Sepsis Flashcards

1
Q

what is an infection?

A

A pathological process caused by an invasion of normally sterile tissue or fluid or body cavity by pathogenic/potentially pathogenic micro-organisms.

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2
Q

infections are caused only by obligate pathogenic bacteria. True/False

A

False.

Infections can be caused also by opportunistic pathogens.

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3
Q

what is an opportunistic pathogen?

A

Opportunistic pathogens can cause an infectious disease in a host with depressed resistance (immunodeficiency) or if they have unusual access to the inside of the body (for example, via trauma).
Examples of opportunistic infections: oral candidiasis, vaginal yeast infection, cytomegalovirus infection, cryptococcal meningitis, pneumocystis jirovecii pneumonia, toxoplasma encephalitis

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4
Q

what is an obligate pathogen?

A

Can only replicate inside the cells of a host and therefore must infect someone in order to survive: e.g., Salmonella, Treponema pallidum, Mycobacterium tuberculosis
If a sufficient amount of bacteria is ingested (e.g., oral or contaminated foods), the disease also occurs in immunocompetent individuals.

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5
Q

Infection can be present without being microbiologically confirmed in the laboratory. True/False

A

True

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6
Q

what are the non-specific signs & symptoms of infection (constitutional signs)

A
Temperature / feels hot + sweaty
Rigors
Anorexia
Fatigue
Myalgia
Arthralgia
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7
Q

what are constitutional symptoms of infection

A

A collection of nonspecific symptoms such as weight loss, fever, chills, night sweats, changes in appetite, changes in sleep, chronic pain, fatigue, and malaise. Typically evaluated on a review of systems with further evaluation based on pertinent positives and negatives.

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8
Q

what are B symptoms?

A

B symptoms refer to systemic symptoms of fever, night sweats, and weight loss which can be associated with both Hodgkin’s lymphoma and non-Hodgkin’s lymphoma. The presence or absence of B symptoms has prognostic significance and is reflected in the staging of these lymphomas.

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9
Q

list examples of the signs and symptoms related to the site of infection

A

Respiratory infection – Shortness of breath, cough, sputum
Urinary infection –frequency, dysuria, flank pain
Skin infection- -erythema, pain
Meningitis–headache, neck stiffness
Abdominal infection –pain, distension

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10
Q

what is the SIRS (systemic inflammatory response syndrome)

A

A syndrome defined by meeting 2 or more of the following criteria: 1) temperature > 38ºC or < 36ºC; 2) heart rate > 90 beats/min; 3) respiratory rate > 20 breaths/min or PaCO2 < 32 mm Hg; and 4) white blood count > 12,000 cells/mm³, < 4,000 cells/mm³, or >1% band forms. These criteria are outdated!!!!!!!!!!; sepsis and septic shock are now evaluated based on Sequential Organ Failure Assessment (SOFA) scoring.

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11
Q

SIRS is characterized by…

A

abnormal vital signs

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12
Q

what are the causes of SIRS?

A
–	Infection
–	Ischaemia
–	Haemorrhage,
–	Inflammation (e.g. pancreatitis)
–	Trauma
–	Burns
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13
Q

define sepsis

A

Sepsis is an acute life-threatening condition characterized by organ dysfunction due to a dysregulated immune response to infection. The previously widely used term “systemic inflammatory response syndrome” (SIRS) is now considered outdated because its criteria were too simplified. Initial infection is generally bacterial and commonly of respiratory, genitourinary, gastrointestinal, dermatological, or soft tissue origin. Risk factors include immunocompromise, chronic comorbidities (e.g., diabetes mellitus), young or old age, and lengthy or invasive medical care. Patients may present with fever, tachycardia, confusion, and signs of the primary infection. Organ dysfunction is determined using a sequential organ failure assessment (SOFA) score that considers multiple parameters but may be quickly evaluated and assumed if two of the following findings are present: tachypnea, hypotension, and altered mental status. Diagnostic workup focuses on determining the responsible pathogen via cultures and identifying the source of infection (e.g., via imaging, ECG, lumbar puncture). Laboratory findings are largely nonspecific. Prompt, aggressive treatment is vital to survival and consists of resuscitation, empiric antibiotic therapy, and control of the infectious source.

