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 Arterial oxygen content Hemoglobin Oxygen Saturation Partial pressure of oxygen dissolved in plasma Stroke Volume Heart rate Preload After load Contractility

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 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 Arterial oxygen content Hemoglobin Oxygen Saturation Partial pressure of oxygen dissolved in plasma Stroke Volume Heart rate Preload After load Contractility

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 1ST hour-20ml/kg/boluses. Correct hypoglycemia and hypocalcemia. Administer 1st 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.