shock in pediatrics ,nelson , pals , shock in children , hypovolemic , cardiogenic , obstructive , distributive

1. SHOCK IN CHILDREN
-Dr.Apoorva.E
PG,DCMS

2. • “ ACUTE CIRCULATORY FAILURE “
with inadequate or inappropriately
distributed tissue perfusion
resulting in generalized cellular
hypoxia

3. • 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

5. CLASSIFICATION
• 5 major types of shock
1.HYPOVOLEMIC
2.CARDIOGENIC
3.OBSTRUCTIVE
4.DISTRIBUTIVE
5.SEPTIC

6. HYPOVOLEMIC SHOCK
• Characterized by fluid loss ( internal / external )
• Decreased preload
Water/electrolyte plasma blood
loss loss loss

7. CARDIOGENIC SHOCK
• Poor myocardial contractility leading to cardiac
pump failure
• Due to :
CHD
Myocarditis
Cardiomyopathies
Arrhythmias

8. OBSTRUCTIVE SHOCK
• Decreased cardiac output secondary to restriction
of all cardiac chambers
• Due to :
Tension pneumothorax
Pericardial tamponade
Pulmonary embolism
Anterior mediastinal masses
Coarctation of aorta

9. DISTRIBUTIVE SHOCK
• Caused by inadequate vasomotor tone
Capillary leak
Maldistribution of fluid into interstitium
• Post-spinal cord or brainstem injury
Anaphylaxis
Poisonings

10. SEPTIC SHOCK
• Complex interaction of
distributive,cardiogenic and hypovolemic
shock
• Bacterial/Viral/Fungal

11. Hypovolemic shock – blood VOLUME
problem
Cardiogenic shock - blood PUMP
problem
Distributive shock – blood VESSEL
problem

12. PATHOPHYSIOLOGY

13. 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

14. 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

15. CLINICAL MANIFESTATIONS
• Tachycardia
• Tachypnoea
• Decreased urine output
• Poor peripheral pulses
• Alteration of mental status
• Low BP

16. COMPENSATED
• Confusion
• Tachycardia
• Normal or mild tachypnoea
• >> CFT
• U/o-adequate
• BP normal

17. UNCOMPENSATED
• Drowsiness
• Marked tachycardia
• Tachypnoea and acidosis
• Very slow CFT
• Oliguria/Anuria
• Hypotension

18. HYPOTENSION FORMULA
Ages – 1 to 10 years
Hypotension is defined as SBP
< 70mmHg + [age in years X 2] mmHg

19. IRREVERSIBLE
• Child is unresponsive
• Bradycardia
• Apnoea
• Cold cyanotic skin
• Anuria
• Unrecordable BP

20. 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

21. HYPOVOLEMIC SHOCK
<< intravascular volume
<< venous return and preload
<< decreased ventricular filling
<< decreased stroke volume
<< CO
<< tissue perfusion
PATHOPHYSIOLOGY

22. ASSESSMENT OF FLUID LOSS

23. 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,start
inotrope (dopamine)
GOAL – RESTORE CIRCULATING VOLUME AND TISSUE
PERFUSION , CORRECT THE CAUSE

24. 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

25. 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

26. 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

27. 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

28. OBSTRUCTIVE SHOCK
PATHOPHYSIOLOGY
Physical obstruction to blood flow
<< CO
<< Tissue perfusion
Compensatory >> in systemic vascular resistance

29. 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

30. 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

31. DISTRIBUTIVE SHOCK
Maldistribution of blood flow
Some tissues inadequately Some tissues
perfused over perfused
(splanchnic circulation) (skeletal muscle,
skin)
PATHOPHYSIOLOGY

32. << 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

33. CLINICAL PRESENTATION
• Tachypnoea without increased work of
breathing
• Hypotension/Normotension
• Bounding pulses/Weak pulses
• Brisk/delayed CFT
• Warm flushed skin/cold pale skin

34. TREATMENT
1. ANAPHYLACTIC SHOCK –
Airway,
IV epinephrine,
Antihistaminics,
Corticosteroids,
Withdrawal of Ag ,
Vasopressors,Inotropes,
Cautious fluid administration

35. 2. NEUROGENIC SHOCK –
Cautious fluid administration,
Vasopressors,Inotropes,
Correct hypothermia,
Treat bradycardia with atropine,
Observe and prevent DVT (due to
peripheral pooling of blood)

36. SEPTIC SHOCK
PATHOPHYSIOLOGY

37. 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

38. INFECTION
• Suspected or proven infection or a clinical
syndrome associated with high probability
of infection
SEPSIS
• SIRS plus a suspected or proven infection

39. SEVERE SEPSIS
• Sepsis plus organ dysfunction,hypoperfusion
or hypotension
(including but not limited to lactic
acidosis,oliguria,acute mental status changes)

40. 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

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

43. 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.

44. DRAW SAMPLE FOR BLOOD C/S
AND START EMPERICAL
ANTIBIOTIC

45. •Antibiotics should be administered within the first hour of
recognition of septic shock
•Selection of antibiotic agents is empirically based on
an assessment of patient's immunity
the potential source of infection
the 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
oGentamicin
o3rd generation cephalosporin
o if pseudomonas is suspected,ceftazidime

46. • 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.

47. DRUGS USED IN
SHOCK

48. 1.Dopamine
-ionotrope at low dose
- peripheral vasoconstriction at
>10mcg/kg/min
- 3-20mcg/kg/min
-arrythmia at higher doses

49. 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

50. 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

52. Drug Indication Dose MOA Principal actions
Dopamine 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

56. THANK YOU