular dysfunction

19. Sepsis or tissue hypoxia with lactic
acidosis
↓ ATP, ↑ H+, ↑ lactate
In vascular smooth muscle
↑nitric
oxide
synthase
↑ vasopressin
secretion
↓ vasopressin
stores
↓ plasma
vasopressin
Open K ATP
Vasodilatation
↑nitric
oxide
Open K
Ca
↓ cytoplasmic Ca
2+
↑ cGMP
↓ phosphorylated
myosin

20. SYSTEMIC INFLAMMATORY RESPONSE SYNDROME
 SIRS is an inflammatory cascade that is
initiated by the host response to an infectious
or noninfectious trigger.
 This inflammatory cascade is triggered when
the host defense system does not
adequately recognize and/or clear the
triggering event
 The inflammatory cascade initiated by shock
can lead to hypovolemia, cardiac & vascular
failure, ARDS, insulin resistance, decreased
CYP450 activity, coagulopathy,..etc

21. Global tissue hypoxia
SIRS
Endothelial activation
Disruption of:
Coagulation
Vascular permeability
Vascular tone
Microcirculatory failure
Precipitated by:
Cytokines
[Over]production
of nitric
oxide
Results in:
Loss of vasomotor
control
Under‐perfusion of
tissues
Hypotension
 Ait‐Oufella H, et al. Intensive Care Med 2010;26:1286‐1298.
Rivers E, et al. NEJM 2001;345:1368‐1377.
Organ dysfunction
Heart
Lungs
Brain
Kidneys
Liver

22.  TNF & other mediators increase vascular
permeability, causing diffuse capillary leak,
decreased vascular tone, and an imbalance
between perfusion and metabolic demands of
tissues
 TNF & IL-1 stimulates the release of pro-inflammatory
and anti-inflammatory mediators
causing fever and vasodilation
 Arachidonic acid metabolites lead to the
development of fever, tachypnea, ventilation-perfusion
abnormalities, and lactic acidosis.

23.  Nitric oxide released from the endothelium or
inflammatory cells, is a major contributor to
hypotension.
 Myocardial depression is caused by myocardium-depressant
factors, TNF, and some interleukins
through direct myocardial injury, depleted
catecholamines, increased -endorphin, and
production of myocardial nitric oxide

24.  The inflammatory cascade is initiated by
toxins or superantigens via macrophage
binding or lymphocyte activation.
 The vascular endothelium is both a target of
tissue injury and a source of mediators that
may cause further injury.
 The balance between these mediator groups
for an individual patient contributes to the
progression of disease and affects the
chance for survival.

25. Focus of
infection
Superantigens
or toxins
Activated
inflammatory cells
Activation of host
defense
Activ. Of
complement
system
Activ. Of
coagulation
system
Endogenous mediator
release
Pro-inflammatory cytokines
Anti-inflammatory cytokines
Platelet activating factor
Arachidonic acid metabolites
Myocardial depressant substance
Endogenous opiates
Activated endothelium
increased expression endothelial
derived adhesion molecules
Decreased thrombomodulin
Increased plasminogen activator
inhibitor
Thrombosis &
antifibrinolysis
Hypovolemia, cardiac & vascular failure, capillary
leak/endothelial damage, ARDS, DIC, decreased steroid
synthesis
Shock
MODS Death

26. INFLAMMATORY MEDIATORS
Pro-inflammatory
mediators
Anti-inflammatory
mediators
Tumor necrosis factor
(TNF)
Interleukin-1
Interleukin-6
Interleukin-8
Interleukin-gamma
HMGB-1 (high mobility
group box chromosomal
protein 1)
Interleukin-4
Interleukin-10
Soluble receptor and
receptor antagonists

27. CLINICAL MANIFESTATIONS
 Categorization is important, but there may be
significant overlap among these groups,
especially in septic shock.
 The clinical presentation of shock depends in
part on the underlying etiology.
 If unrecognized and untreated all forms of
shock progresses ultimately to irreversible
shock and death.

