2. A 73-year-old woman is brought to the emergency center from an assistedliving
facility. The patient has a history of dementia, hypertension, and type II
diabetes mellitus. By report, she has had chills and a productive cough for
several days. In the past 24 hours she has become weaker and does not want to
get out of bed. The physical examination reveals a thin, elderly woman who is
somnolent but arousable. Her rectal temperature is 36.0°C (96.8°F), pulse rate
is 118 beats per minute, blood pressure is 84/50 mm Hg, and respiratory rate
is 22 breaths per minute. Her mucous membranes are dry. Her heart is
tachycardic but regular. She has crackles at her right lung base with a scant
wheeze. Her abdomen is soft and non tender. The extremities feel cool and her
pulses are rapid and thready. The patient is moving all extremities, without
focal deficits.
What is the most likely diagnosis?
3. Systemic inflammatory
response syndrome (SIRS)
• At least two of the following conditions:
1. Oral temperature of >38 or <35
2. Respiratory rate of > 20 breaths/min.
3. Heart rate of > 90/min.
4. Wbc count of > 12000 or < 4000
4. Sepsis syndrome
• Represents the systemic inflammatory
response triggered by an infection in the
host and is mediated by chemical
messengers.
• Tachycardia, tachypnea,fever, and immune
system activation are manifestations.
• Cellular injury, tissue damage, shock,
multiorgan failure or death results if body
is unable to overcome this insult.
5. sepsis
• SIRS that has a proven or suspected microbial
source.
• Severe sepsis: sepsis with one or more signs of
organ dysfunction
1. Hypotension or hypoperfusion.
2. Metabolic acidosis.
3. Acute alteration in mental status.
4. Oliguria
5. Adult respiratory distress syndrome.
6. Septic shock
• Sepsis with hypotension that is
unresponsive to fluid resuscitation plus
organ dysfunction or perfusion
abnormalities.
• Metabolic acidosis. (lactic acidosis).
• Alteration in mental status.
• Oliguria.
• Adult respiratory distress syndrome.
7. Multiple organ dysfunction
syndrome (MODS).
• Dysfunction of more then one organ,
requiring intervention.
• Clinical progression from SIRS – to
sepsis- to severe sepsis- to septic
shock-MODS.
• MORTALITY RATE INCREASES
WITH SEVERITY OF SEPSIS.
8. BACTEREMIA
• Presence of viable bacteria in the blood ,
as evidenced by positive blood culture.
• Positive blood culture are not essential in
the diagnosis of sepsis.
• Culture positive and culture negative
septic patients have similar outcome.
• In recent prospective studies only 17% of
pts with sepsis, 25% of pts with severe
sepsis and 69 % of pts with septic shock
had positive blood culture.
9. sepsis
• Pneumonia ,abdominal abscess, viscus
perforation, pyelonephritis are
primary causes of sepsis.
• Gram positive accounts for 25 to
50%,
• Gram negative 30 to 60 %
• Fungi : 2 to 10 %.
10. Common organism
• E.coli, staph aureus,
pseudomonas, enterococcus
faecalis, streptococci
pnemoniae, klebsiella
pnemoniae, and coagulase
negative staphylococcus.
11. Host factor
• Elderly patients
• Chemotherapy induced neutropenia.
• AIDS.
• STEROID DEPENDENCY
• Indwelling device such as
• Intravascular catheter,
• Prosthetic device
• Et tube
• Increases susceptibility to sepsis
12. epidemiology
• Sepsis is 10th common cause of death in
usa.
• 7,51,000 new cases of sepsis estimated
per year in united states.
• Cost of caring for septic patients is
estimated 17 billion us dollars/year .
• Sepsis accounts for 2 to 10 cases per 100
hospital admission.
• Mortality rate from sepsis are estimated
from 20 to 50 %.
13. pathophysiology
• Sepsis is the endpoint of a complex
process that begins with an infection.
• Initial host response is to mobilize
inflammatory cells , particularly
neutrophils and macrophages, to the
site of infection.
15. pathophysiology
• In the setting of ongoing toxin
release, persistent inflammatory
response occurs with ongoing
mediator activation, cellular hypoxia,
tissue injury, shock, multiple organ
failure, and potentially death.
17. Gram positive organism
• Produce inflammatory response by
direct action of its cell wall
components and indirect action of
secreted soluble substance.
18. Gram positive organism
• Cellular wall components such as
peptidoglycan.
• exotoxin are substance secreted by
bacteria that produce host response
through cell membrane receptors.
19. Mediators of sepsis
• In response to toxins, the body reacts by
secreting substance such as cytokines,
eicosanoids, platelet activation factor,
oxygen free radicals, complement and
fibrinolysins.
