Shock & Sepsis by { Dr. Mohamed Shatat Professor of Internal - - PowerPoint PPT Presentation

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Shock & Sepsis

by

• Dr. Mohamed Shatat

Professor of Internal Medicine

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Shock

 Definition: is a life-threatening medical condition of

low blood perfusion to tissues resulting in cellular injury and inadequate tissue function. The typical signs

• f shock are low blood pressure, rapid heart rate, signs
• f poor end-organ perfusion (i.e., low urine output,

confusion, or loss of consciousness), and weak pulses.

1-distributive



2- cardiogenic



3- hypovolemic



4- obstructive.



However, these are not exclusive, and many patients with circulatory failure have a combination of more than one form

• f shock (multifactorial shock).

: Classification

Four types of shock are recognized:

1- Hypovolemic shock

 Blood loss: 

1- External: -Trauma



GIT bleeding



2- Internal : - Haematoma



Haemothorax



Haemoperitonium

 Plasma loss: e.g.:



Burns



Exfoliative dermatitis

 Fluids and electrolytes loss:  External: -e.g. vomiting and diarrhea  Internal: e.g. pancreatitis, Ascites.

2-Cardiogenic shock

• Arrhythmia
• Heart failure 2ry to myocardial infarction
• r cardiomyopathy.



• Acute valvular dysfunction

3-Obstructive shock

• Tension pneumothorax
• Pericardial disease (cardiac tamponade,

constrictive pericarditis)

• Obstructive valvular disease
• massive pulmonary embolism

4-Distributive shock:

Septic shock Anaphylactic shock Neurogenic shock Vasodilator drugs Acute adrenal insufficiency

Diagnosis of Shock:



• Systolic hypotension: systolic blood

pressure less than 90 mmHg



• End organ hypoperfusion: rapid

thread pulse, decreased urine output, cold bluish mottled extremities, altered mental status, ischemic bowel disease, ischemic hepatitis.



• Altered mental status, agitation,

lethargy, confusion, coma.

Treatment of shock: Goals of treatment: -Central venous pressure (CVP): 11-13

cm water

-O2 saturation above 70% - Cardiac index: 2-4 L/min/m2 - Mean arterial blood pressure: 65-90

mmHg

N.B.: To calculate the Mean arterial blood pressure ( MAP) is to first calculate the pulse pressure (subtract the D BP from the SBP) and divide that by 3, then add the DBP: MAP = 1/3 (SBP – DBP) + DBP

Neurogenic shock

 Infection: Invasion of normally sterile host

tissue by microorganisms

 Bacteraemia: Viable bacteria in blood  Systemic inflammatory response

syndrome (SIRS):The systemic inflammatory

response to a variety of severe clinical insults. The response is manifested by two or more of the following:

• Temperature >38°C or <36°C
• Heart rate >90 beats/min
• Respiratory rate >20 breaths/min or Paco2 <4.3

kPa

• White cell count >12×109/L, <4×109/L or >10%

immature forms

Terminology used in systemic inflammation and sepsis

 Sepsis: SIRS resulting from documented infection  Severe sepsis: Sepsis associated with organ dysfunction,

hypoperfusion or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria or an acute alteration in mental state

 Septic shock: Severe sepsis with hypotension (systolic BP <90 mmHg

• r a reduction of >40 mmHg from baseline) in the absence of other

causes for hypotension and despite adequate fluid resuscitation

Shock is difficult to define. The term is

used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia.

Shock

• A subset of severe sepsis (SIRS) and defined as

sepsis (SIRS) induced hypotension despite adequate fluid resuscitation along with the presence of hypoperfusion that may include, lactic acidosis, oliguria, or an acute alteration in mental status.

• Infectious or non infectious triggers 

Cytokine and inflammatory mediator cascade  cardiovascular dysfunction and microvascular injury  Hypotension and shock

Septic Shock

Sepsis is a form of severe infection (often with bacteraemia &/or their endotoxins contained within the cell wall of gram-negative bacteria or exotoxin released by gram-positive bacteria) in the presence of large areas

• f damaged tissue (e.g. following

trauma or extensive surgery)

Pathogenesis:

with prolonged/repeated episodes of hypoperfusion can trigger an exaggerated inflammatory response with systemic activation of leucocytes and release of a variety

• f potentially damaging

, local vasodilation, mediators' ' increased endothelial permeability, and activation of coagulation pathways.

