SHOCK IN CHILDREN

-Dr.Apoorva.EPG,DCMS

• “ ACUTE CIRCULATORY FAILURE “

with inadequate or inappropriately distributed tissue perfusion

resulting in generalized cellular hypoxia

• Body’s inability to deliver adequate oxygen to meet the metabolic demands of the tissues.

• Initially compensated

• Continued presence of an inciting trigger +

body’s exaggerated response

lead to progression of shock

if untreated,irreversible tissue injury

irreversible shock

CLASSIFICATION

• 5 major types of shock

1.HYPOVOLEMIC

2.CARDIOGENIC

3.OBSTRUCTIVE

4.DISTRIBUTIVE

5.SEPTIC

HYPOVOLEMIC SHOCK• Characterized by fluid loss ( internal / external )

• Decreased preload

Water/electrolyte plasma blood

loss loss loss

CARDIOGENIC SHOCK

• Poor myocardial contractility leading to cardiac pump failure

• Due to :

CHD

Myocarditis

Cardiomyopathies

Arrhythmias

OBSTRUCTIVE SHOCK

• Decreased cardiac output secondary to restrictionof all cardiac chambers

• Due to :

Tension pneumothorax

Pericardial tamponade

Pulmonary embolism

Anterior mediastinal masses

Coarctation of aorta

DISTRIBUTIVE SHOCK

• Caused by inadequate vasomotor tone

Capillary leak

Maldistribution of fluid into interstitium

• Post-spinal cord or brainstem injury

Anaphylaxis

Poisonings

SEPTIC SHOCK

• Complex interaction of distributive,cardiogenic and hypovolemicshock

• Bacterial/Viral/Fungal

Hypovolemic shock – blood VOLUMEproblem

Cardiogenic shock - blood PUMPproblem

Distributive shock – blood VESSELproblem

PATHOPHYSIOLOGY

COMPENSATORY MECHANISMS

• >> Heart rate

• >> Stroke volume

• >> Vascular smooth muscle tone

• >> O2 extraction from the blood

• Redistributing blood flow to brain,kidneys,adrenals and heart at the expense of skin and GIT

To compensate for the metabolic acidosis,

- >> RR with >>CO2 elimination

- Renal excretion of hydrogen ions

- Retention of bicarbonate ions

To maintain intravascular volume,

- Sodium regulation through RAAS

- ADH secretion

- Cortisol and catecholamine synthesis and release

CLINICAL MANIFESTATIONS

• Tachycardia

• Tachypnoea

• Decreased urine output

• Poor peripheral pulses

• Alteration of mental status

• Low BP

COMPENSATED

• Confusion

• Tachycardia

• Normal or mild tachypnoea

• >> CFT

• U/o-adequate

• BP normal

UNCOMPENSATED

• Drowsiness

• Marked tachycardia

• Tachypnoea and acidosis

• Very slow CFT

• Oliguria/Anuria

• Hypotension

HYPOTENSION FORMULA

Ages – 1 to 10 years

Hypotension is defined as SBP

< 70mmHg + [age in years X 2] mmHg

IRREVERSIBLE

• Child is unresponsive

• Bradycardia

• Apnoea

• Cold cyanotic skin

• Anuria

• Unrecordable BP

DIAGNOSIS• Thorough history and physical exam

• Lab findings : thrombocytopenia

prolonged PT and apTT

reduced serum fibrinogen level

>> fibrin split products

anemia

neutrophilia

left shift of leukocytes

electrolyte disturbances

HYPOVOLEMIC SHOCK

<< intravascular volume

<< venous return and preload

<< decreased ventricular filling

<< decreased stroke volume

<< CO

<< tissue perfusion

PATHOPHYSIOLOGY

ASSESSMENT OF FLUID LOSS

TREATMENT

1.Assess airway

2.Administer oxygen

3.Establish IV access

4.Fluid bolus of 20ml/kg isotonic fluid given

5.Continue fluid boluses (maximum of 3) until perfusion improves or hepatomegaly develops

6.In case of shock refractory to fluids,startinotrope (dopamine)

GOAL – RESTORE CIRCULATING VOLUME AND TISSUE PERFUSION , CORRECT THE CAUSE

CARDIOGENIC SHOCK

Impaired pumping ability of LV

Inadequate systolic emptying of LV

>>LV filling pressure << Stroke volume

>>Left atrial pressure << CO

>>Pulmonary capillary pressure

Pulmonary interstitial and intralveolar edema

PATHOPHYSIOLOGY

CLINICAL PRESENTATION

• Tachycardia

• Low volume pulse

• Cold clammy extremities

• >>CFT

• Pulmonary edema,Crackles,RD,Tachypnoea

• Jugular venous distension

• Hepatomegaly

• Hypotension

• Oliguria,changes in mental status

TREATMENT

GOAL - >> CO, treat reversible causes, << myocardial workload

1.Assess airway , administer oxygen/mechanical ventilation

2.IV access

3.Inotropic agents,vasoactive drugs to >> cardiac contractility and to decrease systemic vascular resistance

4.Cautious administration of fluids

(5-10ml/kg boluses over longer time)

5. Morphine to decrease preload and anxiety

6.Vasodilators for afterload reduction

7.Short acting beta blockers for refractory tachycardia

OBSTRUCTIVE SHOCKPATHOPHYSIOLOGY

Physical obstruction to blood flow

<< CO

<< Tissue perfusion

Compensatory >> in systemic vascular resistance

CLINICAL PRESENTATION

• Muffled heart sounds

• Distended neck veins

• Pulsus paradoxus ( << in SBP by

more than 10mmHg on inspiration )

