Needle Phobia: Etiology, Adverse Consequences, and Patient Management

Needle phobia has profound health, dental, societal, and legal implications, and severe psychological, social, and physiologic consequences. There is genetic evidence for the physiologic response to needle puncture, and a significant familial psychological component, showing evidence of inheritance. Needle phobia is also a learned behavior. The dental practitioner must recognize patients with needle phobia before the administration of local anesthetics to identify patients who are potentially reactive and to prevent untoward sequelae. Needle phobia is highly associated with avoidance behavior, and the dentist must exhibit compassion and respect. To avoid bradycardia, hypotension, unconsciousness, convulsions, and possibly asystole, oral premedication with benzodiazepines or other antianxiety agents must be considered for patients who are needle phobic. Management of needle phobiaeinduced syncope includes perioperative monitoring, oxygen administration, positioning, atropine, and vasopressors.

Needle phobia is a formal medical condition affecting approximately 10% of the world population and characterized within the American Psychiatric Association Diagnostics and Statistical Manual of Mental Disorders (DSM-IV) by the presence of fear and the occurrence of avoidance behavior. An individual’s avoidance of health care to eliminate any preconceived exposure to needles is the central premise to the diagnosis of needle phobia. In conjunction with avoidance behavior, there are also physiologic changes in blood pressure, heart rate, electrocardiogram (ECG), and stress hormone levels. Therefore, needle phobia can be defined as a combination of objective clinical parameters as well as subjective symptoms.

Because much of modern medicine depends on the hypodermic needle for medical testing and/or drug therapies, clinicians should be aware that needle phobia is a common condition that may lead to avoidance of medical treatment, severe health and dental problems, and significant social and legal difficulties. Furthermore, there have been reports in peer-reviewed literature of needle phobia–related syncope/vasovagal/fainting reactions that have led to asystole and death. Clinicians should be aware of the underlying pathophysiology, possible severe sequelae, and the prevention and treatment of the possible adverse events that can occur.

Prevalence

In a review of literature, Hamilton states that, because needle phobia has recently been defined, only indirect estimates of its prevalence can be inferred from the literature.

In a Canadian community study completed by Costello, 449 Canadian women were interviewed and administered the Present State Examination (PSE) to allow for a standardized identification of psychiatric classification. The investigators found that 21.2% experienced mild to intense fear, and 4.9% had a phobic level of fear of injections, doctors, dentists, and hospitals. In addition, Agras and colleagues reported findings that estimated that 9% of the population of the United States 10 to 50 years of age have an injection phobia and 5.7% have seen a physician about this phobia. In an English study presented by Keep and Jenkins the dread of a painful injection was present in 11% of 100 British office patients.

Through in-hospital interviews, 22% of 184 teenaged maternity patients in Nashville, Tennessee, were found to have an increased fear of blood drawing that inhibited them from maintaining routine prenatal care within a public clinic. In random questionnaire-based surveys, 23% of 200 Swedish and 27% of 177 American college students reported needle phobia as the main reason for not donating blood.

Several studies have also investigated the associated demographics of needle phobia. It seems that the overall population of needle phobics has a slight female preponderance and is of a younger age. Deacon and Abramowitz recruited 3315 venipuncture participants from hospital-based phlebotomy laboratories. The investigators conducted a series of analyses examining differences between individuals with needle phobia symptoms (n = 72) and those who did not present with any symptoms of needle fear (n = 2787). Compared with those with no needle fear, needle phobics were more likely to be women (68.1% vs 48.9%) and of a younger age (43.3 mean years vs 59.0 mean years). Graham also found a significant correlation of age with anxiety as a predictor for syncope in an older study involving 414 blood donors at a hospital blood bank. This evaluation revealed a definite association between age and the occurrence of fainting. As shown in Table 1 , the younger the blood donor, the more likely he/she was to faint. The pulse rate also proved to be correlated with syncope. Patients with a higher pulse were more likely to have a syncopal episode ( Table 2 ). Anxiety was also a significant factor in predicting syncope. Thirty-two percent admitted to being nervous; of these, 28.6% fainted. Of the remaining 68.2% who denied any anxiety, only 12.9% fainted. Therefore, a donor who admitted to being anxious was twice as likely to faint as to one who denied any anxiety ( Table 3 ). Racial differences in needle phobia are conflicting in the literature. In Graham’s study, 18% of 352 white subjects, but none of the black subjects, fainted while donating blood. There was no obvious explanation for the racial differences. Statistical evaluation showed no significant differences between the means of the 2 groups in age, initial pulse, systolic blood pressure, mean blood pressure, or admission of nervousness. Another study completed by Callahan and colleagues found no racial differences. Further study evaluating the possibility of racial or ethnic genetic characteristics that could predispose one to needle phobia and syncope may be warranted.

