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The association between headache and elevated blood pressure among patients

presenting to an Emergency Department

Benjamin W. Friedman MD, MS, Binoy Mistry MD, Jason West MD,

Andrew Wollowitz MD

PII: S0735-6757(14)00336-2

DOI: doi: 10.1016/j.ajem.2014.05.017

Reference: YAJEM 54300

To appear in: American Journal of Emergency Medicine

Received date: 16 March 2014

Revised date: 13 April 2014

Accepted date: 11 May 2014

Please cite this article as: Friedman Benjamin W., Mistry Binoy, West Jason, WollowitzAndrew, The association between headache and elevated blood pressure among patientspresenting to an Emergency Department, American Journal of Emergency Medicine (2014),

doi: 10.1016/j.ajem.2014.05.017

This is a PDF file of an unedited manuscript that has been accepted for publication.As a service to our customers we are providing this early version of the manuscript.The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production processerrors may be discovered which could affect the content, and all legal disclaimers thatapply to the journal pertain.

http://dx.doi.org/10.1016/j.ajem.2014.05.017






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The association between headache and elevated blood pressure among patients presenting

to an Emergency Department

Benjamin W Friedman, MD, MS

Binoy Mistry, MD

Jason West, MDAndrew Wollowitz, MD

Department of Emergency Medicine, Albert Einstein College of Medicine, Montefiore

Medical Center, Bronx, NY, USADepartment of Emergency Medicine, Johns Hopkins University School of Medicine,

Baltimore, MD, USA

Corresponding author:

Benjamin W. Friedman, MD, MS

Department of Emergency MedicineMontefiore Medical Center

Albert Einstein College of Medicine

111 East 210th

Street

Bronx, NY, 10467 [email protected]

(718) 920-6626

Meetings at which this work has been presented: Society for Academic Emergency

Medicine, Atlanta, Georgia, May, 2013

Grant support: None

Conflicts of interest: NoneWord count for text excluding abstract: 3321

Author contributions:BWF conceived and designed the study. BM, JW, and AW abstracted data and reviewed

the literature. BWF analyzed the data. BWF drafted the manuscript, and all authors

contributed substantially to its revision. BWF takes responsibility for the paper as awhole.



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Background Elevated blood pressure (BP) and headache have long been linked in the medical

literature1 though data on association is conflicting. International guidelines stipulate that

headache should be attributed to elevated BP if the systolic BP rises rapidly to

>180mmHg or if the diastolic rises to >120mmHg and if the headache resolves with

normalization of BP.

2

This guideline statement is supported by ambulatory blood pressure monitoring studies in hypertensive patients, which demonstrate that in general,routine headache is not preceded by atypical fluctuations in blood pressure.

3,4 Left

unclear by these data is the role of elevated BP in headaches of sufficient intensity to

warrant a visit to a medical provider, a not uncommon scenario, and the question of howto manage patients with both an acute headache, such as migraine, and elevated BP.

To help guide care of these patients, we used previously collected data to address these

related aims: 1) Using the National Hospital Ambulatory Medical Care Survey(NHAMCS), a national database, we determined how frequently headache patients

presents to an emergency department (ED) with elevated BP and if elevated BP is more

likely in patients who present to an ED with headache than in patients who present withother complaints; 2) Using data collected in the course of three ED-based migraine

clinical trials, we determined if there is an association between improvement in headache

pain and improvement in BP among patients who present to an ED with migraine and

elevated BP; 3) Using the data from these three migraine clinical trials, we determined ifan elevated baseline BP identifies a group of patients less likely to respond to standard

migraine treatment.



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1) Reason for visit. NHAMCS reports up to three reasons for visit for each patient visit.

We considered patients to have presented to the ED for headache if their primary stated

reason for visit was one of the following: i) Headache, pain in the head; ii) migraine; oriii) sinus problems (pain and pressure). We included sinus problems (pain and pressure)

within our headache categorization because it is clear that many patients with migraine

headache consider their headaches to be attributable to sinus disease.

