The patient’s medical history did not reveal any significant medical findings or conditions. The patient’s vital signs were within normal limits. The patient has smoked since the age of 17. He recently had a physical exam by his primary care physician as a requirement for employment.
The patient has not had a dental exam or prophylaxis in 10 years. He brushes daily with a power toothbrush and does not floss. He noticed that his tongue is discolored and coated, along with “bad breath” and eats sugary mints throughout the day. He does not like the heavy, brown stain on his front teeth.
The patient drinks alcohol on weekends, primarily eats fast food on the run, and smokes a pack of cigarettes daily. He notes that his time is very limited and is very concerned about keeping his new job. He doesn’t like doctors, but will see one if he is in pain.
Extraoral exam revealed no significant findings. Intraorally the patient presents with pale gingiva. The palate appears to have slight nicotine stomatitis. There was: generalized moderate subgingival calculus and moderate stained biofilm with localized bleeding upon probing in the facial and lingual of the lower anterior sextant; generalized maxillary and mandibular probing depths of 3–4 mm; generalized moderate to heavy brown extrinsic stain along the facial and lingual cervical third of the maxillary and mandibular anterior sextants; and Class I malocclusion with slight mandibular anterior crowding.
Dental Hygiene Diagnosis
|Problems||Related to Risks and Etiology|
|Increased caries and periodontal diseases||Dental neglect|
|Extreme apprehension can lead to syncope||Apprehension|
|Oral cancer and delayed healing||Smoker|
|Misuse can lead to cervical abrasion, sensitivity, and ineffective biofilm management||Power toothbrush|
|Differential diagnosis of causes for halitosis||Halitosis|
|Increased caries risk||Use of sugary mints|
(to arrest or control disease and regenerate, restore or maintain health)
|Clinical||Education/Counseling||Oral Hygiene Instruction|
|Scaling and root planing by quadrant
Topical anesthetic as needed
Air‐Powder Polishing with sodium bicarbonate
Full mouth series
Initial exam and study models
Referral to primary care physician to rule out systemic conditions related to halitosis and syncope
|Importance of regular dental visits
Increased risk for caries and periodontal diseases
Smoking cessation counseling and/or referral
Importance of healthy living and stress reduction
Educate and motivate on the importance of biofilm management
|Proper use of power toothbrush
Introduce interdental cleaning either with floss or interproximal brushes
Use of xylitol gum or candies
Use of tongue scraper
Nonalcohol antimicrobial mouthrinse
Patient arrived 20 minutes late for appointment. He was anxious, stressed, and out of breath. Patient was asked to sit in the dental chair and relax before beginning the appointment. Reviewed medical and dental history. Vitals: BP 132/80, 90 BPM, 20 RPM. Extraoral/intraoral examination: An initial comprehensive exam was performed and a full mouth series (FMS) of radiographs was taken. The prophylaxis procedure scheduled for today’s appointment was explained to the patient, and as I spoke, I noticed that he was grasping the arm rests and he complained of dizziness and nausea. He shortly thereafter became pale, lost consciousness, and went limp while in an upright position. I placed him in supine position and immediately initiated our office emergency protocol by calling for help. I kept him in supine position with feet slightly elevated and loosened the collar of his shirt. Respiration was monitored and since patient continued breathing, cardiopulmonary resuscitation (CPR) was not indicated. Oxygen tank and mask were brought into the room by designated staff member and I began oxygen administration. Vitals were monitored and were within normal limits. Patient fully recovered after five minutes of oxygen therapy. Patient was asked to sit in reception area for 20 minutes before driving home. The dentist suggested that I speak to him about premedication prior to the next appointment, and that he consider taking an antianxiety medication and/or the addition of nitrous oxide sedation during the appointment. I called the patient that evening to discuss anxiety management. At that time, he was fully recovered with no additional symptoms.