These mechanisms are in play during septic shock but on a systemic scale, leading to diffuse endothelial damage which itself can further activate inflammatory reactions,vascular permeability, vasodilatation, and coagulation cascades ended by thrombosis of end-organ capillaries and end-organ damage ; with multiple organ failure (MOF).

 Arachidonic acid metabolites  Complement system.  IL-1, IL-6, TNF-alpha - Released by mast cells  Coagulation cascade (DIC) and end-organ damage.  Catecholamines -  Glucocorticoids -  Bradykinin - Contributes to vascular leak  Histamines - Released by mast cells

The following systems and mediators are activated in septic shock:

 The brain and kidneys are normally

protected from swings in blood pressure by autoregulation:

 In early sepsis - autoregulation curve shifts

rightwards (due to increase in sympathetic tone).

 In late sepsis: - vasoparesis occurs

 - autoregulation fails  "Steal phenomena" may occur (areas of

ischaemia may have their blood stolen by areas with good perfusion).

Multiple Organ Failure (MOF) in septic shock:

1-Heart

Depressed myocardial contractility due to: Myocardial oxygen supply is dependent on

diastolic blood pressure (which is decreased).

Increased circulating myocardial depressant

factor. 2-Lungs

Ventilation / perfusion mismatches -Initially

due to increased dead space

• Subsequently due to

shunt

Acidosis - tachypnoea decreased PaCO2 Nosocomial pneumonia (about 70%).

3-Kidneys

Oliguria & Renal failure (pre renal type) due

to intravascular dehydration, circulating nephrotoxins, drugs. 4-Liver

ICU jaundice Uncontrolled production of inflammatory

cytokines by the kuppfer cells (of the liver), primed by ischemia and stimulated by endotoxin (derived from the gut), leads to cholestasis and hyperbilirubinaemia.

• GUT mucosa is usually protected

from injury by autoregulation. * Hypotension and hypovolaemia leads superficial mucosal injury which leads to atrophy and translocation of bacteria into the portal circulation reaching to the liver and stimulate liver macrophages causing cytokine release and amplification of SIRS.

Splanchnic Circulation

• 5

6- CNS

Confusion / stupor / coma secondary to: Hypoperfusion injury Septic encephalopathy Metabolic encephalopathy Drugs

7- Metabolic

Hyperglycaemia due to sepsis &

catecholamines (both cause insulin resistance)

Lactic acidosis Muscular breakdown Generalized catabolic state

 Temperature increased or decreased  White cell count increased or decreased  Rigors  Sweating  Nausea and vomiting  Tachycardia  Hypotension  Tachypnoea (acute lung injury)

Signs and Symptoms of Sepsis:

 Warm pink peripheries  Confusion  Oliguria  increased Glucose  increased Lactate  increasingly negative Base excess  decreased Albumin  increased INR, increased APTT , decreased Platelets, DIC  Jaundice

 Urine: Culture and Sensitivity.  Nasal & throat swabs  Blood cultures  Sputum specimen [protected sample]  Pus / wound swabs  Serological tests  Echocardiogram [heart valves]  Dental examination  X - ray of sinuses  Abdominal ultrasound  Laparotomy  Radiolabelled White Cell Scan

Investigation of sepsis of unknown origin:

 Monitoring of: Blood pressure , Central venous pressure (CVP)

, Pulmonary artery pressure, urine output

 A patent airway must be maintained and oxygen must be

given.

 The underlying cause should be corrected  Preload and volume replacement therapy under monitoring.  Coagulopathy defects should be corrected  Metabolic disturbances (acidosis/alkalosis ) should be

corrected

 impaired Myocardial contractility should be corrected  Good coverage by potent broad spectrum antibiotic

combination

Management of a septic patient: