Shock

Presenter: Preetham R M

Moderator: Narayanappa.D

What is shock?a. BP less than 5th percentile of age normal

b. Uncontrolled fluid loss/blood loss

c. Tachycardia and hypotension

d. Acidosis and increased lactate

e. Signs of organ dysfunction with decreased urine output,

altered mental status.

Pediatric ShockDefinition

Etiology/Types

Pathophysiology

Recognition – early is key!

Investigations

Management- guidelines

Pediatric shockCellular pathology

Has nothing to do with blood pressure (until very late),

cardiac output, heart rate

Inability to meet the metabolic demands (=oxygen) of the

tissue – or inability of the cell to use oxygen

Supply-demand imbalance

DefinitionShock is an acute syndrome characterized by the body’s

inability to deliver adequate oxygen to meet the metabolic

demands of vital organs and tissues.

.

OXYGEN SUPPLY

OXYGEN DEMAND

Requirements for Adequate Tissue

Perfusion

Pump

Fluid

Pipes

Site of exchange

Determinants of tissue perfusionCardiac output is the most important determinant of tissue

perfusion and is defined as volume of blood ejected by the

heart per minute. It is the product of stroke-volume and

the heart rate.

Stroke volume: It’s the amount of blood pumped out by

left ventricle per beat. It depends on

Contractility of left ventricle

Pre load

After load

Preload

Preload refers to the volume of blood filling the ventricle at

the onset of diastole.

It is determined by the volume of venous return to the heart

and myocardial end-diastolic fiber length.

After load

After load is best understood as the sum of forces that the

ventricle must overcome in order to eject blood.

Contractility

It is determined by the total mass of functioning-ventricular

muscle.

Cardiac Output Determination

Distribution of cardiac output

Brain 13%

Skeletal Muscle 20%

Abdominal viscera 25%

Skin 10%

Kidneys 20%

TypesHypovolemic shock

Cardiogenic shock

Distributive shock

Obstructive shock

Septic shock

Hypovolemic shockFluid and electrolyte loss

Diarrhea, vomiting, Excessive sweating

Blood loss

External-Laceration

Internal-

Ruptured viscera,

GI bleed,

Intracranial bleed(neonates)

Plasma loss

Burns

Leaky capillaries

Sepsis, inflammation

Nephrotic syndrome

Dengue

Intestinal obstruction

Endocrine

Adrenal insufficiency

Diabetes insipidus

Diabetes mellitus

Pathophysiology

Hypovolemic

shock

Cardiogenic shock Myocardial insufficiency

Congestive heart failure (Congenital, or acquired heart

disease)

Cardiomyopathies

Myocarditis

Arrhythmias

Hypothermia

Myocardial depressant effect of hypoglycemia, acidosis,

hypoxia

Cardiogenic

shock

Pathophysiology

Distributive shockSeptic shock

Anaphylaxis

Neurogenic shock(Spinal cord trauma)

Drugs/toxin

Tissue injury

Prolonged hypoxia or ischemia

Distributive shock

Pathophysiology

VasodilationVenous

Pooling

Decreased Preload

Mal distribution of regional blood flow

Disruption of sympathetic nervous system

Loss of sympathetic tone

Venous and arterial vasodilatation

Decreased venous return

Decreased stroke volume

Decreased cardiac output

Decreased cellular oxygen supply

Impaired tissue perfusion

Impaired cellular metabolism

Pathophysiology

of Neurogenic

Shock

Obstructive shock

Tension pneumothorax

Pneumopericardium

Cardiac tamponade

Pulmonary embolism

Type of Shock Insult Physiol

ogic

Effect

Compens

ation

Compensation

Heart Rate

Compensation

Contractility

Cardiogenic Heart fails to

pump blood

out

↓CO

↑SVR

↑ ↑

Obstructive Heart pumps

well, but the

outflow is

obstructed

↓CO

↑SVR

↑ ↑

Hypovolemic Heart pumps

well, but not

enough blood

volume to

pump

↓CO

↑SVR

↑ ↑

Distributive Heart pumps

well, but there

is peripheral

vasodilation

↓SVR ↑CO ↑

No Change - in

neurogenic shock

↑

No Change - in

neurogenic shock

To Summarize

Stages of ShockEarly compensated Shock:

Cardiac output and systemic vascular resistance (peripheral vasoconstriction) work to keep BP within normal limits.

Tachycardia; decreased pulses & cool extremities in cold shock; flushing and bounding pulses in warm shock; oliguria; may have mild lactic acidosis

Decompensated Shock: Compensatory mechanisms are overwhelmed.

Hypotension, altered mental status; increased lactic acidosis

Platelet aggregation and release of tissue thromboplastin produce hypercoagulability and DIC.

Irreversible Shock: Irreversible organ damage, cardiac arrest, death.

•bounding pulses in warm shock

Symptoms and Signs of ShockPulse/ heart rate(Most important sign)

Tachycardia, HR > than the expected for age.

Rapid, weak, thready peripheral pulses.

Respiratory rate

Tachypnea

Shallow, irregular, labored.

Age Respiratory rate Heart rate

Per min Per min

Infant 50 160

1-5 yrs 40 140

>5yrs 30 120

Adolescent 20 110

Blood Pressure

May be normal initially !!!

Definition of hypotension according to age(<5th centile)

In children hypotension is a pre-terminal event.

Symptoms and Signs of Shock

Symptoms and Signs of ShockSkin

Cold, clammy (Cardiogenic, Obstructive, Hemorrhagic)

Warm (Distributive shock)

Mottled appearance in children

Look for Petechiae(DIC)

Color: pale, ashen-gray

Capillary refilling time ( > 2 sec)

Increased difference between core and peripheral temperature > 2°C

Dry Mucous membranes.

In infants

Poor tone

Unfocused gaze

Weak cry

Lethargy/Coma

Sunken or bulging fontanelle

Poor feeding

Symptoms and Signs of major

organ dysfunction (late signs)Brain

Level of consciousness

Anxiety

Agitation

Confusion and Delirium

Obtundation and Coma

Kidneys:

Acute renal failure; oliguria, anuria

GIT:

Erosive gastritis,

Decreased bowel sounds

Liver:

Ischemic hepatitis; elevation of transaminases and

bilirubin

Hematologic

Coagulation abnormality,

Elevated PT, APTT

Severe DIC and thrombocytopenia

Lab investigationsInitial laboratory determinations should include those that

may alter immediate therapy, like

Complete blood counts,

Serum electrolytes,

Serum calcium,

Blood sugar,

Arterial blood gases and

Serum lactate.

Additional laboratory parameters should be obtained as

warranted by the patient's condition and the most likely

etiologies for shock state.

Cardiovascular system

ECG

Chest X-ray

Echocardiogram

Gastrointestinal, liver

Gastric pH

Stool occult blood

Liver function tests

Respiratory Metabolic

Lung function tests

Metabolic

Serum proteins

Infection screen

Urine-Sp. Gravity,

Cultures-Blood, Urine, stool and pus

CSF-protein, sugar

Hematologic System

Coagulation screen

Platelet count, fibrinogen degradation products

D-diamers.

Management of ShockThe following are major objectives in the management of shock:

1. Rapid recognition of shock and resuscitation.

2. Correction of initial insult.

3. Correction of secondary consequences of shock.

4. Maintenance of function of vital organs.

5. Identification and correction of aggravating factors.

During the initial resuscitation, therapy should be directed towards achievement of clinical therapeutic endpoint of shock resolution, which are as follows:

Therapeutic endpoints in the

management of shockNormal pulse/heart rate

Capillary refill time < 2 sec

Warm extremities

Normal mental status

Normal blood pressure(MAP>65 mm hg)

Urine output > 1 ml/kg/hr

Decreased serum lactate

Reduced base deficit

SvO2 > 70%

Monitoring of ShockOnce the patient comes with shock continuous monitoring should be done, which serves the following purpose:

1. It allows, definition of pathophysiologic stages of shock, which is helpful in diagnosis, prognosis and treatment.

2. It permits continuous assessment of vital organ function.

3. It provides a means to assess the efficacy of therapeutic intervention.

4. It prevents complications by early recognition of correctable problems.

Approach to undifferentiated shock

in children

Special consideration for different

types of shock(PALS manual)

Airway and Oxygen

administrationThe initial resuscitation involves securing a patent airway,

administration of oxygen and establishment of intravenous

access.

