HYPERTENSION
DEFINITION
Elevated blood pressure. Although this is frequently defined as a
systolic blood pressure greater than 160 mmHg and diastolic blood
pressure greater than 95 mmHg, such absolute figures must be
interpreted in terms of age and ethnicity.
TOXIC CAUSES
Anticholinergics
Corticosteroids: Androgens
Glucocorticoids
Mineralocorticoids (including black liquorice)
Oestrogen
Progesterone
Cyclosporin
Disulfram/ethanol interaction
Envenomations: Scorpions
Spiders: Lactrodectus species
Atrax species
Ethanol
Human Recombinant Erythropoeitin
Ketamine
Metals: Barium
Cadmium
Lead
Lithium
Mercury
Sodium
Thallium
Natural toxins e.g. ephedra alkaloids
Nicotine
Non-steroidal antiinflammatory drugs
Organophosphates
Selective serotonin-reuptake inhibitors
Sympathomimetics (includes pure alpha adrenoreceptor agonists):
Amphetamines
Caffeine
Clonidine (early stages)
Cocaine
Ephedrine
Epinephrine
Ergotamines
Levodopa
Metaraminol
Methoxamine
Monamine Oxidase Inhibitors
Norepinephrine
Oxymetazoline
Phencyclidine
Phenylephrine
Phenylpropanolamine
Pseudoephedrine
Tetrahydralozine
Withdrawal states
Note: Hypertension associated with Monoamine Oxidase Inhibitors is
usually a manifestation of a drug or food interaction. Commonly
implicated drugs include amphetamines, ephedrine, methyldopa and
tricyclic antidepressants. Any tyramine-containing food may be
responsible.
NON-TOXIC CAUSES
Coarctation of the aorta
Essential (idiopathic) hypertension
Hyperadrenergic states (e.g. agitation, exercise)
Hyperaldosteronism
Hypertensive disease of pregnancy
Hyperthyroidism
Phaeochromocytoma
Raised intracranial pressure
Renal parenchymal hypertension
Renovascular hypertension
CLINICAL FEATURES
The diagnosis of hypertension relies upon serial measurements of the
blood pressure using a properly sized cuff.
A toxic aetiology is suggested by the absence of other known causes of
hypertension, in a patient without previous history of hypertension.
The principal signs and symptoms observed are usually those of the
underlying intoxication. Severe elevations of blood pressure may be
complicated by hypertensive encephalopathy, intracerebral haemorrhage,
acute pulmonary oedema or myocardial infarction. Symptoms and signs
such as chest pain, dyspnoea, headache, nausea and vomiting, altered
mental status, visual disturbance, papilloedema, and decreased urine
output may reflect the development of such complications.
DIFFERENTIAL DIAGNOSIS
Artefactual hypertension
Anxiety
RELEVANT INVESTIGATIONS
Serum electrolytes, urea and creatinine
Electrocardiograph
Chest x-ray
CT scan of head if focal neurological signs, evidence of raised
intracranial pressure, or altered mental status without clear evidence
of a toxic ingestion.
Selective toxicological screening, as appropriate or in consultation
with the laboratory.
TREATMENT
Hypertension associated with chronic intoxications is usually mild and
resolves with identification and removal of the offending agent. In
the case of metal intoxications, specific therapy in the form of
chelation may be indicated.
Hypertension associated with the majority of acute intoxications is
mild and requires no more than simple observation until it resolves.
Hypertension associated with acute overdose of cocaine, amphetamines
or MAO inhibitors, or other generalised sympathetic stimulants, will
usually respond to sedation with benzodiazepines, e.g. diazepam 5 to10
mg (0.25 to 0.4 mg/kg in children) intravenously over 1 to 3 minutes.
Repeat this dose as needed, to a maximal total dose of 30 mg (5 mg in
children). Commonly, this is the only therapy necessary.
Where there is evidence of end-organ damage or where the diastolic
blood pressure remains above 120 mmHg despite benzodiazepine sedation,
specific therapy with one of the following short-acting parenteral
hypotensive agents should be instituted. Aim to carefully lower the
diastolic blood pressure to 100 mmHg.
Sodium Nitroprusside
Direct generalised vasodilator.
Dose: Commence continuous IV infusion at 0.5 µg/kg/min.
Titrate to blood pressure to a maximum dose of 10
µg/kg/min.
Must be administered under close observation, ideally with
continuous blood pressure monitoring.
Solution and tubing must be covered to prevent photodegradation.
Phentolamine
Competitive alpha-adrenoreceptor blocker.
Dose: 2.5 - 5 mg (0.05 - 0.1 mg/kg) IV every 5 minutes until
desired effect achieved.
Thereafter, continuous infusion of 25 to 100 mg/12 hours.
CLINICAL COURSE AND MONITORING
Hypertension following acute overdose is usually of short duration
(hours) and parallels the duration of other clinical features of the
intoxication. The blood pressure should be frequently measured,
especially during early phases of the intoxication. In severe cases,
especially where parenteral hypotensive agents are in use, continuous
monitoring via an arterial line is ideal. Very frequent non-invasive
blood pressure measurements are an alternative where such facilities
are unavailable.
During the hypertensive period, the patient should be closely observed
for evidence of the principle acute complications; aortic dissection,
intracranial haemorrhage, left ventricular failure and myocardial
infarction.
LONG TERM COMPLICATIONS
Long-term complications from hypertension of toxic aetiology are rare
but may include those resulting from intracranial haemorrhage, acute
myocardial infarction and retinal haemorrhage.
AUTHOR(S)/REVIEWERS
Author: Lindsay Murray
Senior Lecturer in Emergency Medicine
Queen Elizabeth II Medical Centre
Nedlands, WA 6009
Australia
Tel: 61-8-9346 1665
Fax 61-8-9346 1665
Email: Lindsay.Murray@health.wa.gov.au
Reviewers: Rio de Janeiro 9/97: J.N. Bernstein, E. Birtanov,
R. Fernando, H. Hentschel, T.J. Meredith, Y. Ostapenko,
P. Pelclova, C.P. Snook, J. Szajewski.
London, 15.03.98: T. Della Puppa, T.J. Meredith,
L. Murray, A. Nantel.