Hypertension in Pediatric Emergency

Transient hypertension can occur in a child as a result of stress, fear or pain. Blood pressure (BP) measurements repeated on several different occasions (at least three) are required to diagnose hypertension. The cuff bladder should cover at least 3/4 of the child’s arm length, and the child should be quiet and calm. In children with measured high BP, it is important to differentiate between those who have immediately dangerous hypertension and those who may have long-standing hypertension. In these patients a search for a possible underlying cause should be made. Table 9.3 shows the upper 95th centile measurements for blood pressure.

Causes of hypertension

The causes of hypertension break down into essential hypertension and secondary causes. Secondary causes fall into a few main groups, depending on the system of origin.

These include:

• Renal (75%): postinfectious glomerulonephritis, chronic glomerulonephritis, obstructive uropathy, reflux nephropathy, renovascular, hemolytic uremic syndrome, polycystic kidney disease

• Cardiovascular (15%): coarctation of the aorta

• Endocrine (5%): pheochromocytoma, hyperthyroidism, congenital adrenal hyperplasia, primary hyperaldosteronism, Cushing syndrome

• Other (5%): neuroblastoma, neurofibromatosis, steroid therapy, raised intracranial pressure.

History

The history essentially should contain details of the family history (e.g. pheochromocytoma) and of genitourinary symptoms.

The examination must include the height and weight, blood pressure measurements of both upper and lower limbs, and a full neurological examination. .

Causes of secondary hypertension

• Appearance: Cushingoid, obese

• Skin: café-au-lait spots, neurofibromas, hirsutism, vasculitis

• Fundoscopy: hypertensive retinopathy

• CVS examination: left ventricular hypertrophy, murmurs (particularly interscapular)

• Abdomen: renal/adrenal masses, renal bruits

Investigation

a. Initial investigations should include:

• urine analysis

• urine microscopy

• blood urea and electrolytes

• creatinine

b. Further investigations may include:

• urinary catecholamines

• chest X-ray

• ECG

• renal ultrasound

• gluconate scan

• plasma renin pre- and post-captopril

• thyroid function tests

• cortisol/aldosterone levels

• 17-hydroxyprogesterone

• renal angiography.

Management

a. Asymptomatic hypertension

No urgent treatment is required for asymptomatic hypertension. The child can be investigated and managed as an outpatient and should be referred to the general pediatric outpatient clinic.

b. Acute severe hypertension

These patients require admission to ICU for urgent treatment. Hypertensive encephalopathy presents as severe headache, visual disturbance and vomiting, progressing to focal neurological deficits, seizures and impaired conscious state, with grossly elevated BP, papilledema and retinal hemorrhages. These patients almost always have chronic renal disease and are on dialysis. The differential diagnosis includes uremic encephalopathy and metabolic disturbance. BP should be lowered in a controlled fashion, with anticonvulsants given for seizures.

Antihypertensives. The choice includes the drugs listed below, although this is not an exhaustive list:

• Intravenous labetalol: 0.2 mg kg−1 initially; later by i.v. infusion of labetalol 0.5–3 mg/Kg weight per hour. It should be avoided if there is heart failure, asthma or bradycardia.

• Intravenous hydralazine: 0.1 – 0.2 mg/Kg weight  (max. 10 mg) stat, then 4–6 micro grams/Kg weight  per minute (max 300 micrograms per min). It may cause tachycardia, nausea and fluid

retention.

• Oral captopril: 0.1 mg/Kg weight  initially, increasing to a maximum of 1 mg/Kg weight  (max. 50 mg). Thereafter 0.1–1.0 mg/Kg weight  per dose 8-hourly. Captopril is usually effective within 30–60 minutes.

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Headaches in Pediatric emergency

Headache is a common symptom in children, affecting 80–90% by the age of 15. The common causes are systemic illness with fever, local ENT problems, migraine and tension headache. Meningitis, raised intracranial pressure (ICP), e.g. from tumors, and subarachnoid hemorrhage (SAH) are much rarer causes but these need to be considered. Any headaches that wake a child from sleeping or that are associated with focal signs such as a hemiplegia require investigation as an inpatient

Assessment

History

It is useful to classify headache as acute or recurrent. The following list gives the causes and key features to help make a diagnosis, based on careful history and examination:

Acute

• Systemic: fever and general illness (e.g. ’flu, pneumonia, septicemia)

• Local sinusitis, dental caries, otitis media

• Trauma: head injury

• Meningitis: reduced conscious level, toxicity, photophobia, neck stiffness

• SAH: sudden onset, severe occipital pain; possible reduced conscious level, neck stiffness

Recurrent

• Migraine: aura, nausea, vomiting, pallor, family history

• Tension: throbbing pain (involving neck muscles) at end of day

• Behavioral: family/social/school problems (may be difficult to identify)

• Raised ICP: morning headaches ± vomiting, worse with coughing/sneezing/bending

• Progressively worsening raised ICP: personality or behavioral changes, focal neurological symptoms

• Benign intracranial hypertension, systemic hypertension, uremia, recurrent hypoglycemia, recurrent seizures, lead or CO poisoning.

It may be useful to make out a possible family headache patterns diagram to help identify the nature of the headache.

Examination

As part of the examination it is important to document the following:

• ABC: blood pressure, heart rate

• General: toxic, unwell, temperature, rash

• Neurology: conscious level, fundi, visual fields, cerebellar signs, neurocutaneous stigmata, neck stiffness, cranial bruits

• Local causes: cervical lymphadenopathy, teeth, sinus, ears

• Growth and puberty: head growth, height, weight, growth velocity, pubertal status.

Investigations

In the acute situation, the two most important questions to answer are:

• Does the child need an urgent computerised tomography (CT) scan of the head? and

• Should a lumbar puncture (LP) be performed? In making the decision, you should consider the following factors:

• If the child has altered state of consciousness, focal neurological signs, raised blood pressure or papilledema, consider management of raised ICP and CT scan of head. Discuss this with senior medical staff.

• Consider LP (in the absence of the contraindications) if you are concerned about meningitis or SAH. You may need to do a CT scan first (discuss with consultant).

• If there are no symptoms and signs suggesting raised ICP/SAH/ meningitis and the story is suggestive of migraine, then treat symptomatically (see below).

• If other causes are suspected, do the appropriate investigations (e.g. septic screen, urea, carboxyhemoglobin or lead level [wrist X-rays], blood sugar profile).

Management

If there is a specific diagnosis such as meningitis, SAH, tumor, systemic infection or local infection, then treat as appropriate. Most recurrent headaches can be managed by a pediatrician and do not need to be referred to a neurologist.

Abort attack

Avoid opiates. Initially try simple oral analgesics such as paracetamol (20 mg/kg weight stat then 15 mg/kg weight per dose every 4 hours, to a maximum of 4g per day) or codeine (1 mg/kg weight per dose every 4 hours) or NSAID (ibuprofen 2.5–10 mg/kg weight per dose 6–8 hourly). For adolescents give 1 g of aspirin, 1 g of paracetamol, 10 mg of metoclopramide. Some, but not all, pediatricians use intravenous anti-emetics in severe vomiting. For example, if vomiting is a prominent feature in children over 10 years give slow i.v. prochlorperazine

(0.1–0.2 mg/kg weight).

Prophylaxis

Refer to a local doctor or general pediatric outpatient clinic for long-term management. Consider beta blockers, pizotifen or calcium channel blockers. Non-pharmacological interventions (e.g. avoidance of triggers, relaxation) often play an important role in prevention. Consider getting the child or parents to make a headache diary.

Headache patterns

It may be a good idea with the use of the chart below to explore the pattern of the child’s headaches .

• Acute recurrent includes migraine (common, classical, complicated).

• Chronic non-progressive includes tension (stress related); muscle contraction; anxiety; depression; somatisation headaches.

• Chronic progressive includes headaches from tumor; benign intracranial hypertension; brain abscess; hydrocephalus.

• Acute on chronic non-progressive includes tension headache with coexistent migraine.

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Cardiac Failure and Congenital Heart Disease in Pediatric

Congenital heart disease may present as heart failure with or without shock or cyanosis. However, there are many causes of cardiac failure, including non-congenital reasons such as myocarditis. These may present with signs of heart failure, such as breathlessness, hepatomegaly, pallor and sweating, or may be severe enough to present as cardiogenic shock. Remember that heart failure in an infant can mimic bronchiolitis and the child may have contracted bronchiolitis. This in turn may be the precipitating cause of the heart failure. The likely causes are in picture below.

Causes of Cardiac Failure in Pediatric

In infancy heart failure is usually secondary to congenital structural heart disease. As pulmonary pressures reduce after birth over the first few hours to days of life, increased pulmonary flow from lesions such as VSD or PDA will become apparent. These infants are likely to have a cardiac murmur audible. Rarer duct-dependent lesions, such as pulmonary atresia or transposition of the great vessels, will also present after a few days to weeks as the duct closes. These infants may have a large liver but may not have a cardiac murmur audible. Coarctation and severe aortic stenosis will also present as the duct closes.

Investigation

• CXR may be helpful to demonstrate cardiomegaly with pulmonary plethora or a

characteristic cardiac shape and size

• 12-lead ECG

• Cardiac echocardiography and cardiac consultation

• Infection screen as above

• 4-limb blood pressure

Management Shock 

If there are signs of shock then treat as in the cardiogenic shock section. Heart failure If the ventilation is adequate, then oxygen by facemask will be sufficient. However, if breathing is inadequate, intubation and artificial ventilation with PEEP will be required. 

If oxygenation improves with this maneuver, then the likely problem is that of pulmonary congestion secondary to increased flow from a VSD or PDA etc. A heart murmur may be heard and chest X-ray might be helpful in confirming the diagnosis (see below).

Treatment needs to be discussed with the cardiologists. It will include oxygenation and reducing the preload with diuretics (with, for example, frusemide 1 mg/kg i.v., repeated if no response after 2 hours). Consideration will be given to improving cardiac contractility (using, for example, digoxin or inotropes, such as dopamine or dobutamine) or decreasing the afterload with vasodilatation (using, for example, captopril).

Cyanosis

Increasing breathlessness and cyanosis in the first few days of life is the presentation of the rarer duct-dependent disease, such as tricuspid or pulmonary atresia. In theseconditions, oxygen may cause the duct to close further but, if it is considered necessary for ventilation, it should be carefully titrated. Intravenous prostaglandin El (0.01–0.1 µg/kg per min) should keep the duct open until cardiac opinion is available. Once aresponse occurs, the infusion rate should be titrated down. Prostaglandins may causeapnea and so the child should be ventilated during its administration.

All these children require careful monitoring by ECG, pulse oximetry and non-invasive blood pressure measurement. Remember to check blood pressure in lower limbs as well as upper limbs. It is essential to consider sepsis as a differential diagnosis of cardiacfailure in infancy and most infants will require a full infection screen and possible antibiotic cover. These children need admission and assessment by the cardiology team.

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Cyanotic Episodes in Pediatric

Cyanotic episodes occur in children with cyanotic congenital heart disease, in particular tetralogy of Fallot and pulmonary atresia. There may be a previous history of squatting. The episodes usually occur early in the morning, or in the context of stress or dehydration with periods of increased oxygen demand or increased oxygen use. The pathophysiology is not fully understood, but relates to decreased pulmonary blood flow. Most episodes are self-limiting but cause hypoxic-ischemic brain injury or indeed may be fatal.

Assessment

The assessment includes consideration of the severity of the cyanosis or pallor with either distress and hyperpnea (not tachypnea), or lethargy and a depressed conscious state.

There may be evidence of structural heart disease occasionally with lessening or absence of a previously documented heart murmur.

Treatment and Management

This can be divided into initial measures for short periods of cyanosis and measures for more prolonged problems.

Initial measures

• Put the child in knee to chest position

• Give high flow oxygen via mask or headbox

• Avoid exacerbating distress

• Give morphine 0.2 mg kg−1 s.c.

• Do continuous ECG and oxygen saturation monitoring and frequent blood pressure

measurements

• Correct any underlying cause/secondary problems, which may exacerbate episode, e.g.

cardiac arrhythmia, hypothermia, hypoglycemia.

If the attack is prolonged

• Consult a pediatrician or a cardiologist

• Give intravenous fluids 10 ml/kg bolus followed by maintenance fluids

• Give sodium bicarbonate 2–3 mmol/kg  i.v. (ensure adequate ventilation)

• Consider admission

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Kawasaki Disease in Pediatric

Kawasaki disease is a systemic vasculitis that predominantly affects children under 5 years old. Although the specific etiological agent remains unknown, it is believed that Kawasaki disease is a response to some form of infection (although it is not transmitted from person to person). Diagnosis is often delayed because the features are similar to those of many viral exanthems.

Strawberry tongue Kawasaki Disease in Pediatric

Diagnosis

The diagnostic criteria for Kawasaki disease are fever for 5 days or more, plus four out of five of the following:

• polymorphous rash

• bilateral (non-purulent) conjunctival infection

• mucous membrane changes, e.g. reddened or dry cracked lips, strawberry tongue, diffuse redness of oral or pharyngeal mucosa

• peripheral changes, e.g. erythema of the palms or soles, edema of the hands or feet, and in convalescence desquamation

• cervical lymphadenopathy (>15 mm diameter, usually unilateral, single, non-purulent and painful) and exclusion of diseases with a similar presentation: staphylococcal infection (e.g.scalded skin syndrome, toxic shock syndrome), streptococcal infection (e.g. scarlet fever, toxic shock-like syndrome not just isolation from the throat), measles, other viral exanthems, StevensJohnson syndrome, drug reaction and juvenile rheumatoid arthritis.

The diagnostic features of Kawasaki disease can occur sequentially and may not all be present at the same time. Moreover, it is recognised that some patients with Kawasaki disease do not develop sufficient features to fulfil the formal diagnostic criteria. Clinical vigilance and recognition of this possibility are necessary to recognise these ‘incomplete’ or ‘atypical’ cases. This is important because the atypical cases are probably at similar risk of coronary complications and require treatment. Other relatively common features include arthritis, diarrhea and vomiting, coryza and cough, uveitis, and gallbladder hydrops. Some patients get myocarditis.

Investigations

All patients should have the following investigations:

• ASOT/anti-DNAase B

• echocardiography (at least twice: at initial presentation and, if negative, again at 6–8 weeks)

• platelet count (marked thrombocytosis is common in second week of illness).

Other tests are not diagnostic or particularly useful. The following may be seen:

• neutrophilia

• raised ESR+CRP

• mild normochromic, normocytic anemia

• hypoalbuminemia

• elevated liver enzymes.

Thrombocytosis and desquamation appear in the second week of the illness or later. Their absence earlier does not preclude the diagnosis.

Management

Patients require admission to hospital if Kawasaki disease is diagnosed or strongly suspected. Intravenous immunoglobulin (2 g/kg over 10 hours) should be given, preferably within the first 10 days of the illness, but should also be given to patients diagnosed after 10 days of illness if there is evidence of ongoing inflammation, for instance with fever or raised ESR/CRP.

Aspirin (3–5 mg/kg once a day) should be given for at least 6–8 weeks. Some give a higher dose (10 mg/kg 8 hourly for the first few days) but this probably adds nothing over immunoglobulin.

Follow up

Pediatric follow up should be arranged on discharge. At least one further echocardiogram should be performed at 6–8 weeks. If this is normal, no further examinations are needed

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Syncope in Pediatric

Syncope

A syncopal attack is brief, usually with sudden loss of consciousness and muscle tone caused by cerebral ischemia or inadequate oxygen or glucose to the brain.

Features

• It usually lasts only a few seconds

• The child limp and unresponsive

• Tonic—clonic movements can occur with prolonged unconsciousness

• The patient is back to normal on awakening

Cause

There are several causes, including:

• Vasovagal (fainting)

• Orthostatic or postural hypotension

• Cardiac

• structural (e.g. critical aortic stenosis, tetralogy of Fallot, atrial myxoma etc.)

• arrhythmia (e.g. prolonged QT, AV block, sick sinus syndrome)

• Respiratory (e.g. cough, hyperventilating, breath holding)

• Metabolic (e.g. anemia, hypoglycemia, hysteria etc.)

Management

A history of the surrounding events is important. Orthostatic hypotension usually occurs on standing suddenly. Vasovagal collapse is usually associated with environmental or emotional stresses. Structural cardiac lesion is more likely if the syncope is exertional. 

The patient should be examined for cardiac anomaly (e.g. murmur, heaves etc). Investigations should include an ECG to look for dysrythmias, short/abnormal PR interval (e.g. Wolff-Parkinson-White syndrome) or prolonged QT syndrome.

If unconsciousness lasts more than a few seconds and the patient is not fully awake immediately after the event, then consider seizures as a cause. The patient may need an EEG to clarify this issue. Hysterical syncope generally occurs in front of an audience, patients do not hurt themselves and there is associated moaning or nonrhythmical jerking.

Follow up

All patients who have unexplained syncope should be reviewed in outpatients.

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Supraventricular Tachycardia in Pediatric

Supraventricular tachycardia will usually present with signs of congestive cardiac failure or shock, but will also depend on the age of the child. Sinus tachycardia can be up to about 200 beats per minute. Supraventricular tachycardia (SVT) is usually above 220 beats per minute.

Assessment

Symptoms

Infants usually present with pallor, dyspnea and poor feeding. Older children have palpitations and chest discomfort.

Signs

In SVT there is a regular tachycardia with a heart rate usually 180–300 per minute. Hypotension might be present but is often compensated early on in presentation. Heart failure with hepatomegaly with gallop rhythm occurs, especially in infants. Consult cardiology urgently if tachycardia is broad complex or irregular.

Management and Treatment

The child must be monitored with continuous ECG trace and frequent measurements of blood pressure. The options for treatment are listed below.

• If necessary apply oxygen 10 liter/min by facemask

• If child is shocked (i.e. hypotensive, poor peripheral perfusion, impaired mental state) proceed to direct current cardioversion (see below)

• If child is not shocked treat with intravenous adenosine

Shocked child

If the child is shocked, then direct current cardioversion is needed. You must:

• Call ICU. Ensure experienced staff and full resuscitative measures are present

• Ensure child is on oxygen, and has intravenous access

• Administer diazepam intravenously if there is any chance of awareness

• DC revert using a synchronised shock of 0.5 J/kg. If this is unsuccessful, increase

dose to 1 J/kg and then to 2 J/kg if still unsuccessful

• An unsynchronised shock is necessary for ventricular fibrillation or polymorphic ventricular tachycardia

Stable child

If the child is stable, vasovagal maneuvers and adenosine should be tried:

• Vagal maneuvers: use the Valsalva maneuver if child old enough, the gag or icepack/iced water for infants (apply to face for a maximum of 30 seconds). Do not use eyeball pressure.

• Intravenous adenosine

• Insert cannula into a large proximal peripheral vein (the cubital fossa is ideal) with a 3-way tap attached

• Draw up starting dose of adenosine 50 µg/kg. If necessary dilute to 1 ml with

normal saline

• Draw up 10 ml saline flush

• Turn on the ECG trace recorder

• Administer adenosine as a rapid i.v. push followed by the saline flush

• Repeat procedure at 2-minute intervals, until tachycardia terminated, increasing the dose of adenosine by 50 µg/kg to a total dose of 300 µgµg/kg for infants of less than 1 month, and to a total dose of 500 µg/kg1 to children between 1 month and 12

years.

• Perform 12-lead ECG postreversion

The recorded strip at the time of conversion to sinus rhythm should be inspected and saved, for concealed pre-excitation may only be revealed during the first few beats after conversion to sinus rhythm. After a patient has been reverted, a 12-lead ECG should be performed to look for pre-excitation and other abnormalities. Rapid re-initiation of tachycardia is not uncommon, mostly because of premature atrial contractions stimulated by the adenosine. If this occurs consider trying adenosine again. Side effects including flushing and chest tightness or discomfort are not uncommon but they are usually brief and transient. Rarely atrial fibrillation or prolonged pauses may occur. Adenosine is contraindicated in adenosine—deaminase deficiency (rare immune deficiency) and patients taking dipyridamole (Persantin). Care is required in asthma, as it may cause bronchospasm. If these measures fail to revert the SVT, consult a cardiology specialist.

Disposition

A follow-up plan should be made in consultation with cardiology. Some children may be started on beta blockers. There may be an underlying conduction abnormality such as Wolff-Parkinson-White syndrome.

Source pict: http://www.medscape.org/

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