A Lange Medical Book Pediatrics on call - part 4 ppsx

Problem.A 7-day-old infant is admitted with a history of jitterinessand poor feeding associated with total serum calcium level of 6.0 mg/dLnormal for this age: 7.6–10.9 mg/dL.. Is low se

45.HYPERTENSION 217

5 Enalaprilat.Effective in 5–10 mcg/kg doses q8–24h Becauseneonates have a more active renin-angiotensin system, theyare more sensitive to drug than older children and should begiven dose in lower range Closely monitor renal function andserum potassium level

6 Hydralazine.Old but trustworthy drug given at 0.1–0.5 mg/kg

as a bolus Maximum dose per bolus is 20 mg Can be

repeat-ed q3–4h Monitor heart rate and hold doses if significanttachycardia Watch for resistance to BP-lowering effect

7 Diazoxide.Extremely effective; can cause precipitous drop in

BP and elevate blood glucose concentration If normal salineinfusion is available at bedside to treat acute hypotension, 1–3mg/kg quick IV push works well Second bolus can be givenwithin 5–15 minutes if needed, not to exceed 5 mg/kg com-bined dose Effective dose can be repeated q4–24h

B Hypertensive Urgency.Symptomatic hypertension without dence of end-organ damage Oral treatment is acceptable,although IV medications may also be considered Long-actingoral agents (ie, those recommended in once- or twice-daily doses)should be avoided due to delayed peak concentration

evi-1 “Sublingual” nifedipine.No excessive side effects reported inpediatric literature; frequently administered, convenient drug ofchoice for pediatric hypertensive urgencies if administered inappropriate dose Conventional dose is 0.25–0.5 mg/kg perdose q3–4h, not to exceed 10 mg per dose or 3 mg/kg/day.Although labeled as sublingual, absorption takes place fromstomach, so capsule needs to be opened before being swal-lowing

2 Oral hydralazine.Doses of 0.75–1 mg/kg q4–6h may workwell Maximum one-time dose is 25 mg, with cumulative dailydose of 5 mg/kg

3 Minoxidil.More powerful vasodilator than hydralazine, withmore side effects In acute situations, 0.2 mg/kg may work well.Add diuretic if treatment exceeds a few days

4 Propranolol.Given in doses of 0.12–0.25 mg/kg q6–12h

5 Chronic hypertension.Not within scope of this discussion,but lifestyle changes, such as low-salt diet, exercise, andweight loss, should be part of any comprehensive treatmentplan for patients with chronic hypertension

VI Problem Case Diagnosis.The 13-year-old girl had modest BPelevation, which might be attributed to office hypertension, essen-tial hypertension, or metabolic syndrome Further investigationshowed multiple high BP readings had been obtained by schoolnurse, and patient also had a strong family history of hypertension.Diagnosis of essential hypertension was made, and patient’s BPwas well controlled on salt restriction and hydrochlorothiazide,

25 mg daily

Fivush B, Neu AM, Furth S Acute hypertensive crises in children: Emergencies and

urgencies Curr Opin Pediatr 1997;9:233–236.

Friedman AL Approach to the treatment of hypertension in children Heart Dis

2002;4:47–50.

National High Blood Pressure Education Working Group on Hypertension Control in Children and Adolescents Update on the 1987 task force report on high blood pressure in children and adolescents: A working group report from the National

High Blood Pressure Education Program Pediatrics 1996;98:649–658 Sinaiko AR Hypertension in children N Engl J Med 1996;335:1968–1973.

