Renal Replacement Therapy

Renal Replacement Therapy
Trauma Conference
By:Amanda Wheeler, MD

Principles
4 Main Modalities in ICU
* HD
* PD
* CVVH
* CVVHD

Definition of Terms
* SCUF- Slow Continuous Ultrafiltration
* CAVH- Continuous Arteriovenous Hemofiltration
* CAVH-D- Continuous Arteriovenous Hemofiltration with Dialysis
* CVVH- Continuous Venovenous Hemofiltration
* CVVH-D- Continuous Venovenous Hemofiltration with Dialysis

Indications for Continuous Renal Replacement Therapy
* Volume Overload
* Electrolyte Imbalance
* Uremia
* Acid-Base Disturbances
* Drugs

Hemodialysis vs Hemofiltration Membrane
The hemofiltration membrane consists of relatively straight channels of ever-increasing diameter that offer little resistance to fluid flow.
Hemodialysis membranes contain long, tortuous inter-connecting channels that result in high resistance to fluid flow.
Hemodialysis allows the removal of water and solutes by diffusion across a concentration gradient.

Hemodialysis
* maximum solute clearance
* best tx for severe hyper-K+
* ready availability
* limited anti-coagulation time
* bedside vascular access
* hemodynamic instability
* hypoxemia
* rapid fluid + solute shifts
* complex equipment
* specialized personnel

advantages
disadvantages

Peritoneal Dialysis
* simple to set up + perform
* easy to use
* hemodynamic stability
* no anti-coagulation
* bedside peritoneal access
* unreliable ultrafiltration
* slow fluid + solute removal
* drainage failure, leakage
* catheter obstruction
* respiratory compromise
* hyperglycemia
* peritonitis

advantages
disadvantages

CVVHD vs CVVH
CVVH
* 1. near-complete control of the rate of fluid removal (i.e. the ultrafiltration rate)
* 2. precision and stability
* 3. electrolytes or any formed element of the circulation, including platelets or red or white blood cells, can be removed or added independent of changes in the volume of total body water

CVVH
* easy to use in ICU
* rapid electrolyte correction
* excellent solute clearances
* rapid acid/base correction
* controllable fluid balance
* tolerated by unstable patients
* early use of TPN
* bedside vascular access routine
* systemic anticoagulation *
* citrate anticoagulation new
* frequent filter clotting
* hypotension

advantages
disadvantages

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Bacteria Pathogenicity Ability to Cause Infection

Bacteria Pathogenicity Ability to Cause Infection

Infectious Diseases
* Encounter-bug meets host (reservoir)
* Bug adheres to host
* Entry-bug enters host
* Multiplication- bug multiplies in host
* Damage to host
* Outcome- bug or host wins or
* Coexist- chronic infection

Reservoir
* Exposure to microbe
Virulence Factors
Adherence
* Prevent infection
* Influenza changes adhesions over time
* Neisseria gonorrhoeae -variety of adhesions

Portals of Entry
* Mucous membranes
* Conjunctiva
* Skin
* Bugs have preferred portal
* C. tetani spores in soil --- anaerobic wound

Inoculum

* Number of microbes-dose
* Greater dose, more chance infection will occur
* ID50 or LD50 expresses virulence

Invasins
* Adherence of microbe to surface
* Activates factors that let microbe in-penetration
* Microbes produce invasins (proteins)
* Endocytosis
* Requires multiplication
* Compete with normal flora for space & nutrients
* Overcome local host defenses
* Avoid IgA

Multiplication
* Need Fe to multiply
Avoid Phagocytosis
* Components of cell wall –virulence
Surviving Within Phagocyte

Tuberculosis
* Ancient disease
* 1/3 of world population infected
* 8 million develop active TB each year
* 2 million die each year
* AIDs increases activation of latent TB
* Dependent upon virulence of strain & host resistance
* Produces cell mediated immunity which prevents active disease in many people
* Multi drug resistance has developed

S & S of Pulmonary TB
* Chronic disease
* Progressive weight loss
* Night sweats
* Chronic cough
* Hemoptysis
Mycobacterium tuberculosis
* Acid fast bacillus (AFB)
* Resistant to drying
* Aerobic, slow growth
* Airborne transmission
* Inhale airborne droplets
* Ingested by alveolar macrophages
* Multiply in macrophages even with ongoing immune response

TB Response
* Host immune response-delayed type hypersensitivity reaction
* Tissue damage DT Inflammatory response
TB Conversion
* TST skin reaction is positive
* Occurs within 24 – 48 hours after exposure to TB antigens
* Purified protein derivative of bacillus
* Cell mediated immunity
* Sensitized T cells react with proteins
QuantiferonGold
* Blood test
* Detects interferon gamma

How to Confirm Diagnosis
* Sputum cultures for AFB smear & culture
* Chest xray
Pathogenesis
* LTBI (latent TB infection)
Active Disease

* Low resistance

TB Outcomes
* Primary infection- positive skin test
* 10% progressive primary infection-not controlled
Secondary or Reactivation Infection
* Reinfection-2nd exposure or
* Bacteria escape immune system-reactivation
* Activated macrophages release cytokines
* Delayed hypersensitivity reaction

Prevention of Transmission
* Negative pressure rooms
* Respirator masks-fit tested
* Admit staff aware of symptoms of TB
* Yearly TST of staff
* Conversions treated with 6-9 months of INH

Treatment
* INH for LTBI or TB conversion
* TB disease-active TB
* 9- 12 months of treatment
Resistant TB
* MDR TB
* XDR TB
* DT improper treatment

