SHOCK IN CHILDREN Moderator: Dr. - PowerPoint Presentation

Slide1

SHOCK IN CHILDREN

Moderator: Dr. Kashif AliDepartment of Paediatrics

14

th

December’2019

Slide2

Learning objectives

DefineDescribe the patho-physiology of shockDescribe the severityTypes of shockSystematic approach to evaluation of cardiovascular systemDescribe the Steps of management of shockKnows how- to manage a simulated case of shock

Slide3

Question Which of the following is necessary in the definition of shock?

(a) Hypotension(b) Tissue hypoxia(c) Use of pressors(d) Multiple organ dysfunction3

Slide4

Definition

Is a critical condition that results from inadequate tissue distribution of oxygen and nutrients to meet the tissue metabolic demand.

Slide5

Pathophysiology

Adequate oxygen delivery depends on : Sufficient oxygen content of bloodAdequate blood flow to tissuesAppropriate distribution of blood flow

Slide6

oxygen delivery

Oxygen Delivery (to tissue level) = Cardiac Output x Arterial Oxygen Content (DO2 = C.O. x CaO2)Cardiac output = Stroke volume X heart rate Art Oxygen Content =

Oxygen content of the RBC + the oxygen dissolved in plasma

CaO

2

= (

Hg X SatO

2

X 1.39

) + (

PaO2 X 0.003)

6

Hgb

O

2

Slide7

Blood flow depends on the cardiac output

Cardiac output = Stroke volume X Heart RateOxygen delivery = Cardiac output X oxygen content

Slide8

Cardiac performance

Slide9

Distribution of blood flow depends on Vascular Resistance

Slide10

10

Slide11

Slide12

severity

Compensated shockHypotensive shock

Slide13

Types

HypovolemicDistributiveCardiogenicObstructive

Slide14

Hypovolemic shock

Most common cause of shock.Volume loss – diarrhoea, vomiting, haemorrhage, inadequate fluid intake, diuresis, third space losses, large burnsNarrow pulse pressure, cool pale skinHypovolemic shockpreloadContractilityafterloaddecreasedNormal or increasedincreased

Slide15

SystemMild Blood volume loss (<30%)Moderate blood loss (30-45%)Severe blood loss(>45%)CardiovascularIncrease heart rateWeak peripheral pulsesNormal systolic BPNormal pulse pressureModerate inc. HRWeak central pulsesLow normal BPNarrow pulse pressureTachycardia f/b bradycardiaWeak or absent central pulses Absent peripheral pulsesHypotentionNarrow pulse pressure(undetectable DBP)Central nervous systemAnxious, irritable, confusedLethargic, dulled response to pain

Comatose

Skin

Cool, mottled; prolonged capillary

refill

Cynotic

; marked prolonged capillary refill

Pale and cold

Urine output

Low to very low

Minimal

None Hemorrhagic shock

Slide16

Distributive shock

Mal distribution of blood flowCauses – Septic shock Anaphylactic shock Neurogenic Shock Distributuve shockpreloadconrtactilityafterloadNormal or decreasedNormal or decreasedvariable

Slide17

Bounding peripheral pulse, brisk capillary refill, flushed skin/pale mottled skin, hypotension

Septic shockSeptic shockPreload ContractilityafterloaddereasedNormal to decreasedvariable

Slide18

Anaphylactic shock

Neurogenic shockpreloadcontactiltyafterloaddecreasedvariableLV –decreasedRV - increasedpreload

contactibility

afterload

decreased

normal

decreased

Slide19

Cardiogenic shock

Causes –congenital heart disease, myocarditis, cardiomyopathy arrythmias, sepsis, poisoning/drug toxicity, myocardial injuryIncreased respiratory effort signs of congestive heart failure, cyanosis, cold pale extremitiespreloadcontractilityafterloadvariabledecreasedincreased

Slide20

Obstructive shock

Cardiac tamponadeTension pneumothoraxDuct dependant congenital heart diseaseMassive pulmonary embolismpreloadcontractibilityafterloadvariablenormalincreased

