pathophysiology

Severe sepsis can occur as a result of infection at any body site, including the

lungs, abdomen, skin or soft tissue, or urinary tract and as a result of a primary

blood stream infection, such as in meningococcemia. Bacteria are the pathogens

most commonly associated with the development of sepsis, although fungi,

viruses, and parasites can cause sepsis. The pathophysiology of sepsis can be

initiated by the outer membrane component of gram-negative organisms (e.g.,

lipopolysaccharide [LPS], lipid A, endotoxin) or gram-positive organisms (e.g.,

lipoteichoic acid, peptidoglycan), as well as fungal, viral, and parasitic

components . Signaling by these mediators occurs via a family of

transmembrane receptors known as Toll-like receptors. Within the monocyte,

nuclear factor-κB (NF-κB), is activated, which leads to the production of

proinflammatory cytokines, tumor necrosis factor α (TNF-α), and interleukin 1 (IL-

1). TNF-α and IL-1 lead to the production of toxic downstream mediators,

including prostaglandins, leukotrienes, platelet-activating factor, and

phospholipase A2. These mediators damage the endothelial lining, leading to

increased capillary leakage. Furthermore, these cytokines lead to the production

of adhesion molecules on endothelial cells and neutrophils. Neutrophilic

endothelial interaction leads to further endothelial injury through the release of

the neutrophil components. Finally, activated neutrophils release nitric oxide, a

potent vasodilator that leads to septic shock.

•

• Clinical manifestations

• The clinical manifestations of sepsis may be flagrant or subtle.

Awareness of the signs and symptoms of sepsis allows early recognition and

prompt, appropriate management. The clinical presentation, relative

frequency, and current pathophysiologic understanding of the manifestations

of sepsis are reviewed. Special emphasis is placed on the cardiopulmonary

manifestations, which are examined in a temporal sequence of preshock, early

shock, and late shock states. While therapy for the underlying infection (such

as antibiotics and drainage of abscesses) is often sufficient, therapy for the

specific manifestations of sepsis may also be necessary. Guidelines for

therapy for these manifestations of sepsis are given.

• If a person has sepsis, they often will have fever. Sometimes, though, the

body temperature may be normal or even low. The individual may also have

chills and severe shaking. The heart may be beating very fast, and breathing

may be rapid. Low blood pressure is often observed in septic patients.

Confusion, disorientation, and agitation may be seen as well as dizziness and

decreased urination. Some patients who have sepsis develop a rash on their

skin. The rash may be a reddish discoloration or small dark red dots

throughout the body.

Medical management book based

Sepsis is a medical emergency. If a person has sepsis, treatment is usually given

in the hospital and often in an intensive care unit The patient will likely be placed

on oxygen, either by a tube that is placed near the nose or through a clear plastic

mask. Depending on the results of the tests, the doctor may order medications.

These medications may include antibiotics given by IV (given directly into the

vein). Initially, the antibiotics may be those that kill many different bacteria

because the exact kind of infection the patient has is not known. Once the blood

culture results show the identity of the bacteria, your doctor may select a different

antibiotic that kills the specific microbe. The doctor may also order IV salt solution

(saline) and medications to increase the blood pressure if it is too low. The doctor

will likely admit the patient to the hospital at least until the blood culture results

are known. If the patient is very ill and with low blood pressure, the doctor may

admit the patient to the intensive care unit (ICU) and may consult other doctors to

help in the management of the illness. If results show an infection in the

abdomen, either drainage of the infection by tubes or surgery may be necessary.

Research to discover new treatments for sepsis has failed over the past 20-30

years. Many medications that were thought to be helpful were proven to have no

benefit in clinical trials. However, scientists are working diligently to discover

medications that will modify the body's aggressive immune response to

microbes, which leads to sepsis.

 Laboratory Findings

Random Blood Sugar

September 20, 2010 – 1:25AM – HT- 145 mg/ dl

Blood Chemistry

Results Normal Values

Sodium 141 mmol/L 137-145
Potassium 3.7 mmol/L 3.6- 5.0 mmol/L
Creatinine 328 mmol/L 62- 106 mmol/L

Interpretation: Blood chemistry result on Sodium and Potassium displays

within normal range except for creatinine. High creatinine levels are mainly a

cause of insufficient urine discharge, and in some cases, a blockage in the

kidneys the causes the creatinine to remain in the body. High levels of protein in

the body contribute to an increase in creatinine levels. In relation to the patient’s

case, high creatinine level is one of the pathognomonic sign of sepsis.

Hematology Test

Results Normal Values

Hemoglobin 100 Female: 120- 140 g/l
Eryhrocyte volume fracion 0.39 0.37- 0.43
Leukocyte # 14.0 5.10 x 10 g/l

concentration
>Segmenters 0.98 0.55- 0.65
>Lymphocyte 0.02 0.25- 0.35
Interpretation: Above results were normal except for leukocyte count together

with its components, segmenters which is high and lymphocyte is low on

contrary. An unusually high white blood cell count can indicate an infection or a

blood disorder such as leukemia. In he case of Ms. MN, high leukocyte or WBC

count is a result of sepsis since it is a normal response of the body to any kind of

infection.

Urinalysis

Physical Findings

Color: Amber Sugar: (-)

Transparency: Turbid Protein: ++
Reaction: 5.0
Specified Gravity: 1.030
Microscopic Findings

Cells

Pus Cells: 10-13

RBC:
CASTS:
Coarsely Granular: 10-15/ hpf
Crystals

Amorphous Urates: Abundant

Inerpretation: The urinalysis revealed that the patient has proteins in her urine

that is mainly caused by the kidney damage in relation to her sepsis. Her urine
was found with pus cells that indicates urinary tract infection anywhere from the

kidneys to urethra. Moreover, her urine was seen with amorphous urates or urine

crystals that if formed as a result of the infection in the genitor-urinary tract.