Pathophysiology and Differential Diagnosis of Syncope
Syncope is generally categorized as a brief loss of consciousness, related to a drop in arterial blood pressure and subsequent inadequate supply of blood and nutrients to the brain. Loss of consciousness is characterized by a lack of responsiveness, awareness, and postural hypotension. Patients may have prodromal symptoms and complain of dizziness, but most often syncope occurs without any warning, and can last up to 20 seconds. Patients generally recover without knowledge of the episode or the time that has passed (Brignole and Benditt 2011).
Postural hypotension, or collapse, may be confused or reported by the patient as having fainted, when in fact, the cause may be unknown or unrelated to a syncopal episode. Olshansky reports (Grubb and Olshansky 2005) on a study with 121 patients who were admitted into an emergency room for having fainted or collapsed. Of the 121 patients, only 15 had a true syncopal episode, 15 patients were diagnosed with cardiac arrest, one patient had fallen asleep, and one patient was dead. The remaining patients’ diagnosis was unknown.
The loss or inadequate supply of cerebral nutrients to the brain, is known scientifically as “cerebral hypoperfusion,” or the common “faint,” and has a quick recovery that distinguishes syncope from loss of consciousness from other causes. A firsthand eyewitness account of a syncopal episode may help with the diagnosis. The American Heart Association recommends referral to a physician who can rule out other conditions that may present similar symptoms and have a more serious pathophysiological origin (American Heart Association.org 2016). A syncopal episode should not be taken lightly, and should be of great concern as it may be a symptom of another more lethal or serious systemic disease, such as cardiac arrest (Grubb and Olshansky 2005). In addition, patients who have a history of some previous trauma such as a concussion, or who are having a seizure or stroke may present similar symptoms and lose consciousness. Patients, who have experienced syncope, may not remember the stimulus or origin of the episode. In addition, episodes of syncope can be related to medications, or withheld from disclosure in the medical history because of embarrassment or drug abuse (Brignole and Benditt 2011).
Differential diagnosis of syncope falls within four general categories (Table 3.2.1): reflex syncope (neurally mediated or neurocardiogenic), syncope from orthostatic hypotension, and cardiac and cerebrovascular related syncope (Grubb and Olshansky 2005; Moya et al. 2009). Unknown or undifferentiated causes may include arrhythmias, seizures, and psychiatric causes (Grubb and Olshansky 2005).
Table 3.2.1: Clinical features suggestive of specific causes of syncope.
Source: Courtesy of Brignole (2007).
|Type of syncope||Features|
Reflex syncope (neutrally mediated or neurocardiogenic) is further classified as vasovagal (VVS), situational, carotid sinus syncope (CSS), and atypical syncope (Brignole and Benditt 2011). VVS is a response to emotional stress, pain, or fear and is preceded by dizziness, sweating, pallor, and nausea (Sheldon et al. 2015). Situational syncope is more specific with known triggers such as exercise, defecation, or urination. Carotid sinus syncope is rare and involves direct stimulation of the carotid sinuses. Atypical syncope is absent of triggers or known causes (Brignole and Benditt 2011).
VVS is the most common cause of syncope (Grubb and Olshansky 2005; Brignole and Benditt 2011). The vagus nerve is the 10th out of 12 cranial nerves and supplies the involuntary nervous system. In VVS, the vagus nerve is stimulated, causing a vasovagal response that directs blood to the extremities and increases heart rate in order to maintain homeostasis and an adequate supply of blood to the brain. This response is commonly known as the fight or flight response. In the absence of movement, blood pools in the extremities, and venous return decreases. Heart rate slows (bradycardia) to allow for ventricular filling along with a drop in blood pressure. Homeostasis is disrupted, and the brain is deprived of cerebral nutrients, causing cerebral hypoperfusion that results in hypotension and syncope (Malamed 2015). The elderly (≥ 80yo) have the greatest risk for a syncopal episode that would result in an emergency room visit and/or require medical attention (Soteriades et al. 2002; Grubb and Olshansky 2005).
Syncope resulting from orthostatic hypotension may occur when a patient is raised from a supine to an upright position (Figure 3.2.1) and is the second most common cause of syncope (Grubb and Olshansky 2005; Brignole and Benditt 2011). This type of syncope is often related to diabetes, antihypertensive medications, and dehydration. Autonomic nervous system disturbances, such as Parkinson’s disease and Addison’s disease, may also cause orthostatic syncope (Grubb and Olshansky 2005; Brignole and Benditt 2011).
Cardiovascular syncope is most often related to cardiac arrhythmias and other structural cardiovascular diseases such as myocardial ischemia and infarction (Brignole and Benditt 2011). Findings from the Framingham heart study provide data on the extent and severity of outcomes from syncope. Of the 822 participants included in this subset, VVS was documented as the most common (21.2%) cause of syncope. Cardiovascular syncope was determined to be the cause of syncope in only 9.5% of the participants, this type of syncope was associated with an increased risk for cardiovascular events and premature death (Soteriades et al. 2002).
Management of Syncope in the Dental Office
Patients in a dental office environment are exposed to many potential VVS triggers, such as fear of pain, the sight of blood, sharp instruments that include needles, and shrill sounds. In this case study, the patient wrote in his medical history about a painful past experience at a dental office and demonstrated his apprehension while sitting upright, and clutching the arms of the chair tightly. Knowing that the appointment would continue and sensing pain would be imminent – his fear triggered a vasovagal response. Patients may remain frozen with fear, or determined to stay the course, however, without movement or intervention, hypotension and syncope are inevitable. In a fearful situation, children are generally less inhibited and will move or call out decreasing the likelihood of vasovagal syncope (Malamed 2015).
Response and management of a VVS episode is determined by predisposing factors and symptoms – often referred to in stages. The prodromal period of lightheadedness and dizziness is referred to as pre‐syncope or near‐syncope (Brignole and Benditt 2011; Malamed 2015). The patient is still conscious and is able to breathe on his or her own, therefore, CPR is not indicated. In this situation, the remedy for a patient complaining of dizziness, who is conscious, and who is able to talk, would be to place the patient in supine position until the symptoms are resolved, usually between 15 and 20 seconds. Placing the patient in this position allows gravity to help blood return from the extremities to the heart and brain.
Many dental offices maintain an emergency medical kit that contains ammonia inhalants for use as a secondary measure. Cracking an ammonia inhalant and waving it under the patient’s nose releases the strong smell of ammonia to initiate movement in the body and also aid in restoring blood to the heart. The use of ammonia inhalants to revive patients is highly controversial. A case report in the Journal of Emergency Medical Services (Jems.com 2016) describes the danger of using an ammonia inhalant on a person suspected of syncope. In this case, the person was lying on the ground. When the ammonia inhalant was used, it caused the person to reflex and recoil snapping his neck on the ground. Ammonia is a respiratory irritant and should not be used on people who have a history of any respiratory distress, such as asthma, bronchitis, or emphysema.
It is worthwhile talking with the patient before treatment to allay any concerns. This discussion might include a description of the procedure and available relief for any discomfort. Patients may benefit from pre‐appointment enteral or inhalation sedation (nitrous oxide/oxygen) that would be available during the appointment. In many cases, the trigger for VVS is anxiety, however, ruling out other causes is recommended and referral to a physician is indicated.
Management of a Patient with Reflex Syncope
- Stop the procedure and initiate office emergency protocol.
- Place patient in supine position with feet slightly elevated.
- Patient should recover within 15–20 seconds.
- If consciousness was not lost, and the patient only felt “faint,” treatment may continue if patient and practitioner agree.
- If consciousness does not return quickly or if the patient loses consciousness, assess for Basic Life Support measures until Emergency Medical Services arrive.
- Elderly patients are more likely to be medically compromised and on various drugs. Some drugs such as hypertensive drugs that increase arterial pressure helps to decrease the risk of vasovagal syncope.
- Children who show signs of restlessness rarely experience syncope.
- Most patients who experience syncope require reassurance and education on the triggers and management of syncope.
- Complete medical history assessment will facilitate the preparedness of a medical emergency.
- Follow‐up with referral to physician for evaluation.