Slide21

Cardiac tamponade

Collection of fluid, blood or air in pericardia spaceNarrow pulse, diminished heart sounds, distended neck veins, pulsus paradoxus.Tension pneumothoraxCollection of air in pleural spaceTracheal deviation, hyperresonace on affected side, diminished breath sounds distended neck veins, pulsus paradoxus

Slide22

Duct dependent lesions

Cyanotic – duct dependent pulmonary blood flowLeft ventricular outflow obstruction – duct dependent systemic blood flow.Cyanosis,higher preductal versus post ductal blood pressure, higher preductal versus post ductal oxygen saturation, diminished femoral pulsesMassive pulmonary embolism obstruction of pulmonary artery or its braches by blood clot, fat, air, amniotic fluid, catheter fragment.Cyanosis, systemic venous congestion and RV failure

Slide23

23

Pump failure = Cardiogenic shockRelease valve failure = Obstructive shockHose failure = Distributive shockWater failure = Hypovolemic shockPump failure = Cardiogenic shock

Release valve failure = Obstructive shock

Hose failure = Distributive shock

Water failure =

Hypovolemic

shock

Slide24

Systematic Approach

Clinical signsHypovolemic shockDistributive shockCardiogenic shockObstructive shockAPatencyAirway open and maintainable/ not maintainableBRespiratory rateNormal to increased Laboured

Respiratory sounds

normal

Normal

(crackles +/-)

Crackles, grunting

Systolic blood pressure

Compensated hypotensive

C

Pulse pressure

narrow

variable

NarrowHeart rateIncreased

Peripheral pulse

weakBounding or weak

Weak

SkinPale coolWarm or coolPale or cool

Capillary refill

delayedvariableDelayed

Urine outputDecreased

D

Level of consciousnessEarly – irritableLate – lethargic

E

Temperature

variable

Slide25

Steps in management

Goals of shock management : Improve oxygen deliveryBalance tissue perfusion and oxygen demandReverse perfusion abnormalitiesRestore organ functionPrevent progression to cardiac arrest

Slide26

Optimise oxygen content of blood :

Administer high flow oxygenInvasive or non-invasive mechanical ventilationPacked cell transfusion.

Slide27

Improving volume and distribution of cardiac output :

Crystalloid or colloid fluid bolusReducing oxygen demandDecrease work of breathingRelieve pain and anxietyControl fever

Slide28

Correct metabolic derangements :

HypoglycemiaHypocalcemiaHyperkalemiaMetabolic acidosis

Slide29

Therapeutic end points :

Normal heart rate and blood pressureNormal pulseCapillary refill time <2 secWarm extremitiesNormal mental statusUrine output > 1 ml/kg/ hourDecreased serum lactatesReducing base deficitCentral venous oxygen saturation > 70%

Slide30

General management of shock

Positioning :Responsive and normotensive – most comfortable positionHypotensive and breathing not compromised – Tredelenberg positionAirway and breathing :Oxygen ventilation

Slide31

Vascular access :

Compensated shock – peripheral IV lineHypotensive shock – immediate IO access if IV difficultFluid resuscitation

Slide32

Monitoring :

Oxygen statsHeart rateBlood pressure and pulse pressureMental statusTemperatureUrine output

Slide33

Frequent reassessment :

Evaluate trendsResponse to therapyPlan next interventionsLaboratory studies :CBC, Glucose, Potassium, Calcium, lactate, ABG, ScvO2

Slide34

Medication therapy

: Vasoactive therepy Class Medication EffectInotropes*Dopamine*Epinephrine*DobutamineIncrease cardiac contractilityIncrease HRVariable effect on SVR Inodilators*MilrinoneDecrease SVRImprove coronary artery blood flowImprove contractilityVasodilators*Nitroglycerine*NitroprussideDecrease SVC and venous toneVasopressors*Epinephrine*Norepinephrine

*Dopamine

*Vasopressin

Increase

SVR

Increase myocardial contractility

Slide35

A real life scenario - Things are not so simple though.

