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.
Classification : Four types of shock are recognized: 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).
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/m 2 - 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
Terminology used in systemic sepsis inflammation and 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 × 10 9 /L, <4 × 10 9 /L or >10% immature forms
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 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.
Septic 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
Pathogenesis: 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)
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 ' mediators' , local vasodilation, 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).
The following systems and mediators are activated in septic shock: 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
Multiple Organ Failure (MOF) 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).
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.
5 - Splanchnic Circulation • 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.
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
Signs and Symptoms of Sepsis: Temperature increased or decreased White cell count increased or decreased Rigors Sweating Nausea and vomiting Tachycardia Hypotension Tachypnoea (acute lung injury)
Warm pink peripheries Confusion Oliguria increased Glucose increased Lactate increasingly negative Base excess decreased Albumin increased INR, increased APTT , decreased Platelets, DIC Jaundice
Investigation of sepsis of unknown origin: 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
Management of a septic patient: 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
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