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14
Q

define septic shock

A

A type of distributive shock caused by an excessive inflammatory response to disseminated infection, which leads to fluid extravasation from the vascular space and loss of intravascular volume. Defined as the requirement of vasopressors to maintain a median arterial pressure ≥ 65 mm Hg despite adequate fluid therapy, and lactate > 2 mmol/L (> 18 mg/dL) in a normovolemic patient with sepsis.

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15
Q

define bacteremia

A

The presence of bacteria in circulation. It can be harmless and transient or the result of serious infection, in which case it can lead to disseminated infection, sepsis, and septic shock.

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16
Q

every sepsis has an infection. True/False.

A

not every infection is sepsis however everybody with sepsis has an infection!

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17
Q

Sepsis is a laboratory diagnosis. True/False.

A

False.

It is a clinical diagnosis

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18
Q

sepsis is characterized by organ dysfunction. True/False

A

True

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19
Q

why it is important to define sepsis?

A

• Sepsis is the primary cause of death from infection, especially if not recognised and treated promptly –
• Definitions of ‘sepsis’ provide a framework for clinical intervention
(i.e. facilitates recognition of patients that require resuscitation)

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20
Q

what is the main reason for the poor outcome of sepsis?

A

90% of cases with the poor outcome due to inadequate recognition

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21
Q

what is the etiology of sepsis

A
  • Common primary infections: respiratory, genitourinary, gastrointestinal, skin, and soft tissue infections
  • Pathogens
  • Bacterial: gram-positive bacteria (most common in the US), gram-negative bacteria
  • Fungal, viral, or parasitic infection (rare)
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22
Q

what are the risk factors of sepsis?

A
  • Age: < 1 year or > 75 years
  • Primary comorbidities (diabetes mellitus, cirrhosis, community-acquired pneumonia, bacteremia (presence of bacteria in circulation), alcoholism)
  • Immunosuppression (neutropenia, corticosteroid treatment, cancer, asplenia, HIV, renal failure)
  • Intensive care or prolonged admission (nosocomial infections, immunosuppressive medications)
  • Recent antibiotic or corticosteroid treatment
  • Invasive medical devices (e.g., endotracheal tubes, intravenous lines, urinary catheters)
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23
Q

sepsis is primarily caused by G- bacteria. True/False

A

False

The most common cause are G+ bacteria

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24
Q

what condition is the most common cause of sepsis?

A

Pneumonia is the most common condition leading to sepsis.

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25
Q

define febrile neutropenia

A

A condition characterized by fever in patients with a neutrophil count ≤ 500/μL. Increases risk of severe bacterial infection. Etiologies include chemotherapy, bacterial infection, aspergillosis, candidiasis, and herpes virus infections.

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26
Q

what are the signs of new organ dysfunction in sepsis?

A

1) Lactate>2mmol/L (following adequate initial fluid resuscitation)
2) Systolic BP <90 or MAP <65 or Systolic BP more than 40 below patients normal
3) new need for oxygen to achieve saturation >90%
4) creatinine >170 microMol/L or urine output <0.5 ml/Kg for 2 hours
5) Bilirubin >32microMol/L
6) glucose >7.7 mmol/L (in the absence of diabetes)
7) platelets < 100.000
8) acutely altered mental status

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27
Q

what is the SOFA score?

A

A scoring system used to assess the severity of organ dysfunction and the risk of mortality. Commonly used in intensive care units (ICUs). Considers partial arterial pressure of oxygen, platelet count, bilirubin, mean arterial pressure (or vasopressor requirement), Glasgow Coma scale score, creatinine, and urine output. A simplified version of the SOFA score (the qSOFA score) identifies patients at increased risk for in-hospital mortality with suspected infection outside the ICU.

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28
Q

what is the lactate level in septic shock?

A

> 2mmol/L

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29
Q

how much should be the BP to diagnoses cardiovascular dysfunction in sepsis?

A

Systolic BP <90 or MAP <65 or Systolic BP more than 40 below patients normal

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30
Q

define respiratory dysfunction in sepsis

A

new need for oxygen to achieve saturation >90%

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31
Q

define renal dysfunction in sepsis

A

creatinine >170 microMol/L or urine output <0.5 ml/Kg for 2 hours

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32
Q

define liver dysfunction in sepsis

A

Bilirubin >32microMol/L

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33
Q

what hematological parameters are present in sepsis?

A

platelets < 100.000

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34
Q

define CNS dysfunction in sepsis

A

acutely altered mental status (Glasgow Coma scale)

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35
Q

what is the Glasgow COma scale?