46 HYPOCALCEMIA

I Problem.A 7-day-old infant is admitted with a history of jitterinessand poor feeding associated with total serum calcium level of 6.0 mg/dL(normal for this age: 7.6–10.9 mg/dL)

II Immediate Questions

A Is patient symptomatic?Hypocalcemia can be asymptomatic orassociated with serious life-threatening manifestations Severemanifestations that require immediate treatment include pares-thesias, tetany, laryngospasm, and seizures Diagnostic signssuggesting the need for immediate treatment are positiveChvostek and Trousseau signs

B Is low serum calcium level an artifact or reflective of low ized calcium?Whereas total serum calcium is routinely meas-ured, it is the ionized calcium component that is physiologicallyimportant Ionized calcium can be measured directly or can beestimated by subtracting 0.8 mg/dL for every 1 g/dL by whichserum albumin is < 4 g/dL

ion-C Is serum magnesium level low?Serum calcium will not respond

to correction with IV or oral calcium as long as severe nesemia remains untreated

hypomag-D Pertinent Historical Information

1 Infants.Is there a history of parathyroid or other endocrine eases? What is the gestational history? Pay particular attention

dis-to maternal illnesses (eg, diabetes mellitus, roidism), medications, birth history, and gestational age Whattype of formula or supplements is infant given?

hyperparathy-46.HYPOCALCEMIA 219

2 Children.Is there a history of acute or chronic illnesses, ication use, or surgery? Ask about diet and sun exposure

med-III Differential Diagnosis.Causes of hypocalcemia in infants need to

be distinguished from those in children Neonatal hypocalcemia isclassically divided into early (first 4 days of life) and late, which usu-ally presents at 5–10 days of life In children of all ages, abnormali-ties can be divided into those involving parathyroid hormone (PTH),vitamin D, and binding or distribution of calcium

A Neonatal Hypocalcemia

1 Early neonatal hypocalcemia

a Preterm infants.Transiently decreased PTH secretion

b Neonates with asphyxia.Possibly associated with increasedcalcitonin secretion

c Infants of diabetic mothers.Related to maternal magnesemia

hypo-d Infants whose mothers had preeclampsia.Related tomaternal hypomagnesemia

2 Late neonatal hypocalcemia

a Dietary phosphate loading.Results from inability of ture kidneys to excrete phosphate in infants fed cow’s milkformula

imma-b Hypoparathyroidism.Transient, insufficient PTH secretion

c Hypomagnesemia.Can be associated with rare defects inmagnesium transport

3 Miscellaneous causes of hypocalcemia in infants and neonates

a Congenital hypoparathyroidism.Can be associated with

DiGeorge anomaly or CATCH-22 syndrome (cardiac alies, abnormal facies, thymic aplasia, cleft palate, hypocal- cemia, caused by deletion in chromosome 22q11.2).

anom-b “Late-late” hypocalcemia.Skeletal hypomineralizationand poor mineral and vitamin D intake presenting at 2–4months of age

c Infants of hyperparathyroid mothers.

d Ionized hypocalcemia.Associated with exchange fusions of citrated blood, lipid infusions, or respiratoryalkalosis

trans-B Childhood Hypocalcemia

1 Parathyroid disorders

a Hypoparathyroidism.Associated with chromosome 22q11abnormalities (see A, 3, a, earlier) or autoimmune syn-dromes such as autoimmune polyglandular syndrome

b Pseudohypoparathyroidism.Disorders of activation of thecellular effects of PTH

c Calcium-sensing abnormalities.Occurs when roid gland is abnormally sensitive to serum calcium, causingPTH levels to be low in relation to level of calcium

b Vitamin D–dependent rickets.Block in 1,25-dihydroxyvitamin

D formation (type 1) or abnormal receptor (type 2)

c Renal failure.Acute or chronic, with inadequate formation

of 1,25-dihydroxyvitamin D

d Fanconi syndrome.Proximal renal tubular dysfunction withlow 1,25-dihydroxyvitamin D formation and renal phosphatewasting

e Altered metabolism.Often due to drugs such as barbital, phenytoin, or ketoconazole

pheno-3 Abnormal distribution or binding of calcium

a Tumor lysis syndrome.Hyperphosphatemia, hypocalcemia,and acute renal failure

b Acute rhabdomyolysis.Trapping of calcium into injuredmuscle

c Hungry bone syndrome.Shift of calcium and phosphorusinto bone, often after parathyroidectomy

d Drugs.Foscarnet, bisphosphonates, calcitonin, calciumchelators (citrate, phosphorus)

e Miscellaneous.Acute pancreatitis, toxic shock syndrome,sepsis

IV Database

A Physical Exam Key Points

1 General appearance.Albright hereditary osteodystrophy withpseudohypoparathyroidism (short stature, obesity, round face);large-for-gestational-age infants of diabetic mothers

