SEPTICEMIA

Presentation 2, Group B

GROUP MEMBERS
1) Nor Nadhira binti Mahmod
2) Norsatila binti Saibeh
3) Nor Hanan binti Abd Nasir
4) Nur Aadila Fatihah binti Mazlan
5)
Nik Nur Hakimah binti Nik Mohd Ali

SEPTICE
MIA
Nor Nadhira binti
Mahmod
012012100106

Learning Objectives:
To define what is septicemia, sepsis
and SIRS
To identify the common part of
infection
To know the cause of septicemia
To understand the mechanism of
septicemia

SEPTICEMIA

The presence of bacteria in the blood that

cause disease and local inflammation

SEPSIS
Clinical response to infection that
characterised by systemic
inflammation and widespread tissue
damage

Basically,
Septicemia is a term used to explain the
presence of bacteria in the blood
(bacteremia) that capable to cause disease
and local inflammation
These sepsis need to treat rapidly as the
inflammation can trigger cascade and lead
to multiple organ dysfunction

SIR
S

Systemic Inflammatory Response

Syndrome

Clinicalresponse to a nonspecific insult of

either infectious or non infectious origin.
Due to:
Ischemia.
Inflammation.
Trauma.
Infection.
Several insults
combined

Common parts of infection:

i.
ii.
iii.
iv.
v.
vi.

Abdomen
Lungs (pneumonia)
Urinary tract
Bone (osteomyelitis)
CNS (meningitis)
Heart (endocarditis)

Bacteria involved:
Gram negative bacteria
Escherichia coli
Klebsiella pneumoniae
Enterobacter sp.
Serratia sp.
Salmonella sp.

Condition that can lead to

septicemia:

Human wound infection

Surgical infection
Tooth abscess
Internal injuries
Oral cavity burns

Mechanism

SEPTICAEMIA
NORSATILA BINTI SAIBEH
012012100069

LEARNING OBJECTIVE
To identify the risk factors of getting
Septicaemia

RISK FACTORS
Factors that increase the risk of
developing septicaemia include:
Age - elderly and very young at risk.
Instrumentation or surgery (including
illegal abortion occurring in
unhygienic circumstances).
Chronic or severe illness
Severe bacterial pneumonia
Severe burns to the skin

RISK FACTORS CONT.

Substance abuse, such as alcoholism
Intravenous drug use
Malnutrition, which weakens the
immune system
Long term antibiotic treatment that
changes the ratio of bacteria in the body
by killing some strains and not others
Immune suppression therapy, such as
that used to manage HIV infection
An open wound

Nor Hanan binti Abd

Nasir
012012100064

Outline

Sudden high fever with chills

Generally feeling unwell
Tachycardia
Cyanosis

Advance symptom
-confusion
-red spot on skin
-septic shock

cont
Drowsiness or impairment
consciousness (common in the elderly
but late sign in young children and
young adult)
Sweating
Lympahadenopathy
Hepatomegaly

Diagnostic issue
Localising site of infection
Interpreting microbological finding
Need for early initiation of treatment
( antibiotic and antifungal)

Diagnosis
SEPTICEMIA CAN BE DIAGNOSE BY :
Medical history
Physical examination
Blood test & Full blood count
Blood culture
Coagulative profile
Heamatological test

Physical examination
Infection

SIRS

SEPSIS

SEVERE SEPSIS

DEATH

Physical examination
Low blood pressure
Low body temperature
Sign of related disease eg .
Meningitis epiglottitis, pneumonia or
cellulitis
Chest x-ray
CT scan

Criteria for presence

suspect
respiratory rate > 20 breath/min or
PaCO2<4.3 Kpa
Heart rate > 90 beats/min
Core temperature < 36 or > 38
WBC < 4000 or > 12000 cell/ mm3
or >10% immature form

Blood test
Complete blood count
WBC either high or low
Platelet low in DIC
ESR- high
CRP- high
Lactic acid high due to poor tissue
perfusion and oxygenation
Random blood sugar usually high
except in iver dysfunction

Blood culture
To check for bacteria or other
microorganism in the blood sample
Require in severe sepsis
Only 30%-50% positivity in severe
sepsis or shock
Use
- Blood, tissue, stool, urine

cont
No of blood culture : 2 max 3 should
be obtained
Culture as soon as possible following
onset of fever

Normal and abnormal result

Normal no bacteria
Abnormal infection

Other laboratory test

Urine
-urinary tract infection
Wound secretion
-which antibiotic works best
Repiratory secretion
- Mucus - ? germ

Coagulative profile
It is a screening test for abnormal
blood clotting because it examines
the factors most often associated
with a bleeding problem.
This is done in severe cases to
support other test .
Coagulation profile includes INR,
APTT, platelets and fibrinogen.

