ihgm 27 jan 2015 - hkgs is she dozing off.pdf · complications •increase risk of coronary heart...

Why is she dozing off?

IHGM

27 Jan 2015

Speaker: Dr Karina Mak

Supervisor: Dr Jenny Lee

Background

• F/82

• NKDA

• Lives with family (husband and son)

• Walks with frame outdoor, holding onto furniture at home

Past medical history

• Old CVA with good recovery • Hyperlipidemia • Hypertension • DM on diet • CAD → refused CABG → coro 2009: dLMS 50-60% / mLAD 80% / dLAD

70% / RCA 100% • Tachybrady syndrome with SJM DDDR Apr 2013 • Gout • Post RAI hypothyroidism

Sept 2014

• Recurrent CVA in Sept 2014

• Slurring of speech

• No limbs weakness

• CT brain: left posterior parietal-occipital region subacute infarction; small vessels disease; right parietal lobe and right pons old infarct; bilateral CR lacunar infarcts

• Referred GDH x ADL and cognitive training

3 Oct 2014

• During training in GDH

• Husband c/o ?dozing off when sitting down after breakfast following long morning walk of ~2-3 hrs in recent 2 days

• Home BP at around 9-10am (post meds 1 hr)

–105-131/46-66 mmHg, P 59-60 bpm

• Impression: ?too tired or hypotensive

Medications

• Allopurinol 100mg daily

• Aspirin 160mg daily

• Atorvastatin 10mg daily

• Dipyridamole 25mg tds

• Famotidine 20mg bd

• Thyroxine 100mcg daily

• Amlodipine 5mg daily

• Lisinopril 10mg bd

• Metoprolol 25mg bd

• Isosorbide mononitrate 20mg bd

• Suggest to reduce duration of morning walk

• Reduce lisinopril to 10 mg daily

• Monitor BP and symptoms

• Review 2 weeks later

6 Oct 2014

• ?LOC while sitting before breakfast

• Drooling noted during episode

• No clenching / uprolling eyeballs / tongue biting

• No limbs twitching

• No incontinence

• Spontaneous recovery

• Patient was aware of husband calling her

• Clinical admission for investigation x recurrent near syncope

Physical examination

• BP 166/55 P 62

• No new focal neurological deficit

• No carotid bruit

• HS dual, no murmur

• Chest clear, abdomen unremarkable

Investigations

• CBC normal

• Electrolytes including Na/K/CaPO4/Mg normal

• Cr 130 static

• Spot h'stix 6.2

2015/1/30

Differential diagnosis

• Reflex syncope

– Vasovagal

– Situational

• Orthostatic hypotension

• Post prandial hypotention

• Cardiac syncope

– Arrhythmia

– Structural heart disease eg outflow obstruction

• Epilepsy

Progress

• No significant postural BP drop

• Consulted neurology

– Symptoms not suggestive of epileptic fit

–Not indicated for EEG

• In-patient holter ordered

Patient was well until 9 Oct morning...

• Found patient LOC at bedside chair after having breakfast ~2 hours ago

• BP 82/54 P 63

• No limbs twitching

• Spot h'stix 9.6

• Cardiac mon: no significant arrhythmia

• Regained consciousness after head down position

→ Ddx: orthostatic hypotension

post-prandial hypotension

• Norvasc off

• In-patient 24 hour BP monitoring ordered

• 24 hour BP recording and holter done from 9 Oct 2pm to 10 Oct 2pm

The next morning...

• New right hemiplegia and aphasia

• Power grade 0/5, right side neglect

CT brain

• Urgent CT brain:

– Interval development of hypodense infarction with loss of gray-white differentiation and sulcal spaces effacement in left occipitoparietal lobe, left frontal lobe and left temporal lobe.

–Mild mass effect onto the left lateral ventricle

–No significant MLS

• Aspirin and persantin withheld due to risk of haemorrhagic transformation in view of large infarct

• Plan to resume aspirin 2 weeks later

• Consulted cardiac x ?↑basal PPM rate

– To off betaloc

–but can't affect autonomic response and is unlikely to be benefit x acute drop in BP

– consider ↑basal rate if chronotropic insufficiency eg easy fatigue/malaise, ↓ET, SOB on exertion

7:48 - BP 182/69 p65

8:15 - BP 155/57 p62

8:45 - BP 121/55 p89

23:15 - BP 171/63 p72

00:15 - BP 101/50 p61

Medications

• Lisinopril 10mg daily

• Isosorbide mononitrate 20mg bd

• Metoprolol 25mg bd

• Allopurinol 100mg daily

• Thyroxine 100mcg daily

• Famotidine 20mg bd

Holter study report traced

• SR, PAC +ve, PVC +ve

• HR 59 – 92 bpm

• No non-capture beat

• Episodes of AF, A flutter

DDX

• Watershed infarction due to orthostatic hypotension or post-prandial hypotension

• Cardioembolic stroke

Orthostatic hypotension

• Normal physiology

• Epidemiology and risk factors

• Etiology

• Symptoms

• Diagnosis

• Complications

• Treatment

Normal BP response to standing

• Pooling of 500 - 1000mL of blood in lower extremities and splanchnic circulation

• Decrease in venous return diminished cardiac output and BP

• Baroreceptor reflex to limit the fall in BP

– Fall in SBP (5 to 10 mmHg)

– Increase in DBP (5 to 10 mmHg)

– Increase in pulse rate (10 to 25 bpm)

Baroreflex arc

2015/1/30

Prevalence

• In the Cardiovascular Health study,

– 4931 community-dwelling, non-institutionalized persons aged 65 years and older

– 18 % prevalence

– only 2% were symptomatic Rutan GH, Hermanson B, Bild DE, et al. Orthostatic hypotension in older adults. The Cardiovascular Health Study. CHS

Collaborative Research Group. Hypertension 1992; 19:508.

• Up to 60% of elderly patients in various in-patient series

Feldstein C, Weder AB. Orthostatic hypotension: a common, serious and underrecognized problem in hospitalized patients. J Am Soc Hypertens 2012; 6:27.

Epidemiology and risk factors

• More common in the elderly due to impaired baroreceptor sensitivity

Shibao C, Grijalva CG, Raj SR, et al. Orthostatic hypotension-related hospitalizations in the United States. Am J Med 2007; 120:975.

Hospitalization rates for

orthostatic hypotention

listed as primary discharge

diagnosis

• Use of antihypertensive significantly related to postural hypotension in the elderly

– In elderly hypertensive subjects withdrawal of anti-hypertensive therapy and institution of non-pharmacological treatment can over several months reduce the prevalence of orthostatic hypotension

Fotherby MD, Potter JF. Orthostatic hypotension and anti-hypertensive therapy in the elderly. Postgrad Med J 1994; 70:878.

Etiology

• Autonomic failure

• Volume depletion

• Medications

• Aging

• Cardiac pump failure (aortic stenosis, pericarditis/myocarditis, arrhythmias)

• Adrenal insufficiency

• Up to 1/3 of patients have no identified cause

Gupta V, Lipsitz LA. Orthostatic hypotension in the elderly: diagnosis and treatment. Am J Med 2007; 120:841

Aging

• Decrease in baroreceptor sensitivity

–Diminished response in the older patients to head-up tilt

– In both hypertensive and normotensive subjects

Tonkin AL, Wing LM. Effects of age and isolated systolic hypertension on cardiovascular

reflexes. J Hypertens 1994; 12:1083.

• Both the vagal (heart rate) and adrenergic (total peripheral resistance) components of the baroreceptor reflex became blunted with increasing age, each independent of the other

Huang CC, Sandroni P, Sletten DM, et al. Effect of age on adrenergic and vagal

baroreflex sensitivity in normal subjects. Muscle Nerve 2007; 36:637.

Symptoms

• Lightheadedness, dizziness

• Pre-syncope, syncope

• Weakness, fatigue

• Cognitive slowing, leg buckling, visual blurring

• "Coat-hanger headache": Neck pain and headache localized in the suboccipital, posterior cervical, and shoulder region

• Angina

• Stroke

Diagnosis

• A sustained reduction of

– systolic blood pressure of ≥ 20 mmHg or

–diastolic blood pressure of ≥ 10 mmHg

• within 3 min of standing or head-up tilt to ≥ 60°on a tilt table

Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of

orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res 2011; 21:69.

Delayed orthostatic hypotension

• 108 of 230 patients investigated with tilt table testing had abnormal test results.

• 54% occurred after 3 minutes of tilt

• 40% after 10 minutes

• These patients had milder abnormalities of sympathetic adrenergic function, ?a milder or earlier form of impairment

Gibbons CH, Freeman R. Delayed orthostatic hypotension: a frequent cause of

orthostatic intolerance. Neurology 2006; 67:28.

Postprandial hypotension

• BP fall within 1-2 hours after a meal

• Common in older subjects and in patients with diabetes and different types of autonomic failure

• Etiology not understood completely

– Inadequate sympathetic compensation to meal-induced pooling of blood in the splanchnic circulation

–Vasodilatation induced by insulin or vasoactive gastrointestinal peptides

Evaluation

• Medications

• History of volume loss (vomiting, diarrhea, fluid restriction, fever)

• History of CHF, malignancy, DM, alcoholism

• Signs of parkinsonism, peripheral neuropathy and dysautonomia (eg, abnormal pupillary response, constipation or erectile dysfunction)

• Anemia, dehydration

• ECG , echocardiogram

• Tilt table test to test adrenergic vasomotor function and cardiac sympathetic function

• EMG and NCS if suggestive of neuropathy (distal sensory loss, areflexia)

– Normal NCS does not exclude small-fiber neuropathy

• Fasting blood sugar, syphilis serology, serum protein electrophoresis

• Autonomic testing

–Cardiac response to deep breathing or Valsalva maneuvers and R-R interval

–Quantitative Sudomotor Axon Reflex Testing (QSART) / Thermoregulatory sweat test

• Detailed autonomic testing is not widely available

Complications

• Increase risk of coronary heart disease (HR 1.31) and all-cause mortality (HR 1.22)

Verwoert GC, Mattace-Raso FU, Hofman A, et al. Orthostatic hypotension and risk of cardiovascular disease in elderly people: the Rotterdam study. J Am Geriatr Soc 2008; 56:1816.

