By Adem Lewis / in , , , , , , /


Patient C is a 35 y/o female that presents for a
routine restorative appointment. She became
your patient two years ago when she moved to the area to begin teaching at a local university.
Upon moving to the Ohio Valley, she began to
experience seasonal allergies and asthma. She is currently prescribed the corticosteroid
Flonase, 2 sprays per day, and Albuterol as
needed. She takes OTC Allegra primarily during the spring to treat any remaining symptoms.
Patient C had her tonsils removed at the age of
5 due to recurrent strep infections. She also suffered from an episode of acute pancreatitis at
the age of 16, but has learned to manage her
symptoms through a strict diet and restriction of fats. Her dental record has been impeccable, and she
has regularly scheduled dental cleanings with
your office. At her last appointment, she had her first cavity and received a small composite
filling on tooth #4. At her 6 month follow-up, she
had an additional cavity diagnosed, and has returned today for routine restoration on tooth
#12. The patient is injected with 2% lidocaine with
1:100k epinephrine using an MSA block for local
infiltration anesthesia. Shortly after injection, you notice the patient vigorously scratching her
arm. You inquire if everything is okay, and she
replies “I feel funny and my heart is racing” with wheezing, gasping breaths.
You must act quickly, what do you think has
happened to your patient? A. She is experiencing an acute asthma attack
due to dental phobia
B. She is suffering a severe allergic reaction with anaphylaxis
C. She is experiencing a pain response to the
injection The patient is exhibiting signs and symptoms
related to the cutaneous, respiratory, and
cardiovascular systems, thus it should be assumed that she is having an allergic reaction
to the injection. Systemic anaphylactic
reactions are extremely life-threatening and may be the most acute emergency encountered in
dental practice. Although allergic reactions to
modern anesthetics are rare, patients with a history of asthma and allergies may be
genetically predisposed to have hyperactive
immune responses. However, you might wonder why Patient C did
not have an allergic reaction during her last visit,
when she was initially exposed to the same anesthetic. Most substances in the body have
specific markers on their surface, such as
glycoproteins, that serve as a chemical “nametag” for recognition. These nametags are
called antigens, and allow the immune system
to recognize which substances are supposed to be part of the body, and which substances are
foreign that need to be eliminated. During
Patient C’s last visit, when the anesthetic entered her body, the antigens for the anesthetic
were recognized as foreign by her immune
system. The immune system became activated and began to produce antibodies that could
specifically detect the anesthetic. Today, when
the second exposure to the antigen occurred, her immune system was primed and ready. The
foreign antigens were recognized by the
antibodies. This initiated a reaction in which mast cells in the body release chemicals such
as histamine. Histamine then initiates an
inflammatory reaction, thus causing the anaphylactic reaction.
The widespread inflammation causes a large
variety of detrimental effects throughout the body, with the main concerns being smooth
muscle constriction in the airways of the lungs,
and a sudden loss of blood pressure. For today’s video, we will be focusing on the
cardiovascular effects of an anaphylactic
reaction. In order to understand the role of anaphylaxis on
the vasculature, we must first review the concept
of Starling Fluid Flux in a healthy individual. Here we see a capillary in the body, with the
arteriolar end of the capillary on the left and the
venular end of the capillary on the right. The wall of the capillary is comprised of endothelial
cells, shown here as black dashes. In between
the endothelial cells are clefts that allow the movement of water and other small MW
molecules between the cells.
Filtration is the net movement of water and dissolved solutes from the plasma body fluid
compartment into the interstitial fluid.
Reabsorption is defined as the net movement of water and dissolved solutes from the interstitial
fluid into the plasma. Fluids are constantly
being filtered between the endothelial cells clefts at the arteriolar end of the capillary, and most of
the filtered fluid is then reabsorbed at the venular
end of the capillary. This occurs in response to the balance between four main pressures. This
concept is known in physiology as the Starling
Fluid Flux. The first pressure is called the Blood
Hydrostatic Pressure (BHP). This is the
pressure generated by the heart pumping blood into the enclosed space of the blood vessels.
Blood hydrostatic pressure is the main pressure
promoting filtration across the capillary wall. There is also a pressure called the Interstitial
Fluid Hydrostatic Pressure (IFHP), which is
sometimes referred to as a “back” pressure. It is due to the hydrostatic pressure of fluids from
the interstitial fluid into the plasma. Under
normal physiological conditions, this pressure should be negligible, and is thus represented
here by a smaller arrow. However, in some
pathological conditions it may become significant. Osmotically-active proteins are
compartmentalized within the blood and these
proteins act as sponges, pulling water towards them. The proteins in the plasma compartment
establish a pressure called the Blood Colloid
Osmotic Pressure (BCOP), which also referred to as the oncotic pressure. The BCOP is the
main pressure promoting reabsorption in the
capillaries. Under normal conditions, the endothelial cells
clefts are too small to allow the proteins to
escape from the plasma compartment. This is represented by an index called the reflection
coefficient. A reflection coefficient of 0 means
that a substance is freely permeable to the barrier, while a reflection coefficient of 1 means
that a substance is unable to pass through the
barrier. Proteins typically have a reflection coefficient close to 1, meaning they cannot pass
through the endothelial cell clefts. If proteins did escape into the interstitium, this
would create an Interstitial Fluid Colloid Osmotic
Pressure (IFCOP). Since proteins are usually not able to escape the capillary wall under
normal physiological conditions, this pressure
should typically be low to negligible. Using your knowledge of Starling Fluid Flux,
which of the following pressures would be most
likely to increase in a patient with a severe anaphylactic reaction?