A

A standardized scale used for the assessment of neurological status, consciousness, and degree of brain injury. The scale scores the patient’s eye response (1–4 points), verbal response (1–5 points), and motor response (1–6 points). A maximum score of 15 points corresponds to full consciousness, while a minimum score of 3 points indicates coma or death. The degree of brain injury is classified as follows: Mild brain injury: 13–15 points Moderate brain injury: 9–12 points Severe brain injury: ≤ 8 points (indication for endotracheal intubation)

36
Q

describe the pathophysiology of sepsis

A
  • -Sepsis is the state of a hyperinflammatory systemic reaction
    1) Local activation of inflammatory mediators (complement system, mast cells, macrophages) results in vessel dilation and further release of proinflammatory cytokines (esp. TNFα, IL-1)
    2) Generalized endothelial disruption → capillary leak → generalized edema due to a shift of intravascular fluid and albumin into the surrounding tissue
    3) Intravascular hypovolemia → excessive triggering of the extrinsic coagulation cascade → disseminated intravascular coagulation (DIC) and microvascular thrombosis
    4) Decreased oxygen utilization and tissue ischemia → widespread cellular injury → organ dysfunction (commonly multisystem)
  • -An adequate immune response requires a balance between pro-inflammatory (anti-infectious) and anti-inflammatory signals!
37
Q

what is the response to proinflammatory cytokines?

A

– SIRS response
– Simultaneous activation of coagulation and fibrinolysis
– Uncontrolled/unregulated intravascular inflammation

38
Q

generalized activation of complement, coagulation, and fibrinolytic systems leads to

A

DIC (disseminated intravascular coagulation)

39
Q

what is a DIC?

A

A condition characterized by systemic activation of the clotting cascade, platelet consumption, and subsequent exhaustion of clotting factors that leads to widespread thrombosis and hemorrhage. Often associated with trauma, shock, and sepsis.

40
Q

what are the systemic effects of sepsis?

A

1) tissue ischemia
2) cytopathic injury
3) altered rate of apoptosis
4) immunosuppression

41
Q

what are the effects of tissue ischemia in sepsis

A

– Insufficient oxygen relative to oxygen need
– Microcirculatory lesions (imbalances in coagulation+fibrinolytic systems)
– Endothelial lesions(interactions between endothelial cells and activated polymorphs)

This may be a result of a combination of factors: hypoxic hypoxia, microvascular thrombi, direct cytotoxicity (bacterial endotoxins, TNFα), cell apoptosis, and immunosuppression**.

42
Q

what is the reason for intravascular hypovolemia sepsis?

A

Multifactorial cause assumed: activated adenosine triphosphate (ATP) sensitive potassium channels in endovascular smooth muscles and NO synthase result in arterial vasodilation.

43
Q

how cytopathic injury occurs in sepsis?

A

direct cell injury by proinflammatory cytokines

44
Q

what is the reason for altered apoptosis in sepsis?

A

– Proinflammatory cytokines may delay apoptosis in activated macrophages and neutrophils
– Prolonging/augmenting the inflammatory response = development of multiple organ failure

45
Q

what bacterial components contribute to the progression of a local infection to sepsis?

A

– Bacterial cell wall components (e.g., endotoxin, peptidoglycan, lipoteichoic acid)
– Bacterial products (exotoxins, M protein of group A streptococci

46
Q

wat is a lipoteichoic acid?

A

A cell wall component present in all gram-positive bacteria. Lipoteichoic acid is anchored in the cytoplasmic membrane and extends to the outer cell wall and acts as an antigen that induces TNF-α and IL-1.

47
Q

what is the M protein?

A

A virulence factor expressed on the surface of group A streptococcus that blocks the alternative complement pathway. Shares similar epitopes to human myocardial and nerve proteins, which can lead to an autoimmune attack, which causes acute rheumatic fever.

48
Q

what is the peptidoglycan?

A

A polymer chain of sugars (N-acetylmuramic acid and N-acetylglucosamine) and amino acids that form the cell wall of bacteria, providing protection from osmotic pressure damage.

49
Q

what are the host factors contributing to sepsis?

A
–Age
–Genetic polymorphisms
–Co-morbidities
        •Chronic health status
        •Immuno-modulatory medications
50
Q

what are the clinical effects of sepsis?

