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Pathophysiology , diagnosis and management of septicaemic shock Critical care scoring. Dr. Emeni. University College of Medical Sciences & GTB Hospital, Delhi. Definition Pathophysiology Diagnosis Management . …. Important Clinical Pointers to Impending Shock in a Septic Patient.
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Pathophysiology, diagnosis and management of septicaemic shockCritical care scoring Dr. Emeni University College of Medical Sciences & GTB Hospital, Delhi
Definition • Pathophysiology • Diagnosis • Management
PREDISPOSING FACTORS AND CAUSES • Infections in the aged or malnourished. • Inadequate immune response due to underlying disease eg. hepatic/renal failure, diabetes mellitus. • Iatrogenic infections. • Virulent gram -ve & +ve infections. • Opportunistic infections -prolonged antibiotic therapy -following organ transplants -immunocompromised pt • Fulminant tetanus • Disseminated tuberculosis
Nidus of infection Bloodstream invasion PATHOPHYSIOLOGY Release of mediators Peripheralvascular effects Direct myocardial depression Cellularinjury Poor tissue perfusion & metabolic acidosis Multiple organ dysfunction Death
Classically septic shock is due to “ENDOTOXINS” released by gram negative bacteria - lipopolysaccharide component of outer membrane of bacterial cell. - lipid A-responsible for sepsis Interacts with normal host defences & triggers *release of numerous mediators from cells -IL-1 -Tumournecrosis factor -Procoagulantactivity factor *activates factors within the serum -coagulation cascade
Infection Endotoxin (LPS) Direct cell injury Activation of complement coagulation cascade kallekrein-kinin PMN Macrophages Lymphocyte Monocytes Endothelial cell PROINFLAMMATORY MEDIATORS NO H₂O ₂, OH¯ TNF,IL-6, IL-1 Leukotrienes PG PAF G-CSF CELL INJURY ORGAN FAILURE Heart & vessels GI tract Lungs Kidneys Hematology CNS
If the host defence response is disorganised, unorchestrated,unbalanced and unchecked it fails to defend the host and paradoxically inflicts injury to the host. Inflammation,vasodilation,shock,coagulation disturbances and endothelial injury lead to a chain or network of events that lead to multiple organ failure and death.
HAEMODYNAMIC PROFILE IN SEPTIC SHOCK 1) EARLY STAGE -high cardiac index -low SVR -low PCWP -hypotension -peripheral vasodilatation -LVEF: falls 20-30% in first 24-48hrs 2) LATE STAGE -cardiac function continues to deteriorate -normal or slightly low CI -increasing PCWP -normal or slightly increased SVR
3) PRE-TERMINAL STAGE -low CI -high PCWP -high SVR -hypotension unresponsive to all therapy
OXYGEN DELIVERY & OXYGEN UPTAKE IN SEVERE SEPSIS EARLY STAGE -increase in both DO2 and VO2 -VO2 maintained by local compensatory mechanisms *chiefly by increased oxygen extraction *increased cross-sectional area of capillaries perfusing an organ LATE STAGE VO2 may fall sharply even though O2 delivery is satisfactory. It reflects the inability of the tissues to utilise oxygen.
Decreased O2 extraction is due to * damaged endothelial cells »tissue oedema »increased distance necessary for diffusion of O2 into tissue cells * damaged tissue cells find it difficult to use the O2 for their metabolic needs.
Diagnostic Criteria • Infection, documented or suspected and some of the following----- • General variables • Inflammatory variables • Hemodynamic variables • Organ dysfunction variables • Tissue perfusion variables
General variables - Fever(>38.3⁰ C) - Hypothermia(<36⁰ C) - Heart rate >90bpm - Tachypnea - Altered mental status - Significant edema or positive fluid balance(>20 ml/kg over 24 hrs) - Hyperglycemia(>140 mg/dl in the absence of diabetes) Inflammatory variables - Leukocytosis (WBC > 12,000/µl) - Leukopenia (WBC < 4,000/µl) - Normal WBC count with > 10% immature forms - Plasma CRP > 2SD above normal value - Plasma procalcitonin > 2SD above normal value
Hemodynamic variables - Arterial hypotension(SBP< 90 mmHg, MAP <70 mmHg or SBP decrease > 40mmHg in adults Organ dysfunction variables - Arterial hypoxemia(PaO₂ / FiO₂ < 300) - Acute oliguria (U.O < 0.5ml/kg/hr for atleast 2 hrs despite adequate resuscitation) - Creatinine increase > 0.5mg/dl - Coagulation abnormalities (INR > 1.5 or PTT > 60 secs) - Ileus - Thrombocytopenia (<1,00,000/µl) - Hyperbilirubinemia (Total plasma bilirubin > 4mg/dl) Tissue perfusion variables - Hyperlactatemia (> upper limit of lab normal) - Decreased capillary refill or mottling
Surviving sepsis campaign: International guidelines for management of severe sepsis and septic shock 2008
MANAGEMENT Principles of management Urgent treatment should commence wherever pt is at time of diagnosis before transfer to ICU. Initial resuscitation and infection issues Hemodynamic support and adjunctive therapy Other supportive therapy of severe sepsis Severe sepsis bundles
1.aInitial resuscitation (First 6hrs) Begin resuscitation immediately in pts with hypotension or raised S. lactate >4mmol/L, don’t delay pending ICU admission. Goals • CVP 8-12 mmHg • MAP ≥ 65mmHg • Urine output ≥ 0.5ml/kg/hr • ScvO ₂ ≥ 70% or mixed venous ≥ 65% • If venous O₂ saturation target not achieved : • Consider further fluid • Transfuse packed RBC if required to Hematocrit ≥ 30% and/or • Start dobutamine infusion max 20 µg/kg/min • Higher target CVP of 12-15mmHg is recommended in the presence of mechanical ventilation.
