Cholesterol pneumonia

Chief Complaint: Right arm numbness and weakness

History of Present Illness: A 53-year-old woman with a history of diabetes, hyperlipidemia, and hypertension was in her usual state of health until the evening before admission when she noted the sudden onset of numbness and weakness of her entire right arm while watching television. She could move the arm without difficulty, assumed she had leaned on it, causing it to "fall asleep;" and she went to bed.

The numbness and weakness were present when she awoke the next day, but she went to work. During the morning, she developed the sudden onset of a bilateral frontal pressure headache, unlike her typical migraine symptoms. She also felt disoriented and had difficulty concentrating, particularly when doing simple calculations.

At midday, she felt diffusely weak and lightheaded and fell to the floor without loss of consciousness. She was transported to the Miriam Hospital Emergency Department.

Review of Symptoms: She denied fevers, recent trauma, vision changes, speech or gait difficulty, cough, chest pain, dyspnea, or palpitations.

Prior Medical History: The patient reported a history of hypertension, noninsulin dependent diabetes mellitus, hyperlipidemia, migraine headaches, and irritable bowel syndrome. She had been treated as an outpatient for pneumonia 1 month earlier. Her surgical history included a total abdominal hysterectomy and bilateral oophorectomy, bladder suspension, appendectomy, and tonsillectomy.

Medications: Metformin 1000 mg PO qhs, acetaminophen and ibuprofen prn for headache.

Allergies: Rash with both penicillin and IV dye.

Social History: She worked as a cashier at a sandwich shop. She had no medical insurance and had difficulty paying for antihypertensive and cholesterol-lowering medications. She had a 50 pack-year smoking history, but quit smoking 2 months earlier. She denied alcohol and drug use.

Family History: Positive for coronary artery disease and myocardial infarction, but no history of cancer or stroke.

Physical Exam:

Temp = 36.1C BP = 193/83 HR 72 RR 18 SaO^sub 2^ 98% room air

General: Mildly lethargic but well appearing.

HEENT: No carotid bruit, jugular venous distension, or lymphadenopathy.

CVS: Regular rate and rhythm, normal S1/S2. II/VI systolic ejection murmur at left upper sternal border.

Lungs: Clear to auscultation bilaterally.

Abdomen: Normoactive bowel sounds, soft, nontender, no organomegaly.

Extremities: Trace lower extremity edema bilaterally, palpable pedal pulses.

Neuro: Normal cognition, speech, and language. Cranial nerves intact. Normal gait and cerebellar function. Sensation to light touch decreased in the right arm extending from shoulder to fingertips. Sensation to pinprick and temperature intact. Deep tendon reflexes, motor strength, and fine motor movements intact throughout. Toes downgoing bilaterally.

LABS:

CBC:

WBC count: 10,200 per mL

Hemoglobin: 14.7 g/dL

Hematocrit: 41.8%

Platelet count: 203,000 per mL

Chem 7:

Sodium: 134 mmol/L

Potassium: 4.7 mmol/L

Chloride: 101 mmol/L

Bicarbonate: 24 mol/L

BUN: 19 mg/dL

Creatinine: 0.9 mg/dL

Glucose 290 mg/dL

Cardiac enzymes:

Creatine kinase: 151 IU/L

Troponin I:

Hemoglobin A^sub 1^C: 10.7%

Fasting lipid panel:

Total cholesterol: 251 mg/dL

Triglycerides: 488 mg/dL

High-density lipoproteins: 34 mg/dL

Low-density lipoproteins: unable to quantify

Urinalysis:

Glucose: 1000

Protein: 100

EKG:

Normal sinus rhythm, rate 61 Noncontrasted computed tomography of the brain: no evidence of acute bleeding or mass effect

Hospital Course: While in the emergency department, the patient received 1 liter normal saline, metoprolol 25 mg orally, and ketorolac 15 mg intravenously. Repeat blood pressure was 179/86 mm Hg. She was admitted to the medicine service and placed on aspirin and metoprolol. Neurology consult was obtained, as were several imaging studies. Carotid Doppler studies showed a defect in the medial wall of the left internal carotid artery, suggesting subintimal hemorrhage, occupying one-third of the vessel lumen and extending 1.5 to 2 cm distally from the bifurcation. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) of the brain showed multiple acute embolie infarcts (left frontal, left parietal, and left posterior temporal in both the white matter and at the gray-white junction), as well as a dissection flap of the left internal carotid artery starting 2 cm from the bifurcation and extending 11 mm. 2-D echocardiography showed mild left ventricular hypertrophy and an ejection fraction of 65%.

Anticoagulation was initiated with heparin as well as warfarin. Vascular surgery consult was obtained, but no surgical intervention was recommended. Renal MRA was obtained to evaluate for fibromuscular dysplasia, but showed no significant stenosis. The right arm paresthesias gradually resolved, and the patient was discharged on hospital day 7 on warfarin.

DISCUSSION:

1. What are the risk factors for cervical artery dissection?

Dissection can occur in both the carotid and vertebral arteries. Carotid artery dissection typically affects the extracranial portion of the vessel. The pharyngeal segment (extending from the carotid bifurcation to its entry at the petrous portion of the temporal bone) is mobile, and therefore susceptible to injury. Precipitating events often involve hyperextension and rotation of neck, such as whiplash injuries, but are also associated with benign events such as coughing or sneezing. The role of chiropractic manipulations is controversial. A precipitating event is often not identified, with spontaneous dissections described in more than half of patients in several case series. The role of common risk factors for vascular disease, such as smoking and hyperlipidemia, has not been systematically studied. History of recent respiratory tract infection and migraine headaches have also been proposed as risk factors.

At the tissue level, a defect in the structure of the arterial wall seems to be required, but is not well understood. Not surprisingly, connective tissue disorders such as Marfan's syndrome, osteogenesis imperfecta (type I), and Ehler-Danlos syndrome (type IV) carry an increased risk for cervical artery dissection, but only 5% of dissections can be attributed to these disorders. Fibromuscular dysplasia appears to be the precipitant in about 15% of cases.

Cervical artery dissection can occur in patients of any age. Carotid arteries are involved more commonly than vertebral arteries. The overall incidence for carotid artery dissection is estimated at 2.5 to 3 per 100,000. It most commonly affects those in the fifth decade of life and is a significant cause of stroke (10% to 25% of cases) in young and middle-aged adults.

2. How do the signs und symptoms of cervical artery dissection manifest?

Stroke or transient ischemic attack was the most common presenting feature in one series of 126 patients. With carotid artery involvement, the classic symptom triad includes unilateral head, face, or neck pain associated with an incomplete Homer's syndrome, followed by cerebral or retinal ischemia. However, this symptom complex appears in less than a third of cases. Unilateral pain occurs in approximately half of patients; headache is usually unlike prior migraine symptoms. Cranial nerve palsies, typically affecting the lower cranial nerves, arise in roughly 12% of carotid artery dissections. In some case series, neck pain was more frequently associated with vertebral artery dissection. Ischemic symptoms develop in the vast majority of patients, especially if the dissection is not recognized early in its course.

3. What imaging studies are most useful in the diagnosis of cervical artery dissection?

Ultrasound with Doppler color flow imaging is probably the quickest, most available imaging modality for initial evaluation of suspected cervical artery dissection, with abnormal flow visualized in more than 90% of cases. Magnetic resonance angiography, which has largely replaced conventional angiography, has sufficient resolution to show dissection flaps and intramural hematoma. CT angiography can also image the arterial lumen, but is not as well studied.

4. What is the management of cervical artery dissection?

Anticoagulation - typically intravenous heparin followed by warfarin therapy - is essential to prevent thromboembolic complications, although it has never been studied in a randomized trial. Warfarin therapy, with a goal INR of 2 to 3, is continued for 3 to 6 months with repeat imaging at 3-month intervals, until recanalization is evident. Most dissections heal spontaneously within that time, and most patients recover with no or minimal neurologic deficits. Intra-arterial thrombolytics may be indicated for totally occluded vessels, and surgical intervention may be required for patients with continuing ischemia despite optimal medical therapy. Endovascular stenting is also gaining popularity but is not well studied.

REFERENCES

Bassi P, et al. Cervical cerebral artery dissection. Neural Sd. 2003;24:S4-S7.

Dziewas R, et al. Cervical artery dissection. J Neurol. 2003;250; 1179-84.

Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. NEJM 2001;344-.898-906.

MARY HOHENHAUS, MD

CORRESPONDENCE:

Mary Hohenhaus, MD

E-mail: mhohenhaus@lifespan.org

ACKNOWLEDGEMENTS:

Michael Blundin, MD, Kwame Dapaah, MD, Jeffrey Mazer, MD

Copyright Rhode Island Medical Society Dec 2005
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