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Management of severe
hypertension in children
Dr Nick Plant,
Consultant Paediatric Nephrologist,
Royal Manchester Children’s Hospital
12th June 2015
Follow the department on Twitter: @nephrology_RMCH
Maths GCSE
New treatment for nocturnal enuresis
Overview
• What is severe hypertension?
• How do we measure it?
• How do they present?
• Common causes
• Acute history & examination
• Acute investigations & management
• Transfer
• Management & investigations at RMCH
• Conclusions
What is severe hypertension?
• Nothing agreed regarding a definition
• Usually means: Stage 2 hypertension &
symptoms
How do we measure it?
• Dinamap
– “we can’t get a reading”
• Aneroid – Accoson Green Light
• IA line – gold standard
How do they present?
• Signs/symptoms of heart failure
• Signs/symptoms of pulmonary oedema
• Failure to thrive
• CNS features:
– Nausea, vomiting, seizures (25%), headaches,
encephalopathy (25%), focal neurology,
hemiplegia (8%), VIIn palsy (12%), blindness
(retinal bleeds, acute ischaemic optic neuropathy,
cortical blindness, papilloedema), PRES
CNS features
Common causes
• Renal disease
– Reflux nephropathy
– Glomerulonephritides (esp MPGN)
– AKI
– Polycystic kidney disease (ARPKD, ADPKD)
– CKD5
• Malignancy
– Phaeo
– Wilm’s
– Neuroblastoma
Common causes
• Vascular
– Aortic coarctation
– Renal artery stenosis
– HUS (aHUS > STEC-HUS)
• Others
– Drugs (OCP, MDMA, cocaine)
– Non compliance in children with hypertension
– Rapid withdrawal of clonidine & β blockers
– Fluid overload in dialysis patients
Common causes
• Renal disease
– Reflux nephropathy
– Glomerulonephritides (esp MPGN)
– AKI
– Polycystic kidney disease (ARPKD, ADPKD)
– CKD5
• Malignancy
– Phaeo
– Wilm’s
– Neuroblastoma
Common causes
• Vascular
– Aortic coarctation
– Renal artery stenosis
– HUS (aHUS > STEC-HUS)
• Others
– Drugs (OCP, MDMA, cocaine)
– Non compliance in children with hypertension
– Rapid withdrawal of clonidine & β blockers
– Fluid overload in dialysis patients
Acute history and examination
• Acute history
– PH UTIs, haematuria, poor stream in boys, FTT, rashes, lethargy, headaches, visual disturbances, FH (diabetes, hypertension, sudden death, etc), medication (steroids, cyclosporin, OCP, drugs)
• Acute examination
– Cardiac status, neurological status (eye exam?), volume status, radio-femoral delay, abdominal mass, abdominal bruit, BMI, thyroid enlargement, café au lait spots, Cushingoid, CKD (short stature, anaemia, renal rickets, etc) ambiguous genitalia
Acute investigations and management
• Acute investigations (no need for many)
– CXR, echo(?), blood gas, CT head, FBC, U&E, toxicology screen
• Take care to exclude conditions that mimic
– Seizures, intracranial pathology, dysautonomia
• Acute management
– Not usually PO treatment
– IV labetolol infusion typically (start at 0.5mg/kg/hr, can increase to max of 3.0mg/kg/hr) – bolus alternative
– IV sodium nitroprusside (infusion) or hydralazine (infusion or bolus) are alternatives
Acute investigations and management
• Acute management continued
– Ideally should have IA line
– If not, consider Dinamap, Accoson every 1-2
minutes, initially
– Time now for prompt transfer
Transfer
• Will probably need to involve NWTS
• Try to avoid delays
• Don’t wait for our Bed Manager
• Consider ventilation in the most severely
affected cases
• Usually need transfer to a HDU/PICU
Management & investigation at RMCH
• Management
– Slow reduction in BP - 25% over 8-12 hours, 25%
over next 8-12 hours and remaining 50% in the
following 24 hours, with IV agents
• Labetolol, hydralazine, Nipride, esmolol, diazoxide,
enalaprilat (IM too)
– Switch to PO agents after 2-3 days if possible
• Investigations
– Led by likely cause: huge list…
Conclusions
• Severe hypertension is rare
• It is a medical emergency requiring prompt
treatment
• Slow fall in BP mandatory to avoid significant
complications
• Rapid, safe transfer needed
• Likely to be of renal or vascular aetiology
Conclusions
• Still, JL & Cottom, D. Arch Dis Child 1967 42: 34-39
Conclusion