Management of shock

Presenters
EGLA OLANA
DURETI GIRMA
YONATHAN MERDEKIYOS
Moderator
Dr Mohamed ( Asst. Prof of Pediatrics)
Definition

• Shock is a physiologic state characterized by a

significant, systemic reduction in tissue perfusion
that results in decreased tissue oxygen delivery and
diminished removal of harmful byproducts of
metabolism (eg, lactate)
Epidemiology
• Shock occurs in approximately 2% of all hospitalized infants, children,
and adults in developed countries.
• Mortality rate varies substantially depending on the etiology and
clinical circumstances. among the patients who do not survive most
die due to tha associated complication nd Multi Organ dysfunction
syndrome.
• The most common cause of pediatric shock worldwide is hypovolemia
from diarrhea.
Pathophysiology
• Shock can develop from a variety of conditions that result in the
following:
• Insufficient circulating blood volume (preload)
• Changes in vascular resistance (afterload)
• Heart failure (contractility)
• Obstruction to blood flow
Stages of Shock

• The shock syndrome is characterized by a continuum of physiologic

stages beginning with an initial inciting event that causes a systemic
disturbance in tissue perfusion.
shock usually progress through three major stages
• Compensated shock
• Decompensated shock
• Irreversible shock
Compensated shock
• Compensatory mechanism attempt to maintain blood pressure by
increasing cardiac output and systemic vascular resistance.
• The body also attempts tp to optimize oxygen delivery to the tissue by
increasing oxygen extraction ad redistributing blood flow to the brain,
heart and kidney at the expense of skin and gastrointestinal tract.
Decompensated shock
• During this stage the compensatory mechanisms are overwhelmed if
treatment is not intiated or is inadquate
• Sign and symptom of organ dysfunction such as altered mental status
as aresult of poor brain perfusion appears.
Types of shock

• Hypovolemic
• Distributive
• Cardiogenic
• Septic
• Obstructive
Hypovolemic shock
• Most common type of shock encounteredin children.
• It results from a decreased preload from extravascular fluid loss such
as with diarrhea.
• Since preload is one of the determinants of stroke volume cardiac
output falls when preload falls.
Distributive shock

• It results from decreased SVR, with abnormal distributionof blood

flow with the microcirculation and inadquate tissue perfusion.
• It is normally associated with a normal or increased cardiac output.
• Most common causes of distructive shock in children include sepsis,
anaphylaxis and neurogenic shock.
 Cardiogenic Shock

• Cardiogenic shock results from a pump faliure of the heart causing a

shock-like state with inadequate perfusion to the tissues.
• It is uncommon among children.
• It occurs most commonly in association with, and as a direct result of,
acute ischemic damage to the myocardium.such as Congenital heart
disease ,Cardiomyopathies,Myocarditis and Dysrhythmias
 Septic Shock

• Is often a unique combination of distributive, hypovolemic, and

cardiogenic shock.
• Hypovolemia from intravascular fluid losses occurs through capillary
leak
• Cardiogenic results from the myocardium-depressant effects of sepsis,
• Distributive is the result of decreased systemic vascular resistance.
Systemic Inflammatory Response Syndrome (SIRS)

• Is an inflammatory cascade that is initiated by the

host response to an infectious or non infectious
trigger
• Two of 4 criteria,1 of which must be abnormal
temperature or abnormal leukocyte count
body temperature
heart rate
respiratory function
peripheral leukocyte count
• Sepsis-induced myocardial dysfunction is more common in children,
suggesting that early inotropic support would be more beneficial for
them than adults.
• Initially children will have plethora, warm extremities and bounding
pulses (“warm shock”.) high co/low SVR
• If the shock is not reversed, signs of failure of the compensatory
mechanisms can be noted including cold extremities and prolonged
capillary refill time (“cold shock”) low CO/high SVR
Obstructive Shock

• Stems from any lesion that creates a mechanical barrier that impedes
adequate cardiac output;
• Significant direct obstruction to right or left heart function, or
restriction of all cardiac chambers
• CAUSES;
 Large pulmonary embolism leading to right-sided heart failure,
Critical coarctation of aorta leading to left-sided heart failure
Pericardial tamponade
Tension pneumothorax
Clinical manifestation of shock