8

As we did not wishto include patients presenting primarily with rhinorrhea and congestion, we did notinclude patients whose primary chief complaint was one of the following: i) sinus

problems (unmodified); ii) sinus problems (sinus inflammation, infection); or iii) sinus

problems (sinus congestion). Similarly, we did not include patients whose secondary ortertiary reason for visit was headache because we did not wish to include patients who

presented primarily for a febrile illness that included headache as one of a constellation of

symptoms. In one of our analyses, we compare headache patients to those patients who

presented to the ED for management of abdominal pain. For the abdominal pain analysis,we used the following reason for visit codes: i) stomach and abdominal pain, cramps and

spasms, including gastric pain; ii) abdominal pain, cramps, spasms NOS including

abdominal discomfort, gas pain, and intestinal colic; iii) lower abdominal pain, cramps,spasms, including right lower quadrant pain, left lower quadrant pain, and inguinal pain;

iv) upper abdominal pain, cramps, spasms, including epigastric pain, left upper quadrant

pain, pain in umbilical region, and right upper quadrant pain.

2) Systolic blood pressure. This was the patient’s presenting systolic blood pressure.3) Diastolic blood pressure. This was the patient’s presenting diastolic blood pressure.

4) Anti-hypertensive medication was defined to include any of the following: agents for

hypertensive emergencies; angiotensin converting enzyme inhibitors; antiadrenergicagents, peripherally acting; antiadrenergic agents, centrally acting; anti-anginal agents;

beta-adrenergic blocking agents; calcium channel blocking agents; diuretics; peripheral

vasodilators; antihypertensive combinations; angiotensin II inhibitors; and vasopressin

antagonists5) We included the following co-variates in the regression model described below:

-Age in years. This was a continuous value

-Sex. Reported as male or female-Race/ ethnicity. Reported as Hispanic, non-Hispanic White, non-Hispanic Black,

or non-Hispanic other

-Geographic region. Reported as Northeast, Midwest, Southeast, West-Triage Acuity. Reported as non-urgent, semi-urgent, urgent, emergent,

immediate.

Clinical trials dataset. We extracted the following information from each of our datasets.1) Pain score. Each research subject was asked to describe their headache intensity at

baseline and again 60 minutes later using a 0 to 10 verbal integer scale on which zero

signified no pain and ten signified the worst pain imaginable.

2). Systolic and diastolic blood pressure. Using an automated sphygmomanometer,research associates specifically trained to measure blood pressure assessed it at baseline

and again 60 minutes later.

Analysis.



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Definition of hypertension. We reviewed the medical literature to determine standardized

or evidence-based definitions for moderate and severe acute elevations in blood pressure.

We were unable to identify definitions that met these criteria. We therefore created thefollowing definitions for this analysis:

--Moderately elevated acute blood pressure: systolic BP > 150mmHg or diastolic BP >

95mmHg--Markedly elevated acute blood pressure: systolic BP >165mmHg or diastolic BP>100mmHg

--Severely elevated acute blood pressure: systolic BP >180mmHg or diastolic BP

>110mmHg

NHAMCS.

In NHAMCS, each patient visit is assigned a weight, which incorporates the four stage

sampling strategy and missing data. Using this weight, representative national data can becalculated. Using the complex samples module from SPSS v. 21, we calculated the

frequency, with 95%CI, of elevated blood pressure among patients presenting with a

chief complaint of headache; the odds ratio (OR), with 95%CI, of elevated BP among patients who presented for headache versus those who presented for anything else; and

the frequency, with 95%CI of receipt of anti-hypertensive medications for each level of

elevated BP. We performed a second analysis, in which we compared the frequency of

elevated BP among those patients who presented with headache versus those patientswho presented with a chief complaint of abdominal pain. We identified abdominal pain

as an appropriate comparator group because abdominal pain, like headache, can be

caused by many different benign or malignant process, and like headache, it is oftenassociated with nausea, vomiting, and anorexia, which may result in dehydration and

lower blood pressure. The frequency of elevated blood pressure among headache patients

versus abdominal pain patients is also reported as ORs with 95%CI. Finally, to account

for the influence of socio-demographic variables and severity of illness on therelationship between chief complaint and blood pressure, we built a logistic regression

model in which we included chief complaint (headache or not headache) as the primary

predictor variable and elevated BP (yes or no) as the dependent variable as well as thefollowing co-variates: age as a continuous value in years, sex, geographic region

(Northeast, Midwest, Southeast, West), race/ethnicity (Hispanic, non-Hispanic White,

non-Hispanic Black, non-Hispanic other) and the patient’s triage urgency, using a fivetiered system (Non-urgent,semi-urgent, urgent, emergent, immediate) .

Clinical trials dataset.

For analysis of our clinical trial data, we calculated one-hour improvement in headache as baseline headache score minus one hour headache score. We calculated one hour

improvement in systolic BP as baseline systolic BP minus one hour systolic BP, and

similarly for diastolic BP. We calculated the correlation between these continuous data

using Pearson’s r, reported the r 2 and p value, and plotted the individual values using a

scatterplot. To determine the influence of elevated BP on improvement in headache, we

constructed a linear regression model in which presence of elevated BP was considered

the primary predictor variable, the improvement in headache score was the dependentvariable, and four dummy variables were created to account for the various doses of



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intravenous metoclopramide and the adjuvant therapy used in each of the trials. The

influence of elevated BP on the improvement in pain score is reported with 95% CI.



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Results

In 2010, there were 129.8 million (95%CI: 116.0 million, 143.7 million) patient visits toU.S. EDs. Headache was the primary complaint in 3.7% (95%CI: 3.4, 4.0%) of these

visits, corresponding to 4.8 million (95%CI: 4.2, 5.4 million) patient visits.

Of patients who presented to the ED with a primary complaint of headache, 23.9%(95%CI: 21.4%, 26.7%) had moderately elevated BP (SBP >150mmHg or a DBP

>95mmHg) versus 22.3% (95%CI: 21.3, 23.3%) of the non-headache population. Among

the headache patients, 14.9% (95%CI: 13.0, 17.1%) had markedly elevated BP (SBP>165mmHG or DBP >100mmHg) versus 11.4% (95%CI: 10.7, 12.0%) of the non-

headache population. Similarly, 7.0% (5.6, 8.7%) had severely elevated BP (SBP >

180mmHg or DBP >110mmHg) versus 4.8% (4.4, 5.2%) of the non-headache

population. Odds ratios are presented in Table 1. The association between headache andelevated BP did not change substantially when we changed the comparison group from

all non-headache visits to abdominal pain visits nor when we performed a logistic

regression model controlling for triage acuity and socio-demographic characteristics, inwhich those with a chief complaint of headache were compared to all other chief

complaints (Table 1).

Among patients who presented to the ED primarily for headache with moderatelyelevated BP, 21.7% (16.1, 28.6%) were treated with an anti-hypertensive agent, versus

31.0% (22.4, 41.0%) with markedly elevated BP, and 41.1% (27.9, 55.8%) with severely

elevated BP.

In the RCT dataset, 659 of 664 enrolled research subjects had baseline blood pressures

recorded. Of these, 17% (112) met our criteria for moderately elevated BP, 60 (9.1%) met

our criteria for markedly elevated BP, and 21 (3%) met our criteria for severely elevatedBP.

Among those with moderately elevated BP, there was no correlation betweenimprovement in pain score and improvement in systolic BP (r=-0.07, r

2=0, p=0.465) or

diastolic BP (r=-0.03, r 2=0, p=0.75) (Figure 1a, 1b). Similarly, among patients with

markedly elevated blood pressure, there was no correlation between improvement inheadache and improvement in systolic BP (r=-0.19, r

2=0.04, p=0.89) or diastolic BP (r=-

0.02, r 2=0, p=0.87) (Figure 2a, 2b), nor among patients with severely elevated BP, for

systolic BP (r=0.06, r 2=0, p=0.81) or diastolic BP (r=0.03, r

2=0, p=0.90) (Figures 3a, 3b).

As demonstrated in Figures 1,2, and 3, there was a reduction in BP between baseline and

one hour of 10-30mmHg regardless of improvement in pain score. Since pain

improvement was not driving this reduction, we sought alternative explanations.

Specifically, we determined whether baseline BP was associated with improvement in BPamong patients with elevated BP. Indeed, baseline systolic BP did explain some of the

variability in improvement in systolic BP (r=0.36, r 2=0.13, p<0.01) and similarly with

baseline diastolic BP (r=0.57, r 2=0.33, p<0.01) (Figures 4a &4b). The most plausible

explanation for these observations is regression of abnormal values to values that more



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closely approximate population means.

After adjusting for investigational medication, the presence of elevated BP at baselinehad a small, but statistically significant downward trend on pain relief. Patients with

moderately elevated BP had slightly less improvement in their zero to ten pain score than

patients with BPs below this cutoff (-0.6, 95%CI: -1.2, -0.1, p=0.03). This effect wasmore pronounced among patients with markedly elevated BP (-0.9, 95%CI: -1.7, -0.2).Because only 21 patients had severely elevated BP, we did not repeat this analysis for

those data.



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Limitations

Limitations of working with NHAMCS have been well described previously.9 Primary

among these is the use of data that was collected not for research purposes but for clinical

care. Stated reasons for visit may not have captured the patient’s true concern. Reliability

and accuracy of the listed blood pressure are unknown. Nevertheless, we do not believethere are systematic errors in these variables that would affect our results. Some datasuggest that elevated blood pressures at triage tend to regress to the mean during

subsequent ED course.10,11

Thus, the triage BP may not accurately reflect the BP twenty

minutes later. This is a limitation that cannot be addressed using NHAMCS data. Finally, NHAMCS does not record data on a patient’s past history of hypertension. Thus, we

cannot know how many of these patients with elevated BP had hypertension or were

being treated with anti-hypertensives.

During the migraine clinical trials, we did not collect data regarding diagnosed history of

hypertension, previous blood pressures, or use of anti-hypertensive medications. It is

likely that patients with elevated blood pressure included some with diagnosedhypertension taking multiple anti-hypertensives and others who had never been

diagnosed with hypertension. Similarly, the normal blood pressure group likely contained

patients with a history of hypertension who were well controlled on anti-hypertensives. It

may be that we have lumped distinct populations. However, especially in an ED population, relying on markers of healthcare access to split groups of patients may result

in a socio-economic categorization more than a categorization based on biological

phenomena.



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Discussion

In this manuscript, we used two complimentary databases to explore the relationship between elevated blood pressure and headache among patients presenting to an ED.

NHAMCS, a national probability sample database, provided a wealth of data regarding

ED practice across the country. Our migraine clinical trial database provided prospectively gathered data using a standardized methodology and validated instruments.Using these databases, we found that 1) elevated BP is common among ED patients who

present with a chief complaint of headache; 2) ED patients with headache are more likely

to have elevated BP than are ED patients with other chief complaints; 3) only a minorityof patients who present to an ED with headache and elevated BP are treated with anti-

hypertensive agents; 4) Among patients who present to an ED with migraine and an

elevated BP, there is no correlation between improvement in headache and improvement

in systolic or diastolic BP; and 5) Among patients who present to an ED with migraine,elevated BP at baseline is associated with less headache relief.

The NHAMCS data demonstrate that markedly and severely elevated blood pressure ismore common among patients who present to an ED with headache than among patients

who present to an ED for any chief complaint other than headache or among those who

present specifically for abdominal pain. Some have attributed elevated triage blood

pressures among ED headache patients to pain or anxiety, confounding factors that maydrive both the elevated blood pressure and the need for an ED visit.

12 However, our data

demonstrate that blood pressure is higher among headache patients even when compared

to other ED patients and that this relationship is directly related to degree of blood pressure elevation. Therefore, one can have more confidence that the association is in fact

genuine and not confounded by psychological distress, a finding reflected in the work of

Tanabe et.al., who compared ED BPs to home BPs in a cohort of patients, and found that

the elevation of ED BP above home BP could not be explained by pain or psychologicaldistress.13 However, the directionality of this association between BP and headache, and

the causal pathway are still unknown — one may hypothesize that elevated BP is causing

headache though it is just as likely that headache is causing elevated blood pressure.Alternatively, the relationship may be confounded by a third variable we have not

considered.

The NHAMCS data also demonstrate that even marked elevations of blood pressure in

patients with headache usually are not treated with anti-hypertensive medications.

However, the higher the blood pressure, the more likely the patient is to receive an anti-

hypertensive. Forty percent of headache patients who presented with systolic BP>180mmHg or diastolic >110mmHg were treated with an anti-hypertensive, though 60%

were not. Heterogeneity in clinical practice reflects uncertainty. Until high quality

clinical trial data are available, it will remain unclear how best to manage these patients.

Some clinicians treat patients with acutely elevated BP with anti-hypertensives with thegoal of preventing morbidity or mortality. In our migraine clinical trials, we did not

observe any blood pressure related adverse outcomes,5,6,14

lending some support to the

practice of not treating elevated BP with anti-hypertensive in patients who present to anED with migraine.



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Much to our surprise, among patients with migraine and elevated blood pressure, we did

not identify an association between improvement in blood pressure and improvement inheadache. An often-quoted aphorism in emergency medicine is that if one treats the pain,

the blood pressure will improve, an observation that may rely on regression of abnormal

values to the mean. As depicted in Figures 1, 2, and 3, there was a general improvementin BP of 10-30mmHg. This reflects a regression of abnormal values towards more normalvalues, a phenomenon that explains normalization of blood pressure much better than an

association with relief of pain. Therefore, a therapeutic strategy aimed solely at lowering

BP is unlikely to result in migraine improvement.

Although improvement in blood pressure was not associated with improvement in

headache among patients with elevated BP, a higher baseline blood pressure was

associated with worse pain outcomes. Migraineurs with elevated blood pressure reportedless improvement on a zero to ten pain scale than migraineurs without elevated blood

pressure. This phenomenon was more striking among patients with higher baseline blood

pressure elevations. However, even among patients with higher blood pressures, thedifference in outcomes falls below standard thresholds for minimum clinically significant

difference.15

Therefore, the clinical impact of this finding is unlikely to be substantial. It

is clear that anti-hypertensives prevent headache in outpatient populations.16

Based on

our data, it seems less likely that anti-hypertensives will benefit migraine patients acutely.

The relationship between blood pressure and pain is complex. Since initial reports of anassociation between chronic severe hypertension and headache,

1 there have been

countless attempts to understand this association more completely. There are robust

outpatient data demonstrating that anti-hypertensive agents, regardless of class, prevent

headache, thereby suggesting that lowering blood pressure itself can prevent headache.16

On the other hand, some population data and laboratory work suggest that chronic

hypertension as well as acutely elevated blood pressure moderate nociception, a

phenomenon named hypertension-associated hypalgesia.17

We do not have a readyexplanation for the association between high blood pressure and headache we discovered

in the NHAMCS data. For all those patients who ask us, “Is my high blood pressure

causing my headache?” we can only answer “maybe.”

In conclusion, while there is an association between elevated blood pressure and

headache among patients presenting to an emergency department, it is not clear how best

to address patients who present to an acute care setting with both an elevated blood pressure and headache.



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References

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Intern Med 1913;12:755-98.

2. The International Classification of Headache Disorders, 3rd edition (beta

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ambulatory blood pressure surrounding episodes of headache in mildly

hypertensive patients. Arch Intern Med 2001;161:252-5.

4. Kruszewski P, Bieniaszewski L, Neubauer J, Krupa-Wojciechowska B.

Headache in patients with mild to moderate hypertension is generally not

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44.

