Shock & Sepsis - Minia new... · Sepsis: SIRS resulting from documented infection Severe sepsis:...
Transcript of Shock & Sepsis - Minia new... · Sepsis: SIRS resulting from documented infection Severe sepsis:...
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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 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.
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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:
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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.
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2-Cardiogenic shock -Arrhythmia
-Heart failure 2ry to myocardial infarction or cardiomyopathy.
-Acute valvular dysfunction
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3-Obstructive shock -Tension pneumothorax
- Pericardial disease (cardiac tamponade, constrictive pericarditis)
- Obstructive valvular disease
- massive pulmonary embolism
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4-Distributive shock:
Septic shock
Anaphylactic shock
Neurogenic shock
Vasodilator drugs
Acute adrenal insufficiency
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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.
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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
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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
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Neurogenic shock
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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
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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
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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
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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
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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:
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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.
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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).
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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:
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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:
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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%).
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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.
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• 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
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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
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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:
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Warm pink peripheries
Confusion
Oliguria
increased Glucose
increased Lactate
increasingly negative Base excess
decreased Albumin
increased INR, increased APTT , decreased Platelets, DIC
Jaundice
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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:
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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:
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