Distributive shock

Simple medical student presentation about distributive shock, type and pathophysiology of each septic shock, anaphylactic shock, neurogenic shock
including management, prognosis and disposition of patient..
brief info of type of inotropes and when to start.

1. Distributive shock Inadequate perfusion of tissues through misdistribution of blood flow Cardiac pump and blood volume are normal but blood is not reaching the tissues

2. Etiologies Septic shock (most common) Anaphylactic shock Neurogenic shock

3. Septic Shock

4. S ystemic I nflammatory R esponse S yndrome (SIRS) - a syndrome characterized by presence of two or more of the following clinical criteria Temperature >38, <36 HR>90 Respiratory rate >20b/m , PaCO2 <32 mm of hg WBC <4, >12

5. Sepsis : SIRS with a clearly established focus of infection Septicemia : is a condition when there is prolonged presence of bacteria in the blood accompanied by systemic reaction Septic Shock : refers to severe sepsis which is not responsive to intravenous fluid infusion for resuscitation and requires inotropic or vasopressor agent to maintain SBP

6. Multiple organ dysfunction (MODS) - altered function of more than one organ system in an actually ill patient requiring medical intervention homeostasis.

7. Sou r ce Endo g enou s - Skin Urinary Respiratory Bowel Exogenous- surgical intervention Drapes Imaging machines staff Bacteria: gram negative nearly 2/3 rd , gram positive 1/3 rd E.coli is commonest

8. Risk factors Age <10yr,<70yr Malnutrition Anemia Primary disease, malignancies, DM, CLD, CRF Necrotic issues Hematoma Poor surgical technique Catherization Prolong hospitalization Major surgeries

9. Diagnosis Blood/urine/sputum culture CBC BUN and Creatinine PT and PTT ECG Serum lactate dehydrogenase level Urinalysis ABG

10. T r e a tme n t Septic shock is a medical emergency that requires prompt and sufficient resuscitation Aims To improve hemodynamic s tate Restore tissues perfusion Eliminate toxin from body

11. Preshock or compensated shock Shock or decompensated shock Irreversible shock Reversible with interventions Perfusion and oxygen delivery are relatively normal despite the insult. No overt signs of organ dysfunction ± mild laboratory signs of organ dysfunction (e.g., mildly elevated creatinine, troponin, or lactate) Reversible with interventions Perfusion and oxygen delivery are abnormal. Overt signs of organ dysfunction are present. Permanent organ dysfunction Progression to multisystem organ failure 1. Recognize signs of shock (0-5min)

12. Shock index (SI): heart rate (HR; beats/min) / SBP (mm Hg) SI of 0.5–0.7: Normal SI > 0.9: indicates critical bleeding and transfusion requirement qSOFA (quick Sequential (sepsis-related) Organ Failure Assessments) score: Presence of 2 of the following 3 criteria indicates a worse outcome: SBP < 100 mm Hg Respiratory rate > 22/min Altered mental status

13. Compensated shock: Tachycardia : to compensate for CO Tachypnea : to compensate for metabolic acidosis Hypotension : systolic blood pressure (SBP) < 90 mm Hg, mean arterial pressure (MAP) < 65 mm Hg in normotensive individuals or higher in patients with uncontrolled hypertension Decreased capillary refill Cold and clammy skin

14. Decompensated shock: signs of organ failure Confusion/altered mental status: central nervous system (CNS) hypoperfusion Oliguria (< 0.5 mL/kg/hr) in a patient without a history of renal disease: renal hypoperfusion

15. Bilateral rales : pulmonary edema due to left heart failure or acute respiratory distress syndrome Warm distal extremities, capillary refill in < 2 seconds, and bounding pulses : high CO Cool extremities, delayed capillary refill, weak pulses, and a narrow pulse pressure: low CO Reduced JVP (< 8 cm) : hypovolemic shock

