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DESCRIPTION
Increased diastolic and/or systolic blood pressure at rest defines hypertension.
- Adults and adolescents: greater than 160 mm Hg systolic or 90 mm Hg diastolic
- Children 5 to 10 years of age: systolic blood pressure greater than 120 mm Hg
- Children 1 to 5 years of age: systolic blood pressure greater than 110 mm Hg
- Infants 6 months to 1 year of age: systolic blood pressure greater than 100 mm Hg
PATHOPHYSIOLOGY
- Common toxicologic mechanisms for persistent hypertension include excessive stimulation of alpha- and/or beta-adrenergic receptors.
- The hypertensive response may result from direct receptor stimulation by a toxicant, stimulation of endogenous catecholamine release, or production of a generalized physiologic response (e.g., pain) that produces hypertension.
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DIFFERENTIAL DIAGNOSIS
Toxicologic Causes
Further information on each poison is available in SECTION IV, CHEMICAL AND BIOLOGICAL AGENTS.
- Cocaine. Additional findings may include tachycardia, hyperthermia, agitation, delirium, seizures, track marks, nasal septum erosion or perforation, and rhabdomyolysis.
- Amphetamines. Additional findings may include tachycardia, hyperthermia, agitation, psychosis, seizures, track marks, and rhabdomyolysis.
- Other sympathomimetic agents (ephedrine, phenylpropanolamine, beta-agonist bronchodilator, theophylline). Additional findings may include headache, hypokalemia, tremor, tachycardia, and agitation.
- Anticholinergic agents (diphenhydramine, scopolamine, jimsonweed, hydroxyzine, phenothiazine, dramamine, etc.). Additional findings include tachycardia, dry flushed skin, dilated sluggish pupils, diminished bowel sounds, hyperthermia, hallucinations, agitation, and delirium.
- An alpha-2-adrenergic agonist (clonidine, imidazoline decongestants) may cause initial hypertension, bradycardia, and CNS depression, followed by apnea and hypotension.
- Monoamine oxidase (MAO) inhibitors may cause hyperthermia, hypertension, and altered mental status.
- LSD, phencyclidine, or hallucinogens of any type may cause rhabdomyolysis.
- Ergot alkaloids (ergotamine and dehydroergotamine) often cause signs of vasoconstriction such as pallor or cyanosis of lips and extremities.
- Nicotine causes initial hypertension, usually associated with vomiting, tachycardia, urinary incontinence, lethargy, seizures, and coma.
- Mushrooms may produce hallucinogenic or anticholinergic effects.
- Withdrawal from alcohol, opioids, or sedative-hypnotic agents is associated with a history of abstinence, tachycardia, and hypertension.
Nontoxicologic Causes
Nontoxicologic causes of hypertension include essential hypertension, secondary hypertension (e.g., renal artery stenosis and pheochromocytoma), anxiety (a diagnosis of exclusion), and severe pain.
SIGNS AND SYMPTOMS
Physical signs may help reveal the poison involved when they occur in the setting of hypertension.
Vital Signs
- Tachycardia may indicate sympathomimetic or anticholinergic toxicity, or withdrawal from alcohol or a sedative-hypnotic agent.
- Bradycardia may develop as a physiologic compensation.
- Hyperthermia may indicate intoxication with sympathomimetic, anticholinergic, or MAO inhibitor, drugs, or agents that cause prolonged seizures.
HEENT
- Dilated pupils suggest sympathomimetic, anticholinergic, or hallucinogen toxicity.
- Small pupils may indicate clonidine or nicotine effect.
- Nystagmus may indicate phencyclidine intoxication.
- A perforated nasal septum may indicate chronic drug abuse.
Dermatologic
- Flushed dry skin suggests an anticholinergic agent.
- Pale, sweaty skin may be associated with sympathomimetic drugs or cholinergic agents.
- Track marks suggest chronic parenteral drug abuse.
- Marked peripheral vasoconstriction may indicate ergot alkaloid toxicity.
Cardiovascular
- Tachydysrhythmia may be a sign of toxicity from sympathomimetic drugs, anticholinergic agents, or MAO inhibitors.
- Bradycardia and hypertension may occur early in the course of clonidine or imidazoline decongestant intoxication.
- Transient hypertension followed by hypotension may occur secondarily to severe intoxication with bretylium, cocaine, amphetamines, MAO inhibitors, tricyclic antidepressants, anticholinergic drugs, beta-adrenergic agonists, and nicotine.
Pulmonary
Respiratory depression may indicate clonidine or imidazoline decongestant intoxication.
Gastrointestinal
Diminished bowel sounds suggest an anticholinergic agent.
Renal
Urinary retention suggests an anticholinergic agent.
Fluids and Electrolyte
Hypokalemia suggests a beta-receptor agonist.
Musculoskeletal
Rhabdomyolysis often indicates stimulant or hallucinogen abuse.
Neurologic
- Hallucinations and delirium suggest an anticholinergic agent or abuse of a stimulant or hallucinogen.
- Anxiety, tremor, and seizures suggest theophylline or withdrawal from alcohol or sedative-hypnotic drugs.
- Coma and seizures suggest MAO inhibitors, nicotine, or possible intracranial bleeding due to hypertension.
PROCEDURES AND LABORATORY TESTS
Essential Tests
ECG and continuous cardiac monitoring should be done to detect:
- tachydysrhythmia, caused by sympathomimetic and anticholinergic drugs.
- bradycardia, which may occur as a reflex effect, or with clonidine or imidazoline decongestant poisoning.
- myocardial ischemia.
Recommended Tests
- Serum electrolytes, BUN, and creatinine assist in the assessment of metabolic acidosis and renal insufficiency; hypokalemia is associated with adrenergic agents such as beta-agonist or theophylline.
- A urine toxicology screen should be obtained from patients with persistent hypertension of unknown cause.
- Serum acetaminophen and aspirin levels in an overdose setting should be measured to detect an occult overdose with analgesic medications.
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- Intravenous access should be established.
- The dose and time of exposure should be determined for all substances involved.
- Specific treatment (e.g., sedation, nitroprusside) should be initiated while continuing supportive care.
DIRECTING PATIENT COURSE
Health-care provider should call the poison control center when:
- cause of hypertension is unknown.
- coingestant, drug interaction, or underlying disease presents unusual problem.
Admission Considerations
Nearly all patients with hypertension need hospitalization to assess effectiveness of treatment and underlying cause.
DECONTAMINATION
Out of Hospital
Induction of emesis is not recommended because altered mental status may develop.
In Hospital
- Gastric lavage should be performed in pediatric (tube size 24-32 French) or adult patients (36-42 French) for substantial ingestion presenting within 1 hour of ingestion or if serious effects are present.
- One dose of activated charcoal (1-2 g/kg) should be administered without a cathartic if a substantial ingestion has occurred within the previous few hours.
ADJUNCTIVE TREATMENT
Control of Blood Pressure
Often blood pressure will respond favorably to control of agitation. A benzodiazepine familiar to the clinician should be administered while monitoring the patient's airway closely.
- Diazepam. Adult dose is 5 to 10 mg intravenously, pediatric dose is 0.2 to 0.5 mg/kg intravenously, repeating doses at 5-minute intervals, titrating to effect.
- Lorazepam. Adult dose is 1 to 2 mg intravenously, pediatric dose is 0.05 mg/kg, with doses repeated at 5-minute intervals, titrating to effect.
In general, antihypertensive treatment should be avoided with the following poisons because hypertension is usually not life threatening and resolves with supportive care and hypotension may develop rapidly: clonidine, imidazoline decongestants, bretylium, cocaine, amphetamine, MAO inhibitors, tricyclic antidepressants, anticholinergics, beta-adrenergic agonists, or nicotine.
To control hypertension that is severe and persistent (diastolic pressure more than 130 mm Hg not responsive to sedation) or complicated by end organ effects (CNS bleed, congestive heart failure, myocardial ischemia, or aortic dissection), a short-acting titratable agent such as nitroprusside is recommended.
- Adult and pediatric dose is 0.5 µg/kg/min by continuous infusion, which should be increased by 0.25 to 0.5 µg/kg/min every 5 minutes, titrating the dose until the desired effect is reached.
- An infusion rate over 10 µg/kg/min is rarely required and may produce cyanide toxicity.
- Nitroprusside should be tapered gradually in order to avoid rebound hypertension.
- Intraarterial pressure monitoring is recommended for persistent hypertension requiring nitroprusside treatment.
If hypertension is accompanied by marked tachycardia, refer to SECTION II, Tachycardia chapter.
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PATIENT MONITORING
Cardiac and respiratory function should be monitored continuously.
EXPECTED COURSE AND PROGNOSIS
Toxic causes of hypertension usually respond to treatment without sequelae unless intracranial hemorrhage occurs before treatment.
DISCHARGE CRITERIA/INSTRUCTIONS
Asymptomatic patients with transient, mild hypertension may be discharged after decontamination and a 6-hour observation period and psychiatric evaluation, if needed.
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ICD-9-CM 972Poisoning by agents primarily affecting the cardiovascular system.
See Also: SECTION II, Tachycardia chapter, and SECTION III, Nitroprusside chapter.
RECOMMENDED READING
Hessler R. Cardiovascular principles. In: Goldfrank LR, et al., eds. Goldfrank's toxicologic emergencies, 6th ed. Norwalk, CT: Appleton & Lange, 1998.
Author: Katherine M. Hurlbut
Reviewer: Richard C. Dart