Periodontology 2000, Vol. 46, 2008, 27–41
Printed in Singapore. All rights reserved
Medical emergencies in the
dental practice
MARK GREENWOOD
Medical emergencies can be alarming to any clinician
but these situations are less alarming if proper
preparation has been made. Medical emergencies
occur in dental hospital practice more frequently
than in dental practice, but in similar proportions in
terms of their nature (5). A thorough patient history
can draw the practitionerÕs attention to potential
medical emergencies that could occur (36). It is
particularly important in the history to enquire about
known allergies or adverse reactions to medication so
that these can be avoided (9). Good methods of
practice can prevent many emergencies, for example
prompt treatment of a diabetic patient at a predict-
able time thereby avoiding hypoglycemia. In one
study (4) there was a perceived need for further
training among dental practitioner respondents to a
survey on training in medical emergencies.
Dental procedures themselves can jeopardize the
airway, which must therefore be adequately pro-
tected. Patients with pre-existing medical conditions,
such as asthma or angina, will usually be taking
prescription medications (34) and the practitioner
should always check that these are readily available
and have been taken on the day of treatment (16).
Patients who have an asthma attack and who have
not brought their normal medication will not be
helped significantly by oxygen alone (because of the
bronchoconstriction). It is therefore vital that pa-
tients with asthma bring their inhalers with them or
that they are available in the emergency drug box.
The various national formularies, including the Brit-
ish National Formulary, list the drugs to be included
in an emergency box for the dental surgery (14).
These are shown in Table 1. Similar documents may
be available in different countries (1, 18, 23, 24). A
further addition to the list in the British National
Formulary is the benzodiazepine antagonist, flu-
mazenil.
The common emergencies that may occur in den-
tal practice will be discussed in turn and refer to adult
 2008 The Author.
Journal compilation  2008 Blackwell Munksgaard
PERIODONTOLOGY 2000
patients. In all these situations the basic principles of
resuscitation should be remembered, i.e., attention to
the Airway, Breathing, and Circulation (A, B, C) (7).
Key points in the management of medical emergen-
cies in practice are given in Table 2. Routes of drug
administration are also important (10) and wherever
possible alternatives are given. Drugs are continually
being developed that may be administered by more
ÔconvenientÕ routes (43).
Loss of consciousness
The most common cause of loss of consciousness
in a dental practice is vasovagal syncope (fainting).
If the recovery is not rapid other possibilities
should be considered, such as myocardial infarc-
tion, bradycardia, heart block, stroke, hypoglyce-
mia, or anaphylaxis. If the cause of collapse is
uncertain the following steps should be taken. The
patient should be laid flat, with the legs raised – in
vasovagal syncope this will usually result in rapid
recovery. A clear airway should be ensured and
maintained and the pulse should be checked.
Absence of pulse indicates cardiac arrest and car-
diopulmonary resuscitation (CPR) should start
immediately. If there is a palpable pulse, hypogly-
cemia is a possibility and the patient should be
treated as detailed later in this paper. Hydrocorti-
sone sodium succinate should be given in a dose
of 200 mg intravenously. The management of a
collapsed patient where the collapse is of unknown
cause is summarized in Table 3.
Fainting (vasovagal syncope)
Fainting is the most common medical emergency
encountered in dental practice. It is predisposed to
by factors such as pain and anxiety.
27
Greenwood
Table 1. Contents of the emergency drug box
• Adrenaline (epinephrine) 1 in 1,000
• Aspirin 300 mg
• Chlorphenamine (10–20 mg)
• Diazepam (5 mg ⁄ ml)
• Glucagon (1 mg)
• Glucose intravenous infusion (20% ⁄ 50%)
• Glyceryl trinitrate tablets ⁄ spray
• Hydrocortisone injection (100 mg)
• Oxygen
• Salbutamol
• (Flumazenil)
Table 2. The management of medical emergencies
in practice – key points
• Have well-established drills for emergencies so that
everyone knows their role
• Have emergency phone numbers to hand
• Have an emergency kit that is regularly checked to
ensure it is up-to-date
• Work so as to prevent emergencies as far as possible
• Always ensure that the patients have their own
medication with them, e.g., a glyceryl trinitrate
spray for angina, or ensure that it is to hand in the
emergency kit
Table 3. The management of a patient with collapse
of unknown cause
• Lie the patient flat and raise their legs
• Maintain the airway and administer oxygen
• If no pulse is palpable – cardiac arrest – institute
cardiopulmonary resuscitation
• If a pulse is palpable assume hypoglycemia and treat
by oral or intravenous glucose (depending on the level
of consciousness)
• Give 200 mg of hydrocortisone sodium succinate
intravenously
• Get help
Signs and symptoms
The patient may feel nauseated, with a cold, clammy
skin. There may be visual disturbance together with a
feeling of dizziness. The patientÕs pulse will be ini-
tially rapid and weak and there may be loss of con-
sciousness. The pulse becomes slow on recovery.
28
Management
Before the patient loses consciousness, the possibility
of hypoglycemia should be borne in mind and a
glucose drink may be helpful. The patient should be
laid flat, so that the legs are higher than the head
(heart) and any tight clothing around the neck should
be loosened. Recovery is usually rapid and occa-
sionally the patient may jerk as they regain con-
sciousness in a manner resembling a fit. Prolonged
unconsciousness should lead to consideration of
other causes for the collapse.
The diabetic patient
A thorough history should always be obtained from
a diabetic patient. This should involve an assess-
ment of the degree of diabetic control achieved by
the patient. A history of recurrent hypoglycemic
episodes and markedly varying blood glucose levels
means that a patient attending for dental treatment
is much more likely to develop hypoglycemia. It is
wise to treat diabetic patients first on the operating
list and ensure that they have had their normal
antidiabetic medication and something to eat before
attending the surgery. Hypoglycemia is much more
likely to be encountered in dental practice than
hyperglycemia because the former has a more rapid
onset. Principally seen in diabetics, it may be seen
in very anxious patients who have starved them-
selves for whatever reason before attending for
dental treatment. Diabetic control may be adversely
affected by oral sepsis, leading to an increased risk
of complications (15).
Diabetic emergencies
If hypoglycemia occurs, glucose should be given by
mouth as tablets, syrup, or a sugary drink, if the pa-
tient can cooperate (8). For those patients who are
not able to cooperate, glucose is also available as an
oral gel in a dispenser (GlucoGel). If these measures
are impossible or ineffective, for example in an
uncooperative, semi-conscious or comatose patient,
the usual treatment of first choice is glucagon
(1 mg ⁄ ml injection) 1 mg by intramuscular or
subcutaneous injection (26). Patients who do not
respond to glucagon, or those who have been hypo-
glycemic for some time and may have exhausted
their supplies of liver glycogen, will require up to
50 ml of intravenous glucose solution. Clearly,
patients who have reached this stage should be