Slide36

A 12 year old boy of good build and nutrition from Aligarh, Uttar Pradesh, India was referred from a private hospital to our emergency department of a tertiary level hospital with complains of fever for 7 days, pain and distention of abdomen, vomiting and altered sensorium for one day.

Initial vitals in ED were; PR-144/min, low volume, regular, RR-48/min, with severe increased WOB, Temp- 98.4F (axillary) , BP-80/50mmHg, cold below knees bilaterally, weak central pulses, SPO2-92% at room air. He had petechial rashes

Slide37

he was irritable , with GCS of 10 was E4V2M4 . He had tachypnoea

and crepts on auscultation with decreased air entry on right side. In per abdomen examination there was marked distension of abdomen with fluid thrill and liver was palpable 4cm below costal margin. He had blood tinged UGI aspirates.

Slide38

The initial investigations revealed a hematocrit of 56%,

platelet of 12,000/µl and TLC of 16,000/µl with 54% lymphocytes. Blood urea was 42mg/dl and S. Creatinine 0.7 mg/dl. Total bilirubin 11.6mg/dl with direct 11.3mg/dl , ALT 634 (>10 times UL) and AST 740u/l (>10 times UL) , lactates 7.8 mmol/L, serum sodium 118meq/l and potassium 5meq/l. there was mild metabolic acidosis. He was positive for Dengue NS1 antigen and IgM antibody.

Slide39

Monitoring was started. Fluid resuscitation with Ringer Lactate at 7 ml/kg/hour infusion was given.

Foley catheterization was not done due to high risk of bleeding. Oxygen via nasal prongs was given to target oxygen sats of 94-98. No inotropic support was given. BP increased to 5th centile -10th centile with fluid bolus. One unit PRBC and and 2 units platelets were transfused

Slide40

After 2 hours the patients developed worsened respiratory distress, worsened GCS, desaturation, increasing abdominal distension and hypotensive shock.In view of rapid deterioration he was shifted to

Pediatric Intensive Care unit (PICU) of this hospital.He was intubated I/V/O coma and impending respiratory failureBy that time patient was in multi organ failure.

Slide41

Main issue was SHOCK !

Slide42

Phase 1.He had low volume pulses and cold below knee. His BP was 70/50 on

auscultatory method. USG guided IVC assessment was suggestive of collapsible IVC on respiratory variation. Screening echo was normal. USG abdomen was suggestive of free fluid in peritoneal cavity and bilateral pleural effusion with more on the right side. urine output was 10 ml on catheterization and subsequently 0.4 ml/kg/hr. Left femoral triple lumen CVL of 5f and 15 cm length was inserted. Opening CVP was 26 mm Hg. Intra-abdominal pressure was 22 mm Hg and was suggestive of severe IAH.

Slide43

Classify shock . !

Preload ?Contractility ?Afterload ?

Slide44

Abdominal compartment syndrome

It is a condition caused by abnormally increased pressure within the abdomen.

Slide45

Diagnostic criteria of Abdominal compartment syndrome

:Diagnosis requires two components: (1) Sustained intra-abdominal pressure >20mmHg (2) Organ failure attributable to elevated intra-abdominal pressure.Note: Kidneys are one of the most sensitive organs to increased abdominal pressure

Slide46

Cardiovascular manifestation of Abdominal compartment syndrome

Shock and hypotension, due to reduced preload.Mesenteric ischemia causes bacterial translocation into the bloodstream, which may cause systemic vasodilation and hypotension.

Slide47

Interpreting the abdominal pressure

2-7 mmHg: normal for a non-obese person.>12 mmHg: defined as IAH15-20 mmHg: can cause organ failure >25-30 mmHg: usually cause organ failure, may require emergent decompression. Grading Scale: IAH Grade 1: IAP 12-15 mmHg Grade 2: IAP 15-20 mmHg Grade 3: IAP 20-25 mmHg Grade 4: IAP >25 mmHg ACS Sustained elevation of IAP of >20 mmHg with new organ dysfunction.

