Sudden Headache in a Woman With Hypertension

July 1, 2002
Gary Quick, MD-Series Editor
Gary Quick, MD-Series Editor

Maggie Law, MD
Maggie Law, MD

A 37-year-old woman presents to the emergency departmentwith a diffuse, sharp, pounding headache,which started 2 hours earlier. She rates her discomfort as4 on a scale of 1 to 10. Neck muscle soreness is also present,but the pain does not radiate.

A 37-year-old woman presents to the emergency departmentwith a diffuse, sharp, pounding headache,which started 2 hours earlier. She rates her discomfort as4 on a scale of 1 to 10. Neck muscle soreness is also present,but the pain does not radiate.

The patient has not experienced syncope; visual disturbance;chest pain; light-headedness; dyspnea; difficultyin walking, using her hands and feet, or swallowing; paresthesias;altered mental status; slurred speech; vertigo; face,ear, or jaw pain; nasal discharge; palpitations; diaphoresis;abdominal pain; nausea; vomiting; ordiarrhea. She has not had any acuteillnesses recently.

She has hypertension for whichshe erratically takes antihypertensivemedication, the name of which shehas forgotten. She has no personal orfamily history of migraine or otherheadache syndrome.

She does not smoke or use illicitdrugs; however, she drinks heavily 2or 3 times a week. She is married andlives with her family.

Temperature is 37C (98.6F);pulse rate, 90 beats per minute; respirationrate, 20 breaths per minute;and blood pressure (BP), 190/110 mm Hg. The patient appearsto be in no acute distress.

Scalp and temporal arteries are not tender; pupilsare symmetric and reactive to light. Eye motions are normal,and no cranial nerve deficits are apparent. Speech isclear; gag reflex is intact. Tongue protrudes in the midline.Fundoscopic examination shows the optic disc marginsare sharply defined; no hemorrhages are noted. Venouspulsations are present.

No pronator drift or cerebellar dysfunction. Upperand lower extremity reflexes are equal and symmetric. NoBabinski reflex; Romberg test is negative.

Neck examination reveals no nuchal rigidity or restrictedmotion. Paracervical musculature is tender; flexionof the neck increases neck pain, and the headachecarotid bruits are noted. The remainder of the examinationis normal.

After 30 minutes, the patient's BP is 200/100 mm Hg.She is given oral clonidine, 0.2 mg. A basic metabolicpanel, urinalysis, ECG, and chest film are ordered to detectevidence of progressive end-organ damage caused by uncontrolledhypertension.

The sodium level is 138 mEq/L; potassium, 3.5mEq/L; chloride, 107 mEq/L; carbon dioxide, 22 mEq/L;blood urea nitrogen, 21 mg/dL;and creatinine, 1.6 mg/dL. Urinalysisresults are normal except for traceblood and trace protein. The chestfilm shows no cardiomegaly or congestiveheart failure; the ECG revealsevidence of left ventricular hypertrophy,left axis deviation, and invertedT waves in leads V4 through V6 thatare compatible with a ventricularstrain pattern or ischemia.

BP, which is measured 30 minutesafter clonidine was administered,has risen to 250/130 mm Hg. The patientis given a second dose of oralclonidine, 0.2 mg.

Thirty minutes later her BP is 230/120 mm Hg.Because of both the lack of response to clonidine and theabnormal ECG that indicates hypertensive heart disease,a nitroglycerin drip is initiated.

1. What is the rationale behind the decision to orderthe scan?
2. What does the CT scan show?
3. What should be done next to evaluate and/or treatthis patient?

This patient's presentation was deceptively benign.Many physicians would not have ordered a CT scan inthis setting. Even a patient with minor head trauma whoexperiences a short loss of consciousness might be dischargedwithout a CT scan if the mental status is improvingand the neurologic examination is normal.

Diagnostic clues. Sudden onset of headache suggestsintracranial or subarachnoid hemorrhage, especiallyif the patient experiences syncope or near-syncope. Incontrast to the relatively minor BP elevations that occurin patients with ischemic stroke, intracranial hemorrhageis commonly associated with a profound reactiverise in BP.

Treatment. The identification of ICH in this patientresulted in an immediate switch from oral antihypertensiveagents to parenteral nitroprusside to gain rapid controlof the BP. The treatment of hypertension in the settingof ICH is controversial. Ordinarily, a patient withICH has a stable BP in the range of 220/110 mm Hg anddoes not experience a second hemorrhage even in thepresence of such an elevated reading. This patient's hypertensionwas treated because she had a significantlyhigher reading (250/130 mm Hg) and because her BPwas increasing.

Care must be taken to reduce the BP in this settingby only about 10% to 20% or to a diastolic reading of 100mm Hg, whichever occurs first. The goal of treatment isto restore cerebral autoregulation of BP while simultaneouslyavoiding intracranial hypotension that would lead tofurther CNS damage caused by hypoperfusion of the CNStissue in the area of injury.