ArticlePDF AvailableLiterature Review

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

Authors:
  • University of Maryland, School of Dentistry

Abstract and Figures

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.
Content may be subject to copyright.
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 insufciency,
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 sepsisseptic shock continuum. (J Endod 2021;47:663670.)
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 rst dened
in 1991 as a systemic inammatory response syndrome due to suspected infection with 2 or more
specied clinical criteria. Septic shock includes hypotension and organ dysfunction that persists
despite volume resuscitation, along with the systemic inammatory response syndrome criteria
2
.
Using these denitions, the Surviving Sepsis Campaign developed guidelines for a protocol-driven
model of care
3
. In 2016, the international Sepsis-3 Committee dened 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 uid-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 rst 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 patients
condition rapidly deteriorated
to a medical emergency and
near-death experience
because of sepsis and septic
shock. Signicant 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 inltration
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, difcult 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 uid
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
insufciency, elevated liver enzymes,
leukocytosis, and fever. The transthoracic
echocardiographic nding 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, uctuant swelling in the vestibule
were noted. A diagnosis of acute apical
abscess/canine space infection associated
with tooth #7 was made. After inltrating 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 xed 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 ndings Abnormal ndings
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 0.61.2 mg/dL 1.42 mg/dL*
Lactate 0.51.0 mmol/L 3.4 mmol/L*
Troponin 0.00.04 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 biolm 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
identied 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, inammation 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/
uid 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 insufciency 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
identied 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 ow, and cardiovascular depression
31
.
Hypotension despite adequate uid
resuscitation reects 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 ow
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 inammatory
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 23 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
102107F. 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 sufciently
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
waningGCS 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
uid 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 .101.3F indicate simple
pyrexia, whereas hyperthermia is a term
reserved for body temperatures 105.8F
38
.
We initially recorded temperatures in our
patient as high as 106F. Unfortunately, body
temperature was not recorded when the
patient rst 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 signicant 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 ofce visit due to sepsis/
septic shock. Signicant 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
patients 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 conicts of
interest related to this study.
REFERENCES
1. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference:
denitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis.
Crit Care Med 1992;20:86474.
2. Dugar S, Choudhary C, Duggal A. Sepsis and septic shock: guideline-based management. Cleve
Clin J Med 2020;87:5364.
3. Levy MM, Rhodes A, Phillips GS, et al. Surviving Sepsis Campaign: association between
performance metrics and outcomes in a 7.5-year study. Crit Care Med 2015;43:312.
4. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Denitions for
Sepsis and Septic Shock (Sepsis-3). JAMA 2016;315:80110.
5. Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med 2013;369:84051.
6. Fleischmann C, Scherag A, Adhikari NK, et al. Assessment of global incidence and mortality of
hospital-treated sepsis current estimates and limitations. Am J Respir Crit Care Med
2016;193:25972.
7. Wang HE, Shapiro NI, Angus DC, Yealy DM. National estimates of severe sepsis in United States
emergency departments. Crit Care Med 2007;35:192836.
8. Torio CM, Andrews RM. Statistical nrief #160: National inpatient hospital costs: the most
expensive conditions by payer (2011). In: Healthcare Cost and Utilization Project Statistical
Briefs. Rockville, MD: Agency for Healthcare Research and Quality; 2013. p. 112.
9. Stevenson EK, Rubenstein AR, Radin GT, et al. Two decades of mortality trends among patients
with severe sepsis: a comparative meta-analysis. Crit Care Med 2014;42:62531.
10. Liu V, Escobar GJ, Greene JD, et al. Hospital deaths in patients with sepsis from 2 independent
cohorts. J Am Med Assoc 2014;312:902.
11. Mayr FB, Yende S, Angus DC. Epidemiology of severe sepsis. Virulence 2014;5:411.
12. Kahn JM, Davis BS, Yabes JG, et al. Association between state-mandated protocolized sepsis
care and in-hospital mortality among adults with sepsis. JAMA 2019;322:24050.
668 Mannan et al. JOE Volume 47, Number 4, April 2021
13. Massachusetts Sepsis Consortium. State-based strategies for combating sepsis. 2018.
Available at: https://betsylehmancenterma.gov/assets/uploads/BLC_Sepsis_Landscape_Final
Edit02_v21.pdf. Accessed August 19, 2020.
14. Maryland Department of Health. Report on sepsis public awareness campaign chapter 489 of the
acts of 2018 (HB 1467 / SB 574). Available at: https://phpa.health.maryland.gov/documents/HB-
1467-2018-Report-on-the-Sepsis-Public-Awareness-Campaign-Workgroup.pdf. Accessed
August 11, 2020.
15. Minasyan H. Sepsis and septic shock: pathogenesis and treatment perspectives. J Crit Care
2017;40:22942.
16. Nduka OO, Parrillo JE. The pathophysiology of septic shock. Crit Care Nurs Clin 2011;23:4166.
17. Parrillo JE, Parker MM, Natanson C, et al. Septic shock in humans: advances in the
understanding of pathogenesis, cardiovascular dysfunction, and therapy. Ann Intern Med
1990;113:22742.
18. Campisi L, Brau F, Glaichenhaus N. Imaging host-pathogen interactions. Immunol Rev
2008;221:18899.
19. Minasyan H. Erythrocyte and blood antibacterial defense. Eur J Microbiol Immunol 2014;4:
13843.
20. Minasyan H. Mechanisms and pathways for the clearance of bacteria from blood circulation in
health and disease. Pathophysiology 2016;2:616.
21. Sriskandan S, Cohen J. Gram-positive sepsis: mechanisms and differences from gram-negative
sepsis. Infect Dis Clin North Am 1999;13:397412.
22. Balk RA. Severe sepsis and septic shock. Denitions, epidemiology, and clinical manifestations.
Crit Care Clin 2000;16:17992.
23. Horn KD. Evolving strategies in the treatment of sepsis and systemic inammatory response
syndrome (SIRS). QJM 1998;91:26577.
24. Kakehashi S, Stanley HR, Fitzgerald RJ. The Effects of surgical exposures of dental pulps in germ-
free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol 1965;20:3409.
25. Siqueira JF, Fl
avio RF, Alves FR, R^
oças IN. Pyrosequencing analysis of the apical root canal
microbiota. J Endod 2011;37:1499503.
26. Griffee MB, Patterson SS, Miller CH, et al. The relationship of Bacteroides melaninogenicus to
symptoms associated with pulpal necrosis. Oral Surg Oral Med Oral Pathol 1980;50:45761.
27. House SD, Johnson PC. Diameter and blood ow of skeletal muscle venules during local ow
regulation. Am J Physiol 1986;250:H82837.
28. Olivares-Corichi IM, Ceballos G, Medina-Santillan R, et al. Oxidation by reactive oxygen species
(ROS) alters the structure of human insulin and decreases the insulin-dependent D-glucose-C14
utilization by human adipose tissue. Front Biosci 2005;10:312731.
29. Zhang W, Chen X, Huang L, et al. Severe sepsis: Low expression of the renin-angiotensin system
is associated with poor prognosis. Exp Ther Med 2014;7:13428.
30. Armstrong BA, Betzold RD, May AK. Sepsis and septic shock strategies. Surg Clin North Am
2017;97:133979.
31. Hinshaw LB. Sepsis/septic shock: participation of the microcirculation: an abbreviated review.
Crit Care Med 1996;24:10728.
32. Kumar A. Tumor necrosis factor alpha and interleukin 1beta are responsible for in vitro myocardial
cell depression induced by human septic shock serum. J Exp Med 1996;183:94958.
33. Ullrich R, Scherrer-Crosbie M, Bloch KD, et al. Congenital deciency of nitric oxide synthase 2
protects against endotoxin-induced myocardial dysfunction in mice. Circulation 2000;102:
14406.
34. Lockhart PB, Brennan MT, Sasser HC, et al. Bacteremia associated with tooth brushing and
dental extraction. Circulation 2008;117:311825.
35. Wang H, Liao H, Ochani M, et al. Cholinergic agonists inhibit HMGB1 release and improve survival
in experimental sepsis. Nat Med 2004;10:121621.
36. Annane D, Trabold F, Sharshar T, et al. Inappropriate sympathetic activation at onset of septic
shock: A spectral analysis approach. Am J Respir Crit Care Med 1999;160:45865.
37. qSOFA (Quick SOFA). Score for sepsis. Available at: https://www.mdcalc.com/qsofa-quick-
sofa-score-sepsis#next-steps. Accessed July 31, 2020.
JOE Volume 47, Number 4, April 2021 Dental Abscess to Septic Shock 669
38. Hohl TH, Whitacre RJ, Hooley J, Williams BL. A Self-Instructional Guide: Diagnosis and
Treatment of Odontogenic Infections. Seattle, WA: Stoma Press Inc.; 1983. p. 348.
39. Campanelli CA, Walton RE, Williamson AE, et al. Vital signs of the emergency patient with pulpal
necrosis and localized acute apical abscess. J Endod 2008;34:2647.
670 Mannan et al. JOE Volume 47, Number 4, April 2021
Article
Full-text available
Oral diseases and associated microbes are a risk factor for systemic diseases and can change the courses of these diseases. To date, epidemiological data on microbial oral infections are scarce, and longitudinal reports are lacking.
Article
Full-text available
Importance Beginning in 2013, New York State implemented regulations mandating that hospitals implement evidence-based protocols for sepsis management, as well as report data on protocol adherence and clinical outcomes to the state government. The association between these mandates and sepsis outcomes is unknown. Objective To evaluate the association between New York State sepsis regulations and the outcomes of patients hospitalized with sepsis. Design, Setting, and Participants Retrospective cohort study of adult patients hospitalized with sepsis in New York State and in 4 control states (Florida, Maryland, Massachusetts, and New Jersey) using all-payer hospital discharge data (January 1, 2011-September 30, 2015) and a comparative interrupted time series analytic approach. Exposures Hospitalization for sepsis before (January 1, 2011-March 31, 2013) vs after (April 1, 2013-September 30, 2015) implementation of the 2013 New York State sepsis regulations. Main Outcomes and Measures The primary outcome was 30-day in-hospital mortality. Secondary outcomes were intensive care unit admission rates, central venous catheter use, Clostridium difficile infection rates, and hospital length of stay. Results The final analysis included 1 012 410 sepsis admissions to 509 hospitals. The mean age was 69.5 years (SD, 16.4 years) and 47.9% were female. In New York State and in the control states, 139 019 and 289 225 patients, respectively, were admitted before implementation of the sepsis regulations and 186 767 and 397 399 patients, respectively, were admitted after implementation of the sepsis regulations. Unadjusted 30-day in-hospital mortality was 26.3% in New York State and 22.0% in the control states before the regulations, and was 22.0% in New York State and 19.1% in the control states after the regulations. Adjusting for patient and hospital characteristics as well as preregulation temporal trends and season, mortality after implementation of the regulations decreased significantly in New York State relative to the control states (P = .02 for the joint test of the comparative interrupted time series estimates). For example, by the 10th quarter after implementation of the regulations, adjusted absolute mortality was 3.2% (95% CI, 1.0% to 5.4%) lower than expected in New York State relative to the control states (P = .004). The regulations were associated with no significant differences in intensive care unit admission rates (P = .09) (10th quarter adjusted difference, 2.8% [95% CI, −1.7% to 7.2%], P = .22), a significant relative decrease in hospital length of stay (P = .04) (10th quarter adjusted difference, 0.50 days [95% CI, −0.47 to 1.47 days], P = .31), a significant relative decrease in the C difficile infection rate (P < .001) (10th quarter adjusted difference, −1.8% [95% CI, −2.6% to −1.0%], P < .001), and a significant relative increase in central venous catheter use (P = .02) (10th quarter adjusted difference, 4.8% [95% CI, 2.3% to 7.4%], P < .001). Conclusions and Relevance In New York State, mandated protocolized sepsis care was associated with a greater decrease in sepsis mortality compared with sepsis mortality in control states that did not implement sepsis regulations. Because baseline mortality rates differed between New York and comparison states, it is uncertain whether these findings are generalizable to other states.
Article
Full-text available
The majority of bacteremias do not develop to sepsis: bacteria are cleared from the bloodstream. Oxygen released from erythrocytes and humoral immunity kill bacteria in the bloodstream. Sepsis develops if bacteria are resistant to oxidation and proliferate in erythrocytes. Bacteria provoke oxygen release from erythrocytes to arterial blood. Abundant release of oxygen to the plasma triggers a cascade of events that cause: 1. oxygen delivery failure to cells; 2. oxidation of plasma components that impairs humoral regulation and inactivates immune complexes; 3. disseminated intravascular coagulation and multiple organs' failure. Bacterial reservoir inside erythrocytes provides the long-term survival of bacteria and is the cause of ineffectiveness of antibiotics and host immune reactions. Treatment perspectives that include different aspects of sepsis development are discussed.
Article
Sepsis is a life-threatening organ dysfunction that results from the body's response to infection. It requires prompt recognition, appropriate antibiotics, careful hemodynamic support, and control of the source of infection. With the trend in management moving away from protocolized care in favor of appropriate usual care, an understanding of sepsis physiology and best practice guidelines is critical.
Article
Three therapeutic principles most substantially improve organ dysfunction and survival in sepsis: early, appropriate antimicrobial therapy; restoration of adequate cellular perfusion; timely source control. The new definitions of sepsis and septic shock reflect the inadequate sensitivity, specify, and lack of prognostication of systemic inflammatory response syndrome criteria. Sequential (sepsis-related) organ failure assessment more effectively prognosticates in sepsis and critical illness. Inadequate cellular perfusion accelerates injury and reestablishing perfusion limits injury. Multiple organ systems are affected by sepsis and septic shock and an evidence-based multipronged approach to systems-based therapy in critical illness results in improve outcomes.
Article
The autonomic cardiovascular control was investigated in 10 patients with septic shock, 10 patients with sepsis syndrome, and six tilted healthy subjects. Overall variability, high- and low-frequency components (AUC, HF, and LF, beats/min(2)/Hz or mm Hg-2/Hz) from heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressures spectra were obtained from 5-min recordings. LFHR/HFHR and the square root of LFSBP/LFHR (alpha) were used as indices of sympathovagal interaction and baroreflex control of the heart, respectively. Compared with tilted control subjects and patients with sepsis syndrome, septic shock is characterized by reduction in: (1) HR variability, i.e., decreased AUC(HR) (p = 0.007), LFHR (p = 0.002), and LFHR/HFHR (p = 0.0002); (2) DBP variability, i.e., decreased AUC(DBP) (p = 0.003) and LFDBP (p = 0.001), (3) or (p = 0.003). In septic shock, LFHR/HFHR, alpha, and LFDBP correlated with mean blood pressure (r = 0.67, p = 0.04, r = 0.64, p = 0.03, and r = 0.88, p = 0.0008, respectively), and with plasma norepinephrine levels (r = -0.65, p = 0.03, r = -0.79, p = 0.006, and r = -0.69, p = 0.03, respectively). In conclusion, onset of septic shock is characterized by high concentrations of circulating catecholamines but impaired sympathetic modulation on heart and vessels, suggesting that central autonomic regulatory impairment contributes to circulatory failure.