Test result -CP

APTT( activated partial thromboplastin time )
-measure one part of the clotting pathway known as
the intrinsic pathway it is compared against a
sample of normal blood , the control value. It is
increased by theraphy with intravenous heparin,
haemophilia or DC
INR (International Normalised Ratio)
measures one part of the clotting pathway known as
the extrinsic pathway it is increased by warfarin
therapy, liver dysfunction, orDIC.

Platlet count
the number of platelets in the bloodstream; it is also a routine
component of thefull blood count
Fibrinogen this protein is a precursor to fibrin, which is an essential
part of a blood clot. Fibrinogen may be consumed by conditions such
as DICor some snakebite envenomations. Decreased fibrinogen
results in an increased bleeding tendency.
D- dimer
- sometimes included this is a product of clot breakdown, and is
increased in conditions of increased clotting activity in the body, but
is relatively non-specific because it is often elevated due to different
reasons.
The specific results of the coagulation profile wil help your doctor to
decide whether any further investigations (tests) are required.

Hematological changes
Neutropenia
Thrombocytopenia
Disseminated intravascular
coagulation (DIC)

SUMMARY
Sign and symptom

Diagnosis

REFERENCE
Books
LANGE Medical microbiology
Medical physiology- Guytun & Hall
Clinical medicine Kumar & Clark
A text book of microbiology ( P.CHAKRABORTY)
WEBS
www.criticalcare.org.za ( diagnosis and investigation of sepis)
Surgery.about.com
http://www.medicinenet.com/sepsis/page4.htm
Septicemia. (2011, August 24). University of Maryland Medical
Center. Retrieved June 29, 2012 from http://
www.umm.edu/ency/article/001355trt.htm

MANAGEMENT OF
SEPTICEMIA

NIK NUR HAKIMAH BINTI NIK MOHD ALI

012013050218
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LEARNING OBJECTIVES
UNDERSTAND THE OBJECTIVES OF THE
TREATMENT
KNOW GENERAL MANAGEMENT OF
SEPTICAEMIA
KNOW TYPES OF CRSTALLOID
ABLE TO KNOW,PHARMACOKINETICS, MOA,
CLINICAL USES, ADVERSE EFFECT,
PRECAUTIONS,CONTRAINDICATION AND
DRUG INTERACTION OF CRSTALLOID
TO KNOW PREVENTION FOR SEPTICAEMIA
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BRIEFLY
1 Dental treatment.
2 Endoscopic
procedures
3 Urinary tract
infections.
4 Bacteremia
Bowel infections.
+ SIRS

III
Sepsis+CVS
dysfunction
and/or ARDS
Sepsis+hypoten
sion
despite
adequate fluid
Varies
from a
resuscitation
mild degree to
completely
irreversible
organ failure

Bacteremia
Sepsis
Severe sepsis

Severit
y

Septic Shock
MODS

CREDIT TO:
DR. MOHAMMAD
SAAD ABDUL
MAJID LECTURE

Management
Severe sepsis and septic shock are common,
complicated & deadly conditions within the
same pathophysiologic spectrum.
As defined by the American College of Chest
Physicians/Society of Critical Care Medicine
Consensus Conference in 1992, this spectrum
begins with the Systemic Inflammatory
Response Syndrome or SIRS.
Severity of illness and the inherent mortality
risk escalate from SIRS, through sepsis, severe
sepsis and septic shock to multi-organ failure.
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Management cont.
Two types of death:
Shock
Multi organ failure

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Management cont.
Objectives of treatment
Assure perfusion of critical vascular beds (cerebral,
coronary, renal)
Prescription underlying cause
Start adequate antibiotic therapy (proper dosage &
spectrum) as soon as possible
Resuscitate the patient using supportive measures to
correct hypoxia,hypertension & impaired tissue
oxygenation(hypoperfusions)
Identify and control the source of infection with
specific antimicrobials.
Maintain adequate organ system function
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Fundamental sepsis management

EARLY MANAGEMENT
The first priority in any patient with severe
sepsis or septic shock is stabilization of
their airway and breathing. So, perfusion
to the peripheral tissues should be
restored

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Fundamental sepsis management

cont.
Stabilize respiration
Supplemental oxygen
Intubation and mechanical ventilation required
to
support
the
increased
work
of
breathing(tarcypenea)
Sedative and induction agents (e.g.etomidate)
used to intubate patients
Chest
radiographs
and
arterial
blood
analysis.These studies are used in combination
with other clinical parameters to diagnose acute
respiratory distress syndrome (ARDS), which
frequently complicate sepsis
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Assess perfusion
2 WAYS TO ASSESS PERFUSION
1. Hypotension
2. Serum Lactate