16. 2. Assess ABCs (0-5 min) Provide 100% oxygen at high flow rate (15L) Goal: arterial oxygen saturation of 92%–95% Indications for endotracheal intubation and mechanical ventilatory support: Significant hypoxemia (PaO2 < 60 mm Hg or oxygen saturation < 90%) Hypoventilation (rising partial pressure of carbon dioxide (pCO2)) Significantly altered level of consciousness Inability to protect airways with risk of aspiration Persistent metabolic acidosis with pH < 7.20

17. 3. Establish IV access and place on monitor 2 large-bore peripheral IVs (PIVs) preferred: if difficult IV, place IO access per PALS guidelines; 1 PIV may be sufficient unless vasoactive drugs needed (see Step No. 6, below) Consider labs on IV placement: blood gas, lactate, glucose, ionized calcium, CBC, cultures (glucose check through finger stick preferred for rapid result)

18. 4. Fluid and electrolyte resuscitation (5-15min) Push 20 mL/kg fluid (isotonic crystalloid) IV/IO over 5- 20min or faster if needed (reassess for signs of shock ) Repeat 20 mL/kg bolus push of fluid (up to 60 mL/kg) until clinical symptoms improve or patient develops respiratory distress/rales/ hepatomegaly May continue to require additional fluid above 60 mL/kg (fluid refractory) Fluid needs may approach 200 mL/kg in warm septic shock (warm extremities, flash capillary refill)

19. Correct hypoglycemia: Glucose dosage: 0.5-1 g/kg IV/IO (max that can be administered through a peripheral vein is 25% dextrose in water) (see alternative treatments immediately below) Correct hypocalcemia for low ionized calcium: Calcium gluconate 100 mg/kg IV/IO (max 2g) PRN Calcium chloride 20 mg/kg IV/IO PRN ( Note : central line administration preferred over 60min in nonarrest situation)

20. 5. Infection control (5-60min) Immediate considerations: Administer antibiotics immediately after cultures obtained (blood, urine, +/- CSF/ sputum) Do not delay antibiotics because of delay in obtaining cultures; initial antibiotics should be given within 1h

21. 6. Fluid-refractory shock (persisting after 60 mL/kg fluid) (15-60 min) Central line placement and arterial monitoring if not already established; vasopressors should not be delayed for line placements Warm shock (warm extremities, flash capillary refill): 1st line: Norepinephrine 0.1- 2 mcg/kg/min IV/IO infusion , titrate 2nd line: Vasopressin 0.01U-0.07U/min, fixed dose Cold shock (cool extremities, delayed capillary refill): Epinephrine 0.1-1 mcg/kg/min IV/IO infusion , titrate Normotensive shock (impaired perfusion but normal blood pressure): Dopamine 2-20 mcg/kg/min IV/IO, titrate if continued poor perfusion, consider dobutamine infusion 2-20 mcg/kg/min IV/IO, titrate (may cause hypotension, tachycardia)

22. 7. Shock persists following vasopressor initiation (60 min) SvO2 < 70% (cold shock): Transfuse Hgb >10 g/dL; optimize arterial saturation through oxygen therapy, ventilation; epinephrine 0.1-1 mcg/kg/min IV/IO infusion, titrate to desired effect SvO2 < 70% (normal BP but impaired perfusion): Transfuse Hgb >10 g/dL; optimize arterial saturation through oxygen therapy, ventilation; consider addition of milrinone 0.25-0.75 mcg/kg/min IV/IO (titrate to desired effect) or nitroprusside 0.3-5 mcg/kg/min IV/IO (titrate to desired effect) SvO2 >70% (warm shock): Norepinephrine 0.1-2 mcg/kg/min IV/IO infusion, titrate to desired effect; consider vasopressin 0.2-2 mU/kg/min infusion, titrate to desired effect

23. 8. Fluid refractory and vasopressor-dependent shock (60 min) Consider adrenal insufficiency Hydrocortisone 2 mg/kg (max 100mg) IV/IO bolus; obtain baseline cortisol level; if unsure, consider ACTH stimulation test; duration depends on response, laboratory evaluation 9. Continued shock -> refer Consider cardiac output measurement to direct further therapy Consider extracorporeal membrane oxygenation (ECMO) 10. Supplemental therapies

