Sepsis Critical Care Pathway

Print

Sepsis Critical Care Pathway
Antipyretics should be used cautiously in order
not to damp the essential immune responses of sepsis

By Prof. HR Ahmad

Infection causes acute inflammation. It produces inflammatory mediators and cytokines pouring into the body fluids. Cytokines are also produced by antigen induced leucocytes. These two sources of cytokines cause systemic inflammatory response syndrome [SIRS]. Typical signs of sepsis are heat, pain, redness, and swelling and reduced function of organs. The cytokines responses of bone marrow, liver, kidney, hypothalamus and brain in sepsis should be elucidated. The cytokines response of bone marrow results in immature form of neutrophils. Both leukocytosis [> 12000 cells/mm cube] and leucopenia [<4000 cells/ mm cube] are observed in sepsis. The sepsis leucopenia is dangerous due to bone marrow depression by endotoxins.


Prof. HR Ahmad

The hypothalamic cytokine response is meant to increase the set point of temperature regulation system. Initially, the body and the set point temperature are at 37 degree centigrade. The cytokine increases the normal set point temperature through the action of prostaglandins and neurotransmitters to higher values. In response to this change, body temperature hunts the new set point by rigor and chills. The fever is good for the response of immune system. Antipyretics should be used cautiously in order not to damp the essential immune responses of sepsis. As the hypothalamic set point is reduced to 37 degree, the body core temperature returns to normal while sweating to dissipate the heat current along the core-limbs temperature gradient.

The cytokines responses of hepatocytes are C Reactive Proteins CRP and Serum Amyloid-A Proteins SAAP. The dimers of these two proteins opsonize the bacteria to be engulfed by macrophages. Fibrinogen increases ESR by Rouleaux formation of red cells. The supply of proteins to the liver occurs through the effect of sepsis on skeletal muscle catabolism. High serum creatinine, urea and metabolic acidosis in sepsis signal the signs of kidney failure. Uremia causes edema of lungs and consequently breathing becomes difficult. The sepsis – cytokines – brain axis produces altered mental status. AMS includes disorientation of place, time and person, somnolence, malaise, anorexia, delirium, hallucinations and encephalopathy. Sepsis increases energy demands of the body by increasing glucagon based gluconeogenesis from fats and proteins to increase fasting blood glucose levels of > 7 mmol/l. Increased oxygen demand increases respiratory rate of > 20 breaths per minute, heart rate and blood pressure. Once sepsis is diagnosed, the therapy starts immediately with the following steps: 1. Oxygen supply; 2. Blood culture; 3. Essential biochemical variables; 4. IV antibiotics; 5. Fluid replacement; 6. Pain management; 7. On line recording of vital signs. This therapeutic regimen should be directed to reduce both physical and biochemical signs of sepsis at a hospital settings. Since sepsis is a medical emergency, mortality increases by 1% every ten minutes. Therefore, time is of the essence in sepsis induced multiorgan failure to reverse and to improve survival rate of patients with major cases of sepsis that are from pneumonia and urinary tract infection.

Note: It is dedicated to the fond memories of Nasir Iqbal Chaudhry with a message to develop efficient and humane critical care units throughout Pakistan.

*The author is a professor of Physiology at SIUT and AKU Karachi, Pakistan.

© Professional Medical Publications. All rights reserved.