28.  Shock may initially manifest as only
tachycardia or tachypnea.
Progression leads to;
 Decreased urine output
 Poor peripheral perfusion
 Respiratory distress or failure
 Alteration of mental status
 Low blood pressure

29.  Because of the compensatory mechanisms
hypotension is often a late finding and is not
a criterion for the diagnosis of shock
 Tachycardia with or without tachypnea, may
be the first or only sign of early compensated
shock
 Hypotension reflects an advanced state of
decompensated shock and is associated with
increased mortality.

30. SIGNS OF DECREASED PERFUSION
Organ
dysfunction
↓ Perfusion ↓↓ Perfusion ↓↓↓ Perfusion
CNS __ Restless, apathetic,
anxious
Agitated/confused,
coma
Respiration __ ↑ Ventilation ↑↑ Ventilation
Metabolism __ Compensated
metabolic acidemia
Uncompensated
metabolic acidemia
Gut __ ↑ Motility Ileus
Kidney Decreased urine
volume
Oliguria
< 0.5 mL/kg/hr
Oliguria/anuria
Increased specific
gravity
Skin Delayed capillary refill Cold extremities Mottled, cyanotic,
cold extremities
CVS Increase heart rate 2* increase HR 2* increase HR
Decreased BP, only

31. CRITERIA FOR ORGAN DYSFUNCTION
Organ
system
Criteria for dysfunction
Cardiovascul
ar
Despite administration of isotonic IV fluid bolus ≥ 60 mL/kg in 1
hour: decrease in BP (hypotension) < 5th percentile for age or
systolic BP < 2 SD below normal for age
OR
Need for vasoactive drug to maintain BP in normal range
(dopamine> 5 micro/kg/min or dobutamine, epinephrine, or
norepinephrine at any dose)
OR
Tow of the following:
Unexplained metabolic acidosis: base deficit > 5 mEq/L
Increased arterial lactate: > 2x upper limit of normal
Oliguria: urine output < 0.5 mL/kg/hr
Prolonged capillary refill: > 5 seconds
Core to peripheral temperature gap > 3◦C

32. CRITERIA FOR ORGAN DYSFUNCTION
Organ
system
Criteria for dysfunction
Respirator
y
PaO2/Fio2 ratio < 300 in the absence of cyanotic heart disease or
pre-existing lung disease
OR
PaCO2 > 65 torr or 20 mm Hg over baseline PaCO2
OR
Proven need for >50% FiO2 to maintain saturation ≥ 92%
OR
Need for non-elective invasive or non-invasive mechanical
ventilation
Neurologi
c
GCS score ≤ 11
OR
Acute change in mental status with a decrease in GCS score ≥ 3
points from abnormal baseline

33. CRITERIA FOR ORGAN DYSFUNCTION
Organ
system
Criteria for dysfunction
Hematologi
c
Platelet count < 80,000/mm³ or a decline of 50% in the platelet
count from the highest value recorded over the last 3 days (for
the patient with chronic hematologic or oncologic disorders)
OR
INR > 2
Renal Serum creatinine ≥ 2x upper limit of normal for age or 2-fold
increase in baseline creatinine value
Hepatic Total bilirubin ≥ 4mg/dL (not applicable for newborn)
Alanine transaminase level 2x upper limit of normal for age

34. TYPES OF SHOCK
SHOCK
Hypovole
mic
Cardiogen
ic
Distributiv
e
Obstructi
ve
Septic

35. WHY IS IT IMPORTANT TO IDENTIFY THE TYPE OF
SHOCK?
 Because successful management often depends
on correct interpretation of the classification of
shock, and often, its specific etiology. For
example, the interventions for obstructive or
Cardiogenic shock will be different from the
interventions for distributive shock (which will also
change depending on whether the etiology is
anaphylaxis or sepsis).

36. HYPOVOLEMIC SHOCK
 Most common cause of shock in children
worldwide
 Decreased preload due to internal or
external losses
 Water /electrolyte loss (diarrhea & vomiting)
 Blood loss (hemorrhage)
 Plasma loss (burns & nephrotic syndrome)

37. HYPOVOLEMIC SHOCK
 Tachycardia and an increase in systemic
vascular resistance are the initial
compensatory response to maintain
cardiac output and blood pressure
 Manifests initially as orthostatic
hypotension
 Associated with dry mucous membranes,
dry axillae, poor skin turgor, and
decreased urine output.