A
  • -Patients typically present with a poor overall condition and generalized edema (capillary leak).
  • -Fever, chills, and diaphoresis
  • -Tachycardia
  • -Tachypnea
  • -Features of organ dysfunction (see SOFA score)
    1) CNS impairment: altered mental status
    2) Cardiovascular failure: hypotension
    3) Coagulopathy → disseminated intravascular coagulation → petechiae, purpura
    4) Liver failure: jaundice
    5) Kidney failure: oliguria
    6) Respiratory failure: symptoms of acute respiratory distress syndrome (ARDS)
  • -Additionally in septic shock
    1) Severe hypotension (< 65 mmHg)
    2) Initially warm skin and normal capillary refill time (warm shock) → cold cyanotic, pale, or mottled skin with prolonged capillary refill time (cold shock)
  • -Features of the primary infection
51
Q

what are the cardiovascular effects of sepsis?

A

• Vasodilation
• Increased endothelial permeability
• Hypotension, hypoperfusion
Initially cardiac output increases, but with the progression of sepsis, cardiac output decreases due to myocardia dysfunction caused by lactate

52
Q

what happens to cardiac output in sepsis

A

Initiallycardiac output increases, but with the progression of sepsis, cardiac output decreases due to myocardia dysfunction caused by lactate (extremely important MCQ)

53
Q

what are the respiratory effects of sepsis?

A

Endothelial injury disturbs capillary blood flow + enhances microvascular permeability = pulmonary edema = ventilation-perfusion mismatch = hypoxia

54
Q

what is an ARDS (Acute respiratory distress syndrome)

A

Acute respiratory distress syndrome (ARDS) is a severe inflammatory reaction of the lungs to pulmonary damage. Sepsis is the most common cause, but various other systemic or pulmonary factors – such as pneumonia or aspiration – can lead to ARDS. Patients initially present with acute onset cyanosis, dyspnea, and tachypnea. Over the course of the next weeks, most patients will improve significantly, although some progress to pulmonary fibrosis, which prolongs their hospital stay and delays the resolution of symptoms. The chief finding in ARDS is a hypoxemic respiratory failure with decreased arterial oxygen pressure, which usually progresses to hypercapnic respiratory failure. A chest x-ray typically shows diffuse bilateral infiltrates (“butterfly pattern”). Management of ARDS focuses on maintaining adequate oxygenation, which often requires intubation and (lung protective) mechanical ventilation, as nasal prongs and/or masks ventilation are insufficient. Moreover, any treatable causes of ARDS should be addressed. However, even if adequate treatment is initiated, ARDS remains an acutely life-threatening disease with a high mortality rate.

55
Q

what are the gastrointestinal tract effects of sepsis?

A

Circulatory abnormalities = depress gut’s normal barrier function= bacterial translocation into peritoneum

56
Q

what is the ventilation-perfusion mismatch?

A

n imbalance between the total lung ventilation (airflow; V) and total lung perfusion (blood flow; Q). V/Q mismatch is an indicator of gas exchange and is the most common cause of hypoxemia. The normal V/Q ratio is 0.8 (since lung bases are better ventilated and perfused than the apices). Decreased ventilation (e.g., in pneumonia, atelectasis) decreases the V/Q ratio. Decreased perfusion (e.g., in pulmonary embolism) increases the V/Q ratio.

57
Q

what are the sepsis effects on the liver?

A

• Hepatic failure
• Reduced clearance of bacteria and bacterial products from the portal system (RES)
– Liver reticuloendothelial system (RES) = 1st line defense Vs. bacteria that have entered the portal system from the gut.

58
Q

what are the renal effects of sepsis?

A
  • Acute renal failure. (acute tubular necrosis)
  • Hypoperfusion and/or hypoxemia: systemic hypotension, renal vasoconstriction, the release of cytokines
  • Decreased urine output
59
Q

what is the Acute tubular necrosis?

A

–A form of acute kidney injury that is caused by severe damage to the renal tubules. Accounts for approximately 85% of intrinsic acute kidney injuries. May be due to ischemic/hypoxic (e.g., thromboembolism, prolonged hypotension) or toxic (e.g., contrast-induced nephropathy) damage.
–Damage to a vascular or tubular component of the nephron → necrosis or apoptosis of tubular cells → decreased reabsorption capacity of electrolytes, water, and/or urea (depending on the location of injury along with the tubular system)
–Na+ has multiple reabsorption sites, so its reabsorption is often impaired, which leads to increased Na+ in the urine and increased urine osmolality.
Acute tubular necrosis: necrotic debris obstructs tubules → decreased GFR → sequence of pathophysiological events similar to a prerenal failure

60
Q

what are the central nervous system effects of sepsis?