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Fundamental sepsis management

cont.
Assess perfusion
Once the patient's respiratory status has been stabilized,
the adequacy of perfusion should be assessed. Hypotension
is the most common indicator that perfusion is inadequate
(eg, systolic blood pressure (SBP) <90 mmHg, mean
arterial pressure <70 mmHg, decrease in SBP >40 mmHg).
Therefore, it is important that the blood pressure be
assessed early and often.
An elevated serum lactate (eg, >1mmol/L)can be a
manifestation of organ hypoperfusion in the absence of
hypotension and is an important component of the initial
evaluation. A serum lactate level 4mmol/Lis consistent
with severe sepsis. Additional laboratory studies that help
characterize the severity of sepsis include the platelet
count, international normalized ratio, creatinine, and
bilirubin.
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START OUR MANAGEMENT

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Early Goal-Directed Therapy

Once hypoperfusion exists, early
restoration of
perfusion is
necessary to prevent multiple organ
dysfunction and mortality
Initial
resuscitation
should
be
completed in the first 6 hours
Achieving the following resuscitation
goals is referred to as early goaldirected therapy (EGDT)
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Early Goal-Directed Therapy

cont.
Goals during
resuscitation:

the

first

hours

of

fluid

Used crystalloid fluid 500ml bolus until central

venous pressure (CVP) 8 to 12 mmHg (12-15 mmHg
if incubated on ventilator)
Used vasopressors to attain mean arterial pressure
(MAP) 65 mmHg
Central venous oxygen saturation (Svo2) >70% or
mixed venous more than 65%
Uterine output 0.5 mL/kg/hour

Meeting these goals within the first 6 hours after

onset severe sepsis or septic shock is associated
with an improvement in survival
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Early Goal-Directed Therapy

cont.
Classification of fluid resuscitation in EDGT
CRYSTALLOID or COLLOID
Crystalloid - Normal saline, Ringers solution,
Hartmans solution
Colloid - Albumin solutions, dextran, hetastrach

Vasopressors
Dopamine, Noradrenaline, Adrenaline,
Phenylephrine, Vassopressin

Inotropes
Dobutamine,milirone

Broad spectrum antimicrobials

Vancomycin, Clindamycin, Ciprofloxacin,
MetronidzoleNik Nur Hakimah Binti Nik Mohd Ali
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Crystalloid therapy
The two most commonly
crystalloid solutions are

used

1. Sodium chloride 0.9% solution (normal

saline or NaCl)
2. Lactated ringers solution

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Crystalloid therapy cont.

1. Sodium chloride 0.9% (normal saline) for
intravenous
Pharmacokinetic
Sodium and chloride electrolytes distribute, primarily in
the extracellular fluid. Because the physiological saline
solution is isotonic, it administration will not produce a
change in osmotic pressure of the extracellular fluid ,
whereby water will not pass into with intracellular
compartment and both ions will practically enter the cell.

Mechanism of action
Plasma volume expander
Also expands interstitial fluid volume
Plasma volume effect is only temporary as most of the
saline moves out of the blood vessels quite quickly (low
molecular weight)
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Crystalloid therapy cont.

Clinical uses
Initial replacement fluid, in volume
or

depleted

dehydrated patients. Volume depletion

may
be due to loss of blood, plasma or fluid
and
electrolytes
Maintenance of hydration during prolonged

patient contact time

To keep vein open, as IV route for drugs
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Crystalloid therapy cont.

Contraindications
Hypercholeremic
Metabolic asidosis
Adverse effects
Fluid overload
If an adverse reaction does occur, discontinue the
infusion, evaluate the patient, institute appropriate
therapeutic countermeasures and save remainder
of the fluid for examination if deemed necessary.

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Crystalloid therapy cont.

Precautions
If administering a fluid bolus check BP and
lung sounds every 250cc. Discontinue
bolus if pulmonary edema is discovered, or
once BP is in therapeutic range (generally
SBP
above
90
mm/Hg).
Avoid
hypervolemia.
In patients with diminished renal function,
administration of normal saline may result
in sodium retention.
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Crystalloid therapy cont.

2. Lactated ringers solution for intravenous
Composition
Sodium chloride
Potassium chloride,
Calcium chloride,
Sodium lactate solution at 50%

Pharmacokinetic
This solution diffuses out in extracellular space, thus
enhancing the volume accordingly.
The metabolism of this solution is similar to the different ions
of its composition: sodium, potassium, calcium and chlorides.

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Crystalloid therapy cont.

Mechanism of action
Replaces water and electrolytes

Clinical uses
Used for states of predominantly
extracellular dehydration e.g. vomiting,
diarrhoea
Hypovolemia e.g. hemorrhagic shock,
burns, perioperative electrolyte losses

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Crystalloid therapy cont.

Adverse effects
Redness or pain at the injection site
may occur
Fever, trouble breathing, swelling (in
serious
adverse effect)

Contraindications
Contraindicated in severe metabolic
acidosis or alkalosis, and in severe liver
disease or anoxic states which affect
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lactate metabolism

Crystalloid therapy cont.