BCG
* Live culture of M. bovis
Latent vs Active
* Latent TB
* Active TB
Leprosy
* Hanson’s disease- discovered in 1873
* Seen in tropics and underserved countries
* U.S.-150 new cases per year
* Infection of nervous system
* Infects the peripheral nerves within skin
* 2 forms of disease dependent upon immune response

M. leprae
* Tuberculoid form
Lepromatous Form
* Weak immune response & microbe spreads
* Skin & nerve cells infected
* Shed large #s in nasal secretions and oozing sores-more infectious
Invasion via Enzymes
Kinases
Enzymes
Invasion via Toxins
Exotoxins
A-B Toxins
Superantigens
Naming of Exotoxins
Endotoxin
S & S
Shock
Staphylococci
S. aureus
Successful Pathogen
Biofilm
Capsule
Skin Infections
Invasion via Toxins
Toxic shock syndrome
S. aureus Intoxication
Treatment
CA-MRSA
Outbreaks in Community
PVL Gene
Preventing Transmission
Clostridium botulinum
Neurotoxin
Botulism-Foodborne Disease
Toxin
Clostridium tetani
Neurotoxin
Lockjaw
Clostridium difficile
Epidemiology
Range of Disease
Pathogenesis of CDI
New Issues
Treatment
Transmission
Environment

* Clean and disinfect surfaces in close proximity of the patient
* Patient care equipment.
* Use bleach for C. difficile
* Privacy drapes

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Microbial Interactions with Humans

Microbial Interactions with Humans

Types of Interactions: Symbiosis
* Symbiotic Relationships

Overview of Human-Microbial Interactions
* Pathogens
* Pathogenicity
* Virulence
* Opportunistic Pathogen

Infection Versus Disease
* Infection
* Disease

Opportunistic Pathogens
* Don’t normally cause disease, but may under some circumstances
* 3 circumstances for gaining control/disease

Types of Interactions:
Normal Flora
* Normal Flora
* Factors that influence normal flora

Normal Flora
* Hundreds of different niches associated with human
* Some normal flora are pathogenic
* Resident versus transient flora
* Considered part of the first line of defense!
* Microbial antagonism
* Competitive exclusion

Portals of Entry
* Skin
* Mucous membranes

Preferred Portal
* Many microorganisms have to enter in a specific way and in a certain place to cause disease.
* Skin Portal

Skin
* Epidermis and Keratin
* Hair often deters microbial contact with skin
* Dermis and subcutaneous tissue
* Apocrine and sebaceous glands
* Eccrine glands (sweat)

Skin as a Barrier
Mucous Membranes
* Found in mouth, pharynx, esophagus, GI, respiratory, and urinary tracts
* Epithelial cells coated with protective glycoprotein layer (mucous)
* Less protection than skin
* Cilia and mucous produced by goblet cells

Mucous Membranes
* Respiratory tract Portal
* Respiratory Normal Flora
* Respiratory Barrier Mechanisms
* Gastrointestinal tract portal
* GI Normal Flora

Gastrointestinal Tract
* Large intestine
* GI Barrier
* Genitourinary tract Portal
* Genitourinary Tract Normal Flora
* Genitourinary Tract Barrier

LD50 and ID50
* LD50: Number of microbes in a dose that kill 50% of the organisms infected in a sample
* ID50: Number of microbes in a dose that causes disease in 50% of the organisms infected
* The higher the virulence the lower the ID50 or LD50

Microbial Virulence
Microbe Versus Host
* To cause disease a microbe must…
* Why it is difficult for microbes…
o Skin, antimicrobial sweat
Microorganisms and Mechanisms of Pathogenesis

Line of Defense
* First line: Skin and mucous membranes, normal flora
* Second line: phagocytes, inflammation, fever and antimicrobial substances
* Third line: (specific response) special lymphocytes (B and T cells) and antibodies

Step One: Adherence
* Specific adherence
* Pathogens have attachment structures
* Pathogens have attachment structures

Step 2: Invasion/Colonization
* Increase in numbers beyond the point of attachment.
* Three goals

Step 2: Invasion/Colonization
* Localized versus Systematic infections
* Bacteremia, viremia, toxemia
* Septicemia

Step 3: Cause Damage
* Virulence
* Three Ways to cause damage

Virulence Factors
* Usually help organism colonize and grow
* Coagulase
* Siderophores
* Collagenase
* Protease

Another Way to Classify Exotoxins
* Descriptive classifications
A-B toxin
* Cholera toxin (Vibrio cholera)—cholera

The Action of Chlorea Enterotoxin
More A-B toxin examples
Botulinum Toxin
Tetanus Toxin
Membrane Disrupting Toxins
Superantigens
Endotoxins
* Gram type negatives
* Part of outer portion of cell wall (outer membrane)
* Lipid A portion
* Exert effects when G- microbe lyses
* Same symptoms for different species of microbe
* No antitoxins produced by host
* Very stable—can’t destroy easily
* Rarely fatal
* Disseminated intravascular clotting
* General symptoms

Pyrogenic Response
* Macrophage ingestion
* Release of interleukin-1 in bloodstream
* Interleukin-1 to hypothalamus and production of prostaglandins
* Resetting of bodies thermostat

Susceptibility/Resistance of Host
* Species specificity
* Tissue specificity
* Age
* Stress
* Diet
* Pre-existing disease (Genetic and Infectious)
* Gender
* Behavior
* Weather?
* Your first line of defense—Review this

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