managed under medical supervision and are unlikely
to be seen in dental practice.
Signs and symptoms
There may be uncharacteristic aggression, drowsi-
ness and a moist skin. Pulse may be rapid and full
and blood sugar will be low.
Management
The patient should be laid flat if consciousness is
lost. If the patient is conscious, then oral glucose
(i.e., four lumps of sugar) should be given. If the
patient is unconscious then 20–50 ml glucose should
be given intravenously or 1 mg glucagon intramus-
cularly. Glucagon is more easily administered than
intravenous glucose. Medical help should be sought.
The mainstay of treatment of hyperglycemia is
intravenous rehydration requiring medical inter-
vention and is beyond the scope of this discussion.
The management of diabetic patients
undergoing surgery
In well-controlled diabetics requiring local anesthe-
sia, all that is required is to ensure that these pa-
tients are treated promptly, which usually means
placing them first on an operating list. They should
also have had their normal diet and diabetic medi-
cation. Management becomes more complicated
when the patients have to be fasted (28) and out-
lines of management for patients with type 1 and
type 2 diabetes are given in Tables 4 and 5,
respectively. It is important that such patients are
managed in conjunction with the physician with
responsibility for overall diabetic management. It
should be remembered that the associated illness
will increase basal insulin needs.
Hypersensitivity reactions
Anaphylaxis
Anaphylaxis is a severe allergic reaction. It is a type I
hypersensitivity reaction. Other examples of type I
reactions include asthma and hay fever. In anaphy-
laxis, free antigen binds to immunoglobulin E, which
is fixed on mast cells and basophils; this leads to the
release of vasoactive peptides and histamine. In
dentistry, the most common cause is likely to be
penicillin or latex but non-steroidal anti-inflamma-
Medical emergencies in the dental practice
Table 4. Preoperative management in type 1 diabe-
tes mellitus – fasted patient
• The patient should be first on the list of patients
• All long-acting insulin should be stopped the night
before surgery
• Intravenous access should be obtained at an early
stage
• If surgery is in the morning, all subcutaneous morning
insulin should be stopped
• If surgery is in the afternoon, the usual short-acting
insulin should be given in the morning at breakfast but
no medium or long-acting insulin
• The urea and electrolytes should be checked on the
morning of surgery and an intravenous infusion of
1 litre of 5% dextrose with 20 mmol potassium chlo-
ride over 8 hours should continue until the patient is
eating normally. Dextrose may need constant infusion
to maintain the blood glucose
• 50 units of short-acting insulin should be added to
50 ml 0.9% saline, which can be given by an infusion
pump, and is given according to a sliding scale that
can be adjusted dependent on the blood glucose
measurements
• The blood glucose measurements should be checked
hourly aiming at a level of 7–11 mmol ⁄ l
• Postoperatively the intravenous insulin and dextrose,
potassium chloride and sliding scale should be con-
tinued until the patient is eating
• Finger-prick glucose should be checked every 2 hours
Table 5. Preoperative management in type 2 diabe-
tes mellitus – fasted patient
• These patients may be managed by attention to diet
or, more commonly, use of oral hypoglycemics. A
fasting blood glucose of >10 mmol ⁄ l may require
management along the lines of a type 1 diabetic
• Patients taking a long-acting sulfonylurea should
have the dose halved the day before surgery and the
tablet should be omitted altogether on the day of
surgery. The fasting blood glucose level should be
checked on the morning of surgery and treatment is
only needed if the level is more than 15 mmol. The
blood glucose level should be monitored in any event
using a finger-prick blood sample
• If the blood glucose level is more than 15 mmol,
insulin should be used as described in Table 4
tory drugs can also cause it. Rarely, local anesthetics
may be responsible (33).
Signs and symptoms
There may be facial flushing, pallor, cyanosis or
edema. The skin may be cold and clammy and there
29
Greenwood
may be urticaria (an itchy rash). Wheezing or laryn-
gospasm and tachycardia and hypotension may also
occur.
Management
The patient should be laid flat and 0.5 ml of 1:1,000
epinephrine (adrenaline) should be administered
intramuscularly. Epinephrine administration should
be repeated at 10-minute intervals as necessary. The
epinephrine has both a and b effects; it reverses
peripheral vasodilatation and reduces edema. The
b-activity dilates the airway and increases the force of
myocardial contraction. It also suppresses histamine
and leukotriene release. Adverse effects from epi-
nephrine are rare when appropriate doses are given
intramuscularly.
A clear airway should be ensured and 100% oxygen
should be administered. Ten to 20 mg chlorphen-
amine (antihistamine) should be given intravenously
plus 100 mg of intravenous hydrocortisone sodium
succinate, which helps to reduce edema and stabi-
lizes the mast cells. An inhaled b2-agonist can be
useful to facilitate bronchodilation. The patient
should be admitted to hospital because there may be
a rebound attack.
Chlorphenamine and hydrocortisone need not be
given by non-medical first-responders (2). The
Resuscitation Council (UK) does not define specifi-
cally the position of dentistry but if the practitioner is
confident in drug administration it will do no harm to
administer these drugs. Whatever the status of the
resuscitator, epinephrine must be given and the
preferred injection site is shown in Fig. 1. Many
patients with a history of anaphylactic reactions will
carry an ÔEpipenÕ, which contains 300 lg epinephrine
(Fig. 2).
Fig. 1. The preferred site for epinephrine injection.
30
Fig. 2. An Epipen.
Angioedema
Angioedema is triggered when mast cells release
histamine and other chemicals (essentially vasoactive
peptides) into the blood, producing rapid swelling.
From a medical perspective, angioedema is life-
threatening if the swelling produced compromises
the airway. It may be precipitated by substances such
as latex and drugs including penicillin, non-steroidal
anti-inflammatory drugs and angiotensin-converting
enzyme inhibitors (e.g., captopril and lisinopril).
There is a hereditary component to angioedema.
Swelling of the skin occurs, especially around the
eyes and lips but also in the throat and on the
extremities. Laryngeal edema and bronchospasm
lead to the same clinical situation as anaphylaxis. In
cases of severe angioedema, patients may be pre-
scribed prednisolone. Acute allergic edema of this
type can develop alone or it may be associated with
anaphylactic reactions.
Hereditary angioedema is caused by continued
complement activation resulting from a deficiency of
the inhibitor of the enzyme C1 esterase. The inheri-
tance is usually autosomal dominant and may not
present until adult life. C1 esterase inhibitor con-
centrates are available to supplement the deficiency.
Such supplements should be administered before
dental treatment if such treatment has, in the past,
triggered the onset of angioedema.
Fits
It is important that the practitioner is aware if a
patient has epilepsy; hence the importance of a
thorough history (36). The nature of the seizures,
their frequency, and the degree of control, including
the type of medication used, are important factors to
be elicited.

Signs and symptoms
The signs and symptoms of fits vary widely depend-
ing on the underlying cause. An obvious fit is easily
recognized.
Management
In most cases the main aim of management is to
prevent the patient from injuring themselves during
the fit. If a fit has stopped and the patient is in the
immediate aftermath (Ôpost-ictal phaseÕ) they should
be placed in the recovery position. If the convulsions
are ongoing, 10–20 mg diazepam should be given
intravenously, slowly. The possibility of the patientÕs
airway becoming occluded should be constantly
remembered and the airway must therefore be pro-
tected. It may be appropriate to abort dental treat-
ment if a patient experiences a fit during treatment.
Chest pain
Most patients who are likely to suffer chest pain of
cardiac origin in the dental environment are likely to
have a previous history of cardiac disease. Again, the
history is important as well as recognizing risk factors
for cardiovascular disease, which include smoking,
excess alcohol, diabetes mellitus, hypertension,
hypercholesterolemia, a family history of cardiovas-
cular disease, sedentary lifestyle and obesity. In
addition, symptomatic cardiovascular disease is more
common with increasing age. It is important that if a
patient uses medication to control angina it should
be with them or be readily to hand in the emergency
kit in case the patient needs it. Likewise, it is
important that the patient has taken their normal
medication.
Features which make the pain unlikely to be car-
diac in origin are: pains lasting less than 30 seconds
however severe, stabbing pains, well-localized left
submammary pain and pains that continually vary in
location. A chest pain that is improved by stopping
exercise is more likely to be cardiac in origin than one
that is not exercise-related. Pleuritic pain is sharp and
made worse on inspiration, for example following
pulmonary embolism.
Oesophagitis may cause a retrosternal pain. This
will be worse on bending or lying down. However,
oesophageal pain, like cardiac pain, can be relieved
by sublingual nitrates, for example glyceryl trinitrate.
Hyperventilation may produce chest pain and both
gall bladder and pancreatic disease can mimic car-
Medical emergencies in the dental practice
Table 6. The main causes of chest pain
• Angina
• Myocardial infarction
• Pleuritic, e.g., pulmonary embolism
• Musculoskeletal
• Esophageal reflux
• Hyperventilation
diac pain. Musculoskeletal pain is often accompanied
by tenderness to palpation in the affected region. A
summary of the main possible causes of chest pain is
given in Table 6. Clearly important conditions to
exclude when a patient complains of chest pain are
angina and myocardial infarction (3, 17, 44).
Signs and symptoms
The pain of angina and myocardial infarction may
be very similar comprising a crushing central chest
pain (like a tight band around the chest) radiating
to the left arm (usually) or mandible. Angina is
usually relieved by the patientÕs medication, which
in most cases will be a glyceryl trinitrate spray. The
pain of angina usually lasts for less than 3 minutes
if glyceryl trinitrate is used. Myocardial infarction is
often accompanied by other symptoms, such as
sweating, nausea and palpitations, and is not re-
lieved by glyceryl trinitrate. There may be breath-
lessness and vomiting and the patient may lose
consciousness.
Management
A calm and reassuring manner from the practitioner
is important. If the patient has a history of angina get
the patient to use the normal medication – there
should be a rapid response (within a few minutes) if
the cause was angina. Glyceryl trinitrate should be
part of the emergency drug box in case patients do
not have their own medication with them.
If a myocardial infarction is suspected, help should
be summoned at an early stage and 300 mg aspirin
should be administered to be chewed (if not contra-
indicated). The patient will be most comfortable in a
sitting position. Ensure that the airway is maintained
and administer a 50 ⁄ 50 mix of nitrous oxide and
oxygen, which has analgesic and anxiolytic effects.
A patient who has had a myocardial infarction
attending hospital may be given one of the so-called
Ôclot bustingÕ agents, such as streptokinase. There
31
Greenwood
are strict criteria detailing in which patients this
medication should be used because widespread
bleeding can result. As a consequence of this, a
patient who had undergone recent surgery would be
excluded. More recent management advances in-
clude immediate angioplasty, where facilities and
expertise allow.
Cardiac arrest
The risk factors for developing cardiovascular disease
were given earlier. In addition, it should be remem-
bered that chronic respiratory disorders can lead to
cardiac failure, so-called cor pulmonale. In addition,
a more acute respiratory problem may cause respi-
ratory arrest, which then proceeds to cardiac arrest.
Possible causes of cardiac arrest include: myocardial
infarction, choking, bleeding, drug overdose, and
hypoxia.
Signs and symptoms
The patient loses consciousness and there is no res-
piration or pulse.
Management
Basic life support implies that no equipment is em-
ployed other than a protective device. It has been
suggested (31), that cardiopulmonary resuscitation
can be performed effectively in the dental chair but it
is important that this is confirmed locally. The
Guidelines issued by the Resuscitation Council (UK)
with regard to adult basic life support changed in
April 2006 (2). There are two underlying main themes
– first the need to increase the number of chest
compressions given to a victim of cardiac arrest and
second, the importance of keeping the guidelines
simple.
Interruptions to chest compression in resuscita-
tion are common (20) and are associated with a
reduced chance of survival (25). The ideal situation
is to be able to deliver continuous chest compres-
sions while giving ventilations independently. This is
only possible, however, when an advanced airway is
placed. Chest-compression-only cardiopulmonary
resuscitation is another way to increase the number
of compressions but is only effective for a period of
about 5 minutes (25). For this reason this technique
is not recommended as standard management. The
principle on which compression-only cardiopulmo-
nary resuscitation works is that during the first few
32
UNRESPONSIVE?
Shout for help
Open Airway
NOT BREATHING NORMALLY?
Call 999 (UK)/911 (USA)
30 Chest Compressions
2 rescue breaths
30 compressions
Fig. 3. Algorithm for Adult Basic Life Support; from
Resuscitation Guidelines 2005 – Resuscitation Council
(UK).
minutes after a non-asphyxial cardiac arrest the
blood oxygen content remains high and therefore at
this stage ventilation is less important than chest
compression. Rescuers are now taught to place the
heel of their hand in the center of the chest (ster-
num) with the other hand on top and this is dem-
onstrated by placing the hands in the middle of the
lower half of the sternum. The chest should be
compressed at a rate of about 100 per minute. The
basic algorithm for adult basic life support is given
in Fig. 3.
In Guidelines published in 2000 the concept of
checking for Ôsigns of a circulationÕ was introduced.
Changes were made in 2005 because it had been
found that checking the carotid pulse to diagnose
cardiac arrest can be unreliable, even sometimes
when attempted by some health-care professionals
(6). In Guidelines 2005 the absence of breathing is the
main sign of cardiac arrest (2). Also highlighted is the
need to identify agonal gasps (as well as the absence
of breathing) as a sign to commence cardiopulmo-
nary resuscitation. In the new guidelines, it is still
stressed that before resuscitation attempts are made,
it should be ensured that the environment is safe
before proceeding.
 Medical emergencies in the dental practice

Unresponsive

Call for help

Open airway
Not breathing normally
Send or go for
Automated External
Defibrillator
Call 999 (UK)
CPR 30:2 911 (USA)
Until Automated External
Defibrillator is attached

Automated
External
Defibrillator
assesses

Shock advised No shock advised

1 shock
150-360 J biphasic or
360 J monophasic

Immediately resume Immediately resume

CPR 30:2 for 2 min CPR 30:2 for 2 min

Continue until the

victim starts to breathe Fig. 4. Algorithm for the use of an
normally automated external defibrillator in
cardiac arrest.

The provision of defibrillation has been made easier

Use of defibrillation
Ventricular fibrillation is the most common cause of
cardiac arrest. It is a rapid and chaotic rhythm. As a
result, the heart is unable to contract and therefore
unable to sustain its function as a pump. Defibrilla-
tion is the term that refers to the termination of
fibrillation. It is achieved by administering a con-
trolled electrical shock to the heart; this may restore
an organized rhythm enabling the heart to contract
effectively. It is now well recognized that early defi-
brillation is important. The only effective treatment
for ventricular fibrillation is defibrillation and the
sooner the shock is given, the greater the chance of
survival (30, 39).
by the development of automated external defibril-
lators. These are sophisticated, reliable, safe, com-
puterized devices that use voice and visual prompts to
guide rescuers and are suitable for use by lay people
and health-care professionals (13). The devices ana-
lyse the victimÕs rhythm, determine the need for a
shock and then deliver a shock. The automated
external defibrillator algorithm is given in Fig. 4.
Placement of automated external
defibrillator pads
The victimÕs chest must be sufficiently exposed.
Chest hair will stop the pads adhering properly and if

33
Greenwood
Fig. 5. Carpo-pedal spasm.
excessive it must be rapidly removed if possible.
Resuscitation should never be delayed for this reason,
however. One pad should be placed to the right of the
sternum below the clavicle. The other pad should be
placed in the mid-axillary line, approximately level
with the V6 electrocardiogram electrode position.
This position should be clear of any breast tissue.
Although most automated external defibrillator pads
are labeled, or carry a picture of their position, it does
not matter if they are reversed.
Asthma
Asthma is a potentially life-threatening condition
that should always be taken seriously (35). Exertion,
anxiety, infection, or exposure to an allergen may
all precipitate an attack. Bronchial asthma results
from bronchial hyper-reactivity, which leads to
expiratory wheezing, dyspnea, and cough. Asthma is
paroxysmal and sufferers may therefore be com-
pletely normal between attacks. Again, it is impor-
tant to get an idea of the severity of the condition,
which will usually come from the history. Important
facts to ascertain are the effectiveness of medica-
tion, precipitating factors, hospital admissions as
the result of asthma and the use of systemic
steroids.
It is important that asthmatic patients bring their
usual inhalers ⁄ medication with them to dental
appointments. If the inhaler has not been brought, it
must be in the emergency kit or treatment should be
deferred. If the asthma is in a particularly severe
phase, elective treatment may be best postponed.
The drugs that may be prescribed by dental practi-
tioners, particularly non-steroidal anti-inflammatory
drugs, may worsen asthma and are therefore best
avoided.
34
Signs and symptoms
The patient will be breathless with an expiratory
wheeze and may be using the accessory muscles of
respiration. The patient will usually be tachycardic.
Management
A calm and reassuring presence by the practitioner is
important. The patient will be most comfortable in a
sitting position and should use his ⁄ her normal
asthma medication. Oxygen should be administered
and also hydrocortisone sodium succinate (200 mg)
should be administered intravenously – this will re-
duce edema. If the attack has not responded rapidly
using only the patientÕs usual medication, then the
patient should be admitted to hospital.
It may improve delivery of the patientÕs own
inhaler contents if a spacer device is used. The
method described in the British National Formulary
(14) is to apply the mouthpiece of the inhaler to the
underside of a paper cup through which a hole has
been cut. If the open end of the cup is placed
against the mouth and nose, aerosol delivery should
be improved.
Hyperventilation
Hyperventilation is a more common emergency than
is often thought. When hyperventilation itself per-
sists it is extremely distressing to the patient. Anxiety
is the principal precipitating factor.
Signs and symptoms
The patient may feel weak and light-headed or
dizzy and may complain of paresthesia, for exam-
ple in the hands, or may complain of muscle pain.
The patient may have palpitations and chest pain;
indeed patients are sometimes convinced that they
are having a myocardial infarction. Carpo-pedal
spasm may occur if hyperventilation is prolonged
(Fig. 5).
Management
Clearly a calm and sympathetic approach by the
practitioner is important. The diagnosis is not
always as obvious as it may seem. When other
causes for the symptoms have been excluded
patients should be encouraged to rebreathe their
own exhaled air so as to increase the amount of

Assess Severity
Severe Mild
airway obstruction airway obstruction
(Ineffective Cough) (Effective Cough)
Unconscious Conscious Encourage Cough
Start CPR 5 back blows Continue to check
for deterioration to
5 abdominal ineffective cough
thrusts or relief of
obstruction
Fig. 6. Algorithm for management of choking; from
Resuscitation Guidelines 2005 – Resuscitation Council
(UK).
carbon dioxide being inhaled. Hyperventilation
leads to carbon dioxide being Ôwashed outÕ of the
body, so producing an alkalosis. Rebreathing
exhaled air returns the situation to normal. This is
achieved by breathing in and out of a paper bag
applied over the mouth and nose.
Choking
A foreign body may lead to either mild or severe
airway obstruction. Signs and symptoms that aid in
differentiation are shown in Table 7, which is taken
from the Resuscitation Council UK Guidelines 2005
(2). In the conscious victim it is useful to ask the
question ÔAre you choking?Õ. An algorithm for the
management of a choking patient has been pub-
lished by the Resuscitation Council (UK) (2). This is
shown in Fig. 6. The back blows shown in the
algorithm are given by standing to the side of the
victim and slightly behind. The chest should be
supported with one hand and the victim leant well
forwards so that when the obstruction is dislodged
it is expelled from the mouth rather than passing
further down the airway. Up to five sharp blows
should be given between the shoulder blades with
the heel of the other hand. After each back blow a
check should be made to see if the obstruction has
been relieved.
If the back blows fail to relieve the obstruction, up
to five abdominal thrusts should be given. The
method being as follows: stand behind the victim
and put both arms around the upper part of their
abdomen and lean the victim forwards. The res-
Medical emergencies in the dental practice
Table 7. Management of a choking victim; adapted
from Resuscitation Guidelines 2005 Resuscitation
Council UK
General signs of choking
• Attack occurs while eating ⁄ misplaced dental
instrument ⁄ restoration
• Victim may clutch his neck
Signs of mild airway obstruction
Response to question ÔAre you choking?Õ
• Victim speaks and answers ÔYES!Õ
Other signs
• Victim is able to speak, cough and breathe
Signs of severe airway obstruction
Response to question ÔAre you choking?Õ
• Victim unable to speak
• Victim may respond by nodding
Other signs
• Victim unable to breathe
• Breathing sounds wheezy
• Attempts at coughing are silent
• Victim may be unconscious
cuerÕs fist should be clenched and placed between
the umbilicus and lower end of the sternum. This
clenched fist should be grasped with the other hand
and pulled sharply inwards and upwards; this
should be repeated up to five times. If the obstruc-
tion is not relieved then an alternating pattern of
five back blows with five abdominal thrusts should
be used.
If it is suspected that a foreign body has been
inhaled in the context of dental practice, the patient
must be referred for chest X-ray. Radiographs will be
taken in two planes (postero-anterior and lateral).
The foreign body is most likely to be seen in the right
lung because the right main bronchus is more verti-
cal than the left. Bronchoscopy or even thoracotomy
may be required to retrieve the foreign body.
Adrenal crisis
Adrenal crisis may result from adrenocortical hyp-
ofunction leading to hypotension, shock, and death.
It may be precipitated by stress induced by trauma,
surgery, or infection. Adrenocortical hypofunction
can be primary or secondary. An example of pri-
mary hypoadrenocorticism is AddisonÕs disease, in
which there are circulating autoantibodies to the
adrenal cortex. This results in atrophy and failure
35
Greenwood
of secretion of hydrocortisone and aldosterone.
Tuberculous destruction of the adrenal glands will
produce the same effect. Secondary hypoadreno-
corticism results from adrenocortical hypofunction
as the result of adrenocorticotrophic hormone
deficiency. This occurs through suppression of
adrenocortical function following the use of sys-
temic corticosteroids.
The use of supplemental steroids before dental
surgery in patients at risk of an adrenal crisis is a
contentious issue. The rationale for steroid supple-
mentation is as follows. A normal physiological
response to trauma is to increase corticosteroid
production in response to stress. If this response is
absent, hypotension, collapse, and death will occur.
The hypothalamo–pituitary–adrenal axis will fail to
function if either the pituitary or the adrenal cortex
ceases to function for the reasons mentioned above.
This happens in secondary hypoadrenocorticism
because administration of corticosteroids leads to
negative feedback to the hypothalamus, causing
decreased adrenocorticotrophic hormone production
and adrenocortical atrophy. This atrophy means that
an endogenous steroid boost cannot be produced in
response to stress. Recent studies have suggested that
dental surgery may not require supplementation (38).
More invasive procedures however, such as third
molar surgery or the treatment of very apprehensive
patients, may still require cover. It is wise, even if
supplementary steroids have not been used, to
monitor the blood pressure of patients taking ste-
roids. If the diastolic pressure falls by more than 25%,
then an intravenous steroid injection (100 mg
hydrocortisone) is indicated. Patients who may re-
quire supplementation are those who are currently
taking corticosteroids or have done so in the last
month. A supplement may also be required if steroid
therapy has been used for more than 1 month in the
previous year. If the patient is receiving the equiva-
lent of 20 mg prednisolone daily then extra supple-
mentation is not required.
Signs and symptoms
The patient loses consciousness and has a rapid,
weak, or impalpable pulse. The blood pressure falls
rapidly.
Management
The patient should be laid flat and 200 mg (at least)
hydrocortisone sodium succinate should be admin-
istered intravenously. Ensure a clear airway and
36
administer oxygen. Then call an ambulance or tele-
phone the hospital emergency number.
Stroke
Strokes can be either hemorrhagic or embolic in
etiology but clinically the effects are essentially the
same. Risk factors for stroke include hypertension,
smoking, diabetes mellitus, cardiac and peripheral
vascular disease, atrial fibrillation, obesity, hyper-
lipidemia and excess alcohol intake. Previous tran-
sient ischemic attacks (focal central nervous system
disturbances caused by vascular events such as
microemboli and occlusion leading to ischaemia)
are also risk factors. By definition, symptoms of
transient ischaemic attacks last for less than
24 hours.
Signs and symptoms
These vary according to the site of brain damage.
There may be loss of consciousness and weakness of
the limbs on one side of the body. The side of the face
may be weak, indicating an upper motor neuron
lesion, in which case the forehead will not be affected
on that side.
Management
The airway should be maintained and an ambulance
called.
Local anesthetic emergencies
Allergy to local anesthetic is rare but should be
managed as for any other case of anaphylaxis. When
taken in the context of the number of local anes-
thetics administered, complication rates are low, but
complications can occur (29, 33). The signs and
symptoms are those of anaphylaxis.
Other local anesthetic reactions are rare. Fainting
in association with the injection of local anesthetic
is rather more common and can usually be avoided
by administering the local anesthetic while the
patient is supine. Intravascular injection of local
anesthetic can be avoided by the use of an aspi-
rating syringe. An intravascular injection can in-
duce agitation, drowsiness, or confusion with fits
and ultimately loss of consciousness. Other causes
of local anesthetic-related problems are given in
Table 8.

Table 8. Potential problems with local analgesia
Local anesthetic allergy
Cardiovascular reactions
• Palpitations
• Myocardial infarction
• Hypotension
• Hypertension
Facial palsy or diplopia
Management of an intravascular local anesthetic
injection
• Stop local anesthetic injection
• Lay the patient flat with legs raised
• Maintain the airway
• Reassure the patient that they should recover
within 30 minutes
Cardiovascular problems in association
with local anesthetics
The most common symptoms to be precipitated are
palpitations, which will subside naturally with time. A
myocardial infarction may rarely be precipitated in a
susceptible patient. It is possible for interaction with
antihypertensive drugs to precipitate hypotension. It
is important in these circumstances to ensure that
the airway remains clear and that the patient is
reassured. Medical assistance should be sought.
Hypertension should likewise be managed with
medical assistance. In any circumstance in which a
cardiovascular event is precipitated, treatment
should be deferred for another occasion.
Temporary facial palsy or diplopia
Complications such as these arise from the local
anesthetic agent tracking towards the facial nerve or
the orbital contents. The patient should be reassured
because the effects wear off as the effects of the local
anesthetic diminish. If the temporal and zygomatic
branches of the facial nerve are involved, it is
important to protect the cornea and an eye patch is
indicated as a temporary measure.
Needle breakage
The incidence of needle breakage has decreased
since the advent of single-use needles; however, it is
still a recognized complication. The breakage of a
needle has most commonly been seen in relation to
the inferior alveolar nerve block. The incidence of this
Medical emergencies in the dental practice
Table 9. Management of a broken needle in a dental
patient
If tip is visible
• Remove with artery forceps
If tip is not visible
• Inform the patient
• Arrange immediate maxillofacial referral
• Advise the patient against moving the mandible as
much as possible
• Ensure accurate records and inform Protection
Societies
complication was more common in the 1950s and
before (12).
Needle breakages often occur at the hub of the
needle and are more common with needles of
smaller diameter. If this event does occur the needle
should be retrieved immediately, if possible, using
fine artery forceps. This is only possible if the needle
is not inserted to the hilt while the injection is given
and for this reason the needle should not be inserted
to this degree on any occasion. If immediate retrieval
is not possible the patient should be informed about
what has happened and referred immediately to the
local maxillofacial unit (Table 9). It is important for
medico-legal reasons that the incident is accurately
and clearly documented. The practitionerÕs dental or
medical Protection Societies should also be informed
of such an incident. It is useful if the remaining part
of the needle is sent along with the patient because it
will allow better estimation of the size of the retained
fragment. Although imaging will be carried out at the
hospital, first by plain radiography (two views at right
angles) and then by computed tomography scanning,
the size remaining is still best judged from the frag-
ment left attached to the syringe.
It is important that the needle is retrieved promptly
because there is the potential for pain, trismus, and
dysphagia to develop. There is also the possibility of
migration of the needle. It can be difficult, despite
good imaging, to locate the needle and there is a
school of thought that, because the needle is sterile, if
there is no reason to suspect migration, the needle
should be left in situ unless complications develop
(21).
Sedation emergencies
These are usually avoidable by careful technique, but
may relate to overdose or hypoxia or both. Either of
37
Greenwood
these situations can lead to a respiratory arrest if not
addressed and the patient will be obviously cyanosed
(33). During any dental treatment, the vital signs
should be observed (22) but this is particularly
important during sedation when they should be for-
mally monitored.
Management
No further sedation agent should be given. Open and
maintain the airway and give oxygen; ventilate the
patient. If an overdose is suspected consider the use
of flumazenil.
Emergencies arising from impaired
hemostasis
It is important that any potential problems with
hemostasis are uncovered in the medical history
and therefore can be anticipated and prevented.
Despite this, however, hemorrhage may occur
postoperatively in dental patients and may be
classified into Primary, which is bleeding at the
time of surgery, and Reactionary, which is bleeding
a few hours after surgery. Reactionary hemorrhage
is often attributable to the effects of a vasocon-
strictor-containing local anesthetic wearing off.
Secondary hemorrhage is that which occurs a few
days after the operative procedure and is usually
attributable to infection.
No surgical procedure should be performed on a
patient with a bleeding disorder without consultation
with the patientÕs physician or hematologist. Patients
with congenital bleeding disorders should be treated
in specialist centers that facilitate communication
between surgeon and hematologist. Patients with
hemophilia A, Christmas disease, or von WillebrandÕs
disease may require replacement therapy before
surgery and an antifibrinolytic agent postoperatively
(e.g., tranexamic acid). The use of local measures,
such as suturing and packing with a hemostatic
agent, for example oxidized cellulose (Surgicel) or
collagen sponge (Haemocollagen), both of which
are resorbable, should be considered (11). Bone wax
is a useful method of arresting persistent bony ooz-
ing. The minimum amount of bone wax possible
should be used because of the risk of development of
a foreign body granuloma.
There have been changes in recent years to the
management of patients taking drugs that interfere
with hemostasis. It is unusual in contemporary
practice to withdraw aspirin before surgery, for
example. If aspirin did need to be withdrawn then
38
this should be done 10 days before surgery because
the effect on platelets is irreversible and time is
needed to allow some replacement of the platelet
population. If aspirin is continued, local hemostatic
measures are usually sufficient. Likewise, other anti-
platelet drugs, such as clopidogrel and dipyridamole,
do not need to be stopped before surgery, local
hemostatic measures being adequate.
Data from the literature do not support the
assumption, widely held in the past, that there was
no significant risk to a patient if warfarin therapy
was stopped to facilitate surgical dental treatment
(41). A review of over 500 reports, in which antico-
agulation was stopped before a variety of dental
procedures, reported the following: the majority of
patients had no adverse effects but four patients
experienced fatal thromboembolic events and one
patient experienced embolism which was non-fatal
(40, 41). It cannot be proved conclusively that the
withdrawal of anticoagulant was responsible but it
would appear logical. Reports from the literature
have also suggested that stopping warfarin treat-
ment may lead to a hypercoagulable state as the
result of a rebound phenomenon (41, 42). The
existence of a hypercoaguable state has not been
fully elucidated.
Patients on warfarin therapy should have their
International Normalized Ratio (INR – a measure of
the prothrombin time) measured before any surgical
procedure. This can now be performed in the dental
surgery using a finger-prick sample. The normal
therapeutic international normalized ratio for
warfarinized patients is 2–3, except for those with
cardiac valve replacements in whom the range is
2.5–3.5. There does not appear to be a universally
acknowledged satisfactory international normalized
ratio for dental surgery.
In the United Kingdom, current advice (14) is that
most surgical procedures in dentistry, such as
extractions and simple minor oral surgical proce-
dures, may be carried out if the international
normalized ratio is <3.0 without alteration of the
warfarin dosage. In practice, up to 4 is probably
safe. If the international normalized ratio is >3,
referral to the supervising physician is needed. If
possible, even if the international normalized ratio is
<3 it is advisable to avoid regional block anesthesia,
but not essential. Avoidance may be achieved by the
use of intraligamentary injections. In all warfari-
nized patients local measures for hemostasis must
be employed.
It is important that patients with an international
normalized ratio >3 do not undergo any form of

