Clarification of Answer by
crabcakes-ga
on
05 Oct 2002 20:49 PDT
grenfell,
First let me say, this is a very sad case you are presenting me with.
You did not mention the outcome for this unfortunate infant, but
scenario suggests tragic ending. I’d like to think differently.
I am sorry the first part of my answer was not totally clear, and I
appreciate the additional information. (surgeon-ga also left another
comment on thie clarification)
Sepsis: Simply described, when the body is deprived of oxygen (Whether
from asphyxia, ARDS, hyaline membrane disease of the premature, etc.),
tissue and blood pH changes, blood pressure changes, and anaerobic
metabolism is altered. Lactic acid production increases, causing
acidosis. (The newborn you described did indeed have a lowered pH, of
6.9 . Acidosis is a pH of less than 7.25) With decreased oxygen,
intravascular pressure decreases and body tissues become starved for
oxygen. Gas exchange is greatly compromised at the cellular level.
All of these factors, plus hypothermia, along with the large amount of
meconium provides a fertile ground for bacterial infection. Negative
cultures, especially if improperly collected, can be seen in sepsis.
You stated there was no bacteria present, but lets allow for the
possibility. Sepsis is not the only causative agent of the DIC
process, as outlined in the answer. It is the most common cause.
“Inflammation is the body's normal response to infection. The body's
initial response to an infection is to induce a pro-inflammatory
state. Pro-inflammatory mediators, such as tumor necrosis factor
(TNF-a), interleukin-1 (IL-1), interleukin-6 (IL-6), and
platelet-activating factor (PAF) are released. These mediators have
multiple overlapping effects designed to repair existing damage and
limit new damage. To ensure that the effects of the pro-inflammatory
mediators do not become destructive, the body then launches
compensatory anti-inflammatory mediators, such as interleukin-4 (IL-4)
and interleukin-10 (IL-10), which normally deregulates the initial
pro-inflammatory response.
In sepsis, regulation of the early response to infection is lost, and
a massive systemic reaction occurs. These excessive or inappropriate
inflammatory reactions are detrimental. An excess of the inflammatory
mediators, such as TNF-a and IL-1, are released, triggering an
overwhelming physiologic response, which causes tissue injury and
results in the development of diffuse capillary injury. Finally,
excessive inflammatory reactions interfere with normal tissue
function, leading to tissue damage and organ dysfunction. “
http://www.sepsis.com/pathogenesis.html
Directly from the University of Iowa site, cited below.
“Basically there are 7 causes of (peripheral tissue) hypoxia:
1. Decrease FiO2
2. Decreased alveolar ventilation (VA)
3. Venous admixture (Qva)
4. Shunt (Qs)
5. Decrease venous oxygenation (SvO2) plus shunt (Qs)
6. Cytotoxic hypoxia (CN - in practical terms)
7. Sepsis”
http://www.anesth.uiowa.edu/boezaart/decreasedlex.pdf
From an eMedicine.com article by Linda L Bellig, RN, NNP and Bryan L
Ohning, MD, PhD
“The neonate is unable to respond effectively to infectious hazards
because of deficits in the physiological response to infectious
agents. The neonatal neutrophil or polymorphonuclear (PMN) cell, which
is vital for effective killing of bacteria, is defective in chemotaxis
and killing capacity. Decreased adherence to the endothelial lining of
blood vessels lessens their ability to marginate and leave the
intravascular area to migrate into the tissues. Once in the tissues,
they may fail to deaggregate in response to chemotactic factors. Also,
neonatal PMNs are less deformable; therefore, they are less able to
move through the extracellular matrix of tissues to reach the site of
inflammation and infection. The limited ability of neonatal PMNs for
phagocytosis and killing of bacteria is impaired when the infant is
clinically ill. Lastly, neutrophil reserves are depleted easily due to
the diminished response of the bone marrow, especially in the
premature infant
In the infant with significant risk for sepsis and/or clinical signs
but negative cultures, the clinician must decide whether to provide
continued treatment. Three days of negative cultures should provide
confidence in the data; however, a small number of infants with proven
sepsis at postmortem had negative cultures from initial sepsis workup.
This is further confounded if the mother received antibiotic therapy
prior to delivery, especially close to delivery. This may result in
negative cultures in the infant who still is ill. Review all
diagnostic data, including cultures, maternal/intrapartal risks
factors, CSF results, CBC and differential, x-ray, and clinical
picture to determine the need for continued therapy. Treatment for a
full 7-10 days may be appropriate, even if the infant has negative
cultures at 48 hours.”
http://www.emedicine.com/ped/topic2630.htm
More from the same article:
“Predisposing risk factors also are associated with neonatal sepsis.
They include low Apgar score (<6 at 1 or 5 minutes), maternal fever
greater than 101°F, maternal urinary tract infection, poor prenatal
care, poor maternal nutrition, low socioeconomic status, recurrent
abortion, maternal substance abuse, low birth weight, difficult
delivery, birth asphyxia, meconium staining, and congenital anomalies.
The predisposing risk factors implicated in neonatal sepsis reflect
the stress and illness of the fetus at delivery, as well as the
hazardous uterine environment experienced by the fetus prior to
delivery.
Abnormal neutrophil counts, taken at the time of onset of symptoms,
only are observed in two thirds of infants; therefore, neutrophil
count does not provide adequate confirmation of sepsis”
http://author.emedicine.com/PED/topic2630.htm
A thorough medical explanation of sepsis can be found here:
http://www.sepsis.com/pathogenesis.html
Additional reading:
http://neonatal.peds.washington.edu/NICU-WEB/pphn.stm
http://www.obgyn.net/english/ob/cord_blood_gases.htm
I hope this better explains my answer.
Regards,
crabcakes
