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

3. • Etiologies
- Septic shock (most common)
- Anaphylactic shock
- Neurogenic shock

4. Septic Shock

5. • Systemic Inflammatory Response Syndrome
(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

6. • 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

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

8. Source
Endogenous-
Skin
Urinary
Respiratory
Bowel
Exogenous-
surgical intervention
Drapes
Imaging machines
staff
• Bacteria: gram negative nearly 2/3rd, gram
positive 1/3rd
• E.coli is commonest

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

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

15. Treatment
• Septic shock is a medical emergency that requires
prompt and sufficient resuscitation
• Aims
• To improve hemodynamic state
• Restore tissues perfusion
• Eliminate toxin from body

16. 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)

17. • 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

18. 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

19. 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

20. • 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

21. 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

22. 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)

23. 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)

24. 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)

25. 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

26. 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)

27. 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

28. 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

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

30. Prevention
• Early recognition
• Prompt treatment of infection
• Meticulous surgical treatment
• Pre op antibiotics
• Aseptic technique

31. 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)

32. • 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)

33. Large quantities of inflammatory
mediators released
rapid systemic vasodilation and
vascular permeability
hypotension and extensive
tissue edema
fluid in the lungs and
constriction of airways
shortness of breath and lethal
suffocation
cardiovascular collapse and loss
of consciousness

35. Management
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

36. Management
Steroids IV hydrocortisone 200mg STAT
(up to 500mg)
Anti-
histamines
IV Piriton 10mg STAT
Fluid normal saline bolus 1-2L
can add inotropes (norad)

37. 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)

38. 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

39. Neurogenic Shock

40. • 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.

41. • 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.

42. 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.

45. • Most common causes is
spinal injury above T6.
• Most rare form of shock

46. sign
• Hypothermia, hypotension, decreased CO,
bradycardia, flaccid paralysis

47. Management
• Main aim is to prevent complication and
maintain perfusion

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

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

50. • 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 transvenous
pacing temporarily