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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Hematuria in Pediatric Emergency

Hematuria is the presence of red blood cells in the urine. The presence of 10 or more RBCs per high-power field is abnormal. Urinary dipsticks are very sensitive and can be positive at less than five RBCs per high-power field. In the emergency department it is important in evaluating a child with hematuria to identify serious, treatable and

progressive conditions

.

Red or brown urine does not always indicate hematuria. The discoloration may be as a result of hemoglobinuria, myoglobinuria, some medications and some food. Urate crystals are commonly present in the urine of newborn babies. They can produce a red discoloration of the nappy (‘brick dust’ appearance), which is sometimes mistaken for blood. Blood in the urine can come from sources other than the urinary tract (e.g. vaginal hemorrhage, rectal fissure).

Causes of hematuria

Common causes for microscopic hematuria include an association with viral infections, UTIs, trauma and Henoch-Schönlein purpura. Common causes for macroscopic hematuria include the above, but macroscopic hematuria is more likely to come from the bladder or urethra. Symptomless or ‘benign hematuria’ can occur frequently in children without growth failure, hypertension, edema, proteinuria, urinary casts or renal impairment.

Investigations

The investigation and management of hematuria in Pediatric

Treatment

Many children with isolated microscopic hematuria require no immediate investigation and simply need to be checked to see if the problem persists. This should be arranged with the general practitioner or through outpatient clinic if the family do not have a GP. In the setting of an acute febrile illness, exclude UTI by urine culture and arrange for the urine to be tested again after the acute illness has passed.

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Nephrotic Syndrome in Pediatric Emergency

Nephrotic syndrome is a clinical disorder characterised by edema, proteinuria (>3g per day), hypoalbuminemia and hypercholesterolemia. Minimal change glomerulonephritis accounts for 80–85% of nephrotic syndrome in childhood. Complications include infections, thrombosis and renal impairment.

History

Edema is the primary feature. This may be subtle or gross and is usually noticed in the peri-orbital region, scrotum or labia. It may include, in addition, peripheral edema of the limbs and sacrum. The history is often of weight gain, poor urine output and sometimes of discomfort as a result of the edema. A history of preceding upper respiratory tract infection or diarrhea may be present.

Examination

Examination should confirm the presence of edema. Ascites and pleural effusions may be present when edema is gross. Peripheral perfusion and blood pressure should be assessed. Examination should include a search for signs suggesting the onset of complications such as infected ascites, renal vein thrombosis (e.g. enlarged renal mass, loin tenderness and marked hematuria) and cerebral vein thrombosis. Urinalysis should always be included to make the diagnosis as other causes of edema such as protein losing enteropathy or cardiac failure may occur.

Investigation

Urinalysis usually shows +++ or ++++ protein on dipstick. The degree of proteinuria is variable and is usually of the selective type. Microscopic hematuria is present in 15–20% of patients with minimal change nephrotic syndrome. Microscopy of the urine may show red blood cells or granular casts, which suggests the alternative diagnosis of chronic glomerulonephritis as the underlying cause for nephrotic syndrome.

A timed collection of urine for protein excretion is not necessary when the diagnosis is clear. Blood urea and creatinine tests are important to establish the presence or absence of renal impairment. Blood electrolytes, total protein, albumin, globulin and cholesterol should also be measured.

Treatment

All children should be admitted to hospital with their first presentation of nephrotic syndrome. With relapses, they can sometimes be managed as outpatients after consultation with their treating physician. The components of the treatment will be considered individually

a. Albumin

In nephrotic syndrome, acute renal impairment is due to renal hypoperfusion. Albumin is the treatment of choice. Intravenous albumin is indicated for:

• anuria

• hypotension

• poor skin perfusion with skin mottling

• poor capillary return.

