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Shock & Sepsis by

Dr. Mohamed Shatat

Professor of Internal Medicine

{ 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 of shock are low blood pressure, rapid heart rate, signs of 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 of 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 or 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

or 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 of 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 of 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: