Dental Abscess to Septic Shock – A Case Report and Literature Review

Abstract

Sepsis is a leading cause of death in the United States, with a mortality rate in excess of 215,000 deaths per year. It may lead to septic shock - a complex pathophysiological process with microbial and host response events that progress to multisystem derangement. There is poor documentation of the relationship between dental infection and septic shock, with only a few case reports of septic shock secondary to dentoalveolar abscess. Presented is a review of sepsis/septic shock with a description of a 23-year-old male with signs and symptoms of necrotic pulp, acute apical abscess, and canine space infection that rapidly progressed to an altered mental state, hyperthermia, tachycardia, hypotension, acute respiratory failure, diarrhea, renal insufficiency, lactic acidosis, leukocytosis and hyperglycemia. Once septic shock develops, the mortality rate is nearly 50%. Early antimicrobial intervention is associated with surviving severe sepsis, making it critical for dentists to understand local factors leading to the crisis, and the signs and symptoms of the sepsis-septic shock continuum.

Full text

CASE REPORT/CLINICAL TECHNIQUES
Dental Abscess to Septic
Shock: A Case Report and
Literature Review
ABSTRACT
Sepsis is a leading cause of death in the United States, with a mortality rate in excess of
215,000 deaths per year. It may lead to septic shock, a complex pathophysiological process
with microbial and host response events that progress to multisystem derangement. There is
poor documentation of the relationship between dental infection and septic shock, with only a
few case reports of septic shock secondary to dentoalveolar abscess. Presented is a case of
sepsis/septic shock in a 23-year-old man with signs and symptoms of pulpal necrosis, acute
apical abscess, and canine space infection that rapidly progressed to an altered mental state,
hyperthermia, tachycardia, hypotension, acute respiratory failure, diarrhea, renal insufficiency,
lactic acidosis, leukocytosis, and hyperglycemia. Once septic shock develops, the mortality
rate is nearly 50%. Early antimicrobial intervention is associated with surviving severe sepsis,
making it critical for dentists to understand local factors leading to the crisis and the signs and
symptoms of the sepsis–septic shock continuum. (J Endod 2021;47:663–670.)
KEY WORDS
Bacteremia; dentoalveolar abscess; odontogenic infection; sepsis; septic shock
Sepsis is a serious, complicated medical condition with a high mortality rate. Sepsis and septic shock
are 2 entities occurring as a continuum, with sepsis leading to septic shock
1
. Sepsis was first defined
in 1991 as a systemic inflammatory response syndrome due to suspected infection with 2 or more
specified clinical criteria. Septic shock includes hypotension and organ dysfunction that persists
despite volume resuscitation, along with the systemic inflammatory response syndrome criteria
2
.
Using these definitions, the Surviving Sepsis Campaign developed guidelines for a protocol-driven
model of care
3
. In 2016, the international Sepsis-3 Committee defined sepsis as “a life-threatening
condition caused by a dysregulated host response to infection, resulting in organ dysfunction,”
whereas septic shock is “circulatory, cellular, and metabolic abnormalities in septic patients,
presenting as fluid-refractory hypotension requiring vasopressor therapy with associated tissue
hypoperfusion (lactate .2mmol/L)”
4
.
In the United States, the incidence of severe sepsis is estimated to be 300 cases per 10,000
population
5
, with over 30 million cases of sepsis/annum estimated worldwide
6
. More than 500,000
annual emergency department visits in the United States are related to sepsis
7
. In 2013, sepsis-related
illness was the most expensive reason for hospitalization, costing $23.7 billion
8
. One study reported the
mortality rate of sepsis as 33%–35%
9
, whereas hospital deaths in patients with sepsis from 2
independent cohorts found mortality ranged between 34%–56%
10,11
. With sepsis-related mortality
above 215,000 deaths per year, it is a leading cause of death in the United States
6
.
In 2013, New York state was the first to implement regulations that require hospitals to follow
protocols for treating sepsis, which resulted in a greater decrease in sepsis mortality compared with
control states without regulations
12
. Illinois, New Jersey, and Indiana also have mandatory practices,
whereas other states have introduced bills into legislature as recently as 2020 or use voluntary
programs
13
. In 2018, Maryland developed a public awareness campaign to help prevent sepsis
fatalities
14
.
We report a case of an urgent care visit to a dental school clinic for treatment of an endodontic and
canine space infection that quickly escalated to a medical emergency and near-death experience for the
patient because of sepsis and septic shock.
