Pediatric  Shock Ii
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Pediatric Shock Ii

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Pediatric  Shock Ii Pediatric Shock Ii Presentation Transcript

  •  
  • CARDIOGENIC SHOCK
    • Etiology:
      • Arrhythmias
      • Infection
      • Metabolic
      • Obstructive
      • Drug intoxication
      • Congenital heart disease
      • Trauma
  • CARDIOGENIC SHOCK (cont.)
    • Differentiation from other types of shock:
      • History
      • Physical Exam:
        • Enlarged liver
        • Gallop rhythm
        • Murmur
        • Rales
      • CXR:
        • Enlarged heart, pulmonary venous congestion
  • CARDIOGENIC SHOCK
    • Etiology:
      • Arrhythmias
      • Infection
      • Metabolic
      • Obstructive
      • Drug intoxication
      • Congenital heart disease
      • Trauma
  • CARDIOGENIC SHOCK (cont.)
    • Management:
      • Improve cardiac output::
        • Correct dysrhymias
        • Optimize preload
        • Improve contractility
        • Reduce afterload
      • Minimize cardiac work:
        • Maintain normal temperature
        • Sedation
        • Intubation and mechanical ventilation
        • Correct anemia
  • DISTRIBUTIVE SHOCK
    • Due to an abnormality in vascular tone leading to peripheral pooling of blood with a relative hypovolemia.
    • Etiology
      • Anaphylaxis
      • Drug toxicity
      • Neurologic injury
      • Early sepsis
    • Management
      • Fluid
      • Treat underlying cause
  • OBSTRUCTIVE SHOCK
    • Mechanical obstruction to ventricular outflow
    • Etiology: CHD, massive PE, tension pneumothorax, cardiac tamponade
    • Inadequate C.O. in the face of adequate preload and contractility
    • Tamponade: Narrow pulse pressure and/or EMD
    • Treat underlying cause.
  • DISSOCIATIVE SHOCK
    • Inability of Hemoglobin molecule to give up the oxygen to tissues
    • Etiology: Carbon Monoxide poisoning, methemoglobinemia,dyshemoglobinemias
    • Tissue perfusion is adequate, but oxygen release to tissue is abnormal
    • Early recognition and treatment of the cause is main therapy
  • CLINICAL APPROACH, SOME BACKGROUND & the FUTURE SEPSIS / SIRS MOSF / ARDS
  • 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.
    • CaO 2 – art O 2 content [( 1.34 x Hb x O 2 sat) + (pO2 x 0.003 )].
    • DO 2 - O 2 delivery (CO 2 x CO).
    • VO 2 – O 2 consumption [CO x CO 2 x O 2 extraction].
    • O 2 extraction – the difference in CO 2 between the aorta and the pulmonary artery.
    . . . . . .
  • VOCABULARY II
    • Drugs:
    • Nitroprusside – Nipride [check cyanide or isothiocyanate]
    • Nitroglycerine – NTG [check methemoglobin]
    • Adrenaline – Epinephrine (USA)
    • Noradrenaline – Norepinephrine (USA)
    • Milrinone – Primacor
    • Dobutamine – Dobutrex
  • S E P T I C S H O C K SIRS/Sepsis/Septic shock Mediator release: exogenous & endogenous Maldistribution of blood flow Cardiac dysfunction Imbalance of oxygen supply and demand Alterations in metabolism
  • SEPSIS / SIRS MOSF / ARDS Primary Pro- Inflammatories: LPS; IL-1; TNF Proteases Coagulation factors Kinins Eicosanoids (PGE2) Nitric Oxide, ROS Heat-Shock proteins Anti-Inflammatories: IL-1ra; IL-4; IL-10 INFLAMMATORY EVENTS IN THE SIRS SPECTRUM Secondary Pro- Inflammatories: IL-6; IL-8
  • 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
  • DEFINITIONS OF SHOCK
    • Cold or warm shock: Decreased perfusion including decreased mental status, capillary refill 2 secs (cold shock) or flash capillary refill (warm shock), diminished (cold shock) or bounding (warm shock) peripheral pulses, mottled cool extremities (cold shock), or decreased urine output 1 mL/kg/hr
    • Fluid-refractory/dopamine-resistant shock: Shock persists despite 60 mL/kg fluid resuscitation in first hour and dopamine infusion to 10 g/kg/min
