Extern Conference23/8/50

An 8-year-old Thai boy was admitted due to severe progressive headache and severe hypertension.

History

Present Illness

• He had episodes of headache of few times per month for 1 year. The characteristic was a throbbing frontal headache aggravated from exercise and relieved by resting or analgesic drug such as paracetamol.

• 2 days prior to admission, his headache became progressively severe.

History (2)

Present illness• No nausea, vomiting, dyspnea, and orthopnea

• Vision was normal.

• No fever, cough, or sore throat recently

• Normal urination, no dysuria, hematuria, or oliguria

• No edema, rash, oral ulcer, anemia, abnormal bleeding, or arthralgia

• No history of previous hypertension or urinary tract infection.

History (3)

• No family history of hypertension or renal disease

• Development was normal.

• Complete vaccination as scheduled

• No history of any drug allergy

• No ingestion of any medications

Physical Examination

Vital signs: T 37.5 o C, P 76 /min, no delayed pulse and equal all extremities, RR 24 / min, Blood pressure

Right arm: 170/120 mmHg

Left arm: 165/110 mmHg

Right leg: 170/105 mmHg

Left leg: 170/110 mmHg

BW 23 kg (P10-25) Ht 126.5 cm (P 50)

BMI 14.37 kg/m2

Physical Examination (2)

General appearance: alert and cooperative, not pale, no jaundice, no dyspnea, no orthopnea, no puffy eyelids, no edema, and no cyanosis

Skin: no rash, no petechiae , no ecchymoses, no alopecia, no café au lait spots

HEENT: normal

Physical examination (3)

CVS: PMI at left 5th intercostals space, lateral to midclavicular line, no heaving or thrill, normal first and second heart sound, no murmur

RS: normal

Abdomen: soft, not tender, no palpable mass, liver and spleen not palpable, normal bowel sound , no abdominal bruit

Nervous system : Normal

No superficial lymphadenopathy

Problem list

1. Chronic headache for 1 yr with severe progressive headache for 2 days

2. Severe hypertension

3. Cardiomegaly

Hypertension in childhood

What is hypertension?

• Hypertension=average SBP and/or DBP ≥ 95th percentile for gender, age, and height on ≥ 3 separate occasions

• Prehypertension : BP 90th -95th or BP ≥ 120/80• Normotension : SBP and DBP ≤ 90th by age,

gender, and height or BP ≤ 120/80• Hypertension stage I : SBP and/or DBP 95th -99th

• Hypertension stage II : SBP and/or DBP ≥ 99th

Clinical manifestations of hypertension

• Most of the patients do not have symptom related to hypertension at the presentation.

• Chronic headache (10 %)

• Hypertensive encephalopathy (6.8%)

• Epistaxis (1.4%)

• Visual disturbance (1.4 %)

[ The Study of persistent hypertension in Thai children etiologies and outcome in J med association Thai 2006 ]

Hypertensive Emergency

• No specific level of BP

• Defined as a blood pressure high enough to cause acute injury to target organs

• Children are more prone to hypertensive encephalopathy than adults

Complication of hypertensive emergency

• The most common complications are

- Hypertensive encephalopathy

- Cerebral infarction and hemorrhage

- Facial palsy

- Visual symptoms

- Cardiac failure

- Renal failure

Hypertension etiology

• Primary or early onset of essential hypertension

• Secondary hypertension

The Causes of Secondary Hypertension in Children and Adolescents

Cause Acute hypertension Chronic hypertension Etiology

Renal Acute glomerulonephritis Congenital defects Tumors of the kidney

  Acute renal failure Chronic pyelonephritis Hypoplastic kidney

  Hemolytic-uremic syndrome

Hydronephrosis Collagen vascular disease

Endocrine - Pheochromocytoma Primary aldosteronism

    Hyperthyroidism Neuroblastoma

Vascular Renovascular trauma Coarctation of the aorta Renal arteriovenous fistula

    Renal artery stenosis Neurofibromatosis

    Takayasu arteritis Tuberous sclerosis

Neurogenic Increased intracranial pressure

Dysautonomia -

  Guillain-Barré syndrome    

Metabolic Hypercalcemia - -

  Hypernatremia    

Drugs Cocaine Nonsteroidal Anabolic steroids

  Phencyclidine anti-inflammatory drugs Corticosteroids

  Amphetamines Oral contraceptives Alcohol

Miscellaneous BurnsLeg traction

Heavy metal poisons -

Adapted from Daniels SR, Loggie JM: Essential hypertension. Adolesc Med State Art Rev 2:555, 1991.

The Causes of Secondary Hypertension in Children and Adolescents (2)

Cause Acute hypertension Chronic hypertension Etiology

Metabolic Hypercalcemia - -

  Hypernatremia    

Drugs Cocaine Nonsteroidal Anabolic steroids

  Phencyclidine anti-inflammatory drugs Corticosteroids

  Amphetamines Oral contraceptives Alcohol

Others BurnsLeg traction

Heavy metal poisons -

Adapted from Daniels SR, Loggie JM: Essential hypertension. Adolesc Med State Art Rev 2:555, 1991.

Etiology of Secondary Hypertension in Pediatrics

• 78% renal parenchymal

• 12% renovascular

• 2% coarctation of the aorta

• 0.5% pheochromocytoma

• 7.5% others

Ronald Portman,MD professor and director,division of pediatric nephrology and hypertension, University of Texus Houston, 2003

Cause of the persistent hypertension according to age group in Thailand

Age Cause No. of patient(%) 6-12 yr lupus nephritis 36.1

chronic renal failure 22.2 idiopathic nephrotic syndrome 5.6 IgA nephropathy 2.8 renovascular disase 13.9 drug induced 11.1 coarctation of aorta 2.8 Essential hypertension 2.8 unknown 2.8

[ The Study of persistent hypertension in Thai children etiologies and outcome in J med association Thai 2006 ]

How to approach hypertension

Diagnostic work up & Evaluation for target organ damage

The Causes of Secondary Hypertension as Suggested by History

History Suggests

Known urinary tract infection; recurrent abdominal or flank pain with frequency, urgency, dysuria; secondary enuresis

Renal disease

Joint pains, rash, fever, edema Renal disease, vasculitis

Complicated neonatal course, umbilical artery catheter Renal artery stenosis

Renal trauma Renal artery stenosis

Drug use (e.g., sympathomimetics, anabolic steroids, oral contraceptives, illicit drugs)

Drug-induced hypertension

Aberrant course or timing of secondary sexual characteristics; virilization

Adrenal disorder

Muscle cramping, constipation, weakness Hyperaldosteronism (primary or secondary)

Excessive sweating, episodes of pallor and flushing Pheochromocytoma

Adapted from Hiner LB, Falkner B: Renovascular hypertension in children. Pediatr Clin North Am 40:128-129, 1993.

The Causes of Secondary Hypertension as Suggested by Physical Examination

Adapted from Hiner LB, Falkner B: Renovascular hypertension in children. Pediatr Clin North Am 40:128-129, 1993.

Physical finding Possible secondary cause

Blood pressure

>140/100 at any age Multiple secondary causes

Leg < arm blood pressure Coarctation of the aorta

Poor growth Chronic renal disease

Short stature, features of Turner syndrome Coarctation of the aorta

Multiple café-au-lait spots or neurofibromas Renal artery stenosis, pheochromocytoma

Decreased or delayed pulse in leg Coarctation of the aorta

Vascular bruits  

Over large vessels Arteritis

Over upper abdomen, flank Renal artery stenosis

Flank or upper quadrant mass Renal malformation, renal or adrenal tumor

Excessive virilization or secondary sex characteristics inappropriate for age

Adrenal disorder

Extremities  

Edema Renal disease

Excessive sweating Pheochromocytoma

Adapted from Hiner LB, Falkner B: Renovascular hypertension in children. Pediatr Clin North Am 40:128-129, 1993.

Investigation

The first line

• Urinalysis• Urine culture• BUN , creatinine• 24 hr. urine for

vanillymandelic acid • Renal ultrasound

including Doppler study of renal ateries

• Complete blood count• Electrolyte• Calcium, Phosphate• Chest x- ray • EKG • Retinal examination

Investigation

The second line

• urine catecholamine

• plasma renin and aldosterone

• CT angiography

• ESR and ANA

Investigation in this patient

Investigation

• CBC : Hb 12.1 g/dl Hct 35.3 % WBC 3890 cell/mm3 ( N 46%, L 39%, Mo 9%) Plt 187,000 cell/mm3

• UA : pH 6, Sp.gr. 1.015, protein 2+ ,ketone negative WBC 0-1 cell/HP , RBC 0-1 cell/HP, no dysmorphic RBC, no cast

• Urine protein/creatine : 0.8

• 24 hr. urine protein : 9 mg/kg/day

Investigation

• Blood chemistry : BUN 13.0 mg/dl, Cr 0.7 mg/dl, Na 137 mmol/L, K 3.1 mmol/L, Cl 102 mmol/L, HCO3 22 mmol/L

• Lipid profile : Chol 203 mg/dl, TG 68 mg/dl, HDL 66 mg/dl, LDL 123.4 mg/dl

• EKG : LVH by voltage criteria

• Fundoscopic examination : atherosclerosis grade II BE

• CXR : Cardiomegaly, CT ratio 0.53, no pulmonary infiltration.

Investigation

• Echocardiogram :

no coarctation of aorta, no irregularity or aneurysmal dilatation of abdominal aorta.

concentric LVH without LVOT obstruction.

good LV systolic function.

no structural heart disease.

Investigation

• Throat swab culture : normal flora

• Anti-streptolysin O : 576 IU/ml

• AntiDNAse B : 79.1 U/ml

• C3 : 105 mg/dl

• U/S : Bilateral hydronephrosis and hydroureter UVJ, possibly related with stricture at UVJ from megaureter or stenosis related with ectopic ureter.

VCUG : bilateral vesicoureteric reflux grade 5, suspected bilateral primary megaureter

• Tc-99m MAG3 : hydronephrosis and hydroureter both kidneys with no evidence of obstruction. Mild impair function of left kidney.

Investigation

• Tc-99m DMSA : multiple small renal infarction (function right: left = 51%: 49%)

Renal parenchymal disease

• Acute glomerulonephritis• Lupus nephritis• Acute or chronic renal

failure• Nephrotic syndrome• IgA nephropathy• Henoch-Schonlein

nephritis

• Coarse renal scarring (reflux nephropathy, obstructive uropathy, neuropathic bladder)

• Polycystic kidney disease • Hemolytic uraemic

syndrome.

VESICOURETERAL REFLUX

VESICOURETERAL REFLUX

• The retrograde passage of urine from the bladder into the upper urinary tract

• Incidence : 1 % of children• 2 categories : primary and secondary• Screening with a radionuclide cystogram of all

sibling < 3 year and any sibling with a UTI is appropriate.

older sibling may undergo renal U/S and if an abnormality is found, VCUG is recommended

The length of the submucosal

segment of the distal ureter is an important factor in

determining the effectiveness of the

ureteral valvular mechanism in

preventing VUR.

Clinical manifestation

• Prenatal presentation :

hydronephrosis via U/S (80% are male)

• Postnatal presentation : UTI

• In other children, VCUG is performed during evaluation for pathology of urinary tract

International system of radiographic grading of VUR

Treatment• Goal of treatment are to prevent

complication

• Surgery for severe VUR

• ATB prophylaxis for mild to moderate VUR

Treatment of hypertension

Nonpharmacologic treatment

• dietary salt restriction

• mineral supplementation

• weight control

• regular exercise

• life style modification

Indications for Antihypertensive drugs

• Symptomatic hypertension

• Secondary hypertension

• Hypertensive target-organ damage

• Persistent hypertension despite nonpharmacologic measure

• DM?

Antihypertensive drugs

• ACEI and Ca channel blocker are commonly prescribed in children

• Diuretics are usually adjunct therapy.

• Need regular long term follow up with special attention to target organ injury and underlying disease

Antihypertensive drugs for hypertensive emergency

Most useful

• Esmolol : IV 100-150 ug/kg/min

• Hydralazine : IV or IM 0.2-0.6 mg/kg/dose

• Labetalol : IV 0.2-1.0 mg/kg/dose

• Nicardipine : IV 1-3 mg/kg/min

• Sodium nitroprusside : IV 0.53-10 ug/kg/min

Management in this patient

Management• Antihypertensive drug :

5Enalapril ( mg) ½ tab oral bid ttt tttt tt(30 ) 1

50Atenolol ( mg) ½ tab oral bid pc

• ATB prophylaxis : tttt t ttt tttt tt(80 )1

• At ward , BP 100-130 / 80-90 mmHg ,UA : protein 2+ , wc 0-1/HP

Home medications:

• 80 1Bactrim ( mg of TMP) tab oral hs

• t ttt tttt ttt (5 )• ttt tttt tt(30 ) 1• 50Atenolol ( mg) ½ tab oral bid pc

Progression

Progress Note

Surgery: bilateral re-implantation

(Cohen Cross trigone)

After surgery : no anti-hypertensive medications

(BP 117/80 mmHg)

Medications:– Bactrim (80 mg of TMP) ½ tab oral bid – Paracetamol (500) ½ tab oral prn for pain

q 4-6 hrs

VCUG 1 month after surgery

Tc-99m DMSA : no significant change of bilateral renal cortex compare to the previous study

Special thank

ศ.พญ. อั�จฉรา สั�มบุ�ณณานนท์�

Thank you