SIGNIFICANCE
This is a report of a healthy 23-
year-old male who presented
to the urgent care clinic of a
dental school for treatment of
an endodontic and canine
space infection. The patient’s
condition rapidly deteriorated
to a medical emergency and
near-death experience
because of sepsis and septic
shock. Significant changes in
vital signs are not expected in
localized infections. Hence, all
vital signs should be routinely
checked while examining
infected dental patients.
From the *Endodontics Division,
Department of Advanced Oral Sciences
and Therapeutics, University of Maryland
School of Dentistry, Baltimore, Maryland;
and
†
Department of Endodontics,
Rutgers School of Dental Medicine,
Newark, New Jersey
Address requests for reprints to Dr
Patricia A. Tordik, Endodontics Division,
Department of Advanced Oral Sciences
and Therapeutics, University of Maryland
School of Dentistry, 650 W Baltimore
Street, Baltimore, MD 21201.
E-mail address: ptordik@umaryland.edu
0099-2399/$ - see front matter
Copyright © 2021 American Association
of Endodontists.
https://doi.org/10.1016/
j.joen.2020.12.016
Saurabh Mannan, BDS, DMD,
MPH, MS,*Patricia A. Tordik,
DMD,*Frederico C. Martinho,
DDS, MSc, PhD,*Noah Chivian,
DDS,
†
and Craig S. Hirschberg,
DDS
†
JOE Volume 47, Number 4, April 2021 Dental Abscess to Septic Shock 663

CASE REPORT
Day 1
0900 Hours
A 23-year-old man presented to the
predoctoral urgent care clinic with a chief
complaint of an ongoing “toothache and
severe pain.”His past medical history was
noncontributory with no known drug allergies;
his past dental history included caries in tooth
#7. The patient was taking acetaminophen. His
vital signs are provided in Table 1. A limited oral
examination revealed pulpal necrosis/acute
apical abscess in tooth #7. For pain
management, 1 cartridge of lidocaine with
1:100,000 epinephrine (34 mg lidocaine
hydrochloride/0.017 mg epinephrine) mesial
and distal to the infected area was
administered using a standard local infiltration
technique.
1030 Hours
A dental student was assigned to initiate root
canal treatment of tooth #7 in the predoctoral
endodontics clinic later the same day. With
pain relief, the patient planned to hydrate and
eat a light meal before his appointment.
1415 Hours
The patient presented to the predoctoral
endodontics clinic. Despite having a toxic
appearance, he was alert; was oriented to
person, place, time, and situation; and was in
no respiratory distress. The attending faculty
made a cursory diagnosis of canine space
infection and immediately transferred care to
the on-call postgraduate endodontic resident.
1430 Hours
His past medical and dental history was
reviewed, medications were reconciled, and
no known drug allergies was noted. His vital
signs are presented in Table 1. The clinical/
radiographic data are provided in Table 2.A
periapical radiograph was provided by the
urgent care clinic (Fig. 1). The patient said he
felt cold and was given a blanket.
1440 Hours
Within 10 minutes of evaluation, intense
shivering ensued. The patient was lethargic
and hyperthermic. His tympanic temperature
and vital signs are presented in Table 1.
Emergency medical service (EMS) was
activated. Until the paramedics arrived, the
patient was semireclined, his airway was
maintained, respiration was supported with
100% oxygen, and ice packs were applied to
the forehead and axillae. The patient became
tachypneic, difficult to arouse, and lost
consciousness after EMS arrival. Because of
the suspected contribution of the dental
infection, the attending endodontist requested
the patient be transported to the university
hospital emergency department (ED), where
there is an oral and maxillofacial surgery
service, rather than to the city hospital on call.
The ED consented to accept the patient.
Tachycardia was refractory to 6 mg adenosine
provided en route to the ED. His vital signs are
recorded in Table 1. A review of his systems
are included in Table 3.
1810 Hours
The patient was sedated with propofol and
benzodiazepine and then intubated to protect
the airway. A full-body computed tomographic
scan was ordered because of the sudden
alteration in mental awareness. The differential
diagnosis included meningitis, encephalitis,
septic encephalopathy, toxin/ingestant, and
seizure/postictal. The immediate treatment
plan was for magnetic resonance imaging and
electroencephalography while awaiting the
results of urodynamic studies and lumbar
puncture. To manage possible infection, the
patient was given intravenous cefepime,
vancomycin, and metronidazole, which was
later changed to ceftriaxone, vancomycin,
metronidazole, and acyclovir. A lactated Ringer
solution bolus was administered for fluid
replenishment.