Oxygen in maximal concentration should be administered

initially to all patients in shock to maintain >90% oxygen

concentration in arterial blood, in view of impaired

peripheral oxygen delivery.

Once stabilization is achieved, fraction of oxygen in

inspired air should not exceed 0.6, to reduce the incidence

of pulmonary oxygen toxicity.

Vascular accessStandard techniques like peripheral vein catheterization either percutaneously or by venous cut down are likely to be unsuccessful in a patient with severe shock.

Intraosseous line should be established if three attempts have failed or 90 seconds have elapsed.

Sites for IO line

Proximal tibia-most common site

Distal tibia

Iliac crest

Distal femur

Humorous in older children and adults

Fluid TherapyAdequate volume resuscitation is the most important step in

management of hypovolemic, septic and distributive shock.

Preload is optimized by fluid replacement and the cardiac

output and thus oxygen delivery improves.

The circulating volume must be replaced in boluses of 20

ml/kg within minutes since rapid restoration of cardiac

output and tissue perfusion pressure reduces the chances of

serious organ damage particularly acute renal failure.

The amount of fluid to be administered depends upon the

volume status and ongoing losses of the patient. Initial fluid

resuscitation usually require 40- 60 ml/kg but can be as

much as 200 ml/kg in septic shock and hypovolemic shock

Choice of intravenous fluids

Cardiovascular Support

Cardiogenic shock and late stages of other types of shock

are characterized by impairment of myocardial function.

Inotropic, Vasopressor and Vasodilator are used to

maintain cardiac output in such conditions.

Inotropic and

Vasopressor drug

in Treatment of

Shock

DRUG EFFECT(S)DOSING

RANGECOMMENT(S)

Dopamine

↑ Cardiac

contractility3-20 µg/kg/min

↑ Risk of

arrhythmias at

high doses

Significant

peripheral

vasoconstriction

at >10 µg/kg/min

Epinephrine

↑ Heart rate and ↑

cardiac

contractility0.05-

3.0 µg/kg/min

May ↓ renal

perfusion at high

doses

Potent

vasoconstrictor

↑ Myocardial

O2consumption

Risk of arrhythmia

at high doses

Dobutamine

↑ Cardiac

contractility1-10 µg/kg/min —

Peripheral

vasodilator

Norepinephrine

Potent

vasoconstriction0.05-

1.5 µg/kg/min

↑ Blood pressure

secondary to ↑

systemic vascular

resistance

No significant

effect on cardiac

contractility

↑ Left ventricular

after load

PhenylephrinePotent

vasoconstriction0.5-2.0 µg/kg/min

Can cause

sudden

hypertension

↑ O2 consumption

DRUG EFFECT(S) DOSING RANGE COMMENT(S)

NitroprussideVasodilator (mainly

arterial)0.5-4.0 µg/kg/min

Rapid effect

Risk of cyanide toxicity

with prolonged use (>96

hours)

NitroglycerinVasodilator (mainly

venous)1.0-20 µg/kg/min

Rapid effect

Risk of increased

intracranial pressure

Prostaglandin

E1

Vasodilator

0.01-0.2 µg/kg/min

Can lead to hypotension

Maintains an open

ductus arteriosus in the

newborn with ductal-

dependent congenital

heart disease

Risk of apnea

MilrinoneIncreased cardiac

contractility

Load 50 µg/kg over

15 min

Phosphodiesterase

inhibitor

Improves cardiac

diastolic function0.5-1 µg/kg/min

Peripheral vasodilation

Vasodilators/After load Reducers

Antiarrhythmic TherapyCardiac output in young children is highly dependent on heart

rate.

The wide variation in heart rates associated with metabolic

derangements may significantly impair cardiac performance.

Treatment of arrhythmias includes correction of acidosis,

hypoxia, hypocalcaemia and hypokalemia or hyperkalemia.

Specific cardio-active drugs that may be used are

Atropine and isoproterenol for bradyarrhythmias,

Adenosine, digoxin for supraventricular tachyarrhythmias and

Lidocaine for ventricular ectopy

CORRECTION OF METABOLIC

ABNORMALITIES

Acidosis:

A significant secondary complication in shock of

any etiology is the development of metabolic acidosis

as a consequence of tissue ischemia.