• Hypotension Occurs in the majority of shock patients but is not a

criterion for the diagnosis of shock. in this situation, the main clinical
manifestations are tachycardia and signs of organ hypo perfusion
• Oliguria (<0.5 mL/kg per hour) result from shunting of renal blood
flow to other vital organs, intravascular volume depletion, or both.
Related signs: tachycardia, dry mucous membranes
• Change in mental status due to brain hypo perfusion in shock
-Begins with agitation
-Progresses to confusion/delirium
-Ends in obtundation /coma
• Cool, pale cyanosed or mottled skin vaso constrictive mechanisms
redirecting blood from the periphery to the vital organs
• Metabolic acidosis this implicates decreased clearance of lactate by
the liver, kidneys
Diagnosis
Early recognition and prompt intervention are extremely important
in the management of all forms of shock

• Clinical
• History
• Physical examination
• Laboratory
• Hematologic
• Neutropenia or leukopenia
• Blood lactate levels
General management
Goal-
• To restore adequate organ perfusion and oxygen delivery while
considering/treating the possible cause(s) of shock
Approach:
• ABC of life
• Fluid management
• Inotropic and vasoactive agents
• Hydrocortisone Therapy
• Organ support
Goals during the 1st hour of resuscitation :
a. Maintain and retain heart rate threshold
b. Capillary refill < 2 sec, and

c. Normal blood pressure in the 1st hour/emergency department.

Subsequent ICU Goals /if shock persists/

a, Restore and maintain normal perfusion pressure (MAP , CVP) for age,
b, ScvO2 > 70% and
c, Cardiac index 3.3-6.0 L/min/m2 in PICU.
Goals during the 1st 6 hr of resuscitation:
a. Central venous pressure 8-12 mm Hg
.
b. Mean arterial pressure (MAP) ≥65 mm Hg
c. Urine output ≥0.5 mL kg −1 hr d. Central venous (superior vena
cava) or mixed venous oxygen saturation: 70% or 65%, respectively
2. In patients with elevated lactate levels, targeting resuscitation to
normalize lactate as rapidly as possible.
Recommendations for Shock:

1. Crystalloids fluid of choice

2. Against the use of hydroxyethyl starches
3. Albumin in the fluid resuscitation of severe sepsis and septic shock when
patients require substantial amounts of crystalloids.
4. Initial fluid challenge in patients with sepsis-induced tissue hypoperfusion with
suspicion of hypovolemia, to achieve a minimum of 30 mL/kg of crystalloids
 Vasopressors
1. Vasopressor to target a mean arterial pressure (MAP) of 65 mm Hg.
2. Norepinephrine as the first-choice vasopressor.
3. Epinephrine
4. Vasopressin 0.03 units/min can be added to norepinephrine
5. Phenylephrine is not recommended in the treatment of septic shock except in
some circumstances.
6. Low-dose dopamine should not be used for renal protection.
Inotropic Therapy

1. A trial of dobutamine infusion up to 20 µg/kg/min be administered or added to

vasopressor in the presence of
(a) myocardial dysfunction
(b) ongoing signs of hypoperfusion, despite achieving adequate intravascular
volume and adequate MAP.
2. Not using a strategy to increase cardiac index to predetermined supranormal
levels.
Corticosteroids

• 1. Not using intravenous hydrocortisone to treat adult Septic shock patients

2. Not using the ACTH stimulation test to identify adults with septic shock who
should receive hydrocortisone.
3. In treated patients, hydrocortisone tapered when vasopressors are no longer
required.
4. Corticosteroids should not be administered for the treatment of sepsis in the
absence of shock.
Special Considerations in Pediatric
Patients Initial Resuscitation
1.For respiratory distress and hypoxemia, start with face mask oxygen or,
nasopharyngeal CPAP (NP CPAP).
2. Initial therapeutic end-points of resuscitation of septic shock: capillary refill of ≤2
sec, normal blood pressure for age, normal pulses, warm extremities, urine output
>1 mL kg, and normal mental status.
3. Follow (ACCM-PALS) guidelines for the management of septic shock.
4. Evaluate for and reverse pneumothorax, pericardial tamponade, or endocrine
emergencies in patients with refractory shock.
Antibiotics and Source Control