Precautions
Use of this solution requires that patients clinical
state and laboratory tests be monitored as
follows:
- Severe renal failure
- Oedemas with sodium retention
- Treatment by corticosteroids and their
derivatives.
Since this solution is content-potassium, kalaemia
should be closely monitored in patients who may
develop hyperkalaemia, for example those with
chronic renal impairment
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Colloid therapy
Colloids are higher-molecular-weight solutions
that increase plasma oncotic pressure
It can be classified as either natural (albumin)
or artificial (starches, dextrans, and gelatins)
Colloids include the starches, hetastarch and
pentastarch, human serum albumin, gelatin,
and dextran
Due to their higher molecular weight, colloids
stay in the intravascular space significantly
longer than crystalloids
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Colloid therapy cont.

1. Albumin
Albumin is a protein derived from human plasma. It is
available in varying strengths from 4 to 25%. The Saline
versus Albumin Fluid Evaluation (SAFE) study compared
fluid resuscitation with albumin or saline on mortality and
found similar 28-day mortalities and secondary outcomes
in each arm.
However, a subset analysis of patients with sepsis and
acute lung injury resuscitated with albumin showed a
decrease in mortality, although statistically it was
insignificant. There was a significant increase in mortality
in trauma patients particularly with head injury

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Colloid therapy cont.

2. Hydroxyethyl starch (HES)

Synthetic
colloid
derived
from
hydrolyzed
amylopectin, which has been found to be harmful,
causing renal impairment at recommended doses
and impairing long-term survival at high doses.
HES can also cause coagulopathy and bleeding
complications from reduced factor VIII and von
Willebrand factor levels, as well as impaired
platelet function.
HES increases the risk of acute renal failure among
patients with sepsis and reduces the probability of
survival. HES should be avoided in sepsis

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Colloid therapy cont.

3. Dextrans
Frequently used for rapid plasma
expansion, but rather to lower blood
viscosity. This class can cause renal
dysfunction, as well as anaphylactoid
reactions

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Colloid therapy cont.

4. Gelatins

Produced from bovine collagen. Because they

have a much smaller molecular weight, they
are not as effective expanding plasma volume;
however, they cost less.
Reported to cause renal impairment, as well as
allergic reactions ranging from pruritus to
anaphylaxis.
Gelatins
are
not
currently
available in North America.
Because of the significant calcium content of
Hemaccel, blood should not be infused through
tubing previously used for this product

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5. Statins
Most
commonly
prescribed
agents
for
hypercholesterolaemia and dominate the area of
cardiovascular risk reduction
Moreover, these drugs have a variety of actions that
are independent of their lipid lowering effect. Such
anti-inflammatory, antioxidant, immunomodulatory,
and antiapoptotic features have been collectively
referred to as pleiotropic effects.
By virtue of their pleiotropic effects, statins have also
emerged as potentially useful in various critical care
areas such as bacteraemia, the early phases of
sepsis and septic shock, as well as the management
of serious infections.
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PREVENTION
Immunocompromis
ed patient/Impared
host defence
Patient under
chemotherape
utic drugs

Burn

Geriatrics
Patient

Diabetes
Mellitus
Severe
trauma

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Malignan
cy
Nik Nur Hakimah Binti Nik Mohd Ali

Renal or
Hepatic
Failure
74

Prevention
1.

Immunisation(especially: children)

2.

Prompt treatment of local infections

3. Hospitalized patient: look out for nidus of infection- IV lines,

catheters, E.tubes
4. Shortening the hospital stay
5. Removing indwelling catheters as early as possible
6. Avoiding unnecessary invasive procedures
7. Using aseptic techniques

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Prevention
8. Propylactic antibiotics in the preioperative
phase.
Topical antibiotics around invasive catheter
Topical antibiotics as part of dressings (burn patient)

9. Prevention of sepsis with topical or systemic antibiotics is

suggested for high-risk patients.
Ex:Use nonabsorbable antibiotics in stomach
prevent translocation and occurance of bacteria
10. Early detection of infections and intake of antimicrobial

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References
1. Dellinger RP, Carlet JM, Bion J, Parker MM et al.
(2008)
Surviving
Sepsis
Campaign:
international guidelines for management of
severe sepsis and septic shock: 2008. Crit
Care Med 36: 296-327
2. Gan TJ, Bennett-Guerrero E, Phillips-Bute B, et
al. Hextend, a physiologically balanced
plasma expander for large volume use in
major surgery: a randomized phase III clinical
trial. Hextend Study Group. Anesth Analg
1999; 88:992998
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3. Jones AE, Brown MD, Trzeciak S, et al.