A
  • Encephalopathy
  • Dysfunction of the blood-brain barrier = increased leukocyte infiltration, exposure to toxic mediators, and active transport of cytokines across the barrier
61
Q

what is the blood-brain barrier?

A

A barrier that separates the extracellular fluid of brain tissue from circulating blood. Composed of three layers: pedicles (foot processes of astrocytes), a basal membrane, and capillary endothelial cells bound by tight junctions. The BBB is selectively permeable to certain substances (e.g., glucose, metabolic waste, and gases) and prevents entry of other substances (e.g., bacteria, toxins, certain medications) into the brain parenchyma.

62
Q

what are the most common infective causes of sepsis?

A

respiratory, urinary tract +intra-abdominal

63
Q

what are infective sources of sepsis specific to pregnancy?

A
  • chorioamnionitis
  • endometritis
  • wound infection after cesarean section
  • perineal infection
  • lactational mastitis
64
Q

which infections are exacerbated by sepsis

A
  • listeriosis
  • Urinary tract infection
  • influenza
  • Varicella zoster
  • parvovirus
  • CMV
65
Q

pregnancy is a risk factor for sepsis. True/False

A
True.
•Age > 35
•Premature membrane rupture
•Retained products
•Amniocentesis
•History of 
   –Grp B strep infection
   –pelvic infection
•Group A streptococcal infection in close contacts
66
Q

define premature rupture of membranes during pregancy?

A

The rupture of amniotic membranes before the onset of uterine contractions. Common risk factors include ascending infection and cigarette smoking. Complications include chorioamnionitis, placental abruption, and umbilical cord prolapse.

67
Q

define amniocentesis

A

A prenatal diagnostic procedure in which amniotic fluid is extracted under sonographic guidance via transabdominal puncture. It is optimally performed from 15 weeks of gestation onwards. Used in early pregnancy (e.g., to determine possible chromosomal abnormalities or fetal infections) or in late pregnancy (e.g., to estimate lung maturity). Possible complications are miscarriage, premature rupture of the membranes and infection.

68
Q

what is the most important initial measure of sepsis treatment?

A

fluid resuscitation

69
Q

what are the principles of sepsis management?

A
  1. Optimize organ perfusion
    Fluid resuscitation /Vasopressors to restore BP
  2. Eradicate infection
  3. Support dysfunctional organ systems
70
Q

what you should do at the initial 1st hour of a septic patient?

A
Take:
1)blood and urine cultures
2)blood tests
3)urine output
Give:
1)oxygen
2)IV fluids
3)IV antibiotics
71
Q

how to eradicate the infection in sepsis?

A
  1. Identify source – NB to make sure you pick the correct antimicrobial (s)
  2. Source control
    • Line/device removal
    • Drainage of abscess
  3. Antimicrobial therapy
    • Consider likely source and causative organisms
    • START SMART ‘get it right the first time’
72
Q

what are the general principles of antibiotical therapy of sepsis?

A
  1. Clinical assessment: what is the likely site of infection?
  2. Acquisition: Where do you think the patient got the infection?
    - Is it community, healthcare or hospital-acquired?
    - Local factors e.g. Antibiotic resistance rates
  3. Previous antibiotics
    - including from GP/other hospitals)
  4. Previous microbiology results
  5. History of allergy
73
Q

how to identify the responsible pathogen in sepsis?

A
  • Perform Gram stain and cultures of blood and urine
  • Depending on symptoms, consider other body fluids for culture: e.g., sputum (if coughing), stool (if diarrhea is present), pus (soft tissue infection).
  • at least two distinct peripheral blood cultures and from each indwelling catheter.
  • Blood cultures are negative in ∼50% of patients with sepsis.
74
Q

how to Identify the infectious focus

A
  • Imaging
  • Lumbar puncture if suspected CNS infection
  • Echocardiography if suspected endocarditis
75
Q

Blood cultures are negative in ∼50% of patients with sepsis. True/False

A

True

76
Q

how many blood cultures need to be taken in suspected sepsis?

A

at least two distinct peripheral blood cultures and from each indwelling catheter.

