PEDIATRIC SHOCK

2012

SHOCK

 Shock is a syndrome that results from inadequate oxygen delivery to meet metabolic demands  Sequelae of shock are metabolic acidosis, organ dysfunction and death

SHOCK-OXGEN SUPPLY FAILS TO MEET OXYGEN DEMAND OXYGEN SUPPLY OXYGEN DEMAND

OYGEN DELIVERY CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT Cardiac Output Heart rate Stroke Volume Preload After load Contractility Arterial oxygen content Hemoglobin Oxygen Saturation Partial pressure of oxygen dissolved in plasma

Oxygen Delivery

 Oxygen delivery=CO X Arterial oxygen content  CO=Heart rate X Stroke volume  Stroke volume depends on preload, afterload and contractility  Art Oxygen content= Hb x Sa02 x 1.34 +(0.003 x Pa02)

Factors affecting Oxygen delivery

 Oxygenation-A-a gradient, DPG, acid base balance, Temp, Blockers  Stroke volume-Ventricular compliance, CVP, venous tone, autonomic tone, metabolic milieu, afterload, conduction system

Types of Shock

     Hypovolemic- Hemorrhage, serum or plasma loss Distributive-Anaphylactic, Neurogenic, septic Cardiogenic- Myocardial, dysrrythmia, CHD(duct dependant) Obstructive-Pneumo, tamponade, dissection Dissociative-Heat, CO, cyanide, endocrine RJ has Hypovolemic shock secondary to Hemorrhage

Case 1

 9 year old girl RJ with a history of variceal bleed presents with new onset bleed. O/E-responsive, HR-135, RR-38, BP-88/60, Sats-92%. I stat-7.08/24/80/12/-4. Hb-4.2

 What type of shock is this? Hypovolemic Shock  What is the very first thing you would like to do for this patient?

Oxygen  Is this compensated or uncompensated shock- how does the body compensate?

Compensated

Stages of Shock

   Compensated- Vital organ function maintained, normal BP Uncompensated-Marginal microvascular perfusion.Organ and cellular function deteriorate. Hypotension develops.

Irreversible RJ has compensated shock because her blood pressure is normal

Compensatory Mechanisms

 Baroreceptors-In aortic arch and carotid sinus, low MAP cause vasoconstriction, increases BP, CO and HR  Chemoreceptors- Respond to cellular acidosis, results in vasoconstriction and respiratory stimulation

Compensatory Mechanisms

 Renin Angiotensin- Decreased renal perfusion leads to angiotensin causing vasoconstriction and aldosterone causing salt and water retentions  Humoral Responses-Catecholamines  Autotransfusion-Reabsorption of interstitial fluid

RJ’s Clinical presentation

     Diagnosis is based on exam focused on tissue perfusion Neurological-Fluctuating mental status Skin and extremities-Cool, pallor, mottling, cyanosis, poor cap refill, weak pulses, weak muscle tone Cardio-pulmonary-Hyperpnea, tachycardia Renal-Scant, concentrated urine  Abject hypotension is a late and premorbid sign( and is the flag for uncompensated shock)

Hypovolemic shock

 Commonest cause worldwide  Decreased blood volume, decreased preload, decreased stroke volume  Signs of dehydration-tears, mucous membranes, skin tugor  Site of fluid loss may be obvious or concealed(liver, spleen, intracranial, GI)

Oxygen-What a difference!

 Art Oxygen content= Hb x Sa02 x 1.34 +(0.003 x Pa02)  Pa02 on 100% is approx 650  Pa02 on room air is approx 100 If your Hb is 15 this difference in PaO2 does not make much difference- if your Hb is 5 it makes all the difference!

RJ’s Management

       Increase oxygen delivery, decrease oxygen demand Oxygen Fluid Blood Temperature control Correct metabolic abnormalities Inotrope if needed

Labs

        ABG Blood sugar Electrolytes CBC PT/PTT/Fibrinogen Type and Cross Cultures Imaging

Volume expansion

 Optimize RJ’s preload with NS or RL  10-20cc/kg q 2-10min. RJ is given 2 boluses.

 RJ is given 2 units of blood. Her heart rate stabilizes at 86. BP-112/80.

 RJ is deemed stable and gets sclerotherapy

RJ At Endoscopy

Case 2

  TN is a 5 year old girl with a history of URI symptoms 2 weeks ago presents with decreased effort tolerance, tachypnea . O/E-HR-192, RR-70, BP-45 systolic. Hepatomegaly, b/l rales, no heart murmur on exam but a gallop is heard.

What type of shock is this?

Uncompensated cardiogenic shock  What is the diagnosis? How do you manage this patient?

Myocarditis

Differentiating Cardiogenic Shock

 History  PE-enlarged liver, gallop, murmur, rales  Chest X ray-Enlarged heart, pulmonary venous congestion

Myocarditis

OYGEN DELIVERY CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT Cardiac Output Heart rate Stroke Volume Preload After load Contractility Arterial oxygen content Hemoglobin Oxygen Saturation Partial pressure of oxygen dissolved in plasma

Managing TN

 Increasing Oxygen supply Supplemental Oxygen Improving myocardial output-altering preload, after load and contractility Correct Anemia-Blood  Decreasing oxygen demand Control temperature Sedation Reduce myocardial work and thus oxygen consumption

Fluids in Cardiogenic Shock

 Give small volume boluses of 5-10ml/kg  TN has myocarditis and because of this she has diastolic dysfunction- giving her extra fluid may overload her heart.

Ionotropes/Cardiotonics

 Dopamine-Low dose increases renal and splanchnic blood flow, high dose increases HR and SVR.  Dobutamine- Increases contractility, may reduce SVR, PVR.  Milrinone-Inotropy and venodilation. Improve contractility and decrease after load

Ionotropes/ Cardiotonics

 Epinephrine- Increases HR,SVR and contractility. End point-adequate BP, acceptable tachycardia  Norepinephrine-0.05-1.0mcg/kg/min. Increases SVR. Be hesitant to use either of these drugs for TN as they increase myocardial oxygen consumption

TN’s Hospital Course

 10ml/kg bolus with normal saline results in minimal elevation of blood pressure  Started on Dopamine of 5mcg/kg/min and Milrinone 0.5 mcg/kg/min  Stable for transport to Cardiac ICU  Attempted intubation results in circulatory collapse-TN goes up on ECMO

Other causes of Cardiogenic Shock

 Dysrhythmia  Infection  Metabolic  Obstructive  Drugs  Congenital heart disease  Trauma

Case 3

 4 year old boy RS presents with 3 day h/o fever, malaise. He has a past history of nephrotic syndrome.O/E-Minimally responsive,skin appears flushed and warm, and he has bounding pulses. HR-170 RR-30 BP-40 systolic, sats-88%.  What type of shock does the patient have Uncompensated distributive shock- Warm septic shock  What medications could be used in the management of this patient?

Fluid, antibiotics, pressors, steroids

Septic Shock

 Mediator release- both exogenous and endogenous lead to misdistribution of blood, imbalance of oxygen supply and demand, alterations in metabolism and cardiac dysfunction

Warm Shock

 Early compensated hyperdynamic state of septic shock  Warm extremities, bounding pulses, tachycardia, wide pulse pressure, decreased systemic vascular resistance and increased cardiac output  Often with hyperglycemia

Cold Shock

 Late uncompensated stage of septic shock with drop in cardiac output and increased SVR  Cold and clammy skin, rapid thready pulses, shallow breathing  Associated metabolic acidosis, hypoxia, coagulopathy, hypoglycemia, capillary leak

PALS ALGORITHM

 1 ST hour-20ml/kg/boluses.  Correct hypoglycemia and hypocalcemia.  Administer 1 st dose of antibiotics  Consider vasopressor drip and stress dose hydrocortisone  DETERMINE WHETHER FLUID RESPONSIVE

PALS ALGORITHM

 IF NOT FLUID RESPONSIVE Normotensive-Start Dopamine Hypotensive vasodilated(warm shock) Norepinephrine Hypotensive vasoconstricted(cold shock) Epinephrine EVALUATE MIXED VENOUS SAT, GOAL>70%

RS- Hospital Course

     100ml/kg of fluid is given, BP improves to 60/30 Started on Norepinephrine drip following which BP improves to systolic of 80.

Rt IJ placed ScVO2-74% Hydrocortisone 2mg/kg-1 dose given Starts Vancomycin and Ceftriaxone Microbiology calls to tell you there are Gram Neg rods on blood culture smear

PALS ALGORITHM

   ScvO2>70%, Low BP, warm shock-Additional fluid. Norepinephrine +/- Vasopressin ScvO2<70%, normal BP, poor perfusion-Transfuse to Hb>10g/dl. Consider milrinone/ nitroprusside/dobutamine ScvO2<70%, low BP, poor perfusion-Transfuse to Hb>10g/dl. Consider epinephrine or dobutamine +norepinephrine  ADRENAL INSUFFICIENCY Hydrocrtisone 2mg/kg

How much fluid is to much?

  Fluids in early septic shock- Carcillo, JAMA 1991 Three treatment groups 1-20cc/kg in first hour 2- Upto 40cc/kg in first hour 3- More than 40cc/kg in first hour NO DIFFERENCE IN ARDS BETWEEN GROUPS

Conclusions

 Recognise shock quickly-tachycardia is the first sign, hypotension is late  Gain access quickly-if needed use IO. PIV better than a central line  If patient is not responding the way you think broaden your differential, think about other types of shock.