Sepsis

Question 1

What causes sepsis? What are common sources of infection?

Answer 1

95% bacteria, 5% fungi.

Sources - respiratory, blood, intra-abdominal, urinary tract, skin/other tissue.

Question 2

Discuss what the intrinsic and extrinsic factors for sepsis are.

Answer 2

Intrinsic - extremes of age, co-existing diseases, malignancies, burns, AIDs, diabetes, substance abuse, organ dysfunction, malnutrition.
Extrinsic - invasive devices, drug therapy, fluid therapy, surgical/trauma wounds, immunosuppressive therapy.

Question 3

Define SIRS.

Answer 3

Systemic inflammatory response syndrome. Criteria (at least 2) - temp higher than 38C or lower than 36C, pulse higher then 90 bpm, resp rate higher than 20 breaths/min or PaCO2 lower than 32mmHg, white blood cell count higher than 12,000/µL.

Question 4

Define sepsis.

Answer 4

SIRS plus a documented infection site.

Question 5

Define severe sepsis.

Answer 5

Sepsis associated with organ dysfunction, hypotension or hypoperfusion abnormalities which include lactic acidosis, oliguria or an acute alteration in mental status.

Question 6

Define septic shock.

Answer 6

Septic shock is a diagnosis of severe sepsis characterized by persistent hypotension despite adequate fluid resuscitation.

Question 7

DIscuss the pathophysiology of septic shock.

Answer 7

A systemic response that’s initiated when microorganisms enter the body and stimulate inflammatory immune response. Toxins released damage endothelial cells and a variety of mediators are released. Initially controlled by feedback mechanism however mechanism becomes overwhelmed and capillary membrane permeability, clotting and distribution of blood flow to tissues are affected leading to further endothelail and end-organ damage. Cellular oxygen supply and demand becomes imbalanced and cellular hypoxia, damage and death occurs. Feedback continues to activate release of mediators and increase in permeability and the formation of micro-emboli causing septic process to worsen.

Question 8

Describe the warm phase of septic shock.

Answer 8

SIRS increases permeability and causes massive vasodilation, fluid moves out of the circulation into interstitial space resulting in decreased BP. Body attempts to compensate by increasing HR and heart contractility and peripheral vasoconstriction. Inflammation and mediators cause an increase in temp. Massive maldistribution of circulatory blood volume results in a decrease in cells’ oxygen supply.

Question 9

Describe the cool phase of septic shock.

Answer 9

Body is unable to compensate for the inflammatory response and BP continues to fall. Peripheral shutdown progresses to central circulatory shutdown. Body can no longer sustain increased temp and has a normal temp or hypothermia.

Question 10

Describe typical signs and symptoms of a septic patient.

Answer 10

Fever - hypothalamus resets in in sepsis so that heat production and heat loss are balanced in favour of a higher temp.
Chills/rigors- associated with fever, developing as a consequence of increased muscular activity that produces heat and raises body temp.
Sweating
Anxiety
Confusion
Dyspnoea, increased RR - caused by stimulation of the medullary respiratory center by endotoxins and other inflammatory mediators.

Question 11

Discuss clinical manifestations of a patient with sepsis.

Answer 11

Respiratory - hypoxaemia, low SaO2 and increased RR, crackles (due to pulmonary interstitial oedema), metabolic/respiratory acidosis.
CNS - altered LOC due to decreased cerebral perfusion.
CVS - pink, warm and flushed skin (massive vasodilation), Decreased BP due to reduction in preload and afterload, increased HR, increased temp.
Renal - low UO due to decreased renal perfusion.
GIT - increase in BGLs due to hypermetabolic response.

Question 12

What fluids are commonly administered to a patient in septic shock?

Answer 12

Crystalloid (0.9% sodium chloride, CSL) or colloid (albumin or Gelofusion) solutions.

Question 13

What diagnostic studies are performed on a septic patient?

Answer 13

Blood test - FBC including WBC, INR, aPTT, Prothrombin Time, U&E, LFT.
BGL
Blood cultures, urine specimen, sputum specimen.
Xrays, ultrasound, CT.
Lumbar puncture.
Wound swabs and cultures.
Aspirates.
Cultures of indwelling lines.

Question 14

Identify and discuss potential complications of septic shock.

Answer 14

Disseminated intravascular coagulation - results from abnormally widespread and ongoing activation of clotting. This leads to blockages of blood flow to organs which may result in ischaemia, infarction and necrosis and eventually MODS.
MODS - primary MODS is the result of a well-defined insult in which organ dysfunction occurs early and can be directly attributable to the insult itself. Secondary MODS develops as a consequnce of a host response and is identified within the context of SIRS.

Question 15

Discuss specific nursing care for a patient with sepsis.

Answer 15

Give high flow oxygen, monitor sats.
Blood cultures, sputum & urine specimen to locate source of sepsis.
Accurate fluid balance chart.
Monitor IV fluid administration.
ABGs - aim for PaO2 >70mmHg and normal pH.
IDC and urine output 0.5ml/kg/hr
Vital signs - TPR BP SaO2
Temperature control - active cooling and antipyretic agents.
Monitor BGLs
CVP monitoring aim for >10mmHg for adequate hydration status.
Arterial line monitoring - BP
Administration of inotropes.
Maintain aseptic techniques
Nutritional support.

Question 16

Discuss distributive shock.

Answer 16

Septic shock is a type of distributive shock. Distributive shock is characterized by pathologic vasodilation and shunting of blood from vital organs to non-vital tissues. The endothelial dysfunction and vascular maldistribution characteristic of distributive shock result in global tissue hypoxia.