These are all indicators of a depleted vascular space. Albumin should be given only in consultation with the treating consultant. The dose is 20% albumin 5 ml/kg weight(1 g/kg weight) over 4 hr i.v. Beware of the possibility of hypertension and pulmonary edema. Gross genital edema causing discomfort may also be an indication for albumin.

b. Furosemide

Furosemide (1 mg/kg weight i.v.) should be given only if the peripheral perfusion markedly improves following the albumin or there are signs of pulmonary edema or hypertension.

c. Steroids

Corticosteroids are usually given in the form of prednisolone. Occasionally their use may be delayed until postrenal biopsy at the discretion of the treating physician. The usual dose of prednisolone is 60 mg/m² per day as single dose up to a maximum of 80 mg per day until remission of proteinuria (to trace or negative on urinalysis) for 4 days, then in reducing doses. There are various regimens for dose reduction. One example is:

•  prednisolone 45 mg/m² per day for 8 days then

• 60 mg/m² per alternate day for 8 days (four doses) then

• 45 mg/m² per alternate day for 8 days then

• 30 mg/m² per alternate day for 8 days then

• Reduce by 5 mg every 8 days until finished

d. Antibiotics

The altered immune system in patients with nephrotic syndrome is responsible for their enhanced risk of infection. Oral penicillin 12.5 mg/kg weight per dose b.d. is effective prophylaxis during the edematous phase. If the child is profoundly ill or appears to have sepsis, give cefotaxime 50 mg/kg weight per dose 6 hourly to a maximum of 2 g per dose (to cover Streptococcus pneumoniae, Hemophilus influenzae and Escherichia coli).

e. Anticoagulants

Renal, femoral, cerebral and pulmonary thrombosis can occur in nephrotic patients owing to hypovolemia, high platelet counts and loss of antithrombin III. Thus low-dose aspirin (10 mg/kg weight alternate days) is recommended in edematous nephrotic patients.

General measures

Other general measures include:

• Free fluid intake

• Diet with no added salt

• Strict fluid balance

• Daily weight

Relapses

Over 75% of patients will experience at least one relapse. A relapse is defined as proteinuria ++++ or +++ for 4 days. Management should be discussed with a physician. Prednisolone 60 mg/m² per day should be given until the urine is protein-free for 3 days and then the dose should be slowly reduced as above. If edema is absent, these relapses may not require penicillin and aspirin. Infrequent relapses (less than two relapses within a 6-month period) can be managed in the manner outlined above.

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Urinary Tract Infection (UTI) in Pediatric

The urinary tract is a common site of infection in children. The annual incidence is up to 1% in girls, but less common in boys. Radiological abnormalities are present in about 40% of children with UTIs, the most common being reflux. Asymptomatic bacteriuria in schoolgirls is about 1–2%. It is often difficult to diagnose a UTI on history or examination alone in children and a high index of suspicion must be held. The consequences of missing a UTI in a child with even minor urinary tract abnormalities may be significant.

Positive dipstick for leucocytes and nitrites in a sick child does not exclude another site of serious infection (e.g. meningitis). Organisms may also spread from the urinary tract to elsewhere including the meninges. Therefore further investigations as part of a septic work-up (e.g. LP) should not be omitted in a sick child who returns a positive dipstick.

Source pict: http://www.tipdisease.com/2013/12/urinary-tract-infection-in-children.html

History

Symptoms of serious urinary infections are often non-specific and include fever, irritability, poor feeding and vomiting. More specific features may include loin or abdominal pain, frequency and dysuria. These localising signs are often absent in younger patients. Some children with UTIs may look quite well, while others may appear very unwell.

Examination

This is often normal other than the presence of fever. Loin or suprapubic tenderness may be present. Urinary dipstick testing is only a screening test for a UTI. It has poor sensitivity and specificity (see below).

