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. CLINICAL APPROACH, SOME BACKGROUND

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    1. ???? ?????? ???? (???? 2) ???? ???? ??? ?????? ??? ???? ?"? ?. ????

    2. CLINICAL APPROACH, SOME BACKGROUND & the FUTURE

    3. VOCABULARY I CO - cardiac output = SV x HR AND also CO = ?P / SVR ? ?P (driving pressure) = MAP - CVP SVR systemic vascular resistance . PVR pulmonary vascular resistance. CaO2 art O2 content [(1.34 x Hb x O2sat) + (pO2 x 0.003)]. DO2 - O2 delivery (CO2 x CO). VO2 O2 consumption [CO x CO2 x O2 extraction]. O2 extraction the difference in CO2 between the aorta and the pulmonary artery.

    4. VOCABULARY II Drugs: Nitroprusside Nipride [check cyanide or isothiocyanate] Nitroglycerine NTG [check methemoglobin] Adrenaline Epinephrine (USA) Noradrenaline Norepinephrine (USA) Milrinone Primacor Dobutamine Dobutrex

    5. S E P T I C S H O C K

    7. What do we need to diagnose SEPTIC SHOCK ? Septic shock is suspected in children with the inflammatory triad: fever (or hypothermia), tachycardia & vasodilation (common in benign pediatric infections) + signs of low perfusion such as ? CNS changes (? in mental status, irritability, hypotonia) Prolonged capillary fill (> 2 sec, cold shock) -> common Flash capillary fill (warm shock) -> less common ? urine output

    8. DEFINITIONS OF SHOCK

    9. SEPTIC SHOCK: WARM SHOCK Early, compensated, hyperdynamic state Clinical signs Warm extremities with bounding pulses, tachycardia, tachypnea, confusion Physiologic parameters widened pulse pressure, increased cardiac ouptut and mixed venous saturation, decreased systemic vascular resistance Biochemical evidence: Hypocarbia, elevated lactate, hyperglycemia

    10. Late, uncompensated stage with drop in cardiac output Clinical signs Cyanosis, cold and clammy skin, rapid, thready pulses, shallow respirations Physiologic parameters Decreased mixed venous sats, cardiac output and CVP, increased SVR, thrombocytopenia, oliguria, myocardial dysfunction, capillary leak Biochemical abnormalities Metabolic acidosis, hypoxia, coagulopathy, hypoglycemia

    11. SEPTIC SHOCK (CONT)

    12. GOALS OF 1ST HOUR RESUSCITATION (I) Maintain oxygenation, ventilation, circulation and threshold heart rate (next slide) Therapeutic end points: Capillary refill; no difference between peripheral & central pulses; warm extremities; urine > 1 mL/kg/h; normal mental status & BP for age Monitoring: pulse oximeter; cont ECG; A-line; continuous temp (core & peripheral); bladder catheter; repeated glu & iCa

    14. GOALS OF 1ST HOUR RESUSCITATION (II) Airway & breathing: reasons to intubate ? work of breathing; respiratory acidosis (pCO2 > 60 mmHg, pH < 7.25 with nl BE); hypoxia (pO2/FiO2 < 200); loss of airway protection 2nd to ? mental status. Circulation: two peripherals, intraosseous, cut-down. If inotropes are to be given ? central venous line. Fluids: repeated 20 mL/kg boluses. Follow rales, gallop, hepatomegaly, & ? work of breathing. Sometimes 200 mL/kg were infused. Vasoactive drugs: Dopamine is 1st line. If shock remains resistent: Adrenaline for cold shock (? & ? effects) and Noradrenaline for warm shock (?-effect).

    15. GOALS OF 1ST HOUR RESUSCITATION (III) Hydrocortisone Tx: *adrenal insufficiency should be suspected (purpura fulminans; catecholamine-resistance; hx of CNS abnormality or prior chronic steroid therapy). * adrenal insufficiency = total cortisol < 18 mg/dL. Dose? 1-2 mg/kg for stress coverage to 50 mg/kg for shock bolus followed by same dose as a 24 hour continuous infusion.