A. The Blood Colloid Osmotic Pressure (BCOP)
B. The Blood Hydrostatic Pressure (BHP) C. The Blood Oncotic Pressure (BOP)
D. The Interstitial Fluid Colloid Osmotic
Pressure (IFCOP) E. The Mean Arterial Blood Pressure (MAP)
The correct answer is D, the interstitial fluid
colloid osmotic pressure. Let’s examine the impact that a severe
anaphylactic reaction would have on Starling
Fluid Flux. On the left, we see a normal, healthy individual in which the plasma proteins
are retained in the plasma compartment. During
an anaphylactic reaction, shown on the right, vasodilators such as histamine are released.
Arterioles throughout the systemic circulation
would dilate, increasing blood flow through the capillaries. Additionally, these chemicals cause
a widening of the endothelial cell clefts. This
decreases the reflection coefficient for proteins, and allows plasma proteins to escape into the
interstitial fluid.
Since the proteins are no longer in the plasma, during anaphylaxis the Blood Colloid Osmotic
Pressure drops significantly, and the Interstitial
Fluid Colloid Osmotic Pressure increases. Water is osmotically attracted to the proteins in
the interstitial space, causing a sudden
translocation of fluids from within the capillaries into the interstitial fluid. The swelling of the
interstitial space is called edema. Additionally,
the vasodilation of upstream arterioles exacerbates these effects, by allowing larger
amounts of fluid to pass into the capillaries,
across the capillary walls, and into the interstitial fluid.
While the Interstitial Fluid Hydrostatic Pressure
was minimal under normal conditions, in anaphylaxis the IFHP will increase due to the
edema. Furthermore, during anaphylaxis the
Blood Hydrostatic Pressures will plummet as fluid continues to leave the vasculature.
If we examine an overall picture of the fluid flux,
we would see that in normal conditions most of the filtered fluid (around 85%) is reabsorbed at
the venular end of the capillaries. During
anaphylaxis, the IFCOP increases drastically due to the leakage of plasma proteins into the
interstitial space. A large amount of filtration
occurs, and very little reabsorption occurs. This causes edema of the interstitial space.
Furthermore, these effects lead to a substantial
drop in the arterial blood pressures, which can lead to anaphylactic shock and potentially death
without appropriate treatment. Now that you
have a better understanding of the alterations in Starling fluid flux during anaphylactic shock,
let’s try to answer the following multiple choice
question: During an anaphylactic reaction:
A. The reflection coefficient for proteins in the
systemic vasculature is increased from 0 to 1. B. The interstitial fluid colloid osmotic pressure
(IFCOP) is increased due to the presence of
additional proteins in the interstitial fluid. C. The blood colloid osmotic pressure (BCOP)
is increased due to the vasodilation of systemic
arterioles. D. The systemic mean arterial blood pressure
(MAP) increases drastically, leading to an
increase in the heart rate. E. The blood hydrostatic pressure (BHP) would
be increased due to systemic arteriolar
vasoconstriction. Did you choose B? If so, nice work.
• For response A, the release of histamine and
other inflammatory chemicals would reduce the reflection coefficient from its normal value of 1.
• For response C, the systemic arterioles do
vasodilate during anaphylaxis, but the BCOP should be decreased due to the escape of
proteins from the plasma compartment.
• For response D, a patient in anaphylaxis would experience a large drop in the mean arterial
blood pressure, due to the loss of fluids into the
interstitial space. The heart rate, however, would most likely be increased in an attempt to
bring the blood pressure up to normal values.
• For response E, the systemic arterioles would vasodilate during the anaphylactic reaction.
BHP would also be decreased due to the loss of
plasma fluids into the interstitium. It is critical that a patient suffering from an
anaphylactic reaction be treated promptly.
Generally, the more rapidly that signs and symptoms appear following exposure to the
antigen, the more intense the ultimate reaction
will be. The reaction typically reaches its maximal intensity within 5-30 minutes, but death
can occur within a few minutes. Emergency
personnel should be summoned and basic life support may have to be administered. The most
common treatment for acute anaphylaxis is an
epinephrine auto-injector, commonly referred to as an EpiPen, which is administered in the
muscle of the outer thigh. Epinephrine acts as
a potent vasoconstrictor for the systemic arterioles, and also acts as a bronchodilator.
Thus, it directly opposes the effects of histamine
in the anaphylactic reaction. In severe cases, the patient would most likely have to receive
additional support through hospitalization and
fluid replacement. Hopefully this video has helped to reinforce the
physiological basis for anaphylactic shock.
Systemic anaphylactic reactions are extremely e-threatening and may be the most acute
emergency encountered in dental practice. Thank you for your assistance in solving this
case.


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