38. HYPOVOLEMIC SHOCK
 Depending on the degree of the dehydration,
the patient with hypovolemic shock may
present with either normal or slightly cool
distal extremities, and peripheral or central
(femoral) pulses may be normal, decreased,
or absent.

39. CARDIOGENIC SHOCK
 Cardiac pump failure 2ndry to poor myocardial
function
 CHD
 Cardiomyopathies ( infectious or acquired,
dilated or restrictive)
 Ischemia or arrhythmias
 Myocardial contractility affected leading to
systolic and/or diastolic dysfunction

40. CARDIOGENIC SHOCK
Because of decreased CO and
compensatory peripheral vasoconstriction,
the presenting signs of cardiogenic shock
are:
 Tachypnea
 Cool extremities
 Delayed capillary refill
 Poor peripheral and/or central pulses
 Declining mental status
 Decreased urine output

41. DISTRIBUTIVE SHOCK
 Inadequate vasomotor tone, which leads to
capillary leak and maldistribution of fluid into
the interstitium
 Sepsis, hypoxia, poisonings, anaphylaxis,
spinal cord injury, or mitochondrial
dysfunction.
 ↓ in SVR accompanied with maldistribution
of blood flow from vital organs and a
compensatory increase in CO
 This process leads to decrease in preload
and afterload

42. DISTRIBUTIVE SHOCK
 Distributive shock manifests early as
peripheral vasodilation and increased but
inadequate cardiac output

43. OBSTRUCTIVE SHOCK
 Caused by a lesions that creates a
mechanical barrier that impedes adequate
CO
 Decreased CO secondary to direct
impediment to right or left heart outflow
or restriction of all cardiac chambers.

44. OBSTRUCTIVE SHOCK
 Pericardial tamponade, tension
pneumothorax, pulmonary embolism,
ductus-dependant CHD
 Anterior Mediastinal masses. Critical
coarctation of the aorta

45. OBSTRUCTIVE SHOCK
 Obstructive shock often manifests as
inadequate cardiac output due to a physical
restriction of forward blood flow; the acute
presentation may quickly progress to cardiac
arrest

46.  Regardless of etiology, uncompensated
shock, with hypotension, high vascular
resistance, decreased cardiac output,
respiratory failure, obtundation, and oliguria,
occurs late in the progression of the disease.

47.  Additional clinical findings in shock include
cutaneous lesions such as petechiae, diffuse
erythema, ecchymoses, erythema
gangrenosum, and peripheral gangrene.
 jaundice can be present either as a sign of
infection or as a result of MODS.

48. SEPTIC SHOCK
 Usually involves a more complex
interaction of distributive, Hypovolemic,
and Cardiogenic shock
 Bacterial
 Viral
 Fungal (immunocompromised patients
are at increased risk)

49. SEPTIC SHOCK

50.  Sepsis is defined as SIRS resulting from a
suspected or proven infectious etiology.
 Severe sepsis (the presence of sepsis
combined with organ dysfunction.
 Septic shock (severe sepsis plus the
persistence of hypoperfusion or hypotension
despite adequate fluid resuscitation or a
requirement for vasoactive agents), MODS,
and possibly death.

51. THE PROGRESSION OF SEPSIS
SIRS
From
infection
Sepsis
Severe
sepsis
Death MODS Septic shock
Outcomes improve with early recognition and
treatment

52. SEPTIC SHOCK
 The initial sign and symptoms are;
 Alteration in temperature regulation (hypo or
hyperthermia)
 Tachycardia and tachypnea
 In early stages (hyperdynamic phase or
warm shock) the cardiac output increases in
an attempt to maintain adequate O2 delivery
and meet the metabolic demands

53. SEPTIC SHOCK
 As septic shock progresses, cardiac output
falls in response to the effects of numerous
inflammatory mediators, leading to a
compensatory elevation in SVR and the
development of cold shock