The effect of a quantitative resuscitation
strategy on mortality in patients with
sepsis: a meta-analysis. Crit Care Med
2008; 36:739
4. Kellum JA. Fluid resuscitation and
hyperchloremic acidosis in experimental
sepsis: improved short-term survival and
acid-base
balance
with
Hextend
compared with saline. Crit Care Med
2002; 30:300305
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5. Rangel-Frausto MS, Pitte D, Costigan M et al.

The natural history of the systemic
inflammatory responsive syndromes (SIRS). A
prospective study. JAMA 1995; 237:117
6. Rivers E, Nguyen B, Havstad S, et al. Early
Goal-Directed Therapy Collaborative Group.
Early goal-directed therapy in the treatment
of severe sepsis and septic shock. N Engl J
Med 2001; 345: 136877
7. www.emedicine.medscape.com
8. www.betterhealth.vic.gov.au
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Pharmacology
NUR AADILA FATIHAH BINTI MAZLAN
012012100086

Learning objectives
1. To know the specific drug used to
treat septicemia.
2. To understand the mechanism of
action and pharmacology of drug
use to treat septicemia.
-. Inotropes
-. Antimicrobials
-. Vasopressor

Inotropes

Inotropes
-dobutamine
-Milirinone

Dobutamine
Mechanism of actions:
- it is a derivative of dopamine but not in D1 or
D2 receptor agonist.
( no effect on dopaminergic receptor)
- acts on both alpha and beta adrenergic receptor.
-strong beta 1 and weak alpha effects

Dobutamine
-Strong beta 1 and weak alpha effects
Resulting : increase force of cardiac contraction
increase in cardiac output
increase heart rate
increase blood pressure
decrease peripheral vascular resistance

Dobutamine
- dobutamine is used in early goal-directed
therapy if there is evidence that tissue
hypoperfusion and myocardial dysfunction is
related to sepsis.
- drug of choice for improving cardiac
contractility in hypotensive patients.

Dobutamine
Administration:
-intravenous

Dobutamine
Pharmacokinetics:
Absorption:
- onset : 10 minutes
- duration: 10 minutes
- time to peak effect : ~ 15 minutes
Distribution:
Volume of distribution : 0.2 L/kg

Dobutamine
Metabolism:
- metabolized in tissues and liver by catechol-Omethyl transferase
- metabolites : glucoronide conjugate, 3 - O methylated dobutamine ( inactive)
Elimination:
-Half life : 1-2 minutes
-Clearance: 90mL/kg/min
-Excretion : urine

Dobutamine
clinical use:
- low cardiac output
- congestive heart failure

Dobutamine
Contraindications:
- hypersensitivity
- idiopathic hypertrophy subaortic stenosis
Cautions:
- arrhythmias
- hypovolemia
- myocardial infarction (MI)
- severe coronary artery disease (CAD)

Adverse effect
Tachyarrhythmia
Hypertension
Eosinophilic myocarditis
Premature ventricular beats
Angina
Dyspnea
Fever
Headache
Nausea
Palpation

Antimicrobials

Antimicrobials
Cefotaxime (claforan)
Ticarcillin - clavulanate (carboxypenicillin)
Piperacillin - tazobactam (ureidopenicillin)
Impinem - cilastatin (carbapenems)
Clindamycin (lincosamide)
Metronidazole (nitroimidazole)
Ciprofloxacin , Levofloxacin (fluoroquinolones)
Vancomycin (glycopeptide)

Piperacillin- tazobactam
mechanism of action:
- antipseudomonal penicillin plus beta-lactamase
inhibitor
- inhibits biosynthesis of cell wall mucopeptide
synthesis by binding to 1 or more of the penicillinbinding proteins

Piperacillin- tazobactam
Administration:
-intravenous
-intramuscular

Piperacillin- tazobactam
Pharmacokinetics:
Absorption:
- peak plasma time: 30 minutes following infusion
- bioavailability 71%( piperacillin IM) 84%
(tazobactam IM)

Distribution:
- protein bound:
*piperacillin (25-33%)
*tazobactam (31-32%)
Lungs, intestinal mucosa,skin, muscle, uterus,
ovary, prostate, gall bladder, and bile
-low CSF penetration in noninflammed meninges

Metabolism:
- hepatic to desethyl metabolite (piperacillin) and
inactive metabolite (tazobactam)
Elimination:
-Half- life: 0.7- 1.2 hours
-Excretion:
* piperacillin: urine (68%)
* tazobactam : urine (80%)
Both also excreted in bile

Piperacillin- tazobactam
Uses:
- severe infections
- nosocomial pneumonia
- intra abdominal abscess
- complicated intra abdominal infection
- skin and soft tissue infection
In pediatrics:
- cystic fibrosis
- appendicitis, peritonitis
- complicated intra abdominal infection