24. Prognosis Poor prognostic factor Advanced age Immunosuppression Infection Need for inotropes for >24hrs Availability and mode of treatment

25. P r e v e n tion Early recognition Prompt treatment of infection Meticulous surgical treatment Pre op antibiotics Aseptic technique

26. Anaphylactic shock A type of distributive shock that result from wide spread systemic allergic reaction to an antigen Anaphylaxis: reaction sudden life threatening because the process immunologic of allergen- antibody reaction rapid onset, biphasic course (resolve and return in 1-3h with same severity)

27. Sensitization stage Asymptomatic; 1st antigen exposure Allergen is recognized by antigen-presenting cells → presented to naive T cells → T cells differentiate into Th2 cells Th2 cells release interleukins (IL-4, IL-5, IL-13) → switches B cells to increase IgE antibody production → IgE antibodies bind to mast cells and basophils (via FcεRI receptors) Reaction / effector stage Early (minutes) Late (4-12 hours, peak 6-9 hours)

28. Mana g eme n t Airway head neutral position (slight extended) oxygen supplement Limit exposure Stop drug, remove source Drugs IM Adrenaline /Epinephrine 0.3 -0.5mg, every 5 min, repeated 3 times ) consider IV Glucagon 1mg every 5min if not respond

29. Mana g eme n t Steroids IV hydrocortisone 200mg STAT (up to 500mg) Anti-histamines IV Piriton 10mg STAT Fluid normal saline bolus 1-2L can add inotropes (norad)

30. Complementary treatment Bronchial spasm B-2 agonist: ventolin nebulizer IV MgSO4 2.47g in 20cc NS over 20min Aminophylline 7mg with 10- 20 ml of 0.9& NaCl followed 9mg/kg/24 hours( divided into 3 dose) seizures- diazepam, phenobarbital, midazolam bradycardia- IV Atropine 0.5-1mg (max 3mg)

31. DISPOSITION Unstable/ refractory patient -> ICU Moderate to severe sx -> admit for observation Mild sx -> observe in ED, allow discharge after 4 hours if sx free 3 days antihistamines & prednisolone TCA stat if symptoms not improving/worsening Epinephrine autoinjector Medic-alert bracelet

32. Neurogenic Shock

33. Neurogenic shock is a medical condition which occurs as a result of disturbance in the sympathetic outflow causing loss of vagal tone Experiences neurogenic shock after injury to the spinal cord and when there is disruption in the blood circulation throughout the body due to injury/ illness.

34. It is a serious and life-threatening condition, which requires prompt medical attention without any delay. If the treatment is delayed, then it causes irreversible tissue damage and even death. Out of the different types of the shocks, neurogenic shock is the most difficult to manage, mainly because of the irreversible damage to the tissues. Neurogenic shock mainly affects the spinal cord; the function of which is transmitting neural signals from the brain to the entire body and back.

35. Different! Spinal shock: Temporary loss of spinal reflex activity below a total or near total spinal cord injury Loss of sympathetic tone results in warm & dry skin, no systemic instability Shock usually lasts from 1 to 3 weeks NOT TRUE SHOCK Its either spinal shock only or neurogenic shock associated with spinal shock. No neurologic shock only.

36. Most common causes is spinal injury above T 6 . Most rare form of shock

37. sign Hypothermia, hypotension, decreased CO, bradycardia, flaccid paralysis

38. Mana g eme n t Main aim is to prevent complication and maintain perfusion

39. Hypovolemic- with fluid Observe for fluid overload Vasopressors Hypothermia - thermal blanket Treat hypoxia Maintain ventilator support

40. Observe for bradycardia- major Dysarrthemia Observe for DVT- Venous pooling in extremities make patients high risk Use prevention modalities

41. Alpha agonist to augment tone if perfusion still in adequate Dopamine(>10 mcg/kg per min) Ephedrie(12.5-25mg iv every 3-4 hour) Treat bradycardia with atropine 0.5-1mg doses to maximum 3 mg May need transcutaneous or tran svenous pacing temporarily