20. Mediators of sepsis
• Six categories of cytokines
exists:
• Interleukins 6 &8, tumor
necrosis factor, interferon,
colony stimulating factor,
chemotactic factor, transforming
growth factor beta.
21. cytokines
• Cytokines are primarily pro and anti
inflammatory or growth promoting.
• The main pro-inflammatory cytokines
are IL-1 , TNF, AND IL-8.
• Primary anti-inflammatory cytokines
are IL-10, IL-6, transforming growth
factor beta.
22. Inflammatory response
• If inflammatory response is adequate
, infection is controlled.
• If response is deficient or excessive,
persistent and worsening cascade is
produced leading to shock, organ
failure and potentially death.
23. Organ system
dysfunction
• Neurologic
• Patient with sepsis, manifested by
• Altered mental status
• Lethargy
• Septic encephalopathy.
24. Organ system
dysfunction
• Mortality rate is higher if gcs less then 13
• Causes are endotoxemia, renal hepatic
dysfunction, altered cerebral perfusion,
metabolic derangement.
26. Cardio vascular dysfunction
in sepsis
• Early in sepsis hyperdynamic state causes
increased cardiac output, and decreased
systemic vascular resistance.
• Aggressive fluid resus increases pre load
and ejection fraction.
• Cardio vascular compromise from septic
shock is reversible and normal function
returns with in 10 days.
27. Pulmonary compromise
• Is common and often lethal.
• Common pulmonary end point is ARDS
• Bilateral pulmonary infiltrates on
frontal chest xray.
• Impaired oxygenation
• Arterial hypoxemia
• Alveolar-capillary damage.
28.
29. Gastro intestinal
• Prolonged ilieus due to hypoperfusion
• Blood flow dependant on mean
arterial pressure.
• Little auto regulation of blood flow
• Liver produces some of the mediator
of sepsis
• Aminotranferase and bilirubin are
raised early in sepsis.
30. Endocrine
• IL-1 and IL-6 both activate
hypothalamic-pituitary axis.
• TNF depress pituitary function.
• Adrenal insufficiency due to
decreased blood flow in sepsis
• Decreased pituitary secretion of
ACTH due to severe stress.
31. Hematologic
• SEPSIS causes abnormalities in
coagulation.
• Endotoxin, TNF, IL-1, protein C,
protein S, and fibrinolysin leads to
consumption of essential factors
leading to DIC.
• Activation of coagulation cascade
leads to thrombi, if not corrected
compromise organ perfusion and
contributes to organ failure.
32. Clinical features
• Septic patient manifests signs of
Infection
• TACHYCARDIA
• TACHYPNEA
• HYPERTHERMIA OR HYPOTHERMIA
• HYPOTENSION IF SEVERE SEPSIS
33. CLINICAL FEATURES
• Early signs of sepsis tachycardia and
tachypnea.
• Septic patient have flushed skin with
warm extremities due to early
vasodilatation and hyperdynamic
state.
• Severe septic shock skin appears to
be mottled and cyanotic .
34. Septic shock
• Should be differentiated from
hypovolemic or cardiogenic shock
• Septic patient will classically appear
flushed with warm well perfused
extremities,
• In hypovolemic or cardiogenic shock
patient will appear cool clammy with
poorly perfused extremities. Neck
veins flat, pulse rapid and thready.
35. Risk factors for sepsis
• Immunocompromised state
• AIDS
• DIABETES
• SPLENECTOMY
• CONCURRENT CHEMOTHERAPY
• ELDERLY AGE.
36. RESPIRATORY SYSTEM
• Most common focus of infection
• Productive cough, fever , chills, urti,
throat and ear pain.
• Both presence of pnemonia, tachypnea,
hypoxia are predictors of death in sepsis
• Look for focal infection , exudative
tonsillitis, dullness on lung auscultation,
pharngeal thrush as marker of immuno
compromised state.
37. Gastro intestinal system
• Second most common source of sepsis
• h/o abdominal pain, nausea, vomiting,
diarrhea, fever should be noted.
• Physical examination to r/o peritoneal
irritation, abdominal tenderness,
hyperactive or hypoactive bowel sounds is
critical to find source of sepsis.
38. Physical findings
• Murphy's sign indicating cholecystitis
• Mcburneys point tenderness
indicating appendicitis.
• Left lower quadrant pain suggesting
diverticulitis
• Rectal examination revealing rectal
abscess or prostatitis
39. Neurologic
• Signs of meningitis
• Nuchal rigidity
• Fevers
• Change in consciousness
• Lethargy
• Altered mental status may be due to
Neurologic disease or due to decreased
perfusion from a shock state.
