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Definition
- Nosocomial: Greek word - Nosokomeion = Hospital
- Nosos = disease, Komeo = to take care of
- Also called hospital-acquired infections (HAIs)
- Defined as infections acquired as a result of contact or treatment in the hospital usually manifest after 48 hours of hospitalization or within 30 days of discharge from the hospital but not related to the patient’s original condition
Pathophysiology
Nosocomial infections are infections that are acquired in a healthcare setting. They can be caused by a variety of pathogens, including bacteria, viruses, and fungi. Colonization of the patient's skin, respiratory system, and genitourinary tract by colonies of hospital strains is one of the key steps in the pathophysiology of nosocomial infections.
Colonization is the process by which a pathogen establishes itself on the body surface without causing any symptoms. Hospital strains are pathogens that have adapted to the healthcare environment and are often resistant to antibiotics.
Skin colonization is the most common type of colonization in healthcare settings. It can occur when patients come into contact with contaminated surfaces, such as bedrails, countertops, and medical equipment. Hospital strains of bacteria, such as Staphylococcus aureus and Enterococcus faecalis, are common colonizers of the skin.
Respiratory colonization can occur when patients inhale contaminated air droplets or when they are intubated or ventilated. Common respiratory colonizers include bacteria such as Pseudomonas aeruginosa and Klebsiella pneumoniae, and viruses such as influenza and respiratory syncytial virus.
Genitourinary colonization can occur when patients are catheterized or when they have other types of invasive procedures performed on their urinary tract. Common genitourinary colonizers include bacteria such as Escherichia coli and Enterobacter species.
Once a pathogen has colonized the patient's skin, respiratory system, or genitourinary tract, it can then invade the body and cause an infection. The specific type of infection that develops will depend on the site of colonization and the type of pathogen involved.
For example, skin colonization can lead to surgical site infections, cellulitis, and abscesses. Respiratory colonization can lead to ventilator-associated pneumonia and other types of pneumonia. Genitourinary colonization can lead to catheter-associated urinary tract infections and other types of urinary tract infections.
Risk Factors
Risk factors for invasion are classified into 3:
- Iatrogenic
- Organizational
- Patient-related
Iatrogenic
- Pathogens on the hands of medical personnel
- Invasive procedures e.g., intubation, IV lines, catheters
- Many medical procedures bypass the body's natural protective barriers
- Strict asepsis may not be observed
- Long-term use of broad-spectrum antibiotics
Organizational
- Contaminated air conditioners
- Contaminated water systems
- Open beds close together
- Increases risk of acquisition of infections through droplets, sneezing, and talking
Patient related
- Immuno-suppression state
- Long hospital stay e.g., stroke patients
- Severe illness
Epidemiology
- 5% of all acute hospital admissions in the USA
- Account for about 26,250 deaths annually
- Occurs more frequently in ICU, burns units, neonatal ICU
- No sex predilection
Causes
Viral
- Influenza
- Parainfluenza
- Rotaviruses
- Adenoviruses
Bacteria
- Most patients who have bacterial or fungal nosocomial infections have obvious predispositions such as IV sites or invasive procedures.
- Staphylococcus aureus
- Pseudomonas
- Enterobacter species
- Clostridium difficile
- TB (Tuberculosis)
- Hospital-acquired pneumonia
Treatment and Prevention
- 92% of nosocomial infections are preventable.
- Thorough hand washing
- Use of alcohol rubs before and after examining each patient
- Gloving
- Surface sanitation
- Use of aprons and masks
- Careful use of antibiotics
- Fumigation
- Control and monitoring of hospital indoor air quality
- Antimicrobial therapy - empirical initially but should be pathogen-specific after culture and sensitivity testing (M/C/S).
Definitions
Bacteraemia: Presence of bacteria in the blood, confirmed by a positive blood culture.
Septicaemia: Presence of microbes or their toxins in the blood.
Sepsis: Evidence of infection along with signs and symptoms of systemic inflammatory response (SIRS), which may include fever and tachycardia.
Sepsis Syndrome: Presence of infection, SIRS, and evidence of organ dysfunction, such as confusion, hypoxia, oliguria, and metabolic acidosis.
Septic Shock: Sepsis syndrome accompanied by hypotension that is refractory to volume replacement.
Sepsis
Multiple Organ Dysfunction Syndrome (MODS) is a serious complication of sepsis that can occur when the body's inflammatory response to infection damages multiple organs. MODS can affect any organ system in the body, but the most commonly affected organs include the lungs, kidneys, liver, and brain.
MODS is a complex syndrome with a poorly understood pathophysiology. However, it is thought to be caused by a combination of factors, including:
- Inflammation: Sepsis triggers a systemic inflammatory response, which can damage organ tissues and reduce blood flow to organs.
- Microvascular dysfunction: MODS is often associated with microvascular dysfunction, which is a decrease in blood flow to the smallest blood vessels in the body. This can lead to tissue hypoxia and organ damage.
- Coagulation abnormalities: Sepsis can also lead to coagulation abnormalities, which can increase the risk of bleeding and blood clots. This can further damage organ tissues and reduce blood flow to organs.