1.bDiagnosis • Obtain appropriate cultures before starting antibiotics provided this doesn’t significantly delay antimicrobial administration. • Obtain ≥ 2 blood cultures • ≥1 blood culture should be percutaneous • 1 blood culture from each vascular access device In place ≥ 48 hrs • Culture other sites as clinically indicated • Perform imaging studies promptly in order to confirm or sample any source of infection if safe to do so.
1.c Antibiotic therapy • Begin IV antibiotics as early as possible and always within the first hour of recognizing severe sepsis and septic shock. • Broad spectrum : ≥1 agents active against likely bacteria/fungus pathogens and with good penetration into presumed source. • Reasses antimicrobial regimen daily to optimize efficacy, prevent resistance, avoid toxicity and minimise cost. • Duration of therapy limited to 7-10 days. • Stop antimicrobial therapy if cause found to be non-infective.
CHOICE OF ANTIBIOTIC • SUSPECTED SEPSIS WITHIN ABDOMEN Gram positive & gram negative organisms,anaerobes,streptococcusfecalis Combination of- *3rd gen cephalosporins +aminoglycoside +metronidazole or *Piperacillin + aminoglycoside +metronidazole or *Meropenem/imipenem +aminoglycoside/vancomycin
b) GRAM NEGATIVE INFECTION OUTSIDE ABDOMEN Combination of- *3rd gen cephalosporin +aminoglycoside or *Piperacillin/ticarcillin+aminoglycoside or *Meropenem + aminoglycoside
c) LIFE THREATENING SITUATIONS WHERE SOURCE OF INFECTION IS UNKNOWN • combination of two or more antibiotics • 3rd gen cephalosporin +aminoglycoside/ciprofloxacin +vancomycin +metronidazole/clindamycin • If possibility of Streptococcal/pneumococcal infection cannot be excluded- add Ampicillin 2gram i.v.4hrly till such time as aetiology is known.
d) NOSOCOMIAL INFECTIONS Antibiotics used depend on organisms prevailing in a particular ICU. *Mostly gram negative organisms - respond to 3rd gen cephalosporins +aminoglycoside/ciprofloxacin *Methicillin resistant staphylococcal infections frequent in some ICU’s - add Vancomycin *Antifungal agents used as appropriate.
e) NEUTROPENIC OR IMMUNOCOMPROMISED PATIENTS Gram -ve infections Ticarcillin + clavulanic acid Piperacillintazobactum + aminoglycoside *If fever does not settle within 36 hours -add Vancomycin (possible staphylococcal infection) *Fever persists -amphotericin B ± fluconozole *Possibility of fulminant disseminated T.B.
1.d Source identification and control • Establish specific anatomic site of the infection within first 6 hr of presentation. • Evaluate pt’s for a focus of infection. • Implement source control measures as soon as possible. • Choose the one with max. efficacy and min. physiological upset. • Remove IV access devices if potentially infected.
2. Hemodynamic support and adjunctive therapy 2.a Fluid therapy • resuscitate using crystalloid or colloids. • target a CVP ≥ 8mmHg • Use a fluid challenge technique while associated with a hemodynamic improvement • Give fluid challenges of 1000ml crystalloids or 300- 500ml of colloids over 30mins. More rapid and larger volumes maybe req. in sepsis induced tissue hypoperfusion. • Rate of fluid administration should be reduced if cardiac filling pressures increase without concurrent hemodynamic improvement.
2.b Vasopressors • Maintain MAP ≥ 65 mmHg • Initial vasopressors of choice : norepinephrine or dopamine centrally administered. Epinephrine : use if BP non responsive to NE or dopamine. • Don’t use low dose dopamine for renal protection. • Insert an arterial catheter as soon as practical in pts requiring vasopressors.
2.c Inotropic therapy • dobutamine : use in pts with myocardial dysfunction with Cardiac filling pressure and cardiac output. • Don’t increase cardiac index to predetermine supranormal levels.
2.d Steroids • IV hydrocortisone for adult septic shock when hypotension is unresponsive to fluid resuscitation and vasopressors. • Hydrocortisone dose < 300mg/day.
2.eUSE OF HUMAN RECOMBINANT ACTIVATED (drotrecoginalfa) PROTEIN C PROWESS study (Protein C Worldwide Evaluation in severe sepsis) -demo its use reduced 28day mortality (25% vs 31% in placebo gp) -indicated in septic shock who have ≥ 1 organ dysfunction -continuous i.v.infusion @24µg/kg/hr for 4 days -major side effect - bleeding C/I-deranged coagulation profile -major disadvantage-Cost
3. Other supportive therapy 3.a Blood product administration • Give red blood cells when Hb < 7gm/dl to target a Hb of 7-9gm/dl. • Don’t use erythropoietin to treat sepsis related anemia. • Don’t use FFP to correct clotting abnormalities unless there is bleeding or planned invasive procedure. • Administer platelets when : • < 5000/mm³ regardless of bleeding. • 5000 – 30,000/mm³ and there is significant bleeding risk. • ≥50,000/mm³ is required for surgery or invasive procedure.
3.b Mechanical ventilation of sepsis induced ALI/ARDS • TV of 6ml/kg • Upper limit plateau pressure ≤ 30cm H₂O. • Allow PaCO₂ to increase above normal, if needed to minimize plateau presssure and TV. • PEEP – to avoid extensive lung collapse at end expiration. • Maintain semirecumbent position unless contraindicated. • Use a weaning protocol and Spontaneous Breathing Trial regularily to evaluate for discontinuing mechanical ventilation. • Don’t use pulmonary artery catheter for routine monitoring.
3.c Sedation, analgesia and NMB • Sedation protocol with a sedation goal for the critically ill on ventilator. • Intermittent bolus or continuous infusion sedation to predetermined end points with daily interruption. • Avoid NMB where possible.
3.d Glucose control • Use IV insulin to control hyperglycemia. • Keep blood glucose less than 150mg/dl. • Provide a glucose calorie source and monitor glucose values every 1-2 hrs ( 4hrs when stable ). 3.e Bicarbonate therapy • Don’t use bicarbonate therapy for improving hemodynamics or reducing vasopressor requirements when treating hypoperfusion lactic acidemia with • pH ≥ 7.15
3.f DVT prophylaxis • Use low dose UFH or LMWH. • Compression stockings or an intermittent compression device. 3.g Stress ulcer prophylaxis • H₂ blocker or PPI
Consideration for limitation of support. Discuss advance care planning with patients and families providing relevant information about diagnosis,prognosis and treatment.
4. Severe Sepsis Bundles • 4.aSepsis resuscitation bundle (6 hr bundle) • Serum lactate measured. • Blood culture obtained prior to antibiotic administration. • From the time of presentation, broad spectrum antibiotics administered within 3hrs for ED admissions and 1hr for non ED ICU admission. • In the event of hypotension and/or lactate >4mmol/L (36mg/dl) • Deliver an initial minimum of 20ml/kg of crystalloid (or colloid equivalent) • Apply vasopressor if hypotension still persists to maintain MAP >65 mmHg
If hypotension still persists despite fluid resuscitation and/or lactate > 4mmol/L • Achieve CVP > 8 mmHg • Achieve central venous oxygen saturation > 70% • 4.b Sepsis management bundle (24 hr bundle) • Low dose steroids administered for septic shock in accordance with a standardized ICU policy. • Drotrecogin Alfa (activated) administered in accordance with a standardized ICU policy • Glucose control maintained > lower limit of normal < 150mg/dl • Inspiratory plateau pressure maintained <30 cm H₂O for mechanically ventilated patient
SOFA(sequential organ failure assessment) PIRO(predisposing factors,infection,response And organ dysfunction) APACHE(acute physiology and chronic health evaluation) …to assess severity and risk stratification which affects the therapeutic choices.
Critical care scoring • Optimize distribution of medical and financial resources in the delivery of health care. • To formulate some degree of priority for ICU admission. • However scoring systems have strong limitations and critical care of individual patients should not be influenced by scoring protocols. --APACHE --SOFA --PIRO
APACHE (Acute physiology, Age, Chronic health evaluation) APACHE I • Developed in 1980’s • First illness severity system widely used by ICU’s • 34 physiologic variables and a CHE. • Correlated well with mortality. • Difficult to administer and complex score
APACHE II • Simplified version of APACHE I. • Most commonly used. • 12 physiologic variables, patients age, CHE. • One point increase in score equates to an increase of about 1% in mortality. • Doesn’t take into account the admission diagnosis. APACHE III • Developed in 1991. • 17 physiologic variables, age, CHE. • Weighting for ICU re-admission, patient location and hospital length of stay before ICU admission. • System is complex, more difficult to administer.
Accuracy • Facilitates comparison across ICU and patient population. • To characterize and stratify patient population for research purposes. • Cant be used for decision making in individual patients because the system where designed to predict outcome in a population of patients