Guideline on the Management and

Investigation of Hypertension

Renal Unit
Royal Hospital for Sick Children
Yorkhill Division

Please note: The following guidelines have not been assessed

according to the AGREE (Appraisal of Guidelines for Research and
Evaluation) criteria. This will take place at the next review of this
guideline.

Hypertension Version: 1.1 Page 1 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
 Contents Page Number(s)
1. Introduction 2
2. Definition of Hypertension 2-3
3. Causes of Hypertension in Infants and Children 3
4. Investigation of Hypertension 4
4.1 Initial Investigations 4
4.2 Secondary Investigations 4
4.3 Renal Vein Renin Sampling 4-5
5. The Management of Hypertension 5-6
6. Neonatal Hypertension 6
7. Causes of Neonatal Hypertension 6
8. Investigation of Neonatal Hypertension 7
9. The Management of Neonatal Hypertension 7
9.1 Emergency Treatment 7
9.2 Standard Treatment 7
10. Future Guideline Development 7
Appendix I: Drug Therapy – Oral 8
Appendix II: Intravenous Drug Therapy 9
Appendix III: Reference Ranges: Males 1-17yrs 10
Appendix IV: Reference Ranges: Females 1-17yrs 11
Appendix V: Reference Ranges: Males & 12
Females <1 year
Appendix VI: Reference Ranges: Neonates 13

1. Introduction
The following guideline has been developed and is regularly reviewed by
clinicians within the Renal Unit at Yorkhill. These guidelines are based on
current evidence and best practice relating to the Investigation and
Management of Hypertension in Neonates, Infants and Children. These
guidelines are intended for use by clinicians and nursing staff. For further
discussion of this guideline, please contact a consultant within the Renal
Unit.

2. Definition of Hypertension
As with height and weight there are specific percentiles for blood pressure
measurement available for both sexes. Blood pressure varies according to
both age and height with published values available (Pediatrics
1996;98:649-658) which are included in the appendices.

The “gold standard” for blood pressure measurement is mercury

sphygmomanometry and this should be used to confirm hypertension
found using automated devices.

Hypertension Version: 1.1 Page 2 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
An appropriate sized cuff must be used. The width of the cuff should cover
at least 75% of the upper arm from the acromion to the olecranon,
leaving sufficient space at the antecubital fossa to allow application of the
bell of the stethoscope. The diastolic blood pressure is recorded when the
sound disappears (5th Korotkoff sound) for all ages. In some children
Korotkoff sounds can be heard down to 0mmHg which excludes diastolic
hypertension.

• Normal – Systolic and Diastolic less than 90th percentile for age
and height.

• Borderline – Systolic and/or Diastolic less than 95th percentile for

age and height but occasionally higher.

• Moderate – Systolic and Diastolic consistently greater than 95th

percentile for age and height without evidence of target organ
damage

• Severe - Systolic and Diastolic at least 10-20mmHg greater than

95th percentile for age and height with evidence of target organ
damage.

3. Causes of Hypertension - Infant and Child

Coarctation of the aorta

Chronic Renal failure
Renin Dependent Hypertension Renovascular Disease
Renal Parenchymal Disease
Renal Tumour
Trauma
Catecholamine Excess Phaeochromocytoma
Neuroblastoma
Corticosteroid Excess Congenital Adrenal Hyperplasia
Cushing’s syndrome
Primary Hyperaldosteronism
Low renin hypertension
Essential Hypertension
Drug therapy
Endocrine/ Metabolic Hyperthyroidism
Hyperparathyroidism
Ovarian Tumours
Hypercalcaemia
Porphyria

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Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
4. Investigation of Hypertension
The extent to which hypertension is investigated depends on its severity
and the information obtained from a careful history and examination. A
family history of hypertension, renal disease or endocrine causes may
guide you in a particular direction. Similarly clinical features of any if the
above causes may be detected on examination which should include an
assessment of the target organs, eyes, kidneys, and heart.

4.1 Initial Investigations

a) Urinalysis
b) Urine Culture
c) U&E’s, LFT’s, CRP and FBC
d) ± Peripheral plasma renin and aldosterone (Following 30 minutes of
recumbancy and preferably off treatment)
e) Spot urine for catecholamines
f) CXR
g) ECG and Echocardiograph
h) Renal USS with Doppler

4.2 Secondary Investigations

Secondary investigations are guided by the findings from the above
preliminary investigations along with the clinical findings and include:

1. Renal Aetiology suspected

a) DMSA Scan
b) Direct or indirect cystogram
c) Intravenous Urography
d) Renal Angiography
e) Renal Biopsy

2. Catecholamine Excess suspected

a) I123 MIBG Scan
b) CT/MRI
c) Abdominal Angiography with selective venous sampling

3. Corticosteroid Excess suspected

a) Urinary steroid profile
b) Steroid suppression tests
c) Adrenal CT/MRI
d) Selective adrenal venous steroid sampling

4.3 Renal Vein Renin Sampling

Sampling of 1.5mls of EDTA (pink top) blood should be obtained from the
IVC below the level of the renal veins and from both of the main renal
veins. Biochemistry requires advanced warning, and the specimens should
be transferred immediately on ice to biochemistry.
Hypertension Version: 1.1 Page 4 of 13
Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
Renin secretion should be increased in the ischaemic kidney (as evidenced
by a renal vein renin that is 1.5 times the value from the contralateral
kidney), and suppressed in the contralateral kidney (as evidenced by the
renin from a blood sample obtained from the infrarenal inferior vena cava)
[5].

These values are uncommon in normal subjects, less than 10 percent of

whom have a ratio above 1.5 and less than 20 percent of whom have a
ratio below 1.1 It has also been proposed that the accuracy of these
measurements can be enhanced by the prior administration of an ACE
inhibitor, which will increase renin secretion on the affected side.

There are, however, many false negative and some false positive results.
Although over 90 percent of patients with unilateral renal artery stenosis
and lateralizing renin values will have a positive response to angioplasty
or surgery, approximately 50 percent with nonlateralizing findings will also
benefit from correction of the stenosis. As a result, most physicians rely
on the clinical index of suspicion rather than renal vein renins to estimate
the physiologic significance of a stenotic lesion. One exception may occur
in patients with bilateral renal artery stenosis in whom renal vein renins
can be used to determine which side contributes most to the
hypertension.

5. The Management of Hypertension

Irrespective of the aetiology of the hypertension most hypertensive
patients will benefit if not require general advice on the control of obesity
and increasing the amount of exercise undertaken. Dietary salt restriction
has not been shown to be beneficial in children or adolescents, however
there is a strong association between a high dietary salt intake and
obesity, and therefore attempts should be made to address this.

The aetiology of the hypertension should be considered before

implementing anti-hypertensives e.g. fluid overload would respond best to
volume reduction with a diuretic. Listed below are the commoner drugs
that are used in the management of hypertension.

N.B. Investigations should be undertaken prior to the

commencement of treatment.

Mild Hypertension (One of the following)

Calcium Antagonists – Nifedipine or Amlodipine
β-blocker – Atenolol

Moderate Hypertension (One of the following)

Calcium Antagonists – Nifedipine or Amlodipine
β-blocker – Atenolol
ACE inhibitor - Enalapril

Hypertension Version: 1.1 Page 5 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
Severe Hypertension (One of the following)
Calcium Antagonists – Nifedipine or Amlodipine
β-blocker – Atenolol
ACE inhibitor - Enalapril

May need Intravenous therapy initially.

6. Neonatal Hypertension
There is little data on normal blood pressure values in term and preterm
infants and as hypertension is generally transient therapeutic intervention
mat not be indicated. The incidence of hypertension in NICU is reported to
be 2.6% with figures of over 40% reported in patients with chronic lung
disease.

7. Causes of Neonatal Hypertension

Renovascular Thromboembolism Post UAC

Renal Artery Stenosis
Mid-aortic coarctation
Renal Vein Thrombosis
Renal Parenchymal Disease Polycystic Kidney Disease
Multicystic Dysplastic Kidney Disease
Tuberose Sclrosis
Pelviureteric Junction Obstruction
Acute Tubular Necrosis
Cardiopulmonary Bronchopulmonary Dysplasia
Pneumothorax
Thoracic Aortic Coarctation
Endocrine Congenital Adrenal Hyperplasia
Hyperaldosteronism
Hyperthyroidism
Medication Dexamethasone
Theophylline
Caffeine
Pancuronium
Neurological Intracranial Hypertension
Seizures
Subdural Haematoma
Miscellaneous Total Parenteral Nutrition
Closure of Abdominal Wall Defect
Adrenal Haemorrhage
Hypercalcaemia
ECMO
Birth Asphyxia

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Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
8. Investigation of Neonatal Hypertension
As above but a cranial ultrasound should be undertaken in all
patients as a baseline, but also to exclude intracranial pathology.

9. Management of Neonatal Hypertension

The decision on when to initiate therapy is tempered by the need to
minimise the risks of creating iatrogenic problems. Treatment
should be initiated in the presence of a systolic blood pressure
above the 99th percentile for age, or in the presence of end organ
damage the 95th percentile. Clear guidelines as to the definition of a
hypertensive emergency in neonates is unclear, however if a
recorded blood pressure is 30% greater than expected then
emergency treatment should be initiated.

9.1 Emergency Treatment

• Hydralazine as a continuous intravenous infusion
• Labetalol may be used as a second line agent

9.2 Standard Treatment

• Nifedipine
• Propranolol
• ACE inhibitors – use with care often as little as 10ug/Kg is
sufficient

10. Future Guideline Development

• Should any aspect of this guideline change before the planned
review in January 2007 (i.e. new technology or procedural change)
then this guideline should be updated accordingly.
• Future review of this guideline should make use of the AGREE
document to ensure that up-to-date evidence and best clinical
practice has been used to inform this guideline. For further
information on guideline development please contact the
Chairperson of the Multi-Professional Clinical Practice Committee.

Hypertension Version: 1.1 Page 7 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
Appendix I: Drug Therapy - Oral

Drug Dose mg/kg/day

Initial Max Dosing Tablets Liquid

Adrenergic Blockers
α/β blocker Labetalol 1 3 (AM 600mg) 6-12h 100,200,400 Yes (†)
mg
α blocker Doxazocin 0.02 0.1 (AM 4mg) 24h 1,2,4mg No
α blocker Prazocin 0.05-0.1 0.5 (AM 5mg) 6-8h 0.5,1,2,5mg No
β blocker Atenolol 0.5 2 (AM 50mg) 12-24h 25,50mg Yes
β blocker Propranolol 0.2 1.5 (AM 80mg) 6-12h 10,40,80,16 Yes
0mg
α Agonist Clonidine 0.05-0.1 0.5-0.6 (AM 6-12h 100,300ug No
400ug)
Calcium Antagonists
Nifedipine Bite & Swallow 0.1 0.3 (AM 10mg) 4-6h 5,10mg Yes (‡)
Nifedipine 0.5 1.5 (AM 30mg) 8h 5,10mg Yes (‡)
Nifedipine SR (Adalat 0.5 1 (AM 40mg) 12h 10,20mg No
Retard)
Nifedipine SR (Adalat LA) 0.5 1 (AM 90mg) 24h 20,30,60mg No
Amlodipine 0.05 0.2 (AM 10mg) 24h 5,10mg No
ACE inhibitors
Captopril 12.5,25,50mg No
Children 1.5 6 (50mg) 8h
Neonates 0.03- 2 8-24h
0.15
Enalapril 0.15 1 (AM 40mg) 12-24h 2.5,5,10,20mg No
AII receptor antagonists
Losartan 0.5 2 (AM 100mg) 24h 25mg No
Diuretics
Bumetanide 0.02- 0.3 (AM 5mg) 4-12h 1,5mg Yes
0.05
Frusemide 1 12 (AM 80mg) 4-12h 20,40mg Yes
Hydrochlorothiazide 1 2-3 (AM 50mg) 12h 25,50mg No
Spironolactone 1 3 (AM 25mg) 6-12h 25,50,100mg Yes
Triamterene 2 3 (AM 100mg) 6-12h 50mg No
Vasodilators
Hydralazine 0.75 7.5 (AM 75mg) 6h 25,50mg No
Minoxidil 0.1-0.2 1 (AM 50mg) 12h 2.5,5,10mg No
Centrally Acting
Methyldopa 3 15 (AM 1g) 8-12h 125,250,500 No
mg

Key:
AM – Adult Maximum dose
† - Use IV preparation
‡ - Use Liquid from capsule

Hypertension Version: 1.1 Page 8 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
Appendix II: Intravenous Drug Therapy for the Treatment
of Hypertension

Agent Dose Onset Action Complications

Labetalol 1-5 mg/kg/hr 3-5 min Alpha & beta Hypoglycaemia
blocker Well tolerated
Nifedipine 0.25-0.5 mg/kg 5-10 min Ca channel Headache, nausea,
sublingual blocker syncope
Nitrogylcerin 1-10 ug/kg/min Instant Direct Tachycardia,
as IV infusion vasodilator bradycardia
Sodium 0.5-8 ug/kg/min Instant Direct Thiocyanate
Nitroprusside as IV infusion vasodilator poisoning
Phentolamine 0.1mg/kg stat 5-10 min Alpha blocker Tachycardia,
5-50ug/kg/min vomiting arrythmias
IVI
Clonidine 2-6 ug/kg ~10 Central alpha Depression
min 2 agonist Rebound
Hydralazine 0.2 to 15 5-10 min Direct Headache, vomiting,
mg/dose IV bolus vasodilator tachycardia
4-6ug/kg/min IVI
Frusemide 1-3mg/kg over Diuretic Volume depletion
15min Electrolyte abn
0.1-1mg/kg/hr
IVI
Diazoxide 5 mg/kg (max 3-5 min Direct Hyperglycaemia
300) IV bolus vasodilator Nausea & vomiting

Hypertension Version: 1.1 Page 9 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
Appendix III: Reference Ranges – Males 1-17years

Hypertension Version: 1.1 Page 10 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
Appendix IV: Reference Ranges – Females 1- 17 years

Hypertension Version: 1.1 Page 11 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
Appendix V: Reference Ranges Males and Females age <
1 Year

Girls Boys

Hypertension Version: 1.1 Page 12 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022
Appendix VI: Reference Ranges Neonates

Hypertension Version: 1.1 Page 13 of 13

Author(s): Renal Clinicians Authorised by: Dr J Beattie Issue Date: November 2005
Group
Date of Review: January 2007 Q-Pulse ref: YOR-REN-022