    16. GOALS OF STABILISAZTION Goals: normal perfusion; perfusion pressure normal for age; mixed venous O2 saturation > 70%; 3.3 < CI < 6.0 L/min/m2. Hemodynamic support may be required for days. There are several variations: low C.O. and high SVR ? consider Nipride/NTG + steroids; Milrinone is another option. high C.O. and low SVR ? Norepinephrine + steroids. low C.O. and low SVR ? Adrenaline + steroids. Shock refractory to cathecolamines ? r/o pneomothorax, tamponade, Addison, hypothyroid, ongoing blood loss or an abdominal catastrophy. CONSIDER ECMO

    18. CAN WE CHANGE THE COURSE OF AN INFECTIOUS DISEASE ? OR IS THE PICU IMPORTANT ?

    19. June 1992 December 1997 (n=331) Demographics: Median age 2 y & 8 m (range 5 w to 17.5 y) M / F - 143:188 Septicemia 281; meningitis 50 deaths: In PICU: total 33 [29 (10%) septic, 3 (6%) meningitis] Before arriving PICU: total 29 In 1997 there were 2/111 deaths (predicted 38/111) The proportion of complications remained unchanged (~5.5% for amputations or skin grafting; ~8% for neurological abnormalities)

    20. MD CENTERALIZED CLINICAL MANAGEMENT (I) When dx suspected? prompt PCN injection by the family physician (GP) Continuous telephone advice by PICU attending prior to arrival of mobile team Mobile Intensive Care Team led by PICU attending & nurse transferred all patients to the central unit Elective intubation & ventilation, hemodynamic monitoring, and ongoing resuscitation performed at referring hospital Patient stabilized prior to transport

    21. Photocopies of all documentation done Treatment included Aggressive fluid resuscitation (4.5% Albumin) Early intubation and ventilation Generous use of Inotropes Correction of coagulopathy Correction of metabolic derangements (K, Ca, Mg, Phosph, Bicarb & Glu) Early renal replacement therapy MD CENTERALIZED CLINICAL MANAGEMENT (II)

    24. DO WE HAVE A SPECIFIC TARGET ?

    25. TREATMENT OF GRAM-NEGATIVE BACTEREMIA AND SEPTIC SHOCK WITH HA-1A HUMAN MONOCLONAL ANTIBODY AGAINST ENDOTOXIN. ZEIGLER EJ ET AL N Engl J Med. 1991 Feb 14;324(7):429-36 HA-1A is an IgM monoclonal ab that binds to the lipid A domain of endotoxin. 543 adult patients with sepsis presumed to be of gram-negative origin (not necessarily shock or bacteremia proven !) Total mortality: placebo 43%; HA-1A 39% (p=0.24). Among the 200 who had gram-negative bacteremia mortality was 45/92 (49%) in the placebo group and 32/105 (30%) in the HA-1A group (p=0.014). Follow-up studies ?drug increases mortality and was abandoned.

    26. THE NEXT DECADE SAW DOZENS OF FAILED TRIALS AND MILLIARDS OF $$ WASTED

    29. ACTIVATED PROTEIN C

    33. Xigris 12/2003 ? NO DATA in CHILDREN ! Despite that Eli Lilly insists on full price

    34. HEMODYNAMIC VARIABLES in DIFFERENT SHOCK STATES

    35. FINAL THOUGHTS Recognize compensated shock quickly- have a high index of suspicion, remember tachycardia is first sign. Hypotension is late and ominous. Gain access quickly- if necessary use an IO line. Administer adequate amounts of fluid rapidly. Remember ongoing losses. Correct electrloytes and glucose problems quickly. If the patient is not responding the way you think he should, broaden your differential, think about different types of shock.

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