L10 Shock and Burns Flashcards
Cardiovascular collapse with reduced cardiac output & reduced circulating blood volume?
What does this lead to?
SHOCK = Cardiovascular collapse with reduced cardiac output & reduced circulating blood volume
Leads to:
Systemic hypotension => Hypoperfusion => Tissue hypoxia
Initially, tissue hypoxia/injury is reversible but w/ persistence tissue injury becomes irreversible (hypoxic effects)
Typical signs of Shock?
Typical signs of shock are low blood pressure, rapid heart rate
Also:
weak pulse,
low urine output,
confusion/ loss of consciousness
Causes of Hypovolemic Shock?
- Hemorrage
- Fluid Loss
Causes of Cardiogenic Shock?
- Cardiac Muscle Damage
- Arrythmias
- Mechanical Abnormalities
- Extra-Cardiac Abnormalities
Causes of Distributive Shock?
- Septic Shock (overwhelming Infection)
- Toxic Shock Syndrome (Superantigens from Strep. Pyogenes / Staph Aureus)
- Anaphylactic Shock (IgE Mediated Hypersenentivity Reaction)
- Neurogenic Shock (CNS or Spinal Injury)
What occurs during the First Stage of Shock?
- Non-progressive stage (compensatory)
What occurs during the Progressive (2nd Stage) of Shock?
Progressive stage: compensatory mechanisms overwhelmed =>Widespread tissue hypoxia
Due to persistent oxygen deficit => aerobic respiration replaced by Anaerobic glycolysis → excess production of LACTIC ACID => METABOLIC LACTIC ACIDOSIS
Lowers tissue pH => Impaired Vasomotor Repsonse
=> arteriolar dilatation & pooling of blood in the peripheral circulation
=>Decreases CO
=> Widespread tissue hypoxia
=>Vital organs begin to fail
Worsening hypoxia puts the vascular endothelial cells at risk of developing an anoxic injury
→ development of DIC –Disseminated Intravascular Coagulation.
What does hypoxia during Shock put the vascular endothelial cells at risk of developing?
anoxic injury → development of DIC –Disseminated Intravascular Coagulation.
What occurs during the Irreversible (3rd Stage) of Shock?
Irreversible stage (end organ Disfunction): Hypoxic → Cells begin to die
Widespread cell injury => lysosomal enzyme leakage => worsens shock
Reduced myocardial contractility (in part due to nitric oxide synthesis)
Coma/ Death
____________________:
Destruction of tubular epithelial cells with acute suppression of renal function.
The most common cause of acute renal failure
Causes?
Acute Tubular Necrosis (ATN):
Destruction of tubular epithelial cells with acute suppression of renal function.
Most common cause of acute renal failure
Causes:
Ischemic: As seen w/ shock
Due to inadequate renal blood flow (hypotension and shock)
Ischemia => vasoconstriction => reduced glomerular filtration rate
Nephrotoxic:
Due to:
Drugs (cisplatin, methotrexate, gentamycin)
Hemoglobin (transfusion reaction, malaria)
Myoglobin (from crush injury, myositis, muscle toxins)
Ig light chains (myeloma)
Ethylene glycol, mercury, lead, radiographic contrast agents
Greatest injury is to p_roximal convoluted tubule_s
Examples of Shock Lung?
How does it manifest?
Diffuse Alveolar Damage (DAD)
Adult Respiratory Distress Syndrome (ARDS)
Manifestation:
Rapid onset of severe, life-threatening respiratory insufficiency
Cyanosis
Severe arterial hypoxemia refractory to oxygen therapy
Severe pulmonary edema
Diffuse alveolar infiltration on x-ray
Shock Lung
Causes?
Pathophysiology/Gross?
Microscopy?
Causes: Sepsis, aspiration, diffuse pulmonary infections, mechanical trauma,; also other injury, inhaled irritants, chemical injury, radiation, amiodarone, chemotherapy, acute pancreatitis, burns or uremia
Pathophysiology: Diffuse damage to alveolar capillary walls in both lungs
Gross: Heavy, firm, red, and boggy lung
Microscopy: Congestion and hemorrhage, interstitial and intra-alveolar edema, fibrin deposition, hyaline membrane (composed of edema fluid and cellular debris) foam-like substance inhibiting gas exchange
Cardinal Findings Common to all types of shock? (5)
Clinical/Cardinal Findings Common to all types of shock
Hypotension
- Absolute: systolic BP <90mmHg
- Relative: drop in systolic BP of >40mmHg
Oliguria (Decreases in Urine Production
Altered mental status
Agitation → confusion/delirium → coma
Cool, clammy skin
Metabolic acidosis (LACTATE LEVELS!!!)
____________ Levels are an important indicator of shock
Lactate Levels are an important indicator of shock
Symptoms/Signs of Hypovolemic Shock?
Hypovolemic Shock
Symptoms:
- vomiting*
- diarrhea*
- hematemesis*
- hematochezia*
- trauma*
Signs:
- dry skin/tongue/oral mucosa*
- decreased skin turgor*
- postural hypotension*
Symptoms/Signs of Cardiogenic shock?
