Patient with renovascular hypertension refractory to clinical treatment with hypertensive crisis and acute pulmonary edema
(Portuguese PDF version)

Coordinated by Dr. Fausto Miranda Jr
Telmo P. Bonamigo*

* Head, Service of Vascular Surgery, Irmandade da Santa Casa de Porto Alegre; Associate Professor, Fundação Faculdade Federal de Ciências Médicas de Porto Alegre.

J Vasc Br 2003;2(1):35-36


Part I - CLINICAL CASE

Sixty-five-year-old female white patient, housewife, was admitted to the Emergency Service of a Tertiary Hospital on June 12, 1994, when she complained of intense dyspnea preceded by dry cough and chest pain.

On clinical examination, she was extremely dyspneic (orthopnea) with sweating and cyanosis at the extremities, tachycardia and tachypnea. Arterial pressure was 300/170mmHg and lung auscultation revealed crackles up to the medial third of the chest. ECG traces did not show ischemic abnormalities. The patient's past history included smoking for 40 years (20 cigarettes a day), dyslipidemia and systemic arterial hypertension (SAH) detected six years ago. She reported regular use of hydrochlorothiazide, propranolol, methyldopa and lovastatin. The clinical status was described by the on-call doctor as acute pulmonary edema secondary to hypertensive crisis.

The following treatment was immediately used: oxygen 4l/min., IV morphine 4 mg, SL isosorbide 10 mg, IV furosemide 40 mg, IV aminophylline 240 mg and sodium nitroprusside. The patient was transferred to the ICU. Two hours after that, she showed some clinical improvement, but dyspnea and sweating persisted. Vital signs were as follows: AP= 180/110 mmHg, RF: 28 mrm; HR: 72 bpm and axillary temperature: 36.8 oC.

Lab exams yielded the following results: glycemia 148 mg/dl; creatinine 1.0 mg/dl; Na+ 137mEq/l; K+ 2.8 mEq/l; GOT 9 U/l; CPK 27 U/l and CPK-MB 3.0 U/l.

The patient spent the first two days at the ICU, and received sodium nitroprusside, oral furosemide 40 mg 12/12 h, oral captopril 25 mg 6/6 h, oral nifedipine 10 mg 6/6 h, in addition to IV and oral potassium chloride. Water balance was still negative during this period, and the patient was discharged from the ICU with no symptoms and with normal arterial pressure.

On June 16, she was submitted to abdominal echography, which showed normal liver, pancreas, spleen and gallbladder. Right kidney with approximately 7.8 cm and left one with 9.2 cm at its largest axis. Dilation of collecting ducts was not observed. The abdominal aorta revealed extensive parietal calcifications and no expansive lesions were identified. On the subsequent day, abdominal and renal aortography was performed. (Fig 1). Due to deterioration of renal function (Cr: 3.l mg/dl on January 18), the administration of captopril was discontinued, and replaced with hydralazine and clonidine. On June 20, her creatinine level was 1.9 and endogenous creatinine clearance was 29 ml/min.

A medical conference was held and the following opinions were obtained. The angiographer regarded the case as inadequate for endovascular treatment, due to the risk of thrombosis during the procedure and because of difficult access. The vascular surgeon considered left renal revascularization, as the only alternative to the recovery and treatment of the patient. Without revascularization, the patient would certainly die soon.

Therefore, the patient was discharged from hospital on July 1st, 1994, with the following prescription: oral hydralazine 100 mg every six hours, oral clonidine 0.150 mg every six hours and AAS 200 mg/day.

FOLLOW-UP AT THE OUTPATIENT CLINIC

On the subsequent days, the patient stayed at home and rested, until July 17, when she returned to the emergency service with a new hypertensive crisis, in addition to dizziness, headache and dyspnea, with arterial pressure of 200/100 mmHg. The dose of antihypertensive drugs was increased and lab exams were requested.

On July 27, the patient was dyspneic and hypertensive again with arterial pressure equal to 300/130 mmHg. The lab exams revealed the following: Glycemia: 107 mg/dl, U.: 60 mg/dl. Cr.: 2.0 mg/dl and endogenous creatinine clearance of 14.9 ml/min. The increased dose of antihypertensive drugs was maintained and the patient was kept under observation for two days.

On August 4, 1994, the patient was admitted to Hospital Santa Casa, upon request of her family, for the surgery proposed during her first hospital stay.

CHALLENGE

Patient with long-lasting SAH, refractory to usual medication in the last few months, with administration of three antihypertensive drugs. In the last weeks, the patient was admitted to a cardiological ICU with acute pulmonary edema, event that occurred two more times.

After the etiology of SAH was confirmed and the angiographer considered that endovascular treatment was inappropriate for the patient, the clinician regarded the patient as unfit for the surgical procedure proposed by the vascular surgeon. We reached an impasse. The family was informed about the alternatives, that is, to resume clinical treatment or accept surgical intervention, and the decision was up to them.

This clinical case took place eight years ago.

Our proposal for therapeutic discussion includes some questions:

1. What would you do given the two proposed alternatives?

2. Would you recommend surgical treatment or the clinical one?

3. Should you opt for endovascular treatment, how would you solve the following problems?
a. What vascular access would you use in the presence of stenosing aortoiliac disease?
b. What is the actual success rate?
c. What is the 3-5 year follow-up for similar cases according to the literature?
d. What is the risk of immediate thrombosis of the renal artery?

4. Should you opt for direct conventional surgery, how would you solve the following issues?
a. How would you determine surgical risk?
b. What are the most appropriate survival alternatives?
c. Would you perform isolated endarterectomy of the left renal artery?
d. Would you perform extended endarterectomy of the aorta and left renal artery?
e. Would you opt for aortoiliac _ aortorenal bypass?
f. Would you use an alternative shunt (splenorenal)?
g. Would you suggest another surgical alternative?


Click here for the answer of the therapeutic challenge.

J Vasc Br - Official Publication of the Brazilian Society of Angiology and Vascular Surgery