77
Q

how to assess organ dysfunction in sepsis?

A
  • -Coagulation abnormalities (see disseminated intravascular coagulation): ↑ prothrombin time, ↑activated partial thromboplastin time, ↓ antithrombin III, later ↑ D dimer
  • -Abnormal liver function: hyperbilirubinemia, ↑ INR, ↑ ALT, ↑ AST
  • -Adrenal insufficiency (e.g., ACTH stimulation test)
  • -Impaired kidney function: ↑ BUN and ↑ creatinine
78
Q

what are the non-specific infectious parameters of sepsis?

A
  • -Nonspecific infectious parameters
    1) CBC
    2) Anemia
    3) Leukocytosis or eventual leukopenia
    4) Thrombocytopenia → early prognostic marker of 28-day mortality due to septic shock
    5) Procalcitonin
    6) ↑ CRP
    7) ↑ Serum lactate
    8) Hyperglycemia (plasma glucose > 140 mg/dL or 7.7 mmol/L) in the absence of known diabetes
79
Q

what is the reason for anemia in sepsis?

A

Erythrocytes may be damaged by impaired microcirculation or DIC. Furthermore, bone marrow maturation of erythrocytes is impeded, which is believed to be sepsis-induced.

80
Q

what is the reason for leukopenia in sepsis?

A

Various endotoxins result in increased adherence of leukocytes (especially in the microcirculation), causing leukopenia. Bad prognostic sign

81
Q

what is the role of CRP in sepsis?

A

Useful in follow-up, but no longer the diagnostic parameter of choice because of lower sensitivity in comparison to procalcitonin.

82
Q

what is the indicator of tissue hypoperfusion in sepsis?

A

Lactate.
Lactate is the best indicator of tissue perfusion and is elevated when tissue oxygen demand exceeds supply. Evidence exists that lactate can also be elevated in sepsis in the absence of tissue hypoperfusion, a consequence of mitochondrial dysfunction and downregulated oxidative phosphorylation. Associated with an increase in mortality.

83
Q

what are the indications for intubation in sepsis?

A

Intubation and mechanical ventilation may be required if the following is present: respiratory insufficiency, dyspnea, persistent hypotension, or poor peripheral perfusion

84
Q

define empirical antibiotic therapy in sepsis?

A

begin immediately after blood cultures have been drawn, preferably within 1 hour after recognition
Treat for MRSA until ruled out: vancomycin or linezolid/daptomycin in combination with either:
Piperacillin/tazobactam, cefepime, or carbapenems if Pseudomonas infection is likely
3rd generation cephalosporin (e.g., ceftriaxone or cefotaxime) if Pseudomonas infection is unlikely
Antifungal treatment in cases of documented fungemia (presence of a fungus in the bloodstream)

85
Q

how to control infectious source in sepsis?

A
  • -Remove any foreign bodies
  • -Surgically drain abscesses or perform debridement on infectious wounds
  • -Manage any complications of surgery (e.g., ileus, peritonitis, anastomotic insufficiency, osteomyelitis)
86
Q

what other therapies are used in sepsis?

A
  • -Glucocorticoids (e.g., prednisone or dexamethasone): if there is an increased risk of cerebral edema
  • -Insulin-based control of blood glucose levels: control of stress-induced hyperglycemia results in a shorter length of stay in the ICU, even in non-diabetic patients.
87
Q

what is Critical illness polyneuropathy

A
  • -complication of sepsis
  • -Definition: axonal injury, particularly to the motor neurons, as a sequela of sepsis and multiple organ dysfunction
  • -Clinical features
    1) Predominantly distal, symmetrical, flaccid paralysis of the extremities with muscle atrophy; may affect the diaphragm
    2) Absent or reduced reflexes
    3) Dysesthesias in a glove-and-stocking distribution may be present
    4) Preservation of cranial nerve function
    5) May be associated with critical illness myopathy: flaccid quadriparesis (proximal > distal); facial muscle weakness, sensation normal, tendon reflexes normal or ↑
  • -Diagnosis: typical clinical features, sepsis, and electrophysiological evidence of motor and sensory neuropathy
    1) Electromyography (EMG): spontaneous activity (e.g., fibrillations)
    2) Nerve conduction studies: normal velocity, reduced amplitude
  • -Treatment: no specific treatment available, usually gradual spontaneous resolution (weeks to months)