MODS is a serious condition with a high mortality rate. Early diagnosis and treatment are essential for improving outcomes. Treatment of MODS typically involves supportive care, such as mechanical ventilation, dialysis, and vasoactive medications. In some cases, surgery may be necessary to remove damaged tissue or to repair organ function.
MODS in sepsis
Sepsis is the most common cause of MODS. In fact, MODS is a major cause of death in patients with sepsis.
When sepsis progresses to MODS, the patient's body is no longer able to maintain homeostasis without intervention. This means that the patient's organ systems are failing to function properly, and they may require life support measures, such as mechanical ventilation and dialysis.
The mortality rate for patients with sepsis-related MODS is high, but it has improved in recent years due to advances in critical care medicine. However, MODS remains a serious complication of sepsis, and it is important to identify and treat sepsis early to prevent MODS from developing.
Epidemiology
- Causes about 215,000 deaths in the USA annually.
- Approximately 51 cases per 100,000 people.
- 47% mortality rate.
- There has been a 53% increase in incidence recently.
Clinical Indicators of Sepsis
- Temperature ≥ 38°C or < 36°C: This indicates that the body is trying to fight off an infection or is unable to regulate its temperature.
- Respiratory rate ≥ 20 breaths per minute or hyperventilation as indicated by Pco2 ≤ 4.2 kPa: This indicates that the body is trying to get more oxygen or is unable to remove carbon dioxide effectively.
- Heart rate ≥ 90 beats per minute: This indicates that the body is trying to pump more blood to the tissues or is unable to maintain adequate blood pressure.
- White blood cell count ≥ 12,000 cells/μL or ≤ 4,000 cells/μL, or 10% immature (band) forms: This indicates that the body is fighting off an infection or is unable to produce enough white blood cells.
Note: Pco2 stands for partial pressure of carbon dioxide, and band forms are immature white blood cells. Sepsis is a clinical diagnosis, meaning it is based on the patient's clinical presentation, even if they do not meet all the clinical indicators listed above.
Causes/Risk Factors of Sepsis
- Pneumonia
- Urinary Tract Infection (UTI)
- Typhoid Fever
- Cellulitis
- Meningitis
- Pelvic Inflammatory Disease (PID)
- Intra-abdominal Surgery
- HIV/AIDS
- Steroid Use
- Neoplasms (Cancerous Growth)
- Alcoholism
Effects of Sepsis on Body Systems
- Cardiovascular System (CVS):
- Systolic Blood Pressure (SBP) < 90 mmHg
- Mean Arterial Pressure (MAP) ≤ 70 mmHg
- Central Nervous System (CNS):
- Acute Alteration in Mentation
- Renal System:
- Reduced Urine Output ≤ 0.5 ml/kg/hr despite adequate fluid therapy
- Acute Renal Failure (ARF)
- Hematology:
- Platelet Count < 80
- Disseminated Intravascular Coagulation (DIC)
- Gastrointestinal Tract (GIT):
- Increase in Transaminases
- Increase in Bilirubin
- Metabolic:
- pH ≤ 7.3
- Base Deficit > 5
- Lactate > 1.5
Management Objectives/Targets
- Resuscitation:
- Optimization of Hemodynamic Status and Oxygen Delivery:
- Monitoring:
- MAP (Mean Arterial Pressure):
- Central Venous Pressure (CVP):
- Serum Lactate:
- Packed Cell Volume (PCV):
- Central Venous Oxygen Saturation (ScvO2):
Continuously monitor key parameters for timely intervention.
Target: Maintain MAP >70 mmHg.
Formula: (2 x Diastolic Blood Pressure + Systolic Blood Pressure) / 3.
Target: Maintain CVP within 8-12 mmHg.
Target: Keep serum lactate <4 mmol/L or anion gap <16.
Formula for anion gap: ([Sodium + Potassium] - [Bicarbonate + Chloride]).
Normal anion gap range: 10-18.
Target: Maintain PCV >30% for adequate oxygen-carrying capacity.
Target: Maintain ScvO2 >70% to ensure sufficient tissue oxygenation.
Treatment
- Resuscitation (ABC):
- Oxygen therapy should be initiated.
- Monitoring:
- Laboratory Tests:
- Urgency:
- Intravenous (IV) Crystalloid:
- Blood Transfusion:
- Steroid:
- Glucose Control:
- Broad-Spectrum Antibiotics:
- MAP Maintenance:
Continuous monitoring of vital signs and key parameters, including CVP (Central Venous Pressure) and Swan Ganz catheter.
Perform essential laboratory tests including blood culture, WBC (White Blood Cell count), E/U (Electrolytes/Urea), Cr (Creatinine), and blood gases.
Management demands the same urgency as the treatment of myocardial infarction (MI) or cardiovascular disease (CVD).
Administer IV crystalloid (normal saline or Hartmann's solution) at 20 ml/kg.
Consider blood transfusion if hemoglobin (Hb) is <7 g/dL.
Administer low-dose steroids such as hydrocortisone IV.
Maintain glucose concentration at <8.3 mmol/L.
Initiate treatment with broad-spectrum and potent antibiotics.
If MAP is ≤65 mmHg and the patient is not responding to fluids, consider administering adrenaline, dobutamine, or dopamine.
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