Initial investigations

A UTI cannot be diagnosed on symptoms alone, nor by culture of urine from a bag specimen. A definitive diagnosis can only be made by culture of urine obtained in a sterile fashion from a mid-stream urine (MSU), suprapubic aspiration (SPA), or a catheter specimen of urine (CSU). Prior antibiotic therapy may lead to negative urine culture in patients with UTI. The laboratory will test for antibacterial activity in the urine. Any child who is unwell or is under 6 months old should also have blood culture and electrolytes tested and should be considered for lumbar puncture.

a. Dipstick urine tests

Dipsticks can detect urinary protein, blood, nitrites (produced by bacterial reduction of urinary nitrate), and leucocyte esterase (an enzyme present in white blood cells). They are a screening test only. If you really suspect UTI you must send a specimen for microscopy and culture. Blood and protein are unreliable markers of UTI. Not all organisms produce nitrites and nitrites take time to develop in urine and so have poor sensitivity. Nitrites may appear in the urine in the presence of infections in other body systems.

Not all patients with UTI have pyuria. Leucocyte esterase can only be detected with relatively high WBC counts in urine, so the test has low sensitivity. Leucocytes from local sources (vagina, foreskin) may contaminate urine. Leucocytes appear in the urine in many other febrile illnesses, e.g. upper respiratory tract infection, pneumonia, etc. So the specificity is low. Overall combined sensitivity for both nitrites and leucocytes is around 50%, i.e. dipsticks may miss 50% of infections.

b. Urine specimen collection

There are several ways to collect urine specimens in children, each with its benefits and problems. Practice differs around the world. In the UK, SPA is the method of choice in

infants if a clean catch specimen is not possible. However, in North America, SPA is rarely practised. Parents are offered a choice between awaiting bag screening, confirmed

by CSU on positive specimens, or immediate catheterisation. 

- Urine bag. A urine bag is useful for collecting urine for screening purposes in children who cannot void on request (approximately 0–3 years). The genitalia should be washed with water and dried before application of the bag. Urine is tested with a dipstick for leucocytes and nitrites. If it is positive for either, you should obtain a definitive specimen by SPA (or CSU if SPA fails). If clinical suspicion is high, send a definitive specimen for culture regardless of the dipstick result. A negative dipstick result does not exclude a UTI. Do not send bag specimens for culture in acute presentations. Antibiotics should not be given unless a definitive urine specimen has been obtained.

- Suprapubic aspiration (SPA). SPA remains the preferred method in the UK to collect a minimally contaminated specimen. It should be considered in children too young to obtain an MSU, and with a high probability of UTI, or who are unwell and who warrant a more invasive investigation. The child should be offered fluid to drink. Bedside ultrasound equipment, if available, can improve the success rate of SPA by detecting a full bladder. One author reports 60% success collection rate of SPA and this increases to 80% if bladder ultrasound is used. The specimen should be screened with a dipstick and then sent for culture. Any growth from SPA urine usually indicates infection (but note possible contamination by skin commensals and fecal flora may occasionally produce a mixed growth).

- Catheter specimens. These are useful if SPA fails. The first few drops of the specimen should be discarded and the remaining specimen should always be sent for culture. Any growth of over 103 organisms per ml indicates infection. 

- Mid-stream urine (MSU). A mid-stream urine can be obtained from children who can void on request. The genitalia should be washed with water and dried before the specimen is taken. The first few millilitres should be voided and not collected and then a specimen is obtained. A pure growth of over 108 organisms per ml indicates infection. Apure growth of over 105 organisms per ml may indicate early infection and requires a repeat 

Treatment of UTI

Antibiotics may be given orally or intravenously for a UTI. Oral medication is appropriate for those over the age of 6 months who are not systemically unwell. Cotrimoxazole (200/40 mg in 5 ml) 0.3 ml/ Kg weight b.d. orally for 1 week is a suitable antibiotic. Alternatives include cephalexin 15 mg kg−1 (500 mg) orally three times a day. Any child who is unwell, and most children under 6 months, should be admitted for i.v. antibiotics. Treatment options vary around the world but suitable regimens include cefuroxime 50 mg/Kg weight per dose (maximum 2g) or gentamicin 7.5 mg/Kg weight (maximum dose 240 mg) i.v. daily and benzylpenicillin 50 mg/Kg weight (maximum dose 3 g) i.v. 6 hourly for children over 1 month of age. Gentamicin levels should be taken to ensure appropriate time between subsequent doses. All children should have antibiotic sensitivities checked at 24–48 hours and therapy adjusted accordingly. For children who are still in nappies a prophylactic dose of antibiotic, e.g. co-trimoxazole (200/40 mg in 5 ml) 0.15 ml/Kg weight in a single daily dose, or nitrofurantoin 3 mg/Kg weight at night should be maintained until the child is seen for follow up. If the child is not settling, repeat the urine culture to determine eradication of organism. A shocked child will require fluid resuscitation. Any child with underlying urinary  tract abnormalities should be discussed with the registrar or consultant.

Follow up investigations

All children with proven UTI should be referred for follow up in the general pediatric clinic, or by the child’s own pediatrician. All those with their first UTI should have a renal ultrasound. A micturating cysto-urethrogram (MCU), abdominal X-ray and DMSA (dimercapto-succinoacetic acid) scan may be necessary, but the decision needs to be considered on an individual basis. They are usually done in children under 1 year of age, and may be necessary for older children according to circumstances. For older children, discussion of the need for MCU should be deferred to the outpatient follow up visit. 

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Diabetes in a mildly ill child

Assessment

Occasionally an astute clinician makes the diagnosis of diabetes mellitus in a mildly ill child, with <3% dehydration, no acidosis and no vomiting. Baseline investigations should be carried out, as in the child with ketoacidosis. The diagnosis of diabetes mellitus brings with it a lifetime of treatment. The education and care of child and family should be taken over by a team including a pediatrician, nurses and a dietician. However, management can be initiated without admission to hospital.

Management

Initial insulin treatment. Give 0.25 units/Kg weight of quick-acting insulin s.c. stat. If the child is within 2 hours of a meal, give the meal-time dose only. Halve the dose if he or she is under 4 years old. Before breakfast and lunch (7.30 a.m., 11.30 a.m.) give 0.25 units/Kg weight of quick-acting insulin. Before the evening meal (5.30 p.m.) give 0.25 units/Kg weight of quick-acting insulin and 0.25 units/Kg weight of intermediate-acting insulin. If this is the first insulin dose, give 0.25 units/Kg weight quick-acting insulin only, followed by a further 0.25 units/Kg weight quick-acting insulin at midnight followed by a snack.

Ongoing insulin treatment. Once normoglycemia is achieved and ketonuria disappears, you should change the insulin to a twice daily mixture of short and intermediate insulins usually at 1 unit/Kg weight but this may need modification. It should be given as 2/3 in morning and 1/3 at night; 2/3 of each dose should be intermediate-acting, and 1/3 short-acting. Occasionally older adolescents go onto a basal bolus regimen of 30– 40% intermediate acting insulin given at 10 p.m., with the rest given as short-acting insulin in 3 equal doses before meals.

You must inform your consultant about all admissions of children with diabetic ketoacidosis.

Mildly ill hyperglycemic diabetic patients who are already on insulin Children who have already been diagnosed as having diabetes mellitus and who are already on insulin can present to the Emergency Department with a mild illness and hyperglycemia. They are usually advised to take 10% of total daily dose of insulin as rapid-acting insulin every 2 hours until normoglycemic (in addition to usual insulin). You should notify your consultant if there are any management issues that you want to discuss.

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Diabetes Melitus in Pediatric Emergency

Thirty per cent of children with diabetes present with vomiting and secondary dehydration from the development of acidosis and ketosis. Diabetic ketoacidocis is a medical emergency. The clinical presentation may vary from polydipsia and polyuria or abdominal pain and vomiting to dehydration and weight loss with rapid acidotic breathing. It is important to check the blood glucose in any child who presents with any of these signs or symptoms.

Assessment

Assessment includes the clinical assessment, particularly of the level of dehydration and the laboratory investigations. The level of dehydration is often overestimated.

Degree of dehydration

• Mild-nil (<4%): no clinical signs

• Moderate (4–7%): easily detectable dehydration, e.g. reduced skin turgor, poor capillary return

• Severe (>7%): poor perfusion, rapid pulse, reduced blood pressure, i.e. shock.

Investigations

• Blood glucose, urea, electrolytes.

• Arterial or capillary acid/base

• Urine: ketones, culture

• Check for precipitating cause, e.g. infection (urine, FBC, blood cultures; consider CXR)

• Islet cell antibodies and insulin antibodies in newly diagnosed patients.

Management

Fluid requirements

If hypoperfusion is present, give normal saline at 20 ml/kg weight stat. This should be repeated until the patient is hemodynamically stable with warm, pink extremities and rapid capillary refill time. If more than 30 ml/kg weight is needed, call for senior advice. Rehydration should continue with normal saline.

The child should be kept nil by mouth (except ice to suck) until alert and stable. A nasogastric tube should be inserted if he or she is comatose or has recurrent vomiting. It should be left on free drainage. Rehydration can be completed orally after the first 24–36 hours if the patient is metabolically stable.

Maintenance fluids

If the blood sugar falls very quickly, i.e. within the first few hours, you should change to normal saline with 5% dextrose. When the blood sugar reaches 12–15 mmol/liter, use 0.45% NaCl with 5% dextrose. You should aim to keep the blood sugar at 10–12 mmol/liter. 

If the blood glucose falls below 10–12 mmol/liter and the patient is still sick and acidotic, increase the dextrose in the infusate to 7.5–10%. Do not turn down insulin infusion.

Bicarbonate

Bicarbonate is usually not necessary if shock has been adequately corrected and should not be required in most cases. You must remember that treatment of the dehydration will correct the acid-base disturbance. In extremely sick children (with pH <7.0±HCO3<5 mmol/liter), small amounts of sodium bicarbonate can be given after discussion with the consultant endocrinologist. It should be given over 30 minutes with cardiac monitoring.

The acid base status must then be reassessed.

Note:

• Remember the risk of hypokalemia.

• Continuing acidosis usually means insufficient resuscitation.

Insulin

The insulin should be prepared by adding 50 units of clear/rapid-acting insulin (Actrapid HM or Humulin R) to 49.5 ml 0.9% NaCl (1 unit per ml solution). The insulin infusion may be run as a sideline with the rehydrating fluid via a 3-way tap, provided a syringe

pump is used. Ensure that the insulin is clearly labelled.

You should start at 0.1 units/Kg weight per hour in newly diagnosed children, and in those already on insulin who have glucose levels >15 mmol/liter. Children who have had their usual insulin and whose blood sugars are <15 mmol/liter should receive 0.05 units/kg weight per hour. Adjust the concentration of dextrose to keep the blood glucose at 10–12 mmol/liter.

Adequate insulin must be continued to clear acidosis (ketonemia).

The insulin infusion can be discontinued when the child is alert and metabolically stable (blood glucose <10–12 mmol/liter, pH>7.30 and HCO3>15). The best time to change to subcutaneous insulin is just before meal time. The insulin infusion should only be stopped 30 minutes after the first subcutaneous injection of insulin.

Potassium

Potassium chloride should be added to each bag of i.v. fluid once the patient has urinated. Add this at a rate of 40 mmol/liter if the body weight <30 kg, or 60 mmol/liter if >30 kg. You should measure the levels 2 hours after starting therapy and 2–4 hourly thereafter.

Specimens should in general be arterial or venous. Give no potassium if the serum level is >5.5 mmol/liter or if the patient is anuric.

Admission to ICU

Consider admission to the ICU if the patient is under 2 years of age at onset or if in coma, cardiovascular compromise or is having seizures. Strict monitoring must continue while the child is transferred to ward or to the ICU .

Monitoring during transport to ICU

• Strict fluid balance; check all urine for ketones

• Hourly observations: pulse, BP, respiratory rate, level of consciousness and pupils

• Hourly glucose (Glucometer) during insulin infusion; other biochemistry as clinically indicated

• 4 hourly temperature measurements

Added hazards during the management of ketoacidosis include:

1. Hypernatremia. 

Measured serum sodium is depressed by the dilutional effect of the hyperglycemia. To ‘adjust’ sodium concentration, use the following formula:

i.e. 3 mmol/liter of sodium to be added to the measured result for every 10 mmol/liter of glucose above 5.5 mmol/liter. If Na is >160 mmol/liter, the case should be discussed with the consultant. The sodium should rise as the glucose falls during treatment. If this does not happen or if hyponatremia develops, it usually indicates overzealous volume correction and insufficient electrolyte replacement. This may place the patient at risk of cerebral edema.

2. Hypoglycemia.

 Hypoglycemia can occur during correction of the hyperglycemia. If the blood glucose is <2.2 mol/liter give i.v. 10% dextrose 5 ml/kg weight. Do not discontinue the insulin infusion. Continue with a 10% dextrose infusion until stable. Cerebral edema. Some degree of subclinical brain swelling is present during most episodes of diabetic ketoacidosis. Clinical cerebral edema occurs suddenly, usually between 6 and 12 hours after starting therapy (range 2–24 hours). Mortality or severe morbidity is very high without early treatment.

3. Cerebral edema

Occurrence of cerebral edema is reduced by slow correction of the fluid and biochemical abnormalities. Optimally, the rate of fall of blood glucose and serum osmolality should not exceed 5 mmol/liter per hour, but in children there is often a quicker initial fall in glucose. Patients should be nursed head up. The warning signs are :

Warning signs of cerebral edema

• First presentation, long history of poor control, young age (<5 years)

• No sodium rise as glucose falls, hyponatremia during therapy, initial adjusted hypernatremia

• Headache, irritability, lethargy, depressed consciousness, incontinence, thermal instability

• Very late—bradycardia, increased BP and respiratory impairment

Treatment consists of:

• Mannitol 20% 0.5 g/kg weight i.v. stat if hemodynamically stable. Give immediately when the clinical diagnosis is made—do not delay for confirmatory brain scan.

• Reduce fluid input to 2/3 and replace deficit over 72 hours rather than 24 hours.

• Nurse head up.

• Transfer immediately to ICU.

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Hypoglycemia in Pediatric Emergency

There should be a low threshold for performing a Dextrostix test in the acutely unwell child in the Emergency Department. Beyond the neonatal period, hypoglycemia is defined as a blood glucose less than 2.5 mmol/liter. In children who have had a seizure, hypoglycemia can be the cause of the seizure, or the result of a prolonged seizure.

Effects of hypoglycemia

The effects of the hypoglycemia itself, from whatever cause, are mainly effects on the central nervous system and those of adrenergic overdrive as Table below. Other clinical signs will depend on the cause of the hypoglycemia and a thorough clinical examination is required, including height and weight. 

Hypoglycemia Effects in pediatric

Investigation

Blood and urine must be taken off for metabolic investigation as soon as the child presents, before treatment is commenced. Investigations are listed in Box A.

Note that:

• Hyperinsulinism is the commonest cause of hypoglycemia in children under 2 years old, This diagnosis is excluded by ketonuria.

• ‘Accelerated starvation’ (idiopathic ketotic hypoglycemia) is the commonest cause of hypoglycemia after the age of 2 years, but may present earlier. The diagnosis can be established when fasting-induced hypoglycemia is accompanied by elevated urinary ketones, in the absence of other pathology. It is treated by frequent high protein and carbohydrate meals.

Management

Symptomatic hypoglycemia should be treated with an i.v. bolus of 5 ml/kg weight of 10% dextrose (0.25–0.5 mg/kg weight). The expected maintenance infusion rate is 3–5 ml/kg weight per hour of 10% dextrose (6–8 mg/kg weight per minut). A required infusion rate of 10–20 mg/kg weight per minute is consistent with hyper-insulinism.

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