Piperacillin- tazobactam
adverse effects:
- diarrhea
- headache
- insomnia
- nausea and vomitting
- fever
- pruritus
- hypertension
- rash
- pain

Piperacillin- tazobactam
Contraindications:
- allergy to peniccilins, cephalosporins, impinem, betalactamase inhibitors
Cautions:
Risk of bleeding complications, especially in renal impairment,
discontinue if thrombocytopenia or bleeding occurs
Serious skin reactions reported, including Stevens Johnson
syndrome and toxic epidermal necrolysis, discontinue if
reaction occurs

Ticarcillin- clavulanate
Mechanism of action:
Inhibits cell wall biosynthesis by binding to 1 of
more penicillin binding protein, which
subsequently inhibits bacterial cell wall synthesis
and has a bactericidal effect

Ticarcillin- clavulanate
Administration:
-intravenous
- intramuscular

Ticarcillin- clavulanate
Pharmacokinetics:
Absorbtion :
- absorption : 86% (IM)
- peak plasma time :30 - 75minutes (IM)
- peak plasma concentration: 324mcg/mL
(immediately after 30minutes IV infusion of 3.1g)

Ticarcillin- clavulanate
Distribution:
- protein bound : 45%(ticarcillin) 25%
(clavulanate)
-distributed into bile, low concentrations in CSF
Metabolism :
- liver

Ticarcillin- clavulanate
Elimination:
- half life: 1.1 hr adults , 4.4 hr neonates, 1 hr in
infants/ children
- excretion : 60 - 70% urine (ticarcillin), 35-45%
(clavulanic acid), unchanged in first 6 hr after
administration.

Ticarcillin- clavulanate
Uses:
- septicemia
- lower respiratory infections
- bone and joint infections
- skin & skin structure infections
- urinary tract infections
- intra-abdominal infections
- gynecologic infections
- renal impairment

Ticarcillin- clavulanate
Adverse effects :
- hypersensitivity
- diarrhea
- nephritis
- neurotoxicity
- hematologic toxicities
- cation toxicity

Ticarcillin- clavulanate
Contraindications:
Allergy to penicillins or other beta lactam antibacterials
Cautions:
- serious occasionally fatal hypersensitivity reactions
reported
- risk of bleeding complications
- hypokalemia
- seizures reported when dose exceeded, especially in
presence of renal impairment

Vancomycin
mechanism of action:
-inhibit cell wall biosynthesis,
- alters the membrane permeability and RNA
synthesis

Vancomycin
Administration :
- intravenous

Vancomycin
pharmacokinetics:
Absorption:
- Peak plasma time (IV): 45-65 minutes
Distribution:
- distributed widely in body tissues and fluid
except for cerebrospinal fluid (CSF)
- relative difussion from blood into CSF. Good
only with inflammation.
-protein bound: 10-50%

Vancomycin
Metabolism:
- metabolism of drug is minimal
- hence 90- 100% is excreted by glomerular filtration.
elimination:
- half life: adults = 5 - 11 hours
* in renal impairment: 200 - 250 hours
- excretion :
urine ( 80-90% as unchanged drug)
Primarily feces

Vancomycin
Uses:
Pseudomembranous colitis
Endocarditis
Sirgical site infection(off label)
Dosing modification

Vancomycin
Adverse effects:
Bitter taste
Erythematous rash on face and upper body
Hypotension accompanied by flushing
Nausea and vomitting
Stomatitis
Chills
Drug fever

Vancomycin
Contraindications:
Hypersensitivity
Cautions:
Not absorbed orally, do not use PO for systemic
infection
Endocarditis prophylaxis, use only for high risk
patients

Vancomycin
interactions :
- vancomycin + cyclosporine
* cyclosporine and vancomycin both increase
nephrotoxicity and/or toxicity.

Vassopressor

Vassopressor
- dopamine
- noradrenaline
- adrenaline
- phenylephrine
- vassopressin

Dopamine
mechanism of action:
-endogenous catecholamine, acting on both
dopaminergic and adrenergic neurons
- low dose stimulates mainly dopaminergic
receptors, producing renal and mesentric
vasodilation.