Article
Available data do not support the concept that leukocytes engulf and kill bacteria in the bloodstream. Leukocytes cannot recognize or engulf bacteria in flowing blood; therefore, phagocytosis is impossible in the bloodstream and occurs instead outside of the bloodstream in the body tissues. Erythrocytes capture bacteria in the circulation using an electric charge and kill them using oxidation. The dead bacteria are then disintegrated and digested by the reticuloendothelial system (RES), particularly in the liver and the spleen
Article
Importance Definitions of sepsis and septic shock were last revised in 2001. Considerable advances have since been made into the pathobiology (changes in organ function, morphology, cell biology, biochemistry, immunology, and circulation), management, and epidemiology of sepsis, suggesting the need for reexamination.Objective To evaluate and, as needed, update definitions for sepsis and septic shock.Process A task force (n = 19) with expertise in sepsis pathobiology, clinical trials, and epidemiology was convened by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine. Definitions and clinical criteria were generated through meetings, Delphi processes, analysis of electronic health record databases, and voting, followed by circulation to international professional societies, requesting peer review and endorsement (by 31 societies listed in the Acknowledgment).Key Findings From Evidence Synthesis Limitations of previous definitions included an excessive focus on inflammation, the misleading model that sepsis follows a continuum through severe sepsis to shock, and inadequate specificity and sensitivity of the systemic inflammatory response syndrome (SIRS) criteria. Multiple definitions and terminologies are currently in use for sepsis, septic shock, and organ dysfunction, leading to discrepancies in reported incidence and observed mortality. The task force concluded the term severe sepsis was redundant.Recommendations Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. For clinical operationalization, organ dysfunction can be represented by an increase in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score of 2 points or more, which is associated with an in-hospital mortality greater than 10%. Septic shock should be defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. This combination is associated with hospital mortality rates greater than 40%. In out-of-hospital, emergency department, or general hospital ward settings, adult patients with suspected infection can be rapidly identified as being more likely to have poor outcomes typical of sepsis if they have at least 2 of the following clinical criteria that together constitute a new bedside clinical score termed quickSOFA (qSOFA): respiratory rate of 22/min or greater, altered mentation, or systolic blood pressure of 100 mm Hg or less.Conclusions and Relevance These updated definitions and clinical criteria should replace previous definitions, offer greater consistency for epidemiologic studies and clinical trials, and facilitate earlier recognition and more timely management of patients with sepsis or at risk of developing sepsis.
Article
Rationale: Reducing the global burden of sepsis, a recognised global health challenge, requires comprehensive data on the incidence and mortality on a global scale. Objective: To estimate the worldwide incidence and mortality of sepsis and to identify knowledge gaps based on available evidence from observational studies. Methods: We systematically searched 15 international citation databases for population-level estimates of sepsis incidence rates and fatality in adult populations using consensus criteria and published in the last 36 years. Main results: The search yielded 1553 reports from 1979 to 2015, of which 45 met our criteria. 27 studies from 7 high-income-countries provided data for meta-analysis. For these countries, the population incidence rate was 288 [95%CI, 215-386, τ=0.55] hospital-treated sepsis cases and 148 [95%CI, 98-226, τ=0.99] hospital-treated severe sepsis cases per 100 000 person-years. Restricted to the last decade, the incidence rate was 437 [95%CI, 334-571, τ=0.38] sepsis and 270 [95%CI, 176-412, τ=0.60] severe sepsis cases per 100 000 person-years. Hospital mortality was 17% for sepsis and 26% for severe sepsis during this period. There were no population-level sepsis incidence estimates from lower-income-countries, which limits the prediction of global cases and deaths. However, a tentative extrapolation from high-income-country data suggests global estimates of 31.5 million sepsis and 19.4 million severe sepsis cases, with potentially 5.3 million deaths annually. Conclusions: Population-level epidemiological data for sepsis are scarce, and non-existent for low- and middle-income-countries. Our analyses underline the urgent need to implement global strategies to measure sepsis morbidity and mortality - particularly in low- and middle-income-countries.
Article
Previous studies have demonstrated the presence of myocardial depression in clinical and experimental septic shock. This depression is associated with the presence of a circulating myocardial depressant substance with physical characteristics consistent with cytokines. The present study utilized an in vitro myocardial cell assay to examine the role of various human recombinant cytokines, including tumor necrosis factor (TNF)alpha and interleukin (IL)1beta, in depression of cardiac myocyte contractile function induced by serum from humans with septic shock. The extent and velocity of electrically paced rat cardiac myocytes in tissue culture was quantified by a closed loop video tracking system. Individually, TNF-alpha and IL-1beta each caused significant concentration-dependent depression of maximum extent and peak velocity of myocyte shortening in vitro. In combination, TNF-alpha and IL-1beta induced depression of myocardial cell contractility at substantially lower concentrations consistent with a synergistic effect. Using immunoabsorption, removal of both TNF-alpha and IL-1beta (but not either alone) from the serum of five patients with acute septic shock and marked reversible myocardial depression resulted in elimination of serum myocardial depressant activity. IL-2, -4, -6, -8, -10, and interferon gamma failed to cause significant cardiac myocyte depression over a wide range of concentrations. These data demonstrate that TNF-alpha and IL-1beta cause depression of myocardial cell contraction in vitro and suggest that these two cytokines act synergistically to cause sepsis-associated myocardial depression in humans.