Slide48

Treatment of Abdominal compartment Syndrome

Hemodynamics: *Target MAP >60 *Dont give additional fluid *Consider diuresis/dailysis (if possible)Decompress abdomen: *Ascitis – drain *NPO *decompress bowelSurgical decompression: *Facial release is definitive treatment, but most invasive.

Slide49

Ultrasound guided peritoneal tap with a 20 G IV cannula was done and around 2000 ml of clear fluid was drained over 4 hours. No bleeding was noted from the puncture site. BP improved to 50

th centile and marked improvement in urine output and perfusion. Vent pressure decreased from PP of 38 to 24 cm of water. CVP decreased to 15. Simultaneously USG guided Right pleural tap was done and 600 ml of serous fluid was drained. Peak pressure fell to 18 and CVP was 12 with good BP and perfusion. IVC was turgid with minimal or no respiratory variation. Lasix bolus and infusion was started. His haematocrit settled from 59 to 45 to 29. No fresh bleeding was seen from any site. Antibiotics (cefotaxime/vancomycin) was started.

Slide50

He was extubated after 24hrs of ventilation to oxygen prongs. His GCS was 15/15,

afebrlie, mild tachypnoa and hemodynamically stable. He was subsequently observed further in PICU for 24 hours and was shifted to step down/ therapy room.

Slide51

Phase 2 On day 4 of

hospitalisation he developed fever, worsening tachypnoea, low GCS, tachycardia, bounding pulses with flash capillary refill and hypotension with wide pulse pressure. He was reintubated and put on mechanical ventilation with sedation and paralysis. He developed around 200ml of upper GI bleed. His hematocrit fell to 26 %, platelet to 7000/µl, ALT 1600 u/l and AST 5024 u/l.

Slide52

Arterial line bp monitoring was suggestive of wide pulse pressure and hypotension. CVP was 4. IVC was collapsible. Screening echo was suggestive of

hypercontractile heart with ef of 55 %.

Slide53

Classify shock ?

Preload ?Contractibility ?Afterload ?

Slide54

PALS ALGORITHM FOR SEPTIC SHOCK

Slide55

cryatllaoid

fluid boluses were given and One unit of packed RBC and one unit of Single donor platelet were transfusedNorepinephrine was started and broad spectrum antibiotics (vancomycin and meropenem) were given. Central venous line was resited to right femoral. BP improved initially.But pt again developed narrow pulse pressure hypotensionecho was suggestive of low EF (30%) underfilled IVC. Dobutamine was introduced at 6 mcg/kg/min. Pt was not responding to any fluid bolus and developed worsening hypoxemia and peak pressures. Fluid was restricted.

Slide56

Once BP stabilized norepinephrine was tapered and frusemide was given under CVP monitoring and echocardiography.

Blood cultures showed growth of Enterococcus fecalis sensitive to vancomycin and Candida tropicalis sensitive to fluconazole. Injection Caspofungin was started in view of critical illnessNor adrenaline was stopped and only dobutamine was continued.His vent parameters improved and was extubated successfully to BIPAP.

Slide57

Phase 3 Pt developed hypotension with narrow pulse pressure, new onset

b/l chest crepitations. His CVP was 3. ivc-ci was 50 %.and urine output was borderline . he was refractory to fluid boluses. echo was s/o ejection fraction of 20% and cardiac output of 2L/min.

Slide58

Classify shock ?

Preload ?Contractibility?Afterload ?

Slide59

adrenaline infusion was started

at 0.1 mcg/kg/min .injection levosimendan was added later. Pt improved with ef of 25-30 and pulmonary edema improved.

Slide60

T

ake-Home PointsShock is a progressive process.

I

n

t

e

rv

e

n

e

e

a

rly.

Identifying

the

stage

and

classification

of shock

is

important.Stage:

Compensated,

uncompensated,

or

irreversible?

Classification:

Hypovolemic,

distributive,

cardiogenic,

or

obstructive?



Management

should

be

directed

at

normalizing

tissue

perfusion

and

blood

pressure

.

Slide61