Dopamine
- higher dose stimulates both beta1- adrenergic
and dopaminergic receptors, producing cardiac
stimulation, and renal vasodilation.
- large dose stimulates alpha adrenergic receptors

Dopamine
Administration:
- intravenous

Dopamine
Pharmacokinetics:
Absorption :
Onset: Adults , 5 mins
Duration : 10 minutes
Distribution:
Volume of distribution : 1.8 - 2.45 L/kg

Dopamine
Metabolism:
-metabolized in the liver, kidney, and plasma by
monoamine oxidase and catechol-O-methyl
transferase
- metabolites: norepinephrine (active), inactive
metabolites

Dopamine
Elimination:
Half life : 2 minutes
Total body clearance: 115mL/kg/min
Excretion: urine (80%)

Dopamine
Uses:
- hemodynamic conditions
Treatment of:
- hypotension
- low cardiac output
- poor perfusion of vital organ
- increase mean arterial pressure in septic shock
patients who remain hypotensive after adequate
volume expansion

Dopamine
Adverse effects:
Cardiovascular : ventricular arrhythmia, ectopic
beats , tachycardia, anginal pain, palpitation
Respiratory: dyspnea
Gastrointestinal: Nausea and vomitting
Metabolic/ nutritional: Azotemia
Central nervous system: headache, anxiety
Dermatologic: piloerection

Dopamine
Adverse effects:
- gangrene of extremities
(in higher doses were administered for prolonged
periods) OR
( in patients with occlusive vascular disease
receiving low doses of dopamine hydrocloride)

Dopamine
Contraindications:
Hypersensitivity to dopamine,
pheochromocytoma, ventricular fibrilation or
tachyarrhythmia
Cautions:
Angina pectoris, extravasation, hypovolemia,
occlusive vascular disease, ventricular
arrhythmias, recent use of monoamine oxidase
inhibitor, sensitivity to sulfites

Dopamine
Cautions:
-drug is inactived by alkali
-Use with caution after myocardial infarction
-Monitor blood pressure closely

Adrenaline
mechanism of actions:
- strong alpha adrenergic effects
which cause :
- increase in cardio output and heart rate
- decrease in renal perfusion and pulmonary
vascular resistance
- variable effect on BP (resulting in systemic
vasoconstriction and increase vascular
permeability)

Adrenaline
Strong beta1 and moderate beta2- adrenergic
effects, resulting in:
- bronchial smooth muscle relaxation
Secondary relaxation effect on smooth muscle of
stomach, intestine, uterus, and urinary bladder.

Adrenaline
Administration:
-intravenous

Adrenaline
Pharmacokinetics:
Absorption :
- onset : 5- 10 minutes
- duration: 4 hours
Metabolism:
- metabolized by monoamine oxidase (MAO) and
Catechol-O-methyl transferase in adrenergic
neuron

-metabolites:metadrenaline, sulfate conjugates,

and hydroxy derivatives of mandelic acid
(inactive)
Elimination:
- excretion: urine

Adrenaline
uses:
- cardiac arrest
- asthma, severe/ anaphylaxis
-in pediatrics:
- pulseless arrest
- symptomatic bradycardia
- asthma

Adrenaline
Adverse effects:
- angina
- anxiety
- cardiac arrhthmias
- dizziness
- dyspnea
- flushing
- headache
- tachycardia

Adrenaline
Contraindications:
- hypersensitivity
- organic heart disease or cardiac dilatation
- closed angle glaucoma
- labor

Adrenaline
Cautions:
- cerebrovascular insufficiency
- heart disease
- angina, especially with history of CAD
- hypertension
- thyroid disease
- pregnancy

Noradrenaline
Mechanism of action:
- strong beta1 and alpha- adrenergic effects and
moderate beta2 effects, which :
* increase cardiac output and heart rate
*decrease renal perfusion and pulmonary vascular
resistance
* cause variable BP effects

Noradrenaline
Administration:
- intravenous

Noradrenaline
Absorption:
- onset: 1- 2 minutes
- duration: 1-2 minutes
Metabolism:
-metabolized by monoamine oxidase and catecholO- methyl transferase in adrenergic region
- metabolites: normentanephrine, vanillylmandelic
acid ( inactive)

Noradrenaline
Elimination:
- excretion: urine ( 84-96%)

Noradrenaline
Uses:
- acute hypotension
- cardiac arrest
- sepsis & septic shock
- beta blocker toxicity
- calcium channel blocker toxicity
- tricyclic antidepressant toxicity

Noradrenaline
Adverse effects:
- bradycardia
- hypertension
- arrhythmias
- confusion
- anxiety
- dyspnea
- nausea and vomitting
- headache

Noradrenaline
Contraindications:
- hypersensitivity
- hypotension due to blood volume deficit
- peripheral vascular thrombosis
- concomitant use with same general anesthetics
* chloroform
* trichloroethylene
* cyclopropane
* halothane

Noradrenaline
Cautions:
- mesentric or peripheral vascular thrombosis
- avoid infusion site extravasation
- not for use in profund hypoxia
- sulfite allergy due to presence of metabisulfite
- monitor blood pressure
- extreme caution in concurrent monoamine
oxidase inhibitor use

MCQ
Regarding ticarcillin- clavulanate
a. It inhibits cell wall biosynthesis
b. Has bactericidal effects
c. Metabolised in liver
d. The administration is only by intravenous
e. The adverse effect is hypersensitivity

REFERENCES
Books

LANGE Medical microbiology

Medical physiology- Guytun & Hall
Clinical medicine Kumar & Clark
A text book of microbiology ( P.CHAKRABORTY)

Website
http://emedicine.medscape.com/article/234587medication#showall

SEPTICAEMIA
NORSATILA BINTI SAIBEH
012012100069

LEARNING OBJECTIVE
To describe the complication arise from
septicaemia.
An overview of what is Disseminated
intravascular Coagulation (DIC) and it types.
To identify what are the causes of DIC.
To study the pathophysiology of DIC and it
clinical manifestations.
Discuss the significant laboratory findings in
DIC and along with it treatments
Prevention of Septicaemia.

