Septic shock

Sepsis is one of the most common causes of death in critically ill patients in Intensive Care Units. (Oil by Gabriël Metsu).
Thrombocytopenia with purpura on right hand in patient with septic shock

Potentially fatal medical condition that occurs when sepsis, which is organ injury or damage in response to infection, leads to dangerously low blood pressure and abnormalities in cellular metabolism.

- Septic shock

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Intensive care unit

Intensive therapy unit or intensive treatment unit (ITU) or critical care unit (CCU), is a special department of a hospital or health care facility that provides intensive care medicine.

Intensive care unit
ICU patients often require mechanical ventilation if they have lost the ability to breathe normally.
Nurses in a neonatal intensive care unit (NICU)
A pediatric intensive care unit room at Helen Devos Children's Hospital.
US Army ICU nurse attending to a patient in Baghdad, Iraq
ICU nurses monitoring patients from a central computer station. This allows for rapid intervention should a patient's condition deteriorate whilst a member of staff is not immediately at the bedside.
Mobile ICU of the university hospital in Antwerp, Belgium

Common conditions that are treated within ICUs include acute respiratory distress syndrome, septic shock, and other life-threatening conditions.

Multiple organ dysfunction syndrome

Altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis.

Many of the internal organs of the human body

Sepsis is the most common cause of multiple organ dysfunction syndrome and may result in septic shock.

Bloodstream infections

Bloodstream infections (BSIs), which include bacteremias when the infections are bacterial and fungemias when the infections are fungal, are infections present in the blood.

Micrograph showing a mycosis (aspergillosis). The Aspergillus (which is spaghetti-like) is seen in the center and surrounded by inflammatory cells and necrotic debris. H&E stain.

The immune response to the bacteria can cause sepsis and septic shock, which has a high mortality rate.


Protein complex that controls transcription of DNA, cytokine production and cell survival.

Side view of the crystallographic structure of a homodimer of the RELA protein (green and magenta) bound to DNA (brown).
Mechanism of NF-κB action. The classic "canonical" NF-κB complex is a heterodimer of p50 and RelA, as shown. While in an inactivated state, NF-κB is located in the cytosol complexed with the inhibitory protein IκBα.  Through the intermediacy of integral membrane receptors, a variety of extracellular signals can activate the enzyme IκB kinase (IKK).  IKK, in turn, phosphorylates the IκBα protein, which results in ubiquitination, dissociation of IκBα from NF-κB, and eventual degradation of IκBα by the proteasome.  The activated NF-κB is then translocated into the nucleus where it binds to specific sequences of DNA called response elements (RE).  The DNA/NF-κB complex then recruits other proteins such as coactivators and RNA polymerase, which transcribe downstream DNA into mRNA. In turn, mRNA is translated into protein, resulting in a change of cell function.
Top view of the crystallographic structure of a homodimer of the NFKB1 protein (green and magenta) bound to DNA (brown).
Schematic diagram of NF-κB protein structure. There are two structural classes of NF-κB proteins: class I (top) and class II (bottom). Both classes of proteins contain a N-terminal DNA-binding domain (DBD), which also serves as a dimerization interface to other NF-κB transcription factors and, in addition, binds to the inhibitory IκBα protein.  The C-terminus of class I proteins contains a number of ankyrin repeats and has transrepression activity.  In contrast, the C-terminus of class II proteins has a transactivation function.
NF-κB (green) heterodimerizes with RelB (cyan) to form a ternary complex with DNA (orange) that promotes gene transcription.
Overview of signal transduction pathways involved in apoptosis.

Incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development.

Gram-negative bacteria

Gram-negative bacteria are bacteria that do not retain the crystal violet stain used in the Gram staining method of bacterial differentiation.

Microscopic image of gram-negative Pseudomonas aeruginosa bacteria (pink-red rods)
Gram-negative cell wall structure
Gram-positive and -negative bacteria are differentiated chiefly by their cell wall structure

This toxic reaction may lead to low blood pressure, respiratory failure, reduced oxygen delivery, and lactic acidosis — manifestations of septic shock.


Lipopolysaccharides (LPS) are large molecules consisting of a lipid and a polysaccharide composed of O-antigen, outer core and inner core joined by a covalent bond; they are found in the outer membrane of Gram-negative bacteria.

Structure of a lipopolysaccharide (LPS)
The saccharolipid Kdo2-Lipid A. Kdo residues in (core), glucosamine residues in, acyl chains in black and phosphate groups in.
LPS final assembly: O-antigen subunits are translocated across the inner membrane (by Wzx) where they are polymerized (by Wzy, chain length determined by Wzz) and ligated (by WaaL) on to complete Core-Lipid A molecules (which were translocated by MsbA).
LPS transport: Completed LPS molecules are transported across the periplasm and outer membrane by the proteins LptA, B, C, D, E, F, and G
Toll-like receptors of the innate immune system recognize LPS and trigger an immune response.

When bacterial cells are lysed by the immune system, fragments of membrane containing lipid A are released into the circulation, causing fever, diarrhea, and possible fatal endotoxic shock (also called septic shock).


Genus of rod-shaped Gram-negative bacteria of the family Enterobacteriaceae.

US Food and Drug Administration scientist tests for presence of Salmonella

This can lead to life-threatening hypovolemic shock and septic shock, and requires intensive care including antibiotics.


Life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs.

Skin blotching and inflammation due to sepsis
Blood culture bottles: orange cap for anaerobes, green cap for aerobes, and yellow cap for blood samples from children
Sepsis Steps. Training tool for teaching the progression of sepsis stages
Intravenous fluids being given
Personification of septicemia, carrying a spray can marked "Poison"
Phenotypic strategy switches of microbes capable of provoking sepsis

Septic shock is low blood pressure due to sepsis that does not improve after fluid replacement.

Tumor necrosis factor

Adipokine and a cytokine.

Signaling pathway of TNFR1. Dashed grey lines represent multiple steps.

Kevin J. Tracey and Cerami discovered the key mediator role of TNF in lethal septic shock, and identified the therapeutic effects of monoclonal anti-TNF antibodies.


Low blood pressure.

4) Address the underlying problem (i.e., antibiotic for infection, stent or CABG (coronary artery bypass graft surgery) for infarction, steroids for adrenal insufficiency, etc...)