• Signs of right heart failure plus cyanosis,tachycardia,hypotension

PERICARDIAL EFFUSION

PULMONARY EMBOLISM

TREATMENT

• Pericardial drainage in case of pericardial effusion

• Immediate needle decompression then thoracostomy for chest tube in case of tension pneumothorax

• Anticoagulants or embolectomy for pulmonary embolism

DISTRIBUTIVE SHOCK

Maldistribution of blood flow

Some tissues inadequately Some tissues

perfused over perfused

(splanchnic circulation) (skeletal muscle,

skin)

PATHOPHYSIOLOGY

<< Systemic vascular >> Systemic vascular

resistance & resistance &

>> blood flow to skin << blood flow to skin

Warm extremities, Cold extremities,

bounding peripheral weak pulses

pulses

WARM SHOCK COLD SHOCK

CLINICAL PRESENTATION

• Tachypnoea without increased work of breathing

• Hypotension/Normotension

• Bounding pulses/Weak pulses

• Brisk/delayed CFT

• Warm flushed skin/cold pale skin

TREATMENT

1. ANAPHYLACTIC SHOCK –

Airway,

IV epinephrine,

Antihistaminics,

Corticosteroids,

Withdrawal of Ag ,

Vasopressors,Inotropes,

Cautious fluid administration

2. NEUROGENIC SHOCK –

Cautious fluid administration,

Vasopressors,Inotropes,

Correct hypothermia,

Treat bradycardia with atropine,

Observe and prevent DVT (due to peripheral pooling of blood)

SEPTIC SHOCKPATHOPHYSIOLOGY

DEFINITIONS

SIRS• Requires 2 of the following 4 features to be

present:

o Temperature >38.5° or <36.0° C

o Tachypnea >2SD ABOVE NORMAL FOR AGE

o Tachycardia >2SD ABOVE NORMAL FOR AGE

o WBC ELEVATED OR DEPRESSED FOR AGE/>10%

IMMATURE NEUTROPHILS

INFECTION• Suspected or proven infection or a clinical

syndrome associated with high probability of infection

SEPSIS• SIRS plus a suspected or proven infection

SEVERE SEPSIS

• Sepsis plus organ dysfunction,hypoperfusionor hypotension

(including but not limited to lactic acidosis,oliguria,acute mental status changes)

Identifying Acute Organ Dysfunction as a

Marker of Severe Sepsis

Tachycardia

Hypotension

CVP

PAOP

Jaundice

Enzymes

Albumin

PT

Altered

Consciousness

Confusion

Psychosis

Tachypnea

PaO2 <70 mm Hg

SaO2 <90%

PaO2/FiO2 300

Oliguria

Anuria

Creatinine

Platelets

PT/APTT

Protein C

D-dimer

MODS

• Presence of altered organ function such that homeostasis cannot be maintained without medical intervention

WORK UP

• Laboratory studies

o CBP

o Comprehensive chemistry panel (serum elec,abg,BUN,serum

creat,GRBS,LFT,serum lactate)

o Coagulation studies

o Blood & urine cultures

• Imaging studies

o Chest radiography

o Abdominal radiography

o Others according to the suspected cause.

DRAW SAMPLE FOR BLOOD C/S AND START EMPERICAL

ANTIBIOTIC

•Antibiotics should be administered within the first hour of recognition of septic shock

•Selection of antibiotic agents is empirically based onan assessment of patient's immunitythe potential source of infectionthe most likely responsible organisms.

•Antibiotic choice must be broad spectrum, covering gram-positive, gram-negative, and anaerobic bacteria when the source is unknown

•Regimen for septic shock of unknown cause is oGentamicino3rd generation cephalosporino if pseudomonas is suspected,ceftazidime

• Vancomycin must be added if resistant staphylococci or enterococci are suspected.

• If there is an abdominal source, a drug effective against anaerobes should be included “metronidazole”

• Antibiotics are continued for at least 5 days after shock resolves and evidence of infection subsides

• Abscesses must be drained and necrotic tissues (eg, infarcted bowel) surgically excised.

DRUGS USED IN SHOCK

1.Dopamine

-ionotrope at low dose

- peripheral vasoconstriction at >10mcg/kg/min

- 3-20mcg/kg/min

-arrythmia at higher doses

2. Epinephrine

- >> HR and >> cardiac contractility

- Potent vasoconstrictor

- 0.05 – 3 mcg/kg/min

- << renal perfusion at higher doses,arrythmia at higher doses

3. Norepinephrine

- Potent vasoconstrictor

- No significant effect on cardiac contractility

- 0.05 to 1.5 mcg/kg/min

4. Dobutamine

- >> cardiac contractility

- Peripheral vasodilator

- 1-10 mcg/kg/min

5.Phenylephrine

-potent vasoconstrictor

-0.5 to 2 mcg/kg/min

->> O2 consumption

-can cause sudden hypertension

Drug Indication Dose MOA Principal actionsDopamine Renal perfusion 2-5 mcg/kg/min Dopaminergic Renal a. dilation

hypotension 5-10 mcg/kg/min 1 &dopaminergic

+ inotrope

Hypotension >10 mcg/kg/min 1 vasoconstriction

Dobutamine Cardiogenic shock 2.5-25 mcg/kg/min Selective 1 + inotrope

Norepinephrine Hypotension 2-4 mcg/min 1 & 1 Vasoconstriction

Phenylephrine Hypotension 40-180 mcg/min Selective 1 Vasoconstriction

THANK YOU