2334 Hours
The patient had elevated troponin, lactate, and
creatinine values (Table 3). Primary cardiac
pathology was considered not likely,
transthoracic echocardiography was planned,
and the patient was admitted to the critical
care resuscitation unit.
Day 2
Approximately 8 hours after admission, the
working diagnosis included septic shock,
central nervous system failure or compromise,
metabolic crisis, acute respiratory failure, renal
insufficiency, elevated liver enzymes,
leukocytosis, and fever. The transthoracic
echocardiographic finding was tachycardia
secondary to sepsis, volume depletion, and
fever. Heart rate decreased with volume
resuscitation, leading to the conclusion of
sinus tachycardia. Norepinephrine bitartrate
(Levophed; CIBA, Basel, Switzerland) was
administered to maintain a mean arterial
pressure .65 mm Hg based on the bedside
echocardiogram suggesting myocardial
dysfunction and euvolemia. Full ventilator
support continued until vast improvement
allowed for extubation. Findings of
reconstructed computed tomographic
images, taken with contrast to evaluate for
infection, were unremarkable (Table 4).
TABLE 1 - Vital Signs as Recorded in the Medical Record
Day Time BP Pulse (beats/min) HR R (Rate) R (Rhythm) R (Depth) SpO
2
%
Temperature
(F) Temp (C)
MAP
(mm Hg) Arterial BP
1 0900 155/96*80 12 Regular Normal
1 1430 170/104*100*12 Regular Normal
1 1440 170/100*160*18*Increased Shallow 106*41.1*
1 1533 135/98*183*174*20*Increased Shallow 97*102.9*39.4*
1 1931 113/66 128*114*20*Increased Shallow 100 100*37.8*
2 0200 95/54*79 75 15 Regular Normal 100 98.6 37*67.67*114/53
BP, blood pressure; HR, heart rate; MAP, mean arterial pressure; R, respiration; SpO
2
, oxygen saturation.
*Values outside of the normal range.
TABLE 2 - Clinical and Radiographic Data Collection
Tooth Swelling
Lymphadenopathy upon
palpation ST Cold Hot EPT Percussion Palpation
Mobility
(mm)
Probing
(mm)
Periapical
radiolucency (mm)
7V,CSN NNRNTNTS S 0 ,36!8
CS, canine space; EPT, electric pulp test; N, none; NR, no response; NT, not tested; S, sensitive; ST, sinus tract; V, vestibular.
664 Mannan et al. JOE Volume 47, Number 4, April 2021

Day 3
The oral and maxillofacial surgery service
completed a head/neck examination. Extraoral
swelling with obliteration of the nasiolabial fold
and a broad, fluctuant swelling in the vestibule
were noted. A diagnosis of acute apical
abscess/canine space infection associated
with tooth #7 was made. After infiltrating with
lidocaine/epinephrine, a vestibular, horizontal
incision was made extending from tooth #6 to
tooth #8. Subperiosteal blunt dissection
produced purulent and sanguineous drainage.
Tissues were irrigated with a high volume of
0.9% normal saline, and a gauze pressure
dressing was placed.
Day 4
An improvement in fever, leukocytosis, and
hemodynamics was noted. The clinical course
of infection was improving.
Day 5
The patient was discharged to home with a
7-day course of amoxicillin/clavulanate
potassium 875 mg and 30 mL 0.12%
chlorhexidine gluconate oral rinse. He was
advised to follow up with the dental school,
where the nonsurgical root canal treatment
was completed by the same predoctoral
student, 3 months later (Fig. 2). The discharge
note stated the following: “Because of likely
dental abscess, the patient was hypotensive
on presentation and showed signs of ischemic
end organ damage with lactic acidosis,
transaminitis, troponinemia, acute kidney injury
and altered mental status (AMS), requiring
intubation.”
DISCUSSION
Except when pathogens directly enter the
bloodstream, sepsis occurs in 2 stages:
preseptic and septic. With direct
contamination, the preseptic stage is absent
15
.
Previously, it was believed the immune system
maladaptive response played the predominant
role in presepsis
16,17
. New information
suggests pathogens are also involved
18
.