Cardiogenic shock
Symptoms:
- dyspnea*
- chest pain*
- palpitations*
Signs:
- murmur*
- muffled heart sounds*
- diminished peripheral pulses*
- diffuse crepitations*
Symptoms/Signs of Distributive Shock?
Distributive (Septic /Anaphylactic/ Neurogenic) Shock Manifests as
Symptoms
- chills*
- headache*
- photophobia*
- cough*
- dyspnea*
- dysuria*
- hematuria*
- abdominal pain*
- rash*
Signs:
- fever*
- tachypnoea*
- tachycardia*
- abnormal mental state*
- meningism*
__________ =Presence of bacteria within the bloodstream
Bacteremia =Presence of bacteria within the bloodstream
___________= Microorganisms (bacteria, viruses, fungi) in the blood stream
Septicemia= Microorganisms (bacteria, viruses, fungi) in the blood stream
What is Systemic Inflammatory Response Syndrome (SIRS)?
Systemic Inflammatory Response Syndrome (SIRS): clinical response to an infectious or non-infectious origin (surgical procedures, trauma, medications, and therapies)
Defined as 2 or more of the following variables:
Fever or hypothermia
Tachycardia
Increased blood pressure
Raised WCC
What is Sepsis/ How does it occur?
Sepsis: systemic response to infection and is defined as the presence of SIRS in addition to a documented or presumed infection.
Sepsis occurs when chemicals released into the bloodstream to fight the infection trigger inflammatory responses throughout the body => triggers a cascade of changes damaging organ systems, causing them to fail
What is Septic Shock?
What is its predominant cause?
Septic Shock: results from the spread/expansion of an initially localized infection (abscess, pneumonia/peritonitis) into the bloodstream (septicemia)
70% cases due to Endotoxin-producing gram-negative bacteria (endotoxin shock)
Endotoxin = Lipopolysaccharides (LPS) in walls of bacteria
4 Effects of the Cytokines and Secondary mediators in Septic Shock?
Effects of the cytokines and secondary mediators:
- Systemic vasodilation & hypotension
- Decreased myocardial contractility & decreased CO
-
Widespread endothelial injury & activation resulting in:
- Systemic leukocyte adhesion
- Pulmonary alveolar-capillary damage (DAD/ARDS)
- Activation of the coagulation cascade - Multiorgan failure and Death
3 Cardinal signs of Inflammation?
Cardinal signs of inflammation:
- Leucocyte accumulation (WBC)
- Vasodilation
- Vascular permeability
What is Disseminated Intravascular Coagulation (DIC)?
DIC is a systemic process producing both thrombosis and hemorrhage
An acquired/secondary syndrome characterized by excessive activation of coagulation
=> eventual overwhelming of anticoagulant and fibrinolytic systems
=> Tissue ischemia
What does excessive free, circulating, unopposed thrombin and plasmin as seen in DIC result in?
Excessive free, circulating, unopposed thrombin and plasmin results in:
=> Activation and consumption of platelets, coagulation factors, fibrinogen and fibrin
=> Depletion of anticoagulant proteins (protein C, protein S and antithrombin)
=> Generation of D-dimers and fibrin degradation products
Disseminated Intravascular Coagulation is often associated with ___________
DIC is often associated w/ Obstetric complications (abruption placenta, retained fetus, septic abortion)
Clinical Features of Disseminated Intravascular Coagulation (DIC)? Bloods?
Clinical Features of Disseminated Intravascular Coagulation (DIC)?
Bleeding, Thrombosis or both
BLOODS:
↓Platelets
↓Fibrinogen
↑Prothrombin time (PT)
↑Activated partial thromboplastin time (PTT)
↑D-dimers
Classification of Burns?
1st degree: s_uperficial epithelium_
erythematous w/pain, edema, skin peeling; does not scar
2nd degree: full-thickness epidermis and superficial dermis
skin appendages are spared; blistering, painful; usually do not scar
3rd degree: involves all skin layers, including full-thickness dermis and skin appendages
no pain due to nerve injury; appears white; severe scarring
4th degree: complete destruction of skin, subcutaneous tissue and possibly bone
Guidelines for Documenting Thermal Injury?
Documenting Thermal Injury:
Rule of 9’s (Adults)
Rule of 5’s (Infants)
Mechanism of Death in Thermal Injuries?
Delayed mechanism of death due to thermal injury
–Delayed hypovolemic shock with renal failure
–ARDS
–Infection (pneumonia, sepsis/septic shock, cutaneous)
–Pulmonary embolus due to immobilization
Immediate mechanism of death due to thermal injury
–Neurogenic shock secondary to severe pain
–Hypovolemic shock and acute renal failure due to loss of fluid from skin
–Toxic gas inhalation –Carbon monoxide/CO (most common), cyanide, acrolein, nitrogen dioxide, hydrochloric acid - Often see soot in nose/mouth