2 Skin.Mucocutaneous candidiasis with autoimmune polyglandularsyndrome; alopecia with type 2 vitamin D–dependent rickets

3 HEENT.Facial features of DiGeorge syndrome, laryngospasm,cataracts

4 Skeletal findings. Evidence of bowing with rickets; shortmetacarpals and metatarsals with pseudohypoparathyroidism

5 Neuromuscular exam.Neuromuscular excitability manifested

by irritability, facial grimacing, hyperactive deep tendonreflexes, muscular spasms, twitching and tetany, confusion,seizures

6 Heart.Cardiac abnormalities seen in DiGeorge syndrome

7 Specific tests for tetany of hypocalcemia

a Chvostek sign.Elicited by tapping on the facial nerve belowthe zygomatic arch and 2 cm anterior to the earlobe Positivesign ranges from twitching of the lip at the angle of themouth to contraction of the facial muscles

46.HYPOCALCEMIA 221

b Trousseau sign.Performed by inflating a BP cuff on theupper arm to just above systolic BP for 3 minutes Withhypocalcemia, carpal spasm may occur in response toischemia of the ulnar nerve

B Laboratory Data

1 Serum electrolytes.In addition to total calcium, focus onpotassium, phosphate, and magnesium levels The latter twoare not usually included in standard panels and may have to beordered separately Serum calcium should be interpreted inrelation to serum albumin (see II, B, earlier) Hyperkalemia may

be a sign of tumor lysis Serum phosphate is elevated in renalfailure, tumor lysis, rhabdomyolysis, phosphate enemas, andparathyroid disorders It is also seen in most of the neonatalhypocalcemic disorders Hypophosphatemia is a sign ofvitamin D disorders, hungry bone syndrome, and Fanconisyndrome Severe hypomagnesemia, < 1 mg/dL, is a cause ofrefractory hypocalcemia

2 Serum albumin.As previously described

3 Ionized calcium.Particularly valuable in the presence ofalkalosis and chelators, which may selectively lower ionizedcalcium In confusing cases, ionized calcium can help withdiagnosis and management

4 BUN and creatinine.Signs of renal failure, acute or chronic

5 PTH level.Should be interpreted in relation to serum calciumlevel

6 Vitamin D levels.25-Hydroxyvitamin D identifies deficiency orabnormalities of metabolism whereas 1,25-dihydroxyvitamin Dmay be helpful in patients with vitamin D–dependent statesand renal disease

C Radiographic and Other Studies

1 Bone films.Look for rickets, osteopenia, or renal strophy

osteody-2 ECG.Hypocalcemia may result in prolonged QT interval or Twave inversion

V Plan.Evaluate for symptomatic hypocalcemia that would necessitateimmediate IV treatment with calcium and possibly magnesium.Obtain laboratory studies and initiate oral treatment after patient isstabilized

A Neonates

1 Emergency treatment

a. For symptomatic hypocalcemia or when serum calcium is

< 5–6 mg/dL, give 10–20 mg elemental calcium per kilogrambody weight, or 1–2 mL of calcium gluconate per kilogrambody weight (10% solution) This should be given no fasterthan 1 mL/min under constant cardiac monitoring

b.Treat hypomagnesemia with 0.1–0.2 mL/kg of 50% sium sulfate (0.4–0.8 mEq/kg or 5–10 mg/kg) IV or IM, again

3 Vitamin D.Daily supplement of oral vitamin D at a dose of400–2000 IU/day.

B Children

1 Emergency treatment

a. For acute symptomatic hypocalcemia, give 2–3 mg tal calcium per kilogram body weight or 0.25 mL calciumgluconate per kilogram body weight (10% solution) IV at arate of no more than 1 mL/min under constant cardiac mon-itoring Can continue with a constant infusion at a rate of50–75 mg elemental calcium per kilogram per day untilhypocalcemia is corrected

elemen-b.For hypomagnesemic hypocalcemia, give 6 mg elementalmagnesium per kilogram body weight or 0.12 mL per kilo-gram body weight of 50% magnesium sulfate IM or IV over1–4 hours