    • Catecholamine resistant shock: Shock persists despite use of catecholamines epinephrine or norepinephrine
    • Refractory shock: Shock persists despite goal-directed use of inotropic agents, vasopressors, vasodilators, and maintenance of metabolic (glucose and calcium) and hormonal (thyroid and hydrocortisone) homeostasis
    • Crit Care Med 2002 Vol. 30, No. 6
  • 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
    • 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
    SEPTIC SHOCK: “COLD SHOCK”
  • SEPTIC SHOCK (CON’T)
    • Cold Shock rapidly progresses to MOSF or death, if untreated
    • M ulti- O rgan S ystem F ailure: Coma, ARDS, CHF, Renal Failure, Ileus or GI hemorrhage, DIC
    • More organ systems involved, worse the prognosis
    • Therapy: ABCs, fluid
    • Appropriate antibiotics, treatment of underlying cause
  • 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
  • THRESHOLD HEART RATES AND PERFUSION PRESSURES
  • GOALS OF 1ST HOUR RESUSCITATION (II)
    • Airway & breathing : reasons to intubate –  work of breathing; respiratory acidosis (pCO 2 > 60 mmHg, pH < 7.25 with nl BE); hypoxia (pO 2 /FiO 2 < 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 1 st line. If shock remains resistent: Adrenaline for ‘cold’ shock (  &  effects) and Noradrenaline for ‘warm’ shock (  -effect).
  • 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.
  • GOALS OF STABILISAZTION
    • Goals : normal perfusion; perfusion pressure normal for age; mixed venous O 2 saturation > 70%; 3.3 < CI < 6.0 L/min/m 2 .
    • 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
  • PEDIATRIC ALGORITHM
  • CAN WE CHANGE THE COURSE OF AN INFECTIOUS DISEASE ? OR IS THE PICU IMPORTANT ?
    • 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)
  • 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
    • 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)
  •  
  • NEONATAL ALGORITHM
  • DO WE HAVE A SPECIFIC TARGET ?
  • 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.
  • THE NEXT DECADE SAW DOZENS OF FAILED TRIALS AND MILLIARDS OF $$ WASTED
  • THE SIREN’S SONG OF CONFIRMATORY SEPSIS TRIALS: SELECTION BIAS and SAMPLING ERROR Natanson, Charles MD; Esposito, Claire J. MD; Banks, Steven M. PhD Crit Care Med. 1998 Dec;26(12):1927
  • When confronted with the disappointment of failed sepsis trials, it is alluring to maneuver the data into the conclusion that a given drug was beneficial to certain patients. Unfortunately, the sirens' sweet songs of significance (reached via sampling error and selection bias) may have set back new drug development for sepsis and left the field shipwrecked on the rocks . Overall, vast resources have been expended on sepsis trials in the last 10 yrs. It is important to realize that the small nonsignificant treatment effects found in the primary target populations from large initial sepsis trials have been consistently reproduced in confirmatory trials (PAFra [1,2] , interleukin-1 receptor antagonists [9,10] , anti-TNF-monoclonal antibodies [6-8] , and P-55 soluble TNF receptors [13,14] ) ( Figure 1 and Figure 2 , Table 1 ). Faced with such a persistently high mortality rate from sepsis and new agents with such small beneficial effects, we need to increase our efforts to find better therapeutic agents and do the necessary research to formulate new questions to test these same agents
  • ACTIVATED PROTEIN C
  • Rational for using activated protein C
  •  
  •  
  •  
  • Xigris 12/2003  NO DATA in CHILDREN ! Despite that Eli Lilly insists on full price…
  • HEMODYNAMIC VARIABLES in DIFFERENT SHOCK STATES  or      Septic: Late    Or    Septic: Early  Or   Or   Or    Distributive    Or    Obstructive    Or    Cardiogenic    Or    Hypovolemic CVP Wedge MAP SVR CO
  • 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.
  • תודה על ההקשבה ! שאלות ?