Septic shock {Phase A Written}
Septic shock:
Definition
It may be defined as a shock that is
associated with sepsis or infection by microbes resulting in release of
bacterial endotoxin and the activation of cellular and humeral components of
immune system.
Causes:
1. Surgical
causes-
a. Bowel
preparation and peritonitis
b. Strangulated
intestine
c. Soft
tissue infection, abscess, gangrene
d. Suppurative
biliary condition e.g. empyema of Gall bladder
e. Major
trauma, burn etc.
f. Gas
gangrene
g. Following
operation of large gut
2. Non-surgical
causes
a. Pneumonia
b. Endocarditis
c. Meningitis
d. Hospital
infection
e. Dermatological
infection
Causative organism:
1. Gram
Positive: staphylococcus, streptococcus, pneumococcus, clostridium perfringes
2. Gram
negative: E.coli, Proteus, salmonella, Klebsiella, Bacteroids
3. Some
fungi.
Types of septic shock:
A. Early
septic shock/early warm shock/hyper dynamic stage
B. Late
septic shock/late cold shock/hypo dynamic stage
Patho-physiology of septic shock:
A . Early
septic/ early warm shock/hyper dynamic stage
Release of endotoxin + exotoxin
Acts on plasma proteas, macrophage,
endothelial cells, neutrophils
Rlease
chemical mediators (cytokine IL1,2,6,8, NO, TNF, PAF, PG, LT C5a)
Vasodialation(
reduced systemic vascular resistance)
Hyperdynamic
stage
B. Late
septic shock/late cold shock/hypo dynamic stage:
Delayed improper or maltreatment of early septic shock
Delayed improper or maltreatment of early septic shock
Delayed
action of endotoxin
Increased
vascular permeability
Loss
of fluid from the vascular compartment
Hypovolemia
Reduced
cardiac output
Hypodynamic stage
Clinical features:
1. Early-
a. Patient
is pink and well perfused
b. Increased
JVP
c. Intermittent
sike of fever
d. Reduction
of urine output
e. Increased
pulse rate
f. Decreased
blood pressure
g. Mental
status stable
2. Late-
a. Cold clammy skin
b. Reduced
JVP
c. Reduction
of urine output
d. Increased
urine output
e. Hypotension
f. Anxiety,
restlessness, confusion
Investigation:
1. Laboratory
study: CBC, Coagulation profile, Blood biochemistry, RBS, S. electrolytes,
urea, creatinine, lactate, pro calcitonin, LFT
2. Microbiological
study: Culture and sensitivity
3. Imaging:
Chest X ray, USG, CT, MRI
4. CSF
analysis
Treatment of septic shock:
1. Immediate
resuscitation:
i.
Maintenance of airway-
oropharyngeal suction
ii.
Maintenance of breathing
iii.
Maintenance of
circulation
iv.
Vlood sent for C/S
v.
Broad spectrum antibiotic
vi.
Anti ulcerant
vii.
Steroid – dexamethasone
1.5 mg/Kg, usefull if given within 4 hours, repeat after 4 hours
viii.
Dopamine, dobutamine,
isoprenaline, vaopressin may be needed
ix.
Cathetarization to asses
renal function
x.
If DIC develops
1. Check
fibrinogen level
2. FFP
transfusion
3. Inj
Heparin 100 u/Kg bullous followed by 10 u/Kg hourly,
4. If
bleeding does not stop or platelet count >40,000/mm3- platelet
transfusion.
2. Specific
measures:
a. Debridement
of all dead and gangrenous tissue and proper drainage of pus
b. If
any source of infection amenable to surgery, should be treated as early as
possible.
3. Monitoring:
a. Minimum
i.
Pulse oximetry
ii.
Blood pressure
iii.
ECG
iv.
Urine output
b. Additional
modalities:
i.
Invasive blood pressure
ii.
Central venous pressure
iii.
Cardiac output
iv.
Based deficit and serum
lactate
Complication of septic shock:
SIRS MODS
Death
Conclusion:
Prevention of septic shock is vital as
outcome of treatment is not satisfactory and complications are devastating.
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