54. HEMODYNAMIC VARIABLES IN DIFFERENT SHOCK STATES
Type of
shock
CO SVR MAP CWP CVP
HYPOVOLEM
IC
↓ ↑ ↔ OR ↓ ↓↓↓ ↓↓↓
CARDIOGENI
C:
SYSTOLIC ↓↓ ↑↑↑ ↔ OR ↓ ↑↑ ↑↑
DIASTOLIC ↔ ↑↑ ↔ ↑↑ ↑
OBSTRUCTIV
E
↓ ↑ ↔ OR ↓ ↑↑ Ω ↑↑ Ω
DISTRIBUTIV
E
↑↑ ↓↓↓ ↔ OR ↓ ↔ OR ↓ ↔ OR ↓
SEPTIC:
EARLY ↑↑↑ ↓↓↓ ↔ OR ↓ ‡ ↓ ↓
LATE ↓↓ ↓↓ ↓↓ ↑ ↑ or ↔

55. DIAGNOSIS
 Shock is diagnosed clinically on the basis of
a thorough history and physical exam.

56. DIFFERENTIAL DIAGNOSIS OF THE CHILD
PRESENTING WITH SHOCK
Bleeding shock —History of trauma ,Bleeding site
Dengue shock syndrome —Known dengue outbreak or
season, History of high fever ,Purpura
Cardiac shock —History of heart disease , congested neck
veins and liver
Septic shock —History of febrile illness ,Very ill child
Known outbreak of meningococcal infection
Shock associated with severe dehydration —History of
profuse diarrhea ,Known cholera outbreak

57. CHILD WITH SHOCK

58. TESTING SKIN PINCH FOR ASSESSING
DEHYDRATION

59. LABORATORY FINDINGS
 Thrombocytopenia & anemia
 Prolonged PT & PTT
 Reduced fibrinogen level
 Elevation of fibrin split products
 Elevated neutrophil count and immature
forms, vacuolation of neutrophils, toxic
granulations, and Döhle bodies can be seen
with infection
 Neutropenia & leukopenia are ominous sign
of overwhelming sepsis.

60. LABORATORY FINDINGS
 Glucose dysregulation (hyper or
hypoglycemia) is a common stress response
 Electrolyte abnormalities are hypocalcemia,
hypoalbuminemia, and metabolic acidosis.
 Renal and/or hepatic function may be
abnormal
 Patients with ARDS or pneumonia have
impairment of oxygenation (decreased
PaO2) as well as ventilation (increased
PaCO2) in the later stage of lung injury.

61. LABORATORY FINDINGS
 The hallmark of uncompensated shock is an
imbalance between O2 delivery and O2
consumption.
 This state manifests clinically by increased
lactic acid production (high anion gap,
metabolic acidosis) due to anaerobic
metabolism and a low mixed venous oxygen
saturation

62. LABORATORY FINDINGS
 Serum lactate measurement along with
mixed venous oxygen saturation may be
used as a marker for the adequacy of
oxygen delivery and the effectiveness of
therapeutic interventions.

63. TREATMENT

64. INITIAL MANAGEMENT
 Early recognition and prompt intervention are
extremely important in the management of all
forms of shock.

65. INITIAL MANAGEMENT
 Regardless of the cause: ABC’s
 First assess airway patency, ventilation, then
circulatory system
 Respiratory Performance
 Respiratory rate and pattern, work of breathing,
oxygenation (color), level of alertness
 Circulation
 Heart rate, BP, perfusion, and pulses, liver size
 CVP monitoring may be helpful

66. INITIAL MANAGEMENT
Airway management
 Always provide supplemental oxygen
 Endotracheal intubation and controlled
ventilation is suggested if respiratory failure or
airway compromise is likely
 elective is safer and less difficult
decrease negative intrathoracic pressure
improved oxygenation and O2 delivery and
decreased O2 consumption

67. INITIAL MANAGEMENT
 Neonates and infants in particular may have
profound glucose dysregulation in
association with shock
 Glucose levels should be checked routinely
and treated appropriately, especially early in
the course of the illness.

68. INITIAL MANAGEMENT
 Given the predominance of sepsis and
hypovolemia as the most common causes of
shock in the pediatric population, most
therapeutic regimens are based on
guidelines established in these settings.