Preseptic and Septic Bacterial Role
The primary sources for bacteria entering the
bloodstream include local infection, lungs,
lymphatics, venous system, or intestines. Only
erythrocytes clear bacteria from the
bloodstream
19
. The erythrocyte membrane is
triboelectrically charged to attract bacteria.
Once fixed to the membrane, oxyhemoglobin
is released, killing most bacteria
19,20
.Ifa
bacterium survives oxidation, it can be trapped
in the concave pocket of an erythrocyte. Once
trapped, it is either oxidized and released into
FIGURE 1 – The periapical radiograph provided by the urgent care clinic.
TABLE 3 - A Review of the Systems and Pertinent Values from the Comprehensive Metabolic Panel
Normal findings Abnormal findings
General Febrile, altered mental status:
nonverbal, agitated, incoherent
Skin Diaphoretic
Head and neck No traumatic head injury or cervical
lymphadenopathy
Pulmonary/chest No stridor or wheezes Tachypenia
Cardiovascular Regular rhythm, normal heart
sounds, and intact distal pulses;
no gallop; no friction rub; no
murmur heard
Sinus tachycardia, bedside
echocardiogram grossly
depressed with left ventricular
ejection fraction 525%–35%
Gastrointestinal Normal bowel sounds, no
distention, no mass, no
tenderness, no rebound, no
guarding
Vomiting, diarrhea
Urinary UDS ordered
Genital All
Vascular All
Musculoskeletal All
Neurologic LP and EEG planned
Hematologic Comprehensive metabolic panel
ordered
Endocrine All Thyroid-stimulating hormone and
free thyroxine test planned
Psychiatric Indeterminate signs/symptoms due to altered mental state
Normal range Measured value
Creatinine 0.6–1.2 mg/dL 1.42 mg/dL*
Lactate 0.5–1.0 mmol/L 3.4 mmol/L*
Troponin 0.0–0.04 ng/mL 0.61 ng/mL*
EEG, electroencephalography; LP, lumbar puncture; UDS, urodynamic study.
*Elevated values.
JOE Volume 47, Number 4, April 2021 Dental Abscess to Septic Shock 665

plasma for digestion in the reticuloendothelial
system, released, and removed by the liver and
spleen or uses exotoxin to decompose the
erythrocyte membrane and enter the cell
15
.
Inside an erythrocyte, a bacterium is protected
from immune complexes and exogenous
antibacterial agents. Using hemoglobin, it can
multiply and rupture the membrane, releasing
new bacteria into plasma. This is a critical step
in developing sepsis
15
.
Motile and nonmotile bacteria resistant
to host immunity proliferate in tissue and enter
circulation
15
. Immunity-resistant features
include superoxide dismutase, catalase, and
gonyautoxin production. These enzymes
convert harmful superoxide to nontoxic water
and oxygen
15
. Likewise, a capsule, slime layer,
and biofilm protect against phagocytosis, lytic
enzymes, immune complexes, reactive oxygen
species, and erythrocyte attachment
20
.
Sepsis-causing bacteria must also express a
large quantity/variety of virulence factors and
coordinate individual gene transcription to
maximize virulence potential
16
.
Gram-positive bacteria effectively
invade host tissue
21
and initiate sepsis via
exotoxins and the exposed cell wall
peptidoglycan
22
, whereas gram-negative
bacteria trigger sepsis through
lipopolysaccharide endotoxins
23
. Most sepsis
involves facultative anaerobic bacteria
15
, but
nonfacultative anaerobes also contribute.
Meanwhile, the bacterial etiology of
endodontic infection is well-documented
24
.
Endodontic infections contain both gram-
negative and gram-positive facultative and
obligate anaerobes, with the prevalent phyla
identified as Proteobacteria, Firmicutes,
Bacteroidetes, Fusobacteria, and
Actinobacteria
25
.Prevotella and
Porphyromonas spp. are associated with
symptomatic infected teeth and are thought to
play an essential role in severe infections
26
.Itis
unknown how many cases of sepsis/septic
shock are the result of dental infections.
When erythrocytes are destroyed by
bacteria, inflammation anemia occurs
19
. With
no erythrocytes to deliver oxygen to organs,
cell hypoxia results. The kidneys and liver
detect reduced blood oxygen levels and
secrete erythropoietin to stimulate bone
marrow erythropoiesis. This slightly increases
the blood oxygen transport capacity. Bacterial
attachment to erythrocytes causes premature
oxygen release, platelet activation, and
disseminated intravascular coagulation
27
,
which provides nutrients for bacterial
proliferation
15
. Oxidative hormone inactivation
leads to muscle wasting and impaired
wound healing, whereas insulinlike growth
factor inactivation leads to hyperglycemia
28
.