Table 10. Systemic conditions leading to a potential
deficiency in hemostasis
• Liver impairment and ⁄ or alcoholism
• Renal failure
• Patients receiving cytotoxic medication or radio-
therapy
• Thrombocytopenia, hemophilia, or other known
disorders of hemostasis
surgical procedure without consultation with the
physician who is coordinating the anticoagulation.
In addition, patients taking warfarin who have
concurrent medical problems, listed in Table 10
should not be treated without medical consultation
(32).
Occasionally, patients receiving heparin therapy
may be encountered. The most common group is
patients who are heparinized to facilitate hemodi-
alysis for renal failure. The heparinization is often
carried out about three times per week, but be-
cause of the short half-life of heparin (around
5 hours) treatment can be carried out safely on the
days between dialysis treatments. If a heparinized
patient requires emergency treatment, such as an
extraction, then the effects of heparin can be
reversed by the antagonist protamine sulfate
(10 mg ⁄ ml).
Tranexamic acid is an antifibrinolytic agent whose
primary action is to block the binding of plasminogen
and plasmin to fibrin, thereby preventing fibrinolysis
(37). There is limited published evidence, but has
been suggested that, compared with no local
measures, tranexamic acid mouthwash as a 4.8%
preparation reduces postoperative bleeding in
anticoagulated patients (37).
Problems with medication and
hemostasis
Some drugs that are commonly used in dental
practice interact with anticoagulants. Examples of
analgesics that do this are aspirin, diclofenac, difl-
unisal, ibuprofen, and long-term use of paracetamol;
all of these increase the effect of warfarin. Antimi-
crobials, such as those of the penicillin group, can
increase the prothrombin time in warfarinized pa-
tients but this is uncommon. Erythromycin enhances
the anticoagulant effect of warfarin and nicoum-
alone by reducing the metabolism of the latter drugs.
The combined use of these drugs is not absolutely
Medical emergencies in the dental practice
contraindicated but monitoring of the patients is
required. The interaction between warfarin and
metronidazole is clinically important because the
antibiotic inhibits the metabolism of the anticoagu-
lant (27). Tetracycline may enhance the effect of
warfarin and the other coumarin anticoagulants.
Miconazole can enhance the effects of warfarin even
after topical use and it can lead to catastrophic
bleeding. One case has been reported in which a
patientÕs international normalized ratio increased
from 2.5 to 17.9 following the use of miconazole oral
gel (19). In distinction to the above drugs, carba-
mazepine may reduce the effect of warfarin because
the metabolism of the anticoagulant is increased.
Further details of drug interactions with warfarin are
discussed elsewhere in this volume.
Patients who have liver failure can be difficult to
evaluate with regard to the risk of oral bleeding
postsurgically (32). A relatively small elevation of the
prothrombin time suggests significant liver damage.
There are various methods of improving the
haemostatic picture, for example the intravenous
injection of vitamin K, but this should be carried out
by the hematologist. Fresh frozen plasma will lower
the prothrombin time and platelet transfusion
addresses both quantitative and qualitative prob-
lems. In patients with hepatic problems, care should
be exercised in the use of opioid analgesics, for
example morphine, and sedatives such as diazepam.
Smaller doses should be used for drugs that are
metabolized by the liver. The use of paracetamol
should be avoided in the presence of liver failure and
alcoholism (32).
Acute pain management
Pain results from damage to tissue that induces the
release of chemicals, which include prostaglandins,
serotonin, bradykinin, thromboxane, leukotrienes,
and substance P. It is also a highly subjective phe-
nomenon. Practitioners may find themselves in the
situation where a patient is in acute pain and the
subjective nature of pain is such that the same con-
dition in one patient may effectively produce more
pain than the same condition produces in another.
Wherever possible, attention should be given to
treating the underlying cause of pain. Analgesics may
either act peripherally or centrally. The former acts at
the site of injury whereas the latter attempts to
change the cerebral perception of pain. The decision
with regard to which analgesic should be used is
made with reference to the Ôladder of analgesiaÕ
(Fig. 7).
39
Greenwood
Severe pain - paracetamol and injected opioid e.g. morphine
Moderate pain - paracetamol with or without an oral opioid or non-steroidal
Mild pain - paracetamol
Control of mild pain
The drug of first choice is paracetamol, which acts
peripherally. It has no anti-inflammatory activity. It is
a very useful agent for reducing the temperature in a
pyrexial patient. As long as the correct dose schedule
is adhered to, the drug is safe and does not cause
gastric irritation. Non-steroidal anti-inflammatory
drugs block cyclo-oxygenase and can therefore inter-
fere with hemostasis and cause gastric irritation. Like
paracetamol, non-steroidal anti-inflammatory drugs
act peripherally. As a result of gastric irritation, par-
ticularly in the elderly and those taking corticoster-
oids, caution should be exercised. Some practitioners
would prescribe them in conjunction with a proton
pump inhibitor or H2 antagonists in such patients.
The elderly are also at risk from acute renal failure
because non-steroidal anti-inflammatory drugs block
renal prostaglandin synthesis. Other groups at risk of
renal failure with non-steroidal anti-inflammatory
drugs are those with cardiac failure and pre-existing
renal damage such as diabetic nephropathy.
The original non-steroidal anti-inflammatory drug
is aspirin, which irreversibly inhibits platelet function
and increases the bleeding time. Platelet repopula-
tion is required for the effects to be reversed. In most
cases aspirin is continued and local haemostatic
measures are employed if surgery is undertaken. It
should be remembered that non-steroidal anti-
inflammatory drugs can induce asthma in suscepti-
ble patients and they should therefore be avoided in
this group of individuals.
Control of moderate pain
One of the weak oral opioids, such as codeine, is a
good analgesic that acts centrally. The opioids are
contraindicated in patients who have significant
acute or chronic respiratory disease or who have
been taking monoamine oxidase inhibitors within the
last 14 days. The potential problem with patients who
have a respiratory problem is that respiratory
depression may be clinically significant.
Codeine compound products are now available,
such as co-codamol which is a codeine–paracetamol
preparation. It contains codeine phosphate 8 mg and
paracetamol 500 mg. It is important that if a practi-
tioner prescribes this medication, the patient is in-
40
Fig. 7. The ladder of analgesia.
formed that they must not take it in conjunction with
paracetamol because overdose could easily occur.
Control of severe pain
Attention should be given to addressing the under-
lying cause. Despite this, however, the dental prac-
titioner will sometimes be faced with a situation
requiring the most effective analgesia. Morphine and
pethidine by injection (either intramuscular or
intravenous) can be used but analgesia at this level is
usually restricted to inpatient use, often with medical
consultation. As both of these analgesics can cause
respiratory depression, supplemental oxygen may be
indicated.
One acute presentation of pain to the dental prac-
titioner can be related to temporomandibular joint
pain dysfunction syndrome. Muscle spasm often
seem to be the main source of pain, which can be
treated empirically using a soft lower splint fitted over
the occlusal surfaces of the mandibular teeth. Diaze-
pam can be prescribed on a short-term basis during
an acute phase because it has muscle relaxant quali-
ties in addition to its anxiolytic properties. It is
important to distinguish the temporomandibular
joint pain described above from neuropathic pain,
which occurs as a result of damage to neural tissue.
Summary
Medical emergencies occurring in dental practice can
be alarming. The keys to minimizing alarm are taking
a thorough history so that possible emergencies can
be, to some extent, anticipated, and having a good
working knowledge of how to manage emergencies,
should they arise.
References
1. ADA Council on Scientific Affairs. Office emergencies and
emergency kits. J Am Dent Assoc 2002: 133: 364–365.
2. Adult Basic Life Support Resuscitation Guidelines. London:
Resuscitation Council (UK), 2005.
3. Assael LA. Acute cardiac care in dental practice. Dent Clin
North Am 1995: 39: 555–565.
4. Atherton GJ, McCaul JA, Williams SA. Medical emergencies
in general dental practice in Great Britain. Part 3: percep-