5. Friedman BW, Greenwald P, Bania TC, et al. Randomized trial of IV

dexamethasone for acute migraine in the emergency department. Neurology

2007;69:2038-44.

6. Friedman BW, Mulvey L, Esses D, et al. Metoclopramide for acute migraine: adose-finding randomized clinical trial. Ann Emerg Med 2011;57:475-82 e1.

7. Friedman BW, Garber L, Yoon A, et al. Randomized trial of IV valproate vs

metoclopramide vs ketorolac for acute migraine. Neurology 2014;82:976-83.

8. Eross E, Dodick D, Eross M. The Sinus, Allergy and Migraine Study (SAMS).

Headache 2007;47:213-24.

9. McNaughton CD, Self WH, Pines JM. Annals of Emergency Medicine Journal

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sets: understanding strengths and limitations of the National Hospital Ambulatory

Medical Care Survey: answers to the May 2013 Journal Club questions. Ann Emerg

Med 2013;62:425-30.

10. Pitts SR, Adams RP. Emergency department hypertension and regression tothe mean. Ann Emerg Med 1998;31:214-8.

11. Cienki JJ, Deluca LA, Feaster DJ. Course of untreated high blood pressure in

the emergency department. West J Emerg Med 2011;12:421-5.

12. Denny CJ, Schull MJ. Headache and Facial Pain. In: Tintinalli JE, Strapcyznski

JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli's Emergency Medicine A

Comprehensive Study Guide 7th Edition. New York: McGraw Hill 2011.

13. Tanabe P, Persell SD, Adams JG, McCormick JC, Martinovich Z, Baker DW.

Increased blood pressure in the emergency department: pain, anxiety, or

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14. Friedman BW, Garber L, Yoon A, et al. Randomized trial of IV valproate vs

metoclopramide vs ketorolac for acute migraine. Neurology 2014.15. Todd KH, Funk JP. The minimum clinically important difference in physician-

assigned visual analog pain scores. Acad Emerg Med 1996;3:142-6.

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17. Ghione S. Hypertension-associated hypalgesia. Evidence in experimental

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consequences. Hypertension 1996;28:494-504.



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Table 1. Odds (OR, 95%CI) of headache patients having elevated blood pressure at triage

versus patients with other chief complaints

Blood pressure Headache versus any

other chief complaint

Headache versus

abdominal pain

Headache versus any

other chief complaint,controlling for triage

acuity and socio-demographic

characteristics

Moderately elevated

(SBP >150mmHg or

DBP >95mmHg)

1.10 (0.95, 1.27) 1.06 (0.87, 1.28) 1.27 (1.09, 1.48)

Markedly elevated

(SBP >165mmHg or

DBP >100mmHg)

1.37 (1.16, 1.61) 1.25 (1.01, 1.55) 1.63 (1.38, 1.93)

Severely elevated(SBP > 180mmHgor DBP

>110mmHg)

1.49 (1.17, 1.90) 1.57 (1.12, 2.20) 1.87 (1.46, 2.41)



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Figure 1a. Improvement in systolic blood pressure versus improvement in pain score over

one hour among migraine patients with SBP >150mmHg or DBP >95mmHg. The

relationship between these variables is plotted as a line with 95%CI.



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Figure 1b. Improvement in diastolic blood pressure versus improvement in pain score

over one hour among migraine patients with SBP >150mmHg or DBP >95mmHg. The




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Figure 4a. Baseline systolic BP versus improvement in systolic BP between baseline and


relationship between these variables is plotted as a line with 95%CI. The most likelyexplanation for the association depicted here is regression of abnormal systolic blood pressure values towards the mean systolic blood pressure.



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Figure 4b. Baseline diastolic BP versus improvement in diastolic BP between baseline

and one hour among migraine patients with SBP >150mmHg or DBP >95mmHg. The

relationship between these variables is plotted as a line with 95%CI. The most likelyexplanation for the association depicted here is regression of abnormal diastolic blood

pressure values towards the mean diastolic blood pressure.

the association between headache and elevated blood pressure among patients presenting to an...

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