Lower blood oxidation also affects the
TABLE 4 - Findings of Reconstructed Coronal and Sagittal Computed Tomographic Scans
Airway Bowel
Free air/
fluid Heart/lungs Intracranial
Lymph
nodes
Lytic
lesions Osseous
Other organs/
structures
Posterior
fossa
Soft tissue
planes Thyroid Vasculature
Head and
neck
Patent None Visible lung
apices: clear
Normal Normal Normal Paranasal sinuses,
mastoid air cells:
all well aerated
Visualized
structures:
normal
Normal Normal Intact
Chest and
abdomen
Patent, no
endobronchial
lesions
Normal, no
evidence of
obstruction
of ileum
None No pericardial
or pleural
effusion
Heart/great
vessels: normal
Lungs: clear; no
focal consolidation
atelectasis, nodules,
or masses
Normal
within
mediastinum,
hill, and axilla
Normal Kidney enhancement
and excretion: normal
Liver, gallbladder,
pancreas, spleen,
adrenal glands: normal
Normal
Pelvis None Normal None Urinary bladder collapsed
with Foley catheter in place
666 Mannan et al. JOE Volume 47, Number 4, April 2021

hypothalamic-pituitary-thyroid axis, causing
adrenal and vasopressin insufficiency and
thyroid hormone inadequacy. Vasopressin
oxidation along with low levels of angiotensin II
and angiotensin-converting enzyme contribute
to systemic vasodilation
29
. Resultant albumin
oxidation leads to hypoalbuminemia, which is
identified as an independent predictor of
sepsis mortality
15
. Lastly, inactivation of
immunoglobulins alters immunoreactivity
15
.
Preseptic and Septic Host Role
Prolonged overexpression of chemical
mediators required to recruit immune effector
cells evoke harmful biological effects
16
. Often
referred to as cytokine cascade/dysfunction, it
involves all cell types including antigen-
presenting cells, neutrophils, macrophages,
and lymphocytes. Once the cascade initiates
events, hypoxia and cellular hypoperfusion
lead to transitory organ failure
30
. Profound
oxidative cellular stress results in
catecholamine depletion, hormonal alterations,
vascular dysfunction, neural dysregulation,
and disruptions to immune/metabolic
activities. If the patient is not well managed,
health rapidly deteriorates. Symptoms include
cardiovascular depression, delirium, acute
respiratory distress syndrome, acute renal
failure, and hepatic dysfunction
31
. A nonlinear,
exponential relationship between cellular injury
and organ failure leads to a high level of
mortality
30
.
The effect of septic shock on the
cardiovascular system can be divided into 3
major events: vasodilation, maldistribution of
blood flow, and cardiovascular depression
31
.
Hypotension despite adequate fluid
resuscitation reflects the end of progressive
deterioration
17
. Myocardial depressant factors
tumor necrosis factor alpha and interleukin 1
beta participate in cardiovascular
depression
32
. These factors produce
abnormal amounts of nitric oxide and cyclic
guanosine monophosphate. Excessive nitric
oxide leads to decreased vascular resistance,
resulting in maldistribution of blood flow
33
.It
also interacts with superoxide to form
peroxynitrite, which directly injures intracellular
structures
34
. Mitochondrial injury limits the
ability of the cytochrome system to generate
adenosine triphosphate, leading to myocardial
depression. Excessive acetylcholine secretion
also leads to myocardial depression, but it can
inhibit tumor necrosis factor alpha expression,
improving survival
35
.
High concentrations of circulating
catecholamines produced in the early stages
of septic shock enhance the inflammatory
response. Continuous elevated levels result in
depletion, perhaps because of apoptosis of
adrenal medullary cells
36
. Once depleted, the
patient is predisposed to peripheral
vasodilation, compromised myocardial
contractility, and myocardial depression
36
.
Hypotension, hypoperfusion, and organ
dysfunction follow. The concomitant abnormal
adrenergic modulation of heart/vessels during
septic shock indicates that adrenergic
regulation impairment contributes to
cardiocirculatory failure
36
.
Signs and Symptoms of Septic
Shock
Sequential (Sepsis-Related) Organ Function
Assessment (SOFA) scoring is an objective
method to determine dysfunction based on
oxygen levels, platelet count, Glasgow Coma
Scale (GCS) score, bilirubin level, creatinine
level, and mean arterial pressure
2
. Quick SOFA
(qSOFA) is simpler and predicts death risk
2
.