COMPLICATIONS
Without medical treatment, the bacteria in the
bloodstream can cause serious and potentially lethal
complications, including:
Endocarditis - inflammation of the inner lining of the
heart (endocardium).
Pericarditis - inflammation of the membrane that
encloses the heart (pericardium).
Meningitis - inflammation of the membranes that
enclose the brain and spinal cord (meninges).
Osteomyelitis - bone infection.
Infectious arthritis - joint infection.
Septic shock - severe drop in blood pressure, which
can lead to organ failure. This is also known as sepsis.

COMPLICATIONS CONT.
Multiorgan failure, eg: renal failure or
cardiorespiratory failure.
Disseminated intravascular
coagulation (DIC).

WHAT IS DISSEMINATED
INTRAVASCULAR
COAGULATION (DIC)
Disseminated = widely spread
Intravascular = inside the blood
vessel
Coagulation = activation of the
blood clotting system

Disseminated Intravascular
Coagulation (DIC)

TYPES OF DIC

CAUSES OF DIC

PATHOPHYSIOLOGY OF DIC

CLINICAL MANIFESTATIONS
OF DIC
Bleeding signs and symptoms:
Petechiae
Purpura
Venipuncture site bleeding

CLINICAL MANIFESTATIONS
OF DIC
Organ damage
Skin, bone and bone marrow necrosis
may be seen

SIGNIFICANT LABORATORY
FINDINGS IN DIC
TEST

NORMAL RANGE

DIC

D-dimer

0-100 ng/mL

>500 ng/mL

Fibrinogen

200-400 mg/dL

<200 mg/dL

Platelets count

200-400 x 109/L

<200-400 x 109/L

Peripheral blood smear----------Fragmented RBCs

Thrombin Time----------------------Prolonged

Fragmented RBCs

There are numerous fragmented RBC's seen here.

Some of the irregular shapes appear as "helmet" cells.
Such fragmented RBC's are known as "schistocytes. .

TREATMENTS
Replacement of coagulation factors
and platelets
Inhibition of clotting process with
heparin and other agents

PREVENTION OF
SEPTICAEMIA
Bacterial infections are the underlying cause of septicemia.
Therefore, one of the best ways to prevent this condition is
to see a doctor right away if you suspect you have an
infection.
Getting treated for infections can prevent septicemia. The
Haemophilus influenza B (HIB) vaccine and S. pneumoniae
vaccine have already reduced the number of septicemia
cases in children. Both are recommended childhood
immunizations.
If your infection can be effectively treated with antibiotics in
the early stages, you may be able to prevent the bacteria
from entering the bloodstream. In rare cases, people who
are in close contact with someone who has septicemia may
be prescribed preventive antibiotics.

REFERENCES
Acute respiratory distress syndrome. (2012, March 3).
National Library of Medicine National Health Institutes.
Retrieved June 29, 2012 from
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001164/
Septic shock. (2010, January 4). National Library of Medicine
National Health Institutes. Retrieved June 29, 2012 from
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001689/
Septicemia. (n.d.) Johns Hopkins Medicine. Retrieve July 3,
2012, from
http://www.hopkinsmedicine.org/healthlibrary/conditions/adul
t/nervous_system_disorders/septicemia_85,P00802/
Septicemia. (2011, August 24). University of Maryland
Medical Center. Retrieved June 29, 2012 from
http://www.umm.edu/ency/article/001355trt.htm

MCQ-1
1) All above are sample use for
diagnose septicemia except?
a) Saliva
b) Tears
c) Urine
d) Stool

MCQ-2
Which of the following symptom of
septicemia?
a) Neutrophilia
b)Lack of energy
c) Bardycardia
d) Neutropenia

MCQ-3
Which of the following would not be
considered a sepsis risk factor?
A. Presence of a central venous
catheter
B. An indwelling Foley catheter
C. Decreased length of hospital stay
D. Extremes of age of patients
Answer: C

MCQ-4
Regarding ticarcillin- clavulanate
a. It inhibits cell wall biosynthesis
b. Has bactericidal effects
c. Metabolised in liver
d. The administration is only by intravenous
e. The adverse effect is hypersensitivity