Toxaemia

Presence of toxins in the bloodstream

Resulting from spread of bacterial products by the bloodstream
Or resulting from metabolic disturbances
Clinical signs: depression, lethargy, separating from group, reduced appetite,
slow growth, poor production, low fecal output, weak pulse of normal rate,
weakness, albuminuria
Localizing signs such as pressure by an abscess
Toxaemic shock presence of large quantities of potent toxins in the
bloodstream
o Peripheral vasodilation
o Fall in blood pressure
o Mucosal pallor
o Hypothermia
o Tachychardia
o Muscle weakness
Coliform toxicosis

Septicaemia

Condition in which toxic bacteria invade the bloodstream

Organisms + toxin become widely distributed
o Every organ affected
o Results in death if late treatment or if bacterium resistant to antibiotic

Bacteraemia

Presence of viable bacteria in blood stream

Sepsis

Systemic inflammatory response to the infection

Systemic inflammatory response syndrome

Clinical syndrome caused by sepsis or system inflammation of noninfectious

origin
Tachycardia, tachypnea, hypothermia or hyperthermia, and leukocytosis,
leucopenia, or bands

Severe sepsis

SIR to infection associated with organ dysfunction and manisfestations of

hypoperfusion or hypotension

Septic shock

SIR to infection with hypotension despite adequate fluid resuscitation along

with manifestations of hypoperfusion

MODS

Altered function of two or more organs secondary to SIRS such that

homeostasis cannot be maintained without intervention

ARDS

Pulmonary inflammatory disorder characterized by noncardiogenic pulmonary

edema, neutrophilic inflammation, and hypoxaemia

MODS

Devastating consequence of sepsis

Pathogenesis of organ failure during sepsis
o Multifactorial but centers around the development of mitochondrial
dysfunction
Circulatory collapse, microcirculatory changes, hypoxaemia and inflammation
o Tissue ischemia, reduced mitochondrial and then cellular function
o Organ damgemay be permanent or may resolve when sepsis is
resolved
Some forms of Org dysfunction like ARDS
o Result of inflammation
o Not circulatory collapse and mitochondrial damage
o during the initiation of ARDS:
o inflammatory mediators and microbial products activate pulmonary
macrophages
o result in vasodilation, vascular leak, pulmonary edema and neutrophilic
inflammation

SEPTIC SIRS

anaerobic bacte
fungi
products of gm negative or positive bact
protozoa
virusesc

NON SEPTIC SIRS

burns
chemical aspiration
heatstroke
immune mediated dz
ischemic organ necrosis
neoplasia
pancreatitis
trauma

SHOCK
3 stages of shock
1. Compensatory stage
BP Normal limits, shunted from the kidney, skin and GIT to the vital organs such as
the brain and the liver
In stage one of shock, when low blood flow (perfusion) is first detected, a number of
systems are activated in order to maintain/restore perfusion, the result is that the
heart beats faster, the blood vessels throughout the body become sslightly smaller
in diameter, and the kidney works to retain fluid in the circulatory system. All this
serves to maximize blood flow to the most important organs and systems in the
body. The patient in this stage of shock has very few symptoms, and aggressive
treatment may slow progression.
2. Early decompensatory stage (progressive stage)
Regulate BP can no longer compensate and the mean arterial. The overworked
heart become dysfunctional
In stage 2 of shock, these methods of compensation begin to fail. The systems of
the body are unable to improve perfusion any longer, and the patients symptoms
reflect that fact. Oxygen deprivation in the brain casues the patient to become
confused and disorientated.
3. Decompensatory stage (irreversible stage of shock)
There is severe organ damage that patient do not respond anymore to treatment.
Survival is almst impossible
In stage 3 of shock, the length of time that poor perfusion has existed begins to take
a permanent toll on the bodys organs and tissues. The hearts functioning
continues to spiral downward, and the kidneys usually shut down completely. Cells
in organs and tissues throughout the body are injured and dying. The endpoint is
patient death

Shock
Hypovolemic

Definition
Decreased
effective
circulating blood
volume

Pathophysiology
Decreased
effective
circulation volume

Treatment
IV fluids (lrs, ns,
blood)
Electrolyte
replacement

Decreased venous
return
Decreased stroke
volume

Obstructive

Physical
impediment to
blood flow in large
vessels

Decreased cardiac
output and blood
delivery to tissues.
Physical blockage
to venous/ blood
trapped distal to
obstruction
Decreased stroke
volume

Cardiogenic

Distributive

Heart unable to
pump blood (lack
of contractility)

Decreased cardiac
output and blood
deliver to the
tissues
Decreased
contractility

Decreased cardiac
output and blood
deliver to tissues
Multifactorial(one or more of following)
Vasodilation
Vasodilation
(peripheral
vessels)
Blood trapped in
peripher
Decreased venous
return
Decreased stroke
volume
Decreased cardiac
output and blood
deliver to tissues

Antiarrythmatics,
inotropic drugs,
sedative and
diuretics

IV therapy and
crystalloids
Antibiotics for
sepsis

Increased vessel
permeability

Increased wall
permeability
Decreased
effective
circulating blood
volume
Decreased venous
return

Decreased cardiac
contractility due to
effects of cytokine
mediators or
platelets
activating factor
Activation of the
coagulation
system

Decreased cardiac
output and blood
deliver to tissues
(same as
cardiogenic)

Multiple clot
formation
Small vessel
occluded
Decreased venous
return
Decreased cardiac
output and blood
deliver to tissues