One point each is awarded for AMS (GCS
,15), respiratory rate 22 breaths/min, and
systolic blood pressure (BP) 100 mm Hg.
Patients with qSOFA scores of 2–3 are
associated with a 3- to 14-fold increase in
hospital mortality and should be further
assessed with blood testing, including serum
lactate, and full SOFA scoring
37
. When our
patient suffered from AMS and tachypnea, he
had a qSOFA score of 2.
Our patient presented with serious,
general signs of sepsis including all
components of a toxic appearance
38
. This
included an ill presentation, shivers/chills,
lethargy, diaphoresis, rapid pulse, and fever of
102–107F. Upon arrival to the ED, our
patient was suffering from acute respiratory
failure.
Questioning an infected dental patient
can reveal if he or she is eating or sufficiently
hydrated. Dentists should recognize the signs
and symptoms of dehydration, including a
drawn facial appearance, dry mucous
membranes, fever, loss of skin turgor, oliguria,
postural hypotension, serum electrolyte
changes, thirst, and weakness
38
. Our patient
was experiencing at least 6 of these signs and
symptoms.
FIGURE 2 – The immediate postobturation periapical radiograph. The nonsurgical root canal treatment was completed
by the predoctoral dental student.
JOE Volume 47, Number 4, April 2021 Dental Abscess to Septic Shock 667

Another symptom of sepsis is central
nervous system changes. Although our patient
was initially alert and oriented, his best eye,
verbal, and motor responses diminished over a
short period of time. Within 30 minutes, his
GCS score was 15, then 11, and then
unresponsive. A declining or “waxing and
waning”GCS is concerning, and the airway
should be reassessed for intervention
38
. Our
patient was intubated upon arrival in the ED.
Our patient had elevated creatinine
(1.42 mg/dL), lactate (3.4 mmol/L), and
troponin (0.61 ng/mL) values. Elevated
creatinine indicates kidney disease, shock,
dehydration, or congestive heart failure
38
. The
high lactic acid level was interpreted as
secondary to hypoperfusion, and intravenous
fluid replenishment was continued. Elevated
lactate signals anaerobic metabolism and
indicates sepsis, shock, cardiac arrest, liver
disease, seizure, asthma, trauma, bowel
dysfunction, medication-related damage, or
cancers
38
. Troponin values between 0.04 and
0.39 ng/mL may indicate cardiac problems,
with values over 0.4 ng/mL indicating possible
cardiac arrest. Other reasons for elevation
include sepsis, kidney failure, pulmonary
embolism, myocarditis, drug abuse, or
trauma
38
.
An elevated body temperature highly
predicts acute infection. Moderate to severe
infections always produce an elevated
temperature, whereas a localized acute apical
abscess with or without swelling will not
39
.
Temperatures .101.3F indicate simple
pyrexia, whereas hyperthermia is a term
reserved for body temperatures 105.8F
38
.
We initially recorded temperatures in our
patient as high as 106F. Unfortunately, body
temperature was not recorded when the
patient first arrived. If it had been, a referral
could have occurred sooner.
Although there are no or minor changes
in BP during localized infections, sepsis/septic
shock produce significant BP changes
attributed to shock, decreased blood volume,
vasodilatation, or severe dehydration (low BP).
Our 23-year-old patient presented with severe
pain, no known medical conditions, a normal
body mass index of 22.8 kg/m
2
, and elevated
BP readings that steadily decreased to
hypotension by day 2. The normal
physiological heart rate response to infection
and shock is rapid and weak. Our patient had
recorded rates of 100 beats/min and then 160
beats/min before EMS arrival.
CONCLUSION
Presented is a healthy 23-year-old male whose
condition rapidly deteriorated during an
emergency dental office visit due to sepsis/
septic shock. Significant changes in vital signs
are not expected in localized infections. Hence,
all vital signs should be routinely checked while
examining infected dental patients. BP, pulse,
respiration, and temperature should be
thoughtfully assessed within the context of the
patient’s overall medical and dental conditions
and sudden alterations in mental state,
respiration, and systolic BP quickly acted on.
ACKNOWLEDGMENTS
The authors thank Dr. Michael A. Steinle for his
valuable input.
The authors deny any conflicts of
interest related to this study.
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