Severe acidosis impairs metabolic processes and

prevents effective pharmacologic actions of various

Vasopressor and inotropic agents administered to the

patient.

Correction is indicated when marked metabolic acidosis

exists (arterial blood, pH < 7.15).

Rx

Sodium bicarbonate is usually given in an initial dose of 1 to

2 mEq/kg.

Subsequent doses are based on body weight and base

deficit.

Calcium:

Sustained decrease in ionized calcium as seen in course of

any acute hemodynamic deterioration is associated

with depressed myocardial function, tachycardia,

hypotension, alteration in sensorium.

Therapeutic intervention is justified when serum ionized

calcium level falls below normal (less than 3.0 mg/dl).

Rx

An intravenous infusion of 1-2 ml/kg of 10 percent calcium

gluconate under cardiac monitoring is the usual dose.

Phosphate:

Phosphorus is essential to muscle, nervous system and

functioning of blood cells.

Consequences of severe hypophosphatemia include acute

respiratory failure, altered myocardial performance,

platelet dysfunction, hemolytic anemia,

hepatocellular damage and neurologic abnormalities.

Rx

To correct hypophosphatemia, 5 to 10 mg/kg of potassium

phosphate is given intravenously over six hours.

Blood Glucose:

At the time of resuscitation, hypoglycemia is of major

concern for its negative inotropic effect and associated severe

neurological damage.

Blood glucose < 60 mg/ dL can be used to define

hypoglycemia (beyond the neonatal period).

So Hypoglycemia should be identified rapidly and corrected

immediately.

Rx

IV dextrose may be administered as 25% dextrose (2-4 ml/kg)

or 10% dextrose (5-10 ml/kg).

Ventilatory SupportThe lung is the one of the most sensitive organ that is

affected by shock. Respiratory failure can develop rapidly

and is frequently the cause of death.

In a patient with shock the work of breathing is

substantially increased, which may result in respiratory

muscle fatigue and respiratory failure.

Indications for mechanical ventilation in the management

of a patient in shock are:

1. Apnea or ventilatory failure (acute respiratory acidosis).

2. Failure to achieve adequate oxygenation with high flow

oxygen-with venturi masks or nasal prongs.

3. Respiratory fatigue-for relief of metabolic stress of the

work of breathing.

4. Adjunctive therapy for other interventions

(postoperative state).

Prevention of Acute Renal

FailureThe hypotension and hypoperfusion that are associated

with shock may often lead to oliguria and acute renal

failure.

Aggressive fluid replacement is necessary to support urine

output.

Gastrointestinal SupportGastrointestinal disturbances, as a consequence of shock,

include bleeding and ileus.

Ileus may result from hypokalemia and may lead to

abdominal distention with respiratory compromise.

Gastrointestinal blood loss can be prevented by using

antacids, an H2 receptor blocker, or sucralfate

Hematological SupportPacked RBCs should be transfused if SvO2 is < 70% and

if Hb is < 10 g% even after achieving optimal CVP, urine

output > 1 ml/kg/hour and normal capillary refill.

Once tissue oxygen delivery has resolved, red cell

transfusion is recommended only when hemoglobin falls

to < 7g%.

Coagulation abnormalities and thrombocytopenia are

common in patients with sepsis and shock. It should be

corrected with FFP and platelet transfusion only if

bleeding is present.

Nutritional SupportNutritional support is a frequently overlooked but

extremely important aspect of the care of the shock

patients.

Excessive catabolism with destruction of lean body mass

is the most common nutritional abnormality in shock

states.

Close monitoring of daily caloric intake and determination

of serum albumin, electrolytes and liver function tests

should be done.

Pediatric sepsis and Septic shockInternational Consensus Definitions for Pediatric Sepsis and septic shock

Systemic

inflammatory

response

syndrome (SIRS)Can be due to

•Infection or

• Non infectious (trauma,

burns, ischemia,

pancreatitis, trauma,

adrenal insufficiency)

2 out of 4 criteria, 1 of which must be abnormal temperature or

abnormal leukocyte count:

1.Core temperature >38.5°C or <36°C (rectal, bladder, oral, or

central catheter)

2.Tachycardia:

Mean heart rate >2 SD above normal for age in absence of

external stimuli, chronic drugs or painful stimuli

OR

Unexplained persistent elevation over 0.5-4 hr

OR

In children <1 year old, persistent bradycardia over 0.5 hour

3.Respiratory rate >2 SD above normal for age or acute need

for mechanical ventilation not related to neuromuscular disease

or general anesthesia

4.Leukocyte count elevated or depressed for age (>14000 or

<4000)

Sepsis SIRS plus a suspected or proven infection

Severe

sepsis

Sepsis plus 1 of the following:

1.Cardiovascular organ dysfunction, defined as:

Despite >40 mL/kg of isotonic intravenous fluid in 1 hour:

Hypotension <5th percentile for age

OR

Need for vasoactive drug to maintain blood pressure

OR

2 of the following:

• Unexplained metabolic acidosis: base deficit > 5 mEq/L

• Increased arterial lactate: >2 times upper limit of normal

• Oliguria: urine output <0.5 mL/kg/hr

• Prolonged capillary refill: >5 sec

• Core to peripheral temperature gap >3°C

2.Acute respiratory distress syndrome (ARDS) as defined by the presence of a Pao2/Fio2 ratio

≤300 mm Hg, bilateral infiltrates on chest radiograph, and no evidence of left heart failure

3. Sepsis plus 2 or more organ dysfunctions (renal, neurologic, hematologic, or hepatic)

Septic shock

Sepsis plus cardiovascular

organ dysfunction as defined

above

Multiple organ dysfunction

syndrome (MODS)

Presence of altered organ

function such that homeostasis

cannot be maintained without

medical intervention

Pathophysiology

Warm

Shock

Cold Shock Fluid-

Refractory/

Dopamine

resistant

Catecholamine

Resistant

Refractory

Shock

Early,

compensated

Clinical Signs

-Inc.HR

-Warm

extremities,

bounding pulses

Physiologic

Parameters

-Wide PP

-Inc. C.O.

-Inc. MvO2

-Dec.SVR

Lab Data

-Inc. Lactate

-Inc.Glucose

Late, Uncompensated

Clinical Signs

-Cold, clammy

extremities

-Rapid, thready pulses

-Shallow breathing

Physiologic Parameters

-Narrow PP

-Dec.CVP, C.O

-Dec. MvO2 sat

-Inc. SVR

-Oliguria

-Capillary Leak

Lab Data

-Metabolic Acidosis

-Hypoxia

-Coagulopathy

-Hypoglycemia

Persistence of

shock despite >

60cc/kg fluid

resuscitation

Persistence of

shock despite

Dopamine at

>10mcg/kg/mn

Persistence of shock

despite administration

of direct acting

catecholamines

Epinephrine/

Nor-Epinephrine

Persistence of shock

despite:

-Goal direct

inotropic/ pressor

therapy

-Use of vasodilators

-Maintenance of

metabolic and

hormonal

homeostasis

Algorithm for management of

septic shock

2

Special Aspects of Management

of Septic ShockAntibiotics

Therapy with antibiotics should be initiated as soon as

possible, preferably after sampling for cultures.

It is preferable to provide empirical broad spectrum

antibiotic coverage taking into consideration the primary

site of infection, local bacterial sensitivity pattern and

immunocompetence of the host.

Corticosteroids:

They reduce generation of various mediators of

inflammation and reduce further deterioration of the patient.

The clear indication for use of steroids include children who

have proven adrenal insufficiency or who are at risk for

adrenal insufficiency.

In these cases, it is preferable to obtain a baseline cortisol

level and adrenal insufficiency may be assumed if random

cortisol level is less than 18 μg/dL.

Rx

Stress doses of hydrocortisone should be given intravenously

(2 mg/kg or 50 mg/m2) followed by 50 mg/m2/day in four

divided doses intravenously for 5 to 7 days

NEWER MODALITIES OF TREATMENT

FOR SEPTIC SHOCK

ECMO(Extra corporeal membrane oxygenation)

It is an extracorporeal technique of providing both cardiac and respiratory support to patients whose heart and lungs are so severely diseased or damaged that they can no longer serve their function.

Types

1. Veno-arterial

Right common Femoral vein to right femoral artery

2. Veno- venous

Right common femoral vein to right internal jugular vein

In both modalities, blood drained from the venous system is oxygenated outside of the body and then transfused back.

Thank you