40. Genitourinary
• History of flank pain
• Dysuria
• Polyuria
• Discharge
• Foley catheter placement
• Genitalia should be evaluated for ulcer, discharge,
penile or vulvar lesion.
• Rectal examination to r/o rectal abscess, tender
boggy prostrate t/ r/o prostatitis
41. Musculoskeletal
• Redness swelling and warmth over joint
• Decreased ROM of joint
• Cellulitis
• Abscess
• Wound infection
• Fasciitis
• Crepitus indicates gas forming organism
• Lymphadenopathy,
42. Diagnostic strategy
hematology
• White blood cells marker of
inflammation
• Leucocytosis
• Febrile neutropenic patient are at risk
of increased severe infection
43. Diagnostic strategy
hematology
• WBC < 500 cells/ cubic mm should be
admitted, isolated and iv antibiotics
• Hemoglobin Hb > 10 and haematocrit
HCT > 30 % should be maintained
44. DIC
• Thrombocytopenia
• Elevated prothrombin time
• Elevated activated partial thromboplastin
time.
• Decreased fibrinogen
• Increased fibrin split products.
• Are associated with DIC and severe sepsis
syndrome
45. chemistry
• Low bicarbonate level suggests acidosis
and inadequate perfusion
• Elevated anion gap acidosis represent
lactic acidosis or diabetic ketoacidosis.
• High creatinine level : renal dysfunction
• Elevated Lactate level: poor prognosis
• Elevated amylase and lipase : pancreatitis
• LFT : to identify liver failure
46. microbiology
• Blood, sputum, urine, csf , tissue
culture are important to identify
organism
• Gram stain of sputum, csf, abscess,
help early prediction of organism
• Urinalysis showing Leucocytosis : UTI
• CSF Leucocytosis : meningitis
47. radiology
• Chest xray : focal infiltrate : pneumonia
• Fluffy bilateral infiltrate : ARDS
• upright chest x ray : to r/o gas under
diaphragm , suspected bowel perforation
• Pneumomediastinum : esophageal
perforation, mediastinitis
• Soft tissue x ray of infected area : looking
for air , TO r/o gas forming organism
48. CT SCAN
• Diverticulitis, appendicitis, necrotizing
pancreatitis, micro perforation of
stomach or bowel , intra abdominal abscess
best diagnosed by CT scan
• MRI scan to identify soft tissue infection
, necrotizing Fasciitis or epidural abscess.
• USG for cholecystitis, tubo ovarian
abscess.
51. Management of sepsis
• Early detection and aggressive
management reduces mortality.
• Primary goal :Adequate tissue oxygenation
and perfusion .
• AIRWAY management, intravenous access,
oxygen, antibiotics, fluid resuscitation .
52. Resus in emergency dept
• Early fluid resus,
• Normalization of blood pressure
• Adequate oxygen delivery
• Proper tissue oxygenation
• In septic shock bp <90, fluid challenge 20-
30 ml/kg or lactic acid > 4 mmol/l
• Aim is to normalize preload and to prevent
hypoxia
53. preload
• Patient in sepsis or septic shock are often
in a state of fluid deficit.
• On an average 5 liters of fluid are needed
in first 6 hours of resuscitation.
• CVP should be maintained at a level of 8-
12 mm hg .
• Intubated patient with positive pressure
ventilation the level should be 12-16 mm
Hg
54. PERFUSION PRESSURE
• AIM is to maintain an adequate blood
pressure.
• Mean arterial pressure ( 2/3 diastolic+ 1/3
systolic) should be kept between 60-90
mm Hg.
• IF mean arterial pressure is below 60 mm
Hg in the presence of adequate preload ,
vasopressor should be started.
55. Oxygen delivery
• Once preload and pressure is
normalized
• Focus should be on oxygen delivery
56. Oxygen delivery
• Hemoglobin should be maintained 8-10
g/dl, haematocrit of 30%.
• Oxygen delivery by non rebreather mask
or intubation,
• If this is normalized , and patient not
tachycardia, doputamine can be added to
increase cardiac contractility and increase
cardiac output resulting improved oxygen
delivery
57. Respiratory support
• Patients with respiratory rate >30
are likely to develop respiratory
collapse.
• 85 % of pts with severe sepsis needs
mechanical ventilation.
• Improved oxygen delivery is achieved
by mechanical ventilation, sedation
and paralysis.
59. Cardio vascular support
fluid resus
• Pts with sepsis require large volume
of iv fluid to maintain perfusion.
• Intra vascular Hypovolemia is due to
vasodilatations and diffuse capillary
leak.
• 6-10 liters of crystalloid may be
required in first 24 hours.