Table 1
Frequency of fainting according to age
Age (y) Proportion Fainted (%)
50–59 0/21 (0)
40–49 8/79 (10)
30–39 24/125 (19)
20–29 28/117 (24)
10–19 3/10 (30)

Data from Graham DT. Prediction of fainting in blood donors. Circulation 1961;23:903.

Table 2
Frequency of fainting according to initial pulse rate
Pulse Rate (bpm) Proportion Fainted (%)
>100 15/35 (43)
90–99 15/73 (21)
80–89 21/155 (14)
70–79 8/72 (11)
60–69 4/17 (24)

Abbreviation: bpm, beats per minute.
Data from Graham DT. Prediction of fainting in blood donors. Circulation 1961;23:903.

Table 3
Combination of pulse, age, and anxiety
Age (y) Pulse Rate (bpm) Anxiety Level Proportion Fainted (%)
<30 ≥90<100 Not nervous 16/46 (35)
<30 ≥90<100 Nervous 11/23 (48)
<30 ≥100 Not nervous 6/12 (50)
<30 ≥100 Nervous 5/7 (71)

Data from Graham DT. Prediction of fainting in blood donors. Circulation 1961;23:904.

A familial predilection for needle phobia has been shown in various research. Hamilton reports that approximately 80% of patients who have needle phobia report strong needle fear in a first-degree relative (ie, a parent, child, or sibling). Numerous other studies have shown that patients with needle phobia have family members with similar traits. A Swedish study showed that 68% of patients with needle phobia had biologic relatives who were needle phobic, a rate that was 3 to 6 times higher than the frequency of corresponding phobias among the relatives of patients treated for agoraphobia, social phobia, dental phobia, or animal phobia. In an American study, 27% of patients with needle phobia had a family history of needle fear. By means of a comparative twin study (monozygotic and dizygotic twins), Torgersen investigated the etiology and nosology of phobic fears. The study established that, apart from separation fears, genetic factors have a consistent role in the strength as well as content of phobic fears.

Etiology

Evolution of the Needle Phobic Trait

Hamilton postulates the presence of a genetic trait that probably evolved among the human species in response to piercing, stabbing, and cutting injuries. He speculates that most violent deaths in our species’ evolutionary history have been caused by penetrations from teeth, claws, fangs, and tusks, and from sticks, stone axes, knives, spears, swords, and arrows. He surmises that a deep-rooted, evolutionally developed psychological reflex resulted in a strong fear of skin puncture and provided selective values in teaching humans to avoid such injuries. He concludes that, in the past 4 million years or more of human evolution, genes controlling blood pressure, heart rate, cardiac rhythm, and stress hormone release developed to maintain the survival of the human species.

However, not all humans suffer an extreme response to needles. Hamilton concludes his hypothesis of etiology by likening it to other human traits such as weight, height, and intelligence, which vary with each individual human. Therefore, he suggests that the gene for needle phobia is distributed in a normal bell-shaped distribution curve that affects individuals to varying degrees.

Inherited or Learned

There is clear evidence that supports the hypothesis of a hereditary component to needle phobia. Both the vasovagal reflex and needle phobia tend to run strongly in families. The heritability of blood-injury phobias that include fear of injections, wounds, blood, and pain have been estimated at 48% in twin studies. The heritability in electrocardiographic variations such as PR, QRS, and QT intervals, as well as heart rate, is at 30% to 60%, respectively. The autonomic control of the cardiovascular system in general, based on these twin comparisons, can be considered genetically influenced. Therefore, during a needle phobic response, a correlation may exist between abrupt decreases in blood pressure, heart rate and ECG changes, and genetic influences.

In addition to genetic factors, there is a learned component to needle phobia. There are several publications that discuss the needle fear that arises after a negative experience at a physician’s or dentist’s office. A study completed by Ost of 56 subjects who had injection phobia showed that 56% could trace their fear back to negative conditioning from a health care experience. The mean onset of age was 8.06 years and often correlated with a first-time health care–related appointment. This study also determined that 24% of the subjects could trace their phobias to having seen another child, often a sibling, have a negative experience to needles. It has been surmised that over time, with more needle exposures, this learned fear tends to organize itself and form into a conscious phobia that leads to an anticipatory anxiety before various medical procedures involving needles. This fear then becomes generalized toward objects that are frequently associated with needles, such as syringes, doctors, white laboratory coats, examination rooms, nurses, and even the antiseptic smells of offices and hospitals.

Based on these studies, it can be hypothesized that the trait of needle phobia is both inherited and learned. A vasovagal reflex is seen in all patients with needle phobia who have been tested, and medical histories show that most have had learning experiences that triggered the needle fear. A reasonable theoretic model might propose that needle phobia depends on both an inherited reflex that is hardwired in neurovascular and neuroendocrine pathways and on the learning of a conscious fear.

Other investigators have reached similar conclusions. Marks reports that emotional fainting in response to a needle stimulus may have evolved from the tonic immobility reaction (ie, playing dead) that is seen in many species. In a recent animal study completed by Gabrielsen and colleagues, grouse were found to have an emotional bradycardia when they freeze on being approached. Predators tend to attack prey that is moving, and tend to lose interest when the prey becomes still. Marks continues by saying that emotional faints in humans, and tonic immobility in animals, may be mediated by a depressor pathway related to survival that has been found in cats and monkeys. Pool and Ransohoff reviewed the physiology of a tonic immobility reaction in which the rostral cingulated gyrus in the brain serves as the primary action sector. He found that stimulation of that area led to autonomic responses, motor effects, and a suppressor action. In the same report, the autonomic responses were evaluated and there was a marked respiratory slowing and arrest up to 25 seconds. Marked cardiovascular effects were also observed, consisting of vagal slowing of the heart, cardiac arrest, and a marked decrease in blood pressure. Kremer suggested the existence of different functional areas in the cingulated gyrus that were related not only to autonomic responses but emotional responses.

Etiology

Evolution of the Needle Phobic Trait

Hamilton postulates the presence of a genetic trait that probably evolved among the human species in response to piercing, stabbing, and cutting injuries. He speculates that most violent deaths in our species’ evolutionary history have been caused by penetrations from teeth, claws, fangs, and tusks, and from sticks, stone axes, knives, spears, swords, and arrows. He surmises that a deep-rooted, evolutionally developed psychological reflex resulted in a strong fear of skin puncture and provided selective values in teaching humans to avoid such injuries. He concludes that, in the past 4 million years or more of human evolution, genes controlling blood pressure, heart rate, cardiac rhythm, and stress hormone release developed to maintain the survival of the human species.

However, not all humans suffer an extreme response to needles. Hamilton concludes his hypothesis of etiology by likening it to other human traits such as weight, height, and intelligence, which vary with each individual human. Therefore, he suggests that the gene for needle phobia is distributed in a normal bell-shaped distribution curve that affects individuals to varying degrees.

Inherited or Learned

There is clear evidence that supports the hypothesis of a hereditary component to needle phobia. Both the vasovagal reflex and needle phobia tend to run strongly in families. The heritability of blood-injury phobias that include fear of injections, wounds, blood, and pain have been estimated at 48% in twin studies. The heritability in electrocardiographic variations such as PR, QRS, and QT intervals, as well as heart rate, is at 30% to 60%, respectively. The autonomic control of the cardiovascular system in general, based on these twin comparisons, can be considered genetically influenced. Therefore, during a needle phobic response, a correlation may exist between abrupt decreases in blood pressure, heart rate and ECG changes, and genetic influences.

In addition to genetic factors, there is a learned component to needle phobia. There are several publications that discuss the needle fear that arises after a negative experience at a physician’s or dentist’s office. A study completed by Ost of 56 subjects who had injection phobia showed that 56% could trace their fear back to negative conditioning from a health care experience. The mean onset of age was 8.06 years and often correlated with a first-time health care–related appointment. This study also determined that 24% of the subjects could trace their phobias to having seen another child, often a sibling, have a negative experience to needles. It has been surmised that over time, with more needle exposures, this learned fear tends to organize itself and form into a conscious phobia that leads to an anticipatory anxiety before various medical procedures involving needles. This fear then becomes generalized toward objects that are frequently associated with needles, such as syringes, doctors, white laboratory coats, examination rooms, nurses, and even the antiseptic smells of offices and hospitals.

Based on these studies, it can be hypothesized that the trait of needle phobia is both inherited and learned. A vasovagal reflex is seen in all patients with needle phobia who have been tested, and medical histories show that most have had learning experiences that triggered the needle fear. A reasonable theoretic model might propose that needle phobia depends on both an inherited reflex that is hardwired in neurovascular and neuroendocrine pathways and on the learning of a conscious fear.

Other investigators have reached similar conclusions. Marks reports that emotional fainting in response to a needle stimulus may have evolved from the tonic immobility reaction (ie, playing dead) that is seen in many species. In a recent animal study completed by Gabrielsen and colleagues, grouse were found to have an emotional bradycardia when they freeze on being approached. Predators tend to attack prey that is moving, and tend to lose interest when the prey becomes still. Marks continues by saying that emotional faints in humans, and tonic immobility in animals, may be mediated by a depressor pathway related to survival that has been found in cats and monkeys. Pool and Ransohoff reviewed the physiology of a tonic immobility reaction in which the rostral cingulated gyrus in the brain serves as the primary action sector. He found that stimulation of that area led to autonomic responses, motor effects, and a suppressor action. In the same report, the autonomic responses were evaluated and there was a marked respiratory slowing and arrest up to 25 seconds. Marked cardiovascular effects were also observed, consisting of vagal slowing of the heart, cardiac arrest, and a marked decrease in blood pressure. Kremer suggested the existence of different functional areas in the cingulated gyrus that were related not only to autonomic responses but emotional responses.

Clinical findings/physiology

The physical symptoms of needle phobia include syncope, near syncope, light-headedness, or vertigo on needle exposure, along with other autonomic symptoms such as pallor, diaphoresis, and nausea.

The Vasovagal Response

The neurophysiology of the vasovagal reflex is both a vagal bradycardia and a vasodilation from withdrawal of α-sympathetic arteriolar tone, which together cause hypotension. Some studies have shown that the vasovagal reflex is a biphasic response in which there is an anticipatory reaction of increased heart rate and blood pressure before needle puncture followed by a sudden decrease in both heart rate and blood pressure after a needle puncture. However, Hamilton has observed that some patients with needle phobia do not show this initial cardiovascular increase.

The onset of the vasovagal response can be immediate, within 2 to 3 seconds, and is usually brief. However, not all cases of syncope are short lived. Hamilton presented a prospective study demonstrating that of 84 blood donors that fainted, 16.7% experienced syncope from 5 to 30 minutes. Another series of 64 blood donors who fainted found that 14% fainted after leaving the phlebotomy site, sometimes several hours later. Furthermore, although those who faint only do so for several seconds, a survey of 298 fainting patients showed that several had lost consciousness for 10 to 30 minutes, and a few from 1 to 2 hours. These studies show that blood pressure returns to normal after 2 hours and most patients feel well enough to return to their normal activity after several hours. However, some have reported anxiety, malaise, and weakness for 1 to 2 days after the syncopal episode.

Cardiovascular Implications

There are several reports of ECG changes during the vasovagal reflex. They include sinus arrhythmias; premature atrial contractions; premature junctional contractions; unifocal and multifocal premature ventricular contractions; bigeminy; first- and second-degree heart block; changes in P waves, ST waves, and T waves; sinus bradycardia; sinus tachycardia; ventricular tachycardia; ventricular fibrillation; and asystole. Some experts presume that these ECG changes are secondary to vagal influence on the sinoatrial and atrioventricular nodes, and that they also relate to the antagonism between the activated sympathetic and parasympathetic systems on the heart. Such evidence should indicate to the clinician that patients who have needle phobia require cautionary management. Although the condition is rare, any prolonged syncopal event indicates prolonged bradycardia and hypotension, and is thus associated with hypoperfusion of cardiac and brain tissue. Such events always expose the patient to a greater incidence of cardiac or cerebral ischemia.

Hormonal Relationships

Epinephrine and norepinephrine levels do not always become increased during episodes of needle phobia. They have been observed to decrease in 8 patients who fainted after venipuncture. This is presumably related to the withdrawal of sympathetic vascular tone. In another study, 21 young women receiving dental treatment had increased levels of epinephrine, but not norepinephrine. This was likely the result of a severe situational stress response in which epinephrine is secreted by adrenal medullary cells in the manner of a fight-or-flight response. Sympathetic activity can be decreased before or during syncope, which may decrease norepinephrine outflow. As the shutdown of norepinephrine reduces vascular tone, epinephrine selectively produces vasodilation in skeletal muscle, which causes pooling of blood in the periphery, reduces venous return, and results in profound sudden hypotension.

Vasopressin or antidiuretic hormone (ADH) has been shown to increase in response to the vasovagal reflex associated with venipuncture. This may be caused by a reduction in intravascular volume by the pituitary gland during vasovagal shock. Renin also increased by 200% in one patient with needle phobia, which could be an attempt by the body to compensate for syncope by increasing the circulating blood volume. ADH, a potent vasoconstrictor, is responsible for the pallor seen during the vasovagal reflex and also contributes to a nausea effect. The ADH hormone acts during the vasovagal response by sharply decreasing cutaneous blood flow, and its increase may be considerable, reaching 46 times normal levels. This extensive increase may be responsible, along with the cathecholamine increase, for the intense fear that victims of needle phobia learn in response to their vasovagal reflex.

Bispectral Index

There were also reports of cases in which there was a decrease in bispectral index (BIS) as an indicator of syncope. BIS provides a numerical value that has been correlated with the patient’s hypnotic state and is related to the patient’s electroencephalogram (EEG). The EEG is a recording of electrical potentials generated by cells in the cerebral cortex of the brain. Data measured by the EEG are taken through a computer-generated algorithm that results in a numerical readout that correlates with the depth of hypnosis. BIS values of 65 to 85 have been related to varying levels of sedation, whereas patients are considered to be unconscious with BIS values ranging from 40 to 65. The BIS monitoring device is a tool used extensively in anesthesiology to aid the anesthesiologist in gauging a patient’s depth of anesthesia.

Win and colleagues reported 2 patients with decreased BIS indexes that were associated with syncope during venipuncture. One patient had a reduced BIS score that occurred during the development of hypotension and bradycardia, and the other patient lost consciousness with decreasing BIS scores before hypotension and bradycardia could occur. Using these case studies as means of analysis, it seems that the cortical processing of emotional fear, stress, and pain may be conveyed to the medullary cardiovascular center through the limbic system. The limbic system regulates emotions, and stimulation of the limbic sympathoinhibitory center can cause hypotension and bradycardia.

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Oct 29, 2016 | Posted by in General Dentistry | Comments Off on Needle Phobia: Etiology, Adverse Consequences, and Patient Management
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