69. INITIAL MANAGEMENT
 Immediately after establishment of IV or IO
access, aggressive, early goal-directed
therapy (EGDT) should be initiated unless
there significant concerns for cardiogenic
shock as an underlying pathophysiology.

70. INITIAL MANAGEMENT
 Rapid IV administration of 20 mL/kg isotonic
saline or, less often colloid should be initiated
in an attempt to reverse the shock state
 Bolus should be repeated quickly up to 60-80
mL/kg.
 Rapid fluid resuscitation using 60-80 mL/kg
or more is associated with improved survival
without an increased incidence of pulmonary
edema.

71. INITIAL MANAGEMENT
 Fluid resuscitation in increments of 20 mL/kg
should be titrated to normalize HR, urine
output (to 1 mL/kg/hr), capillary refill time(<2
seconds), and mental status.
 Normalization of BP alone is not a reliable
endpoint for assessing the effectiveness of
resuscitation.

72. INITIAL MANAGEMENT
 Although the type of fluid (crystalloid vs
colloid) is an are of debate, fluid resuscitation
in the first hour is unquestionably essential to
survival in septic shock, regardless of the
fluid type administered.
 If shock remains refractory following 60-80
mL/kg resuscitation, inotrope therapy should
be instituted while additional fluid are
administred

73. INITIAL MANAGEMENT
 Inotropic and vasoactive drugs are not a substitute
for fluid, however...
 Can have various combinations of hypovolemic
and septic and cardiogenic shock
 May need to treat poor vascular tone and/or poor
cardiac function

75. CARDIOVASCULAR DRUG TREATMENT OF SHOCK
Drug Effects Dosing range comments
Dopamine ↑ cardiac contractility 3-20
microg/kg/min
↑ risk of
arrhythmias with
high doses
Significant peripheral
vasoconstriction at > 10
micro/kg/min
Epinephrine ↑ HR, ↑ cardiac
contractility
0.05-3
mic/kg/min
May ↓ renal perfusion
at high doses
Potent
vasoconstrictor
↑ myocardial O2 consumption
Risk of arrhythmias at high
doses
Dobutamine ↑ cardiac contractility 1-10
micro/kg/min
___
Peripheral vasodilator
Norepinephri
ne
Potent
vasoconstriction
0.05-1.5
micro/kg/min
↑ BP 2ndry to ↑ SVR
No significant effect
on cardiac
contractility
↑ left ventricular
afterload

76. VASODILATORS/AFTERLOAD REDUCERS
Drug Effects Dosing range comments
Nitroprossid
e
Vasodilator (mainly
arterial)
0.5-4 mic/kg/min Rapid effect
Risk of cyanide
toxicity with use
>96hr
Nitroglyceri
ne
Vasodilator (mainly
venous)
1-20 mic/kg/min Rapid effect
Risk of ↑ ICP
Prostagland
in E1
vasodilator 0.01-0.2
mic/kg/min
Can lead to
hypotension
Risk of apnea
Maintain an open ductus
arteriosus
Milrinone Increased cardiac
contractility
Load 50 mic/kg
over 15 min
Phosphodiestrase
inhibitor – slow
cyclic adenosine
monophosphate
breakdown
Improves cardiac
diastolic function
0.5-1 mic/kg/min
Peripheral vasodilation

77. GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK
System Disorder Goals therapies
Respiratory ARDS Prevent/treat;
hypoxia &
respiratory acidosis
Oxygen
Respiratory muscle
fatigue
Prevent
barotrauma
Early endotracheal
intubation & mechanical
ventilation
Central apnea Decrease work of
breathing
PEEP
Permissive hypercapnia
High-frequency
ventilation
ECMO

78. GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK
Syste
m
Disorder Goal Therapies
Renal Prerenal
failure
Renal failure
Prevent/treat; hypovolemia,
hypervolemia, hyperkalemia,
metabolic acidosis,
hypernatremia/hyponatremia,
& hypertension.
Monitor serum electrolytes
Judicious fluid
resuscitation
Low-dose dopamine
Establishment of normal
urine output & BP for age
Furosemide (Lasix)
Dialysis, ultrfiltration,
hemofiltration

79. GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK
System Disorder Goal Therapies
Hematologi
c
Coagulopathy (DIC) Prevent/treat; bleeding Vitamin K
Fresh frozen
plasma
Platelets
Thrombosis Prevent/treat; abnormal
clotting
Heparinization
Activated protein C

80. GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK
Syste
m
Disorder Goal Therapies
GIT Stress ulcer Prevent/treat; gastric
bleeding
Avoid aspiration, abdominal
distension
Histamine H2
receptor-blocking
agents or proton
pump inhibitors
Nasogastric tube
Ileus
Bacterial
translocation
Avoid mucosal atrophy Early enteral
feedings

81. GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK
System Disorder Goal Therapies
Endocrin
e
Adrenal
insufficiency,
primary or
secondary to
chronic steroid
therapy
Prevent/treat;
adrenal crisis
Stress-dose steroid in patients
previously given steroids
Physiologic dose for presumed
primary insufficiency in sepsis
Metabolic Metabolic
acidosis
Correct
etiology
Normalize pH
Treatment of hypovolemia (fluids) &
poor cardiac function (fluids,
inotropic agents)
Improvement of renal acid excretion
Low-dose (0.5-2 mEq/kg) sodium
bicarbonate if the patient is not
showing response, pH < 7.1, and
ventilation (CO2 elimination) is
adequate.

82. SEPTIC SHOCK
 Early administration of broad spectrum
antimicrobial agents is associated with a
reduction in mortality.
 Neonates should be treated with ampicillin
plus cefotaxime and/or gentamicin. Acyclovir
should be added if herpes simplex virus is
suspected clinically.

83. SEPTIC SHOCK
In infants and children
 Community acquired N. meningitides can be
treated with 3rd generation cephalosporin
(Ceftriaxone or cefotaxime) or high dose
penicillin.
 H. influenzae can be treated with ceftrixone
or cefotaxime
 The presence of resistant S. pneumoniae
often requires the addition of vancomycin

84. SEPTIC SHOCK
 Suspicious of community or hospital acquired
MRSA infection warrants the coverage with
vancomycin.
 If intra-abdominal process is suspected,
anaerobic coverage should be included with
an agents such as Metronidazole,
Clindamycin, or piperacillin-tazobactam.

85. SEPTIC SHOCK
 Nosocomial sepsis should generally be treated
at least 3rd or 4th generation cephalosporin or
piperacillin-tazobactam. An aminoglycoside
should be added as the clinical situation
warrants.
 Vancomycin should be added to the regimen if
the patient has an indwelling medical device,
gram positive cocci are isolated from the blood,
or MRSA is suspected or as empiric coverage
for S. pneumoniae.

86. SEPTIC SHOCK
 Empirical coverage for fungal infections should
be considered for selected
immunocompromised patients.
 These broad, generalized recommendations
must be tailored to the individual clinical
scenario and to the local resistance pattern of
the community and/or hospital

87. HYPOVOLEMIC SHOCK
 Mainstay of therapy is fluid
 Goals
 Restore intravascular volume
 Correct metabolic acidosis
 Treat the cause
 Degree of dehydration often underestimated
 Reassess perfusion, urine output, vital
signs...
 Isotonic crystalloid is always a good choice

88.  Regardless of the etiology of shock,
metabolic status should be meticulously
maintained.
 Electrolytes should be monitored closely and
corrected as needed.
 Hypoglycemia is common and should be
promptly treated.
 Hypocalcemia which may contribute to
myocardial dysfunction, should be treated.

89. STEROIDS
 Hydrocortisone replacement may be beneficial
in pediatric shock.
 Up t0 50% of critically ill patient may have
absolute or relative adrenal insufficiency.
 Patients at increased risk for adrenal
insufficiency include those with congenital
adrenal hyperplasia, abnormalities of
hypothalamic-pituitary axes, recent therapy with
corticosteroids, and should receive stress doses
of hydrocortisone.

90. STEROIDS
 Steroids may also be considered in patients
with shock that is unresponsive to fluid
resuscitation and catecholamines.

91. THANK YOU