60. Fluid resus
• Fluid replacement must be • NORMAL SALINE and
titrated to clinical ringer lactate are equally
parameter such as: effective and neither
• Heart rate worsens lactic acidosis
• Blood pressure
• Change in mental status • Colloids are as effective as
• Capillary refill crystalloids
• Cool skin
• Urine output(0.5-1 • Colloids are expensive
ml/kg/hr)
61. vasopressor
• If fluid resus fails ,. Vasopressor
support may be required
• Septic patient requiring vasopressor
should have an arterial cannula so
that blood pressure can be monitored
more accurately
• Mean arterial pressure should be
maintained 60-70 mm Hg.
63. Management
recommendation for
hemodynamic support
• Basic principle
• Admission to ICU
• Arterial cannulation in pts with shock
• Resus to target tissue perfusion
• Central venous or pulmonary arterial
catheter placement to assess cardiac
filling.
64. Fluid resus
• Fluid are primary modality to resus
• Colloids and crystalloids equally effective
• Invasive monitoring for patients not
responding to initial resus with target
pulmonary wedge pressure of 12-15 mm hg
• HB concentration should be maintained 8-
10 g/dl
65. Vasopressor therapy
• Dopamine is first line agent in shock
unresponsive to fluid resus
• Routine low dose dopamine is not
recommended
• Epinephrine is reserved for refractory
shock.
• Vasopressin may be considered in
refractory shock not responding to fluid
resus and other vasopressor.
66. Inotropic therapy
• Dobutamine is the first choice for
pts with refractory low cardiac index
• Dobutamine may improve cardiac
index and organ perfusion
• Vasopressor and inotropes can be
titrated separately to maintain mean
arterial pressure
• Epinephrine and dopamine can be
used as inotropes.
67. antibiotics
• Antibiotics should target nidus of
infection.
• Mortality is reduced by 50 %
• If pts condition permits , culture before
starting antibiotics.
• Double cover for virulent organism such as
pseudomonas.aeruginosa and
• Multiple organism infection such as
peritonitis
69. Suggested antibiotics
• if MRSA : add vancomycin
• CSF: ceftriazone+ vancomycin
• Iv drug abuse: nafcillin
+aminoglycoside
70. Steroid therapy
• random cortisol level should be
measured in the emergency dept , to
guide inpatient therapy ,
• If steroid administered , it should be
low dosed < 300mg/day of
hydrocortisone.
71. disposition
• Pts with sepsis syndrome should have
consultation with admitting service while in
emergency dept.
• Once emergency dept management is
complete , antibiotics are given, need for
emergency operative intervention and
procedure has been excluded,
• Patient should be admitted.
72. disposition
• Pts with severe sepsis and septic
shock , MODS should be admitted to
ICU
• Pts with SIRS can be admitted in
high dependency ward monitored with
closed supervision .
73. Key concepts
• Sepsis is a progression of disease
ranging from SIRS to sepsis to
severe sepsis to septic shock to
MODS.
• Elderly, Immunocompromised,
neutropenic pts are at increased risk
for development of sepsis syndromes.
74. Key concepts
• Early administration of appropriate
antibiotics is essential in the
treatment of sepsis syndromes.
• Patients with septic shock should be
treated with aggressive fluid
resuscitation and vasopressor
therapy as needed.
76. A 73-year-old woman is brought to the emergency center from an assistedliving
facility. The patient has a history of dementia, hypertension, and type II
diabetes mellitus. By report, she has had chills and a productive cough for
several days. In the past 24 hours she has become weaker and does not want to
get out of bed. The physical examination reveals a thin, elderly woman who is
somnolent but arousable. Her rectal temperature is 36.0°C (96.8°F), pulse rate
is 118 beats per minute, blood pressure is 84/50 mm Hg, and respiratory rate
is 22 breaths per minute. Her mucous membranes are dry. Her heart is
tachycardic but regular. She has crackles at her right lung base with a scant
wheeze. Her abdomen is soft and non tender. The extremities feel cool and her
pulses are rapid and thready. The patient is moving all extremities, without
focal deficits.
What is the most likely diagnosis?
77. Answer case 5 is SEVER SEPSIS
Summary: A 73-year-old woman presents from an
assisted-living facility with
cough, lethargy and hypotension of unknown
etiology.
Most likely diagnosis: Severe sepsis.
Most likely etiology: Pneumonia, nursing-home
acquired`
78. This woman appears to be suffering
from severe sepsis, a clinical entity
on the continuum from systemic
inflammatory response syndrome to
septic shock with multiorgan system
dysfunction (see below for
definitions). In her case, the etiology is
likely pneumonia, an extremely
common cause of sepsis in elderly
patients. Sepsis caused by a urinary
tract infection (ie, urosepsis) is another
important cause of sepsis in this
population.