• Congestive heart failure (HR 1.54) Jones CD, Loehr L, Franceschini N, et al. Orthostatic hypotension as a risk factor for incident heart failure: the atherosclerosis

risk in communities study. Hypertension 2012; 59:913.

• Atrial fibrillation (HR 1.3) Fedorowski A, Hedblad B, Engström G, et al. Orthostatic hypotension and long-term incidence of atrial fibrillation: the Malmö

Preventive Project. J Intern Med 2010; 268:383.

• Predictive of ischemic stroke (HR 2.0)

Eigenbrodt ML, Rose KM, Couper DJ et al. Orthostatic hypotension as a risk factor for stroke: The Atherosclerosis Risk in Communities (ARIC) study, 1987–1996. Stroke 2000;31:2307–2313.

• Recurrent falls (RR 2.6)

Ooi WL, Hossain M, Lipsitz LA. The association between orthostatic hypotension and recurrent falls in nursing home residents. Am J Med 2000; 108:106.

Treatment

• Regardless of the cause, treatment of orthostatic hypotension is symptomatic

• Non-pharmacological

• Pharmacological

Non-pharmacological

• Withdraw offending medication (either substitution or discontinuation)

• Rise slowly from supine to sitting to standing position

• Avoid straining, coughing, and prolonged standing in hot weather

• Cross legs while standing


• Squat, stooping forward

• Raise head of bed 10 to 20 degrees

• Small meals and coffee in the morning

• Elastic waist high stocking

• Increase salt and water intake

• Exercise, eg, swimming, recumbent biking, and rowing


Pharmacological

• Fludrocortisone

– Synthetic mineralocorticoid to reduce salt loss and increase blood volume

– Initial: 0.1mg daily; Max: 1mg daily

– Increments of 0.1 mg every week until development of trace pedal edema

– Supine hypertension, hypokalemia, HF, headache

Hussain RM, Mcintosh SJ, Lawson J, Kenny RA. Fludrocortisone in the treatment of hypotensive disorders in the elderly.

Heart. 1996;76: 507-509

Chobanian AV, Volicer L, Tifft CP, et al. Mineralocorticoid-induced hypertension in patients with orthostatic hypotension. N

Engl J Med 1979; 301:68.

Pharmacological

• Midodrine

–Alpha-agonist with selective vasopressor properties

– Initial: 2.5 mg tds; Max: 10 mg tds

–Contraindication: Coronary heart disease, HF, urinary retention, thyrotoxicosis, acute renal failure

– Supine hypertension, piloerection, pruritus, paresthesia

Low PA, Gilden JL, Freeman R, et al. Efficacy of midodrine vs placebo in neurogenic orthostatic hypotension. A

randomized, double-blind multicenter study. Midodrine Study Group. JAMA. 1997;277: 1046-1051

Pharmacological

• Synergistic effects of fludrocortisone and midodrine

Pharmacological

• NSAIDs

–Block the vasodilating effects of prostaglandins

–GI & renal side effects

– Limited use in elderly

Pharmacological

• Caffeine

– Inhibit adenosine receptor induced vasodilatation

–200 mg every morning as 2 cups of brewed coffee or by tablet

–GI irritation, insomnia, agitation, nervousness

Pharmacological

• Erythropoietin

– Effective in a subgroup of patients with anemia and autonomic dysfunction

Hoeldtke RD, Streetan DHP. Treatment of orthostatic hypotension with erythropoietin. N Engl J Med. 1993;329:611-615

– Unknown exact mechanism of action, ?due to increased red cell mass and blood volume

– Parenteral route of administration

– Contraindication: uncontrolled HT

– Hypertension, stroke, myocardial infarction

Concurrent supine hypertension

• Maximize nonpharmacologic measures

• Use drugs that might raise the supine blood pressure only to the degree that permits the patient to ambulate

• Transdermal nitroglycerin patch (0.025 to 0.1 mg/hour) at night

Shannon J, Jordan J, Costa F, et al. The hypertension of autonomic failure and its treatment. Hypertension 1997; 30:1062

Jordan J, Shannon JR, Pohar B, et al. Contrasting effects of vasodilators on blood pressure and sodium balance in the hypertension of autonomic failure. J Am Soc Nephrol 1999; 10:35

• Short-acting antihypertensive agents (eg, captopril, hydralazine)

Back to our patient

• MFAC 1/7, ADL D, MBI 0/100

• Transferred to TPH

• Referred MSW x placement

• Discharged home eventually

• Admitted 3 weeks after d/c x chest infection/ CD diarrhea

• Eventually succumbed

Take home message

• Orthostatic hypotension is not uncommon in the elderly

• Can cause debilitating complications

• Treatment is symptomatic

• Thanks

ihgm 27 jan 2015 - hkgs is she dozing off.pdf · complications •increase risk of coronary heart...

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