SEPSIS

GROUP MEMBERS

 ABENA YEBOAH KWARTENG

 GIDEON ANTWI BOADI
 BENEDICTA ABENA YALLEY
 JOSEPH ANSAH KWAME
 STEPHANIE SOSU DELALI
PRESENTATION OUTLINE

 INTRODUCTION
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 CLINICAL MANIFESTATION
 RISK FACTORS
 COMPLICATIONS
 INVESTIGATION
 DIAGNOSIS
 MANAGEMENT.
 REFERENCES.
INTRODUCTION

 Sepsis also known as septicemia is a life threatening complication of an

infection.
 It arises when the body’s response to an infection injures its own tissues and
organs.
 When the infection- fighting processes turn on the body, they cause organs to
function poorly and abnormally.
 Sepsis can lead to shock, multiple organ failure and death especially if not
recognized early and treated promptly
 Sepsis remains the primary cause of death from infection despite advances in
modern medicine, including vaccines, antibiotics and acute care.
EPIDEMIOLOGY

The incidence of sepsis varies among the different racial and ethnic group, but
appears to be highest among African-American males
The incidence is also greatest during the winter, probably due to the increased
prevalence of respiratory infections.
Older patients of 65 years or more account for majority (60 to 80 percent) of all
episodes of sepsis; with an increasing aging population, it is likely that the
incidence of sepsis will continue to increase in the future.
EPIDEMIOLOGY

 Gram positive bacteria are most frequently identified in patient.

 Cases of Gram negative sepsis remains substantial.
 The incidence of fungal sepsis has increased over the past decade , but
remains lower than bacterial sepsis.
 In half cases of sepsis, an organism is not identified.
EPIDEMIOLOGY
CLINICAL MANIFESTATIONS

 Fast Heart Rate

 Fever or Hypothermia(very low body temperature)
 Shaking or Chills
 Warm or sweaty skin
 Confusion or Disorientation
 Hyperventilation(rapid breathing or shortness of breath)
PATHOPHYSIOLOGY

 Multiple Organ Dysfunction and results from diffuse cell injury

 Mechanisms of cell injury/Death:
1. Cellular Necrosis(ischemic Injury)
2. Apoptosis
3. Leukocyte-mediated tissue injury
4. Cytopathic Hypoxia
SIGNS AND SYMPTOMS OF SEPSIS

 To be diagnosed of sepsis, one must have a probable or confirmed infection

and all of the following signs ;
 Change in mental status
 Change in systolic blood pressure – the first number in a blood pressure
reading is less than or equal to 100mmHg
 Respiratory rate higher than or equal to 22 breaths a minute.
CAUSES OF SEPSIS

 While any type of infection bacterial, viral or fungal can lead to sepsis.
 Infections that more commonly can lead to sepsis include infections of;
 Lungs such as pneumonia
 Kidney, bladder and other parts of the urinary system.
 Digestive system
 Bloodstream (bacteremia)
 Catheter sites
 Wounds or burns
RISK FACTORS

 Several factors increase the risk of sepsis, including

 Older age
 Infancy
 Compromised immune system
 Diabetes
 Chronic kidney or liver disease
 Admission to intensive care unit or longer hospital stays
 Invasive devices such as intravenous catheters or breathing tubes
 Previous use of antibiotics or corticosteroids.
INVESTIGATIONS

 Blood Tests are used to test for:

1. Evidence of infection
2. Clotting problems
3. Abnormal liver or kidney function
4. Impaired oxygen availability
5. Electrolyte imbalances
 Urine Tests
 Wound Secretions
 Respiratory secretions
 Imaging Tests(X-Ray, Ultrasound, Computerized Tomography etc.)
COMPLICATIONS

 As sepsis worsens blood flow to vital organs such as the brain, heart and
kidneys becomes impaired.
 Sepsis may cause abnormal blood clotting that results in small clots or burst
blood vessels that damage tissues
 MANAGEMENT