2 Chronic treatment

a Calcium.Oral calcium at a dose of 500–1000 mg elementalcalcium per dose q6h This can be given as liquid (calciumcarbonate, 100 mg/mL; calcium glubionate, 25 mg/mL) orone of many tablet forms

b Vitamin D.Treat vitamin D deficiency with ergocalciferoldrops at a dose of 800–8000 IU/day Doses have beendescribed in the literature up to 600,000 units given in asingle day For patients with renal failure, calcitriol can begiven at a dose of 0.25–1 mcg/day Patients withhypoparathyroidism, pseudohypoparathyroidism, and vita-min D–dependent rickets type 1 also require calcitriol thera-

py rather than ergocalciferol This can be given orally orintravenously

VI Problem Case Diagnosis.The 1-week-old infant had late neonatalhypocalcemia, and a phosphorus level of 9.2 mg/dL Infant was treatedwith IV calcium gluconate and placed on Similac PM 60/40 There was

no evidence of DiGeorge syndrome or recurrence of hypocalcemia

VII Teaching Pearl: Question.In most cases of vitamin D–deficiencyrickets, is the level of 1,25-dihydroxyvitamin D high, normal, or low?

VIII Teaching Pearl: Answer.The 1,25-dihydroxyvitamin D levels areusually in the normal range, but this is inappropriate for the level of

Bone and Mineral Research, 2003:286–288.

Koo W Hypocalcemia and hypercalcemia in neonates In: Umpaichitra V, Bastian W,

Castells S Hypocalcemia in children: Pathogenesis and management Clin Pediatr 2001;40:305.

47 HYPOGLYCEMIA

I Problem.A previously healthy 3-year-old boy is brought to the gency department in the early morning after his parents found himdifficult to arouse The family had been traveling and the child had aprolonged fast His blood glucose level is 28 mg/dL

emer-II Immediate Questions

A What constitutes a low serum glucose level in a patient of this age?Hypoglycemia in children is defined as follows

1 Term neonate.Serum glucose < 50–60 mg/dL

2 Infants and young children.Serum glucose < 45–60 mg/dL

3 Older children and adolescents.Serum glucose < 60 mg/dL

B What is patient’s mental status?An unconscious patient mustfirst be stabilized Quickly assess ABCs (airway, breathing, andcirculation) and obtain access to draw samples for laboratoryanalysis and provide glucose

C Is patient diabetic?Excess insulin administration or tion of insulin in a patient who is not eating can induce hypo-glycemia

administra-D Has patient had adequate intake? Was TPN abruptly tinued?Often children who are sick have decreased oral intakeand may not have had anything to eat or drink for several hours.Abrupt discontinuation of dextrose-containing fluids can also lead

discon-to hypoglycemia

E Is ingestion a possibility?Many different agents can inducehypoglycemia, including salicylates, alcohol, and oral hypo-glycemic agents

F Is patient a newborn, an infant of a diabetic mother, ine growth retarded (IUGR), or small or large for gestational age (SGA or LGA)?Infants of diabetic mothers are often hyperin-sulinemic at birth and when glucose stores from the placenta areremoved can become hypoglycemic SGA infants (defined as < 10thpercentile or < 2.5 kg at term) and LGA infants (defined as > 95thpercentile or > 4.0 kg at term) are at increased risk of hypoglycemia

intrauter-G What symptoms are associated with hypoglycemia?

Symptoms include anxiety, diaphoresis, jitteriness, weakness,

224 I:ON CALL PROBLEMSnausea, headache, and confusion Infants with hypoglycemia canpresent with few symptoms.

III Differential Diagnosis

A Medications

1 Insulin.Check for administration error, including patient

identi