tions of training and competence of GDPs in their man-
agement. Br Dent J 1999: 186: 234–237.
5. Atherton GJ, Pemberton MN, Thornhill MH. Medical
emergencies: the experience of staff of a UK dental teach-
ing hospital. Br Dent J 2000: 188: 320–324.
6. Bahr J, Klingler H, Panzer W, Rode H, Kettler D. Skills of lay
people in checking the carotid pulse. Resuscitation 1997:
35: 23–26.
7. Bassi GS, Cousin GC, Lawrence C, Bali N, Lowry JC. Im-
proved resuscitation training of senior house officers in
oral and maxillofacial surgery. Br J Oral Maxillofac Surg
2002: 40: 293–295.
8. Bavitz JB. Emergency management of hypoglycaemia and
hyperglycemia. Dent Clin North Am 1995: 39: 587–594.
9. Becker DE. Management of immediate allergic reactions.
Dent Clin North Am 1995: 39: 577–586.
10. Bennett JD. Emergency drug therapy. Drugs and routes of
administration. Dent Clin North Am 1995: 39: 501–521.
11. Blinder D, Manor Y, Martinowitz U, Taicher S. Dental
extractions in patients maintained on continued oral an-
ticoagulants, comparison of local haemostatic modalities.
Oral Surg Oral Med Oral Pathol Oral Radiol Endodont
1999: 88: 137–140.
12. Blum T. A Report of 100 cases of hypodermic needles
broken during the administration of oral local anaesthetic.
Dent Cosmos 1928: 70: 865–874.
13. Boyd BC, Fantuzzo JJ, Votta T. The role of automated
external defibrillators in dental practice. N Y State Dent J
2006: 72: 20–23.
14. British National Formulary. Royal Pharmaceutical Society
of Great Britain, 20-5 Prescribing in Dental Practice. Lon-
don: BMA and Royal Pharmaceutical Society of Great
Britain, 2006.
15. Chandu A, Macisaac RJ, Smith AC, Bach LA. Diabetic
ketoacidosis secondary to dento-alveolar infection. Int J
Oral Maxillofac Surg 2002: 31: 57–59.
16. Chapman PJ. A case report of acute heart failure caused by
a patient delaying taking his diuretic medication. Aust Dent
J 2002: 47: 66–67.
17. Chapman PJ. Chest pain in the dental surgery; a brief
review and practical points in diagnosis and management.
Aust Dent J 2002: 47: 259–261.
18. Chapman PJ. An overview of drugs and ancillary equipment
for the dentistÕs emergency kit. Aust Dent J 2003: 48: 130–133.
19. Colquhun MC, Daly M, Stewart B, Beeley L. Interaction
between warfarin and miconazole oral gel. Lancet 1987: I:
694–696.
20. Eftestol T, Sunde K, Steen PA. Effects of interrupting pre-
cordial compressions on the calculated probability of
defibrillation success during out-of-hospital cardiac arrest.
Circulation 2002: 105: 2270–2273.
21. Faura-Sole M, Sanchez-Garces MA, Berini-Aytes L, Gay-
Escoda C. Broken anaesthetic injection needles: report of
five cases. Quintessence Int 1999: 30: 461–465.
22. Fukayama H, Yagiela JA. Monitoring of vital signs during
dental care. Int Dent J 2006: 56: 102–108.
23. Haas DA. Emergency drugs. Dent Clin North Am 2002: 46:
815–830.
24. Haas DA. Management of medical emergencies in the
dental office: conditions in each country, the extent of
treatment by the dentist. Anesth Prog 2006: 53: 20–24.
Medical emergencies in the dental practice
25. Hallstrom A, Cobb L, Johnson E, Copass M. Cardiopul-
monary resuscitation by chest compression alone or with
mouth-to-mouth ventilation. N Engl J Med 2000: 342:
1546–1553.
26. Jowett NI, Cabot LB. Diabetic hypoglycaemia and the
dental patient. Br Dent J 1998: 185: 439–442.
27. Kazmier FJ. A significant interaction between metronida-
zole and warfarin. Mayo Clin Proc 1987: 51: 782–784.
28. Keene JR, Kaltman SI, Kaplan HM. Treatment of patients
who have type 1 diabetes mellitus: physiological miscon-
ceptions and infusion pump therapy. J Am Dent Assoc 2002:
133: 1088–1092.
29. Koerner KR, Taylor SE. Emergencies associated with local
anaesthetics. Dent Today 2000: 19: 72–79.
30. Leitch J, Schmulian C, Scott A. Automatic external
defibrillators – time for a change? Br Dent J 2005: 198: 209–
210.
31. Lepere AJ, Finn J, Jacobs I. Efficacy of cardiopulmonary
resuscitation performed in a dental chair. Aust Dent J 2003:
48: 244–247.
32. Lockhart PB, Gibson J, Pond SH, Leitch J. Dental man-
agement considerations for the patient with an acquired
coagulopathy. Part I: coagulopathies from systemic dis-
ease. Br Dent J 2003: 195: 439–445.
33. Meechan JG, Skelly AM. Problems complicating dental
treatment with local anaesthesia or sedation: prevention
and management. Dent Update 1997: 24: 278–283.
34. Pyle MA, Faddoul FF, Terezhalmy GT. Clinical implications
of drugs taken by our patients. Dent Clin North Am 1993:
37: 73–90.
35. Shafer DM. Respiratory emergencies in the dental office.
Dent Clin North Am 1995: 39: 541–554.
36. Shampain GS. Patient assessment and preventive measures
for medical emergencies in the dental office. Dent Clin
North Am 1999: 43: 383–400.
37. Sindet-Pederson S, Ramström G, Bernvil S, Blombäck M.
Hemostatic effect of tranexamic acid mouthwash in anti-
coagulant treated patients undergoing oral surgery. N Engl
J Med 1989: 320: 840–843.
38. Thomason JM, Girdler NM, Kendall-Taylor P, Wastell H,
Weddell A, Seymour RA. An investigation into the need for
supplementary steroids in organ transplant patients
undergoing gingival surgery. J Clin Periodontol 1999: 26:
577–582.
39. Van Alem A, Sanou B, Koster R. Interruption of CPR with
the use of the AED in out-of-hospital cardiac arrest. Ann
Emerg Med 2003: 42: 449–457.
40. Wahl MJ. Dental surgery in anticoagulated patients. Arch
Intern Med 1998: 158: 1610–1616.
41. Wahl MJ. Myths of dental surgery in patients receiving
anticoagulant therapy. J Am Dent Assoc 2000: 131: 77–81.
42. Webster K, Wilde J. Management of anticoagulation in
patients with prosthetic heart valves undergoing oral and
maxillofacial operations. Br J Oral Maxillofac Surg 2000: 38:
124–126.
43. Yamada T. The potential of the nasal mucosa route for
emergency drug administration via a high-pressure nee-
dleless injection system. Anesth Prog 2004: 51: 56–61.
44. Young ER, Saso MA, Pulver E. Acute chest pain during
dental treatment – a case report. J Can Dent Assoc 1990: 56:
437–440.
41