1. Empirical antibiotics within 1 hr in severe sepsis

2. Clindamycin and antitoxin therapies = TSS with refractory hypotension.
3. Early source control.
4. Clostridium difficile colitis with enteral antibiotics if. Oral vancomycin is preferred
for severe disease.
Blood Products and Plasma Therapies
1. Similar hemoglobin targets in children as in adults. During resuscitation of low
superior vena cava oxygen saturation shock (7.0 g/dL) can be considered
reasonable.
2. Similar platelet transfusion targets in children as in adults.
3. Use plasma therapies in children to correct sepsis-induced thrombotic purpura
disorders.
Glycemic Control
1. Control hyperglycemia using a similar target as in adults (≤180 mg/dL). Diuretics
and Renal Replacement Therapy 1. Use diuretics to reverse fluid overload when
shock has resolved.
Nutrition
1. Enteral nutrition given to children who can be fed enterally, and parenteral feeding
in those who cannot (grade 2C).
Management of specific types of shock

35
Management of septic shock
All patients — All patients with suspected septic shock should receive continuous
monitoring of heart rate, breathing, and pulse oximetry and frequent
measurements of blood pressure, timely support of airway and breathing, and
rapid fluid resuscitation
ABC of life
Treat Hypogycemia and hypocalcemia
 Rapid recognition of septic shock or sepsis-associated organ dysfunction.

Recognition Bundle
Screen acutely unwell for septic shock by sepsis screening tool
Clinician assessment within 15 minutes for positive screen
Initiate Resuscitation Bundle within 15 minutes for confirmed suspicion of septic
shock.
1st hour resuscitation bundles
For diagnosed septic shock
- secure an IV/IO line
- obtain sample for culture and lactate
- start fluid resuscitation
- empiric antimicrobial therapy
- start vasopressor for those with fluid refractory shock
1st hour Stabilization Bundle:
1) monitoring to attain a normal perfusion pressure (MAP-CVP)
and SCVO2 > 70% and/or Cardiac Index 3.3-6.0 L/min/m2

2) Administration of appropriate antibiotic therapy and source control

3 hour care bundle

In case of sepsis induced organ dysfunction but no shock

1. Obtain blood cultures

2. Measure lactate level.

3. Administer broad-spectrum antibiotics.
4. Administer 30 mL/kg crystalloid for

hypotension or lactate =4 mmol/L

6 hour care bundle:

5. vasopressors: to maintain (MAP) =65 mm Hg.

