Consultations

Hypertension

History

HPC :
Symptoms of uncontrolled hypertension – chest pain, visual disturbance, headache, haematuria, weakness in
limbs?
Symptoms of end organ damage – chest pain, palpitations, dyspnoea, ankle swelling, neurological symptoms?
MACROVASCULAR

• CAD – chest pain, breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea, ankle oedema
• Peripheral vascular disease – cold extremities, claudication
• Cerebrovascular disease – neurological deficit, visual disturbances

MICROVASCULAR

• Retinal disease – visual disturbance
• Renal disease – nausea, lethargy, ankle swelling, pruritus

– Symptoms of underlying medical disorder causing secondary hypertension

o Hyperthyroidism – sweating, anxiety, palpitations, weight loss, heat intolerance, tremor, diarrhea
o Acromegaly – change in appearance, high blood sugars – polyuria/polydipsia, sweating,
headaches, glove and shoe size, visual field disturbance, joint pains, carpal tunnel
o Cushing’s syndrome – abdominal striae, weight gain, steroid use, proximal muscle weakness,
centripetal fat, bruising thinned skin
o Conn’s syndrome – weakness, lethargy, muscle cramps (hypokalemia)
o Phaeochromocytoma – palpitations, sweating, weight loss
o Renal disease – urinary symptoms, obstructive symptoms, uraemia – lethargy, nausea, pruritus

– White coat syndrome anxiety ever measured blood pressure at home?

Relevant medical and family history

– Conditions which predispose to HTN – thyroid disease, kidney disease, hormonal disease
– Complications of HTN – stroke, heart disease, kidney disease, heart failure, peripheral vascular disease
– Family history – essential hypertension, endocrine disease MEN 2, heart disease and risk factors
hyperlipidemia

Medications and interactions

– NSAIDs – sodium retention resistance to hypertension treatment

o Decongestants and nasal sprays

– Oral contraceptive drugs
– Corticosteroids
– Ciclosporin – progressive HTN
– Recreational drugs – cocaine, ecstasy, MDMA, amphetamines, anabolic steroids

– Compliance to prescribed medication and adverse reactions

o Thiazide – impotence, gout, headache
o CCB – ankle swelling, constipation
o ACE – cough

Social Issues

– Alcohol excess and obesity
– Diet – caffeine and salt intake
– Smoking risk factor to CHD
– RCD
– Occupation
– Life stressors or recent life events

Formulating plan of action

– Explain diagnosis of HTN, although not serious control of BP, is essential to prevent serious complications
like heart disease, stroke, kidney disease and peripheral vascular disease.
– There are two types of HTN primary and secondary

o Third type called white coat hypertension can be excluded by monitoring blood pressure at
home regularly for a week or 24hour ambulatory blood pressure monitor

– Blood test investigations will help identify an underlying cause
– An ECG to look for evidence of heart involvement (LVH, LV strain pattern)
– Advise on lifestyle factors and modifications
– Follow-up appointment to discuss results and monitor blood pressure long-term

Causes of secondary hypertension:
Renal
– Renal parenchymal disease
– Renovascular disease
– Chronic kidney disease
Endocrine
– Hyperthyroidism
– Acromegaly
– Cushing’s syndrome
– Conns syndrome – Hyperaldosteronism (decrease renin aldosterone ratio, hypokalemia)
– Phaeochromocytoma – plasma metanephrines, 24hr urinary metanephrines
– Adrenal Hyperplasia
Cardiorespiratory
– Coarctation of aorta – cold legs and feet, muscle weakness in legs, cramps, headaches, nosebleeds
– Obstructive Sleep Apnea
– HOCM – Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy (LVH) and
increased risk for sudden cardiac death.
– Thus, hypertension may exacerbate the phenotype of HCM and blood pressure control is important to
prevent worsened LVH and diastolic dysfunction in this population.
Drug-induced
– Steroids
– NSAIDs
– COCP
Treatment
– 10year CHD risk Qrisk score > 10%

o Age, gender, smoking, BMI, Total and HDL Cholesterol, systolic blood pressure

– Treat all with pre-existing CVD, diabetes, familial hypercholesterolemia or renal disease
Targets
– Non diabetic: 140/90
– Diabetic: 130/90

2. Headaches
Exclude serious causes of headache before diagnosis of primary headache type made

HPC:
– Onset – sudden or gradual
– Progression – worsening severity
– Previous Episodes – chronic or acute
SOCRATES
Site – where did the pain first start
– Tension headache – bilateral pain across foreahead
– Migraine – unilateral and fronto-parietal, can be bilateral or global
– Cluster headache – unilateral and retroorbital, lacrimation
– Temporal arteritis – temporal in location, pain on combing hair, chewing jaw claudication
– SAH and meningitis – occipital, meningism (sudden onset – SAH, associated features – meningitis)
– Trigeminal neuralgia – severe pain in cheek or lower jaw, electric shock like sharp shooting pain, unilateral
97%, short duration second to minutes, recurrent in day, episodic remission for weeks to months, provoked by
light touch to face, chewing, talking, cold

o Autonomic associated features: lacrimation, conjunctival injection, nasal congestion or
rhinorrhea, eye lid oedema, ptosis, facial sweating
o Trivial stimuli: washing, dressing, smoking, talking, brushing teeth
Character

– Describe the pain to me!

o Throbbing? – migraine
o Sharp?
o Shooting?
o Stabbing?
o Tight band like? – tension headache

Radiation

– Pain radiates to neck and shoulders – meningism?
Exacerbating / Relieving Factors
– Analgesia – how often used? For how long? Overuse?
– Precipitating factors – hunger, sleep deprivation, sounds and bright lights, menstruation, sexual activity
– Exacerbating factors – alcohol in cluster headaches

o Worse when bending forward, straining or coughing? – Increased ICP / SOL? Benign
intracranial hypertension, normal pressure hydrocephalus (elderly – ataxia, urinary incontinence,
memory impairment)
o Light, noise, certain smells and movement – migraine

– Relieving factors

o Sleep, quiet, darkened room
o Analgesia – frequency of use more than 3x week?

Timing – Duration and Temporal pattern
– Headache duration? – Migraine 12-24 hours may persist up to 72 hours

o Cluster headache minutes to hours (every night before bedtime for weeks to months then –
remission for months)

– Temporal pattern

o Tension headache worse towards end of the day
o Pain worse on waking up in morning – raised ICP
o Pain wake you up from sleep? Does it occur at same time each day? – Cluster Headache

Associated Symptoms
– Aura – feature of migraine 30% patients

o Zig zag lines or flashing lights – fortification spectra
o Areas of loss of vision with bright edges – Scintillating Scotoma
o Positive sensory, motor, olfactory aura

– Photophobia/ phonophobia / osmophobia – migraines (senisitivity to light, sounds, smell, movement)
– Limb weakness – CVD or migraine
– Visual disturbance

o Sudden loss of vision – amaurosis fugax, giant cell arteritis, optic neuritis, retinal migrain,
carotid dissection (headache, facial or eye pain, neck pain, horners ipsilateral)
o Diplopia – pituitary masses or apoplexy
o Visual disorders – refractive errors can cause headaches last visited optician?

§ Acute angle glaucoma – red eye and unilateral headache

– Fever, neck stiffness, photophobia and rash – Meningitis
– Scalp tenderness and jaw claudication – GCA
– Lacrimation, rhinorrhea, sweating, drooping of eyelid, conjunctival suffusion – Cluster headache, trigeminal
neuralgia
– Ear, tooth, facial and neck pain – referred headache e.g. sinusitis

o Recent ear, eye, throat or sinusitis infection?

– Nausea and vomiting – meningitis, ICP / profuse projectile vomiting – SOL
– Confusion, béhavioral change and seizures – Encephalitis, SOL brain tumours
– Constitutional symptoms – weight loss, anorexia, night sweats – neoplastic disease

o Fever – infection
o Proximal muscle weakness – polymyalgia rheumatic/ GCA

Severity and Progression
– Scale 1 – 10
– Progression – is the headache the same as when it first started, worse or better?

Alarm symptoms

– Sudden onset reaching maximal intensity within minutes – SAH

o Change in nature of headache chronic headaches but severe episode out of keeping with
chronic episodes – SAH

– Progressive increase in severity of headache – Space Occupying Lesion, Subdural Haemorrhage,
Analgesia overuse headache
– Focal neurological symptoms other than typical visual or sensory aura – SOL or Vascular Lesion
– Change in conscious levels
– New headache in high risk groups – hx of malignancy (cerebral metastasis), HIV (opportunistic infection/
lymphoma), pregnancy (OCP-venous sinus thrombosis, pituitary apoplexy)
– Recent head injury, fall or neck injury?

Frequency and analgesia – Bried Headache Screen

1. How often do you get severe headaches – severe enough to impair daily functioning? – Migraines
2. How often do you get milder headaches? – medication overuse
3. How often do you take painkillers for headaches? – medication overuse headaches more than 3x a week)

Relevant Medical and Family History
– Personal history of

o Migraines
o Autosomal dominant polycystic kidney disease
o Previous malignancy
o HIV and immunosuppression
o Depression and anxiety
o Bleeding disorders or coagulopathies – hemorrhage or venous sinus thrombosis

– Family history

o SAH
o Migraine
o Thrombosis
o CTD – Marfans, Ehler Danlos

Medications
– Headache causing medication

o Thiazides
o CCB
o Nitrates
o Dipyridamole
o Tetracyclines
o Steroids – Idiopathic Intracranial Hypertension

– Anticoagulants or antiplatelets patients with thrombophilia
– What analgesics type – dose – frequency à frequent headaches despite use of analgesics = analgesia
overuse headache à confirmed if headache subsides within 2 months on discontinuing analgesics
– OCP – increased risk of venous sinus thrombosis (further risk if migraine with aura)
– RCD use – cocaine withdrawal – SAH

Social

– Occupation? Particular stressors at work, life stressors?

o Impact of headaches of daily living and work

– Recent travel abroad
– Smoking history cessation attempts nicotine withdrawal
– Caffeine history
– ICE

Plan of Action

– Explain that in any sudden onset headache out of keeping with previous history of headaches warrants
further investigations and full clinical examination
– Investigations include:

o Blood tests including:

§ full blood count to check for infection
§ ESR and CRP to exclude GCA
§ Pituitary hormone profile in cases of pituitary adenoma or apoplexy

• • • Prolactin
    • TSH and T4
    • Cortisol and ACTH
    • LH and FSH
    • IGF, oral glucose suppression test

§ Consider thrombophilia screen in patients with likely cerebral venous thrombosis
symptoms – Assays for: Activated protein C resistance, Protein S/C deficiency, Factor V
Leiden PCR, Antithrombin, anti-cardiolipin antibody, lupus anticoagulant

o Imaging studies include:

§ If history of injury plain x-ray of cervical spine and skull
§ CT scan of head in case of

• • • New sudden onset headache or change in character of headache
    • Clinical suspicion of SOL – postural headache, seizures, focal neuro,
      papilloedema on examination (95% sensitivity within 12 hours sx onset)
    • Confusion, behavioural change and impaired consciousness

§ MRI in suspected pituitary disease with CONTRAST T2/gadolinium
§ Magnetic Resonance Venography – Cerebral Venous thrombosis

• • • Angiography (CT, MRI, digital subtraction) – integrity of extracranial vasculature –
      carotid or vertebral dissection à performed after positive scan for SAH on CT or
      xanthochromia in CSF to detect presence and site of intracranial aneurysms
      amenable to neurosurgical intervention

o Lumbar puncture

§ Opening pressure – raised ICP in SOL / idiopathic intracranial hypertension
§ Appearance: turbid, cloudy – infection
§ Cell count: red cell, white cell count and differentials
§ Biochemistry: protein and glucose
§ Microbiology: Ziehl Nielson stain for tuberculosis, Gram Stain, India ink for Cryptococcus
and Cryptococcal antigen
§ Xanthochromia – SAH à atleast 12 hours from symptom onset (bilirubin formation) 75%
sensitivity up to 2 weeks post hemorrhage
§ Simultaneous blood sample for serum glucose, total protein and bilirubin at time of LP

o Throat swab, stool culture, viral PCR – bacterial or viral meningitis
o Temporal artery biopsy – within 7 days of starting steroids for definitive diagnosis (skip lesions
common)

SAH Treatment
– Adequate analgesia
– Prevention of vasospasm induced ischaemia – nimodipine and hydration
– Maintenance of normal blood pressure – nimodipine and labetolol
– Prevention of rebleeding – neurosurgical interventions – endovascular clipping or coiling

Migraine Medical Management
– Treatment of acute attackes

o Simple analgesia – paracetamol, NSAIDs
o Anti-emetics – ondansetron, cyclizine
o Triptans – sumatriptan
o Ergot derivatives – ergotamines if contraindication to triptans

– Prevention of further attacks – 3 or more migraines per month

o Propanolol or atenolol (first-line)
o Amitriptyline, Topiramate, Sodium Valproate
o Promethazine