 MEDICATIONS
 Antibiotics :Treatment with antibiotics begins as soon as possible. Broad-
spectrum antibiotics, which are effective against a variety of bacteria, are
usually used first.
 Drugs such as;
 Azithromycin(Tab 250mg OD)
 Amoxicillin with clauvinic acid(Tab 375mg QID)
 Ceftriaxone(IV 2g BD)
 Piperacillin
 Cefotaxime(Claforan)
 Gram-Positive Bacilli
Most gram-positive bacilli live harmlessly on your body without causing problems.
 Treatment of Gram-Positive Bacilli
 Gram-positive bacilli infections are treated with antibiotics. Penicillin, cloxacillin, and 
erythromycin treat over 90% of gram-positive bacteria.
 Gram-Negative Bacteria
Gram-negative bacteria have a hard, protective outer shell. Their peptidoglycan layer is
much thinner than that of gram-positive bacilli. Gram-negative bacteria are harder to kill
because of their harder cell wall. 
 Treatment of Gram-negative organisms
The aminoglycosides, particularly gentamicin, were historically the antibiotics of choice in
the treatment of Gram-negative infections.
The use of broad-spectrum antibiotics for treatment of infections in hospitalized patients
has been widespread and often empiric. These antibiotics include cephalosporins
(ceftriaxone-cefotaxime, ceftazidime, and others), fluoroquinolones (ciprofloxacin,
levofloxacin), aminoglycosides (gentamicin, amikacin), imipenem, broad-spectrum
penicillins with or without β-lactamase inhibitors (amoxicillin-clavulanic acid,
piperacillin-tazobactam)
 Intravenous fluids; the use of intravenous fluids begins as soon as possible

 Vasopressors; if the blood pressure remains too low even after receiving
intravenous fluids you may be given a vasopressor medication. This drug
constricts blood vessels and helps increase blood pressure.
 Also, other medications include low doses of corticosteroids,
 Insulin to help stabilize blood sugar levels
 Drugs that modify the immune system responses
 Painkillers or sedatives. Examples of sedatives include benzodiazepines
COUNSELING

 NON-PHARMACOLOGICAL
 Wash your hands often with soap.
 Try to stay away from people who have a cold or flu
 PHARMACOLOGICAL
 Antibiotics should not be taken with milk. This is because the calcium in the
milk binds the antibiotic and prevents gut absorption.
 Sedatives such as benzodiazepines should not be taken with alcohol.
 Do not allow the total course of antibiotics to exceed 3 weeks, except fo
specific clinical scenarios, which may require prolonged courses of oral
antibiotics.
REFERENCES

 Gupta, S., Sakhuja, A., Kumar, G., McGrath, E., Nanchal, R. S., & Kashani, K. B.
(2016). Culture negative severe sepsis: nationwide trends and outcomes. Chest,
150(6), 1251-1259.
 Kumar, A., Roberts, D., Wood, K. E., Light, B,. Parrillo, J.E., Sharma, S., …& Gurka,
D. (2006). Duration of hypotension before initiation of effective antimicrobial
therapy is the critical determinant of survival in human septic shock. Critical Care
Medicine, 34(6), 1589-1596.
 Levy, M. M., Evans, L. E., & Rhodes, A. (2018, June). The Surviving Sepsis Campaign
bundle: 2018 update. Critical Care Medicine, 46(6), 997-1000.
 Mayr, F. B., Talisa, V. B., Balakumar, V., Chang, C. C., Fine, M., & Yende, S. (2017).
Proportion and cost of unplanned 30-day readmissions after sepsis compared to other
medical conditions. Journal of the American Medical Association, 317(5), 530-531.

 Nguyen, H. B., Rivers, E. P., Knoblich, B. P., Jacobsen, G., Muzzin, A.,
Ressler, J. A., & Tomlanovich, M. C. (2004). Early lactate clearance is
associated with improved outcome in severe sepsis and septic shock. Critical
Care Medicine, 32(8), 1637-1642.
 Pruinelli, L., Westra, B. L., Yadav, P., Hoff, A., Steinback, M., Kumar, V., . . .
Simon, G. (2018). Delay within the 3-hour Surviving Sepsis Campaign guideline
on mortality for patients with severe sepsis and septic shock. Critical Care
Medicine, 46(4), 500-505.
 Shapiro, N. I., Howell, M. D., Talmor, D., Nathanson, L. A., Lisbon, A., Wolfe,
R. E., & Weiss, J. W. (2005). Serum lactate as a predictor of mortality in
emergency department patients with infections. Journal of Emergency
Medicine, 45(5), 524-528.