6. In persistent hypotension despite fluid resuscitation or initial lactate =4

mmol/L (36 mg/dL):
Measure central venous pressure (CVP).
Measure central venous oxygen saturation (ScvO 2 )
7. Remeasure lactate if initial lactate was elevated.
SEPTIC SHOCK
Early Considerations In septic shock specifically, early (within 1 hr ) administration
of broadspectrum.
Neonates
Ampicillin plus cefepime and/or gentamicin.
Nosocomial sepsis
Third- or Fourth generation cephalosporin
FUID MANAGMENT
 Patients without signs of fluid overload should receive 10 to 20 mL/kg of
balanced crystalloid solution such as lactated Ringer's solution OR 0.9% normal
saline Fluid volume should be calculated based upon ideal body weight (eg, 50
percentile for age . If the patient develops signs of fluid overload, the fluid bolus
should be omitted or reduced (eg, 5 to 10 mL/kg given over 15 minutes).
Patients with fluid-refractory shock
Vasoactive agents are indicated in patients with fluid-refractory septic shock and
are frequently necessary in the initial resuscitation of children with septic shock
while hypovolemia is corrected. The choice of agent is determined by whether
the blood pressure is normal or hypotensive for age.
Patients with catecholamine-resistant
shock
Patients with catecholamine-resistant shock warrant evaluation for unrecognized
morbidities. Etiologies to evaluate during initial management include
pneumothorax, pericardial effusion, intra-abdominal hypertension, ongoing
blood loss, and overt adrenal insufficiency
Septic shock and hypotension
 In patients with septic shock and hypotension and without severe anemia
(hemoglobin <5 g/dL [hematocrit <15 percent]) or severe acute malnutrition,
bolus fluids should be administered judiciously in aliquots of 10 to 20 mL/kg up to
40 mL/kg in the first hour.
DISTRIBUTIVE SHOCK
Neurogenic Shock:
ABC of life
Initial focus is hemodynamic stabilization
Phenylephrine or vasopressin to increase SVR
IV fluid is first line for hypotension
Vasopressors and inotropes if hypotension persists
Norepinephrine is first line, 0.05-0.5mcg/kg/minute
Epinephrine for refractory cases of hypotension
If bradycardic give atropine[0.2 mg/kg IV] to oppose
vagal tone
Methylxanthine (theophylline, aminophylline) for
refractory cases of bradycardia
corticosteroids may also be considered
Anaphylactic shock
• Anaphylactic reactions Can be mild moderate sever
Evaluate Airway, Breathing and Circulation
High flow oxygen
FLUID:: start with 20 ml/kg over 10–20 min. can be repeated.
 If more than 40 ml/kg is required, inotropic support (dopamine or adrenaline)
Epinephrine is the medication of choice for anaphylactic
episodes
corticosteroid: Hydrocortisone 4mg/kg IV
Antihistamine
If no response in 5-10 minutes: Repeat I.M. adrenaline,
repeat fluid bolus, Set up adrenaline I.V.
cardiogenic Shock
Patients with cardiogenic Shock Smaller boluses of fluid (5-10 mL/kg) should be
given in cardiogenic shock to replace deficits and maintain preload. Early
initiation of epinephrine or dopamine is important, and early consideration
should be given to administration of an inodilator.Target clinical end-points,
including increased urine output, improved peripheral perfusion, resolution of
acidosis, and normalization of mental status..
Hypovolemic shock
Hypovolemic shock — Intravascular fluid loss is the principal feature of
hypovolemic shock. For hypovolemic shock, most children should receive 20
mL/kg per bolus, repeated as needed. Each bolus should be infused over 5 to 10
minutes. Rapid infusion of fluids should be performed with caution in children
with severe malnutrition.
Physiologic indicators of perfusion
mental status
Quality of central and peripheral pulses
 Skin perfusion (warm, with capillary refill <2 seconds)
Urine output (≥1 mL/kg per hour)
Blood pressure
Considerations for children who have not improved after
receiving a total of 60 mL/kg over 30 to 60 minutes include:
The amount of fluid loss may have been underestimated (as with
burn injury) or there may be significant ongoing fluid loss
Other conditions may be causing or contributing to shock
Although controversial, colloid is a reasonable option for patients
with hypoalbuminemia (albumin<3g/dL) or hyperchloremic metabolic
acidosis who have not improved after initial therapy with at least 60
mL/kg of crystalloid solutions. However, hydroxyethyl starch solutions
may be harmful and should beavoided.
For hemorrhagic

• Targeting transfusion to a hemoglobin goal of greater than 10 g/dl

• Packed red blood cells should be infused in 10 mL/kg boluses

• A recent proposed protocol recommends a ratio of 1:1:1 units of

PRBC:FFP: platelets as a massive transfusion protocol
Risks of Aggressive fluid administration
• Fluid overload
• In hemorrhagic
• Elevation of blood pressure will increase bleeding from open vessels
• Dilute native clotting factors and red cell mass
• Result of increased hemorrhage and mortality
Obstructive shock
For patients with obstructive shock , fluid resuscitation may be briefly
temporizing in maintaining cardiac output, but the primary insult
must be immediately addressed.Regardless of the etiology of shock,
metabolic status should be meticulously maintained. Electrolyte levels
should be monitored closely and corrected as needed. Hypoglycemia
is common and should be promptly treated.
Obstructive shock
ABC of life
 fluid resuscitation to maintain CO
primary insult must be immediately addressed.

PERICARDIAL pneumothorax Pulmonary Ductus dependent

EFFUSIION embolism cardiac lesions

pericardiocentesis Pleurocentesis thrombectomy/ Prostaglandin

or thrombolysis infusion
Chest tube
placement
Clinical end-points serve as global markers for organ perfusion and
oxygenation.
1 Laboratory parameters such as SvO 2 (or ScvO2 >70%)
2 serum lactate concentration,
3 cardiac index, 3.3-6.0 L/min/m2
4 Hemoglobin should be generally maintained at 10 g/dL,
 PROGNOSIS
• Prognosis In septic shock, mortality rates are as low as 3% in
previously healthy children and 6–9% in children with chronic illness
(compared with 25–30% in adults). With early recognition and
therapy, the mortality rate for pediatric shock continues to improve,
but shock and MODS remain one of the leading causes of death in
infants and children. The risk of death involves a complex interaction
of factors, including the underlying etiology, presence of chronic
illness, host immune response, and timing of recognition and therapy.
ReferenceS
• Nelson Textbook of Pediatrics 21 edition

• Up To Date 2023

64
THANKYOU