Septic shock.pptx

A quick review of sepsis and septic shock

1. Define and classify shock. Discuss the current concepts in the pathophysiology and management of endotoxic shock Dr Eretare C. Odjugo

2. Introduction Definition of terms Classification of shock Bacteriology Aetiology of septic shock Pathophysiology of septic shock Clinical features of septic shock Evaluation Outline

3. Treatment of septic shock Prognosis Prevention Conclusion References Outline

4. Infections are a continuous challenge in medical practice especially in resource limited areas The extent of the infection is affected by the persons co-morbidities, virulence of the infective organism, hosts immune response and other factors. Introduction

5. Infection: An infection is the invasion of an organism's body tissues by disease-causing agents, their multiplication, and the reaction of host tissues to the infectious agents and the toxins they produce. Shock: A state of cellular and tissue hypoxia due to either reduced oxygen delivery, increased consumption, inadequate oxygen utilisation or a combination of these processes. Terminology

6. Sepsis is defined as life-threatening organ dysfunction due to dysregulated host response to infection. Organ dysfunction is defined as an acute change in total Sequential Organ Failure Assessment (SOFA) score of 2 points or greater secondary to the infection cause. Terminology

7. Systemic Inflammatory Response Syndrome (SIRS): Adult: Manifestations of SIRS include, but are not limited to: Body temperature <36 °C or >38 °C Heart rate >90 beats per minute Tachypnea (high respiratory rate), with >20 breaths per minute; or, an arterial PaCO 2 less than 4.3 kPa (32 mmHg) White blood cell count <4 x 10 9 cells/L or >12 x 10 9 cells/L; or the presence of >10% immature neutrophils (band forms). Band forms >3% is called bandemia or a "left-shift.” Terminology

8. In children Heart rate >2 SD above normal for age in the absence of stimuli such as pain and drug administration, or unexplained persistent elevation for >30 minutes to 4 hours. Body temperature obtained orally, rectally, <36 °C or >38.5 °C. Respiratory rate >2 SD above normal for age or the requirement for mechanical ventilation not related to neuromuscular disease or the administration of anesthesia . White blood cell count elevated or depressed for age not related to chemotherapy, or >10% bands plus other immature forms. Terminology

9. Septic shock: Septic shock is defined by persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mm Hg or higher and a serum lactate level greater than 2 mmol /L (18 mg/ dL ) despite adequate volume resuscitation Terminology

10. Aetiology

11. Hypovolaemic Distributive Obstructive Cardiogenic Classification of shock

12. From loss of blood volume or plasma Seen in major bleeding, trauma and burns Characterised by  tachycardia, cool clammy extremities, hypotension, dry skin and mucous membranes, and poor turgor. Hypovolaemic shock

13. Caused by an extrinsic or intrinsic impedance to circulation Pulmonary embolism Cardiac tamponade Obstructive shock

14. Caused by primary myocardial dysfunction despite normal intravascular volume. Normal cardiac output not maintained Characterised by cool clammy extremities, poor capillary refill, tachycardia, a narrow pulse pressure, and low urine output. Cardiogenic shock

15. Excessive vasodilation Impaired blood flow Reduced vasomotor resistance or increased capacitance It’s characterised by high cardiac output, hypotension, a large pulse pressure, a low diastolic pressure, and warm extremities with good capillary refill Distributive shock

16. Septic shock Anaphylactic shock Neurogenic shock Distributive shock

17. Bacteriology

18.  The normal physiologic response to localized infection includes activation of host defence mechanisms that result in the influx of activated neutrophils and monocytes, release of inflammatory mediators, local vasodilation, increased endothelial permeability, and activation of coagulation pathways. Pathophysiology

19. These responses are brought about by the interaction between the host responses and the infective agent In sepsis, there is an exaggeration of these host responses.  leading to diffuse endothelial disruption, vascular permeability, vasodilation, and thrombosis of end-organ capillaries Pathophysiology

20. In Gram negative bacteria, the Lipid A moiety of the lipopolysaccharide molecule leads to cytokine induction via the lipoteichoic acid. For Gram positive bacteria they may also bring about production of cytokines by secretion of super-antigens. Pathophysiology

21. Sepsis induced ARDS

22. Septic encephalopathy

23. Sepsis induced coagulopathy

24. This is the system responsible for the progression too septic shock The main components are the vascular response Arteriolar vasodilatation Increased capacitance And Myocardial activity Chronotrophic Ionotrophic Circulatory dysfunction in sepsis

25. Circulatory dysfunction in sepsis

26. The hypotension is initially compensated by an increased cardiac output but over time this also fails. Myocardial suppression is brought about by Beta adrenergic receptor downregulation Nitric oxide Pulmonary hypertension Circulatory dysfunction in sepsis

27. There is also a challenge with oxygen utilisation at tissues Mitochondrial dysfunction which leads to anaerobic respiration with resultant lactate production Diminished offloading at the tissues There is loss of the normal auto-regulatory function of the autonomic nervous system and thus vital organs (brain and heart) which normally receive preference do not Circulatory dysfunction in sepsis

28. Major site of bacteria Hypoperfusion leads to failure of gut mucosal barrier Translocation of bacteria and endotoxin Propagation of sepsis Sepsis also causes ileus GI dysfunction

29. Hypoxic hypoxia: Decrease oxygen supply Histotoxic hypoxia Apoptosis Coagulopathy Immunosuppression Organ dysfunction in sepsis

30. Clinical features Temperature abnormalities (fever or hypothermia) Elevated pulse rate with warm or cold extremities Altered mental status Dyspnoea Malaise and lethargy Localizing symptoms referable to organ systems may provide useful clues to the etiology of sepsis.

31. Full blood count ( Leukocytosis with left shift) Blood culture (not always positive) Serum electrolytes, urea and creatinine Liver function test including total protein and albumin Clotting profile Serum lactate (assessment of perfusion) Blood glucose monitoring (predictor of mortality) Urinalysis and urine culture Evaluation

32. Specialised investigations to confirm source of infection CT scans/MRIs of various regions Plain radiographs Ultrasound scans Evaluation

33. SOFA scoring

34. Based on the current literature, include the following: Early recognition Source control Early and adequate antibiotic therapy Early hemodynamic resuscitation and continued support Proper ventilator management with low tidal volume in patients with acute respiratory distress syndrome (ARDS) Management principles

35. Resuscitation Venous access Fluids ( Iso -osmotic crystalloids) 20 -40ml/kg over the first hour. Respiratory and ventilator support Urethral catheterisation Correction of anaemia Circulatory support Antimicrobial therapy Source control Temperature control Nutritional support Treatment

36. Haemodynamic support Aim for MAP >65mmHg Fluid Crystalloids Colloids (4% Albumin) Must be monitored for overload Vasopressors Norepinephrine Epinephrine Dopamine Phenylephrine Ionotropes Dopexamine Dopamine Dobutamine

37. Crystalloids ( 30ml/kg over 1 st hour) Normal saline Ringers lactate (not preferred due to interaction with lactate assays) Colloids 4% Albumin: as effective as normal saline at less volume more expensive Not readily available Fluids

38. Vasopressor First line Dopamine 5 – 10mcg/kg/min Tachyarhythmias May be increased to 20mcg/kg/min Norepinephrine 5 – 20mcg/min Not weight dependent Predictable response Shorter hospital stay with less mortality Alpha agonist thus potent vasoconstrictors 0.2 – 1.5mcg/kg/min

39. Second line Synthetic Human Angiotensin 2 (25ml/kg) improves response when used with 1 st line Epinephrine potent inotrope Causes myocardial and splanchnic ischemia Phenylephrine Selective potent vasopressor Causes reduce myocardial contractility and rate ADH Reserved for salvage therapy thus should not be used alone More potent when acting with nor epinephrine Vasopressors

40. Dobutamine : Recommended only when there is hypoperfusion despite fluid targets and MAP targets have been met. Given at 20mcg/kg/min Dopamine Inotropes

41. Initial therapy should be combination broad spectrum for suspected causative agents. Daily evaluation for effectiveness De-escalation to monotherapy later. An aminoglycoside ( e.g gentamicin) should be used for “antibiotic-experienced” patients. Cephamycins ( Cefotetan ) and Carbapenems are preferred for ESBL producing bacteria ( Kliebsiella and E. coli ) Immunocompromised patients should receive carbapenems or 4 th gen Cephalosporins ) Anti-microbial therapy

42. Intra-abdominal infection Antibacterials Metronidazole – Meropenem Imipenem – Cilastin Levofloxacin or Ciprofloxacin Piperacilin or Tazobactam Ceftazidim or Cefepime Antifungals Caspofungin Micafungin Fluconazole in C. albicans Antimicrobial therapy

43. The American College of Critical Care Medicine recommends Avoidance of ACTH suppression test Use of Hydrocortisone as first line Use in patients with suspected adrenal insufficiency Do not use dexamethasone therapy for septic shock or ARDS Treatment of septic shock 200 mg/day in 4 divided doses or 100mg bolus then 10mg/hour. If given for >14 days, it should be tapered off Corticosteroid use

44. Target is between 80 - 110 mg/dl (4.4 – 6.1mmol/l) Hyperglycaemia confers a 10% rise in mortality. Glycaemic control

45. In absence of bleeding Unfractionated heparin LMW heparin can be used. Dalteparin used in severe renal dysfunction CrCl <30ml/min Compression stockings and intermittent compression devices may be used. DVT prophylaxis

46. Treat underlying cause Transfuse with plasma or platelet concentrate Don’t treat prophylactically DIC

47. Treatment of ARDS Intubation and mechanical ventilation 5 – 8 l/min Use of PEEP to prevent lung injury Extra-corporeal Membrane Oxygenation

48. Ubi pus, ibi evacua . Antibiotic therapy alone may not suffice for some causes of septic shock The source of infection should be controlled if not all therapies will eventually fail. Abscesses should be drained either percutaneously or an open drainage. Necrotic tissue should be debrided. Surgery

49. Renal dysfunction (AKI) may require dialysis For hepatic dysfunction, therapy is mostly supportive Other modalities

50. In the past decades, recovery and survival from septic shock is on the rise. Some countries have as high as 50% (Australia) while others 30% most developed countries. In our setting, septic shock is almost invariably fatal due to challenges with finance, resources and personnel. Prognosis

51. Basic measures to prevent nosocomial infections include the following Shortening the hospital stay Removing indwelling catheters as early as possible Avoiding unnecessary invasive procedures Using aseptic techniques Prophylactic antibiotics for GI surgeries are also of benefit Prevention

52. Sepsis and septic shock are major contributors to surgical morbidity and mortality Early recognition and intervention are key to improving outcomes. The best form of treatment still remains prevention by eliminating risk factors as much as possible Conclusion

53. https://jamanetwork.com/journals/jama/article-abstract/2598892 accessed last 3/8/20. https://emedicine.medscape.com/article/168402-overview#a1 accessed on 4/8/20 Surviving Sepsis: Guidelines for management of sepsis and septic shock 2012 https://www.uptodate.com/contents/definition-classification-etiology-and-pathophysiology-of-shock-in-adults accessed 03/08/20 Images obtained from https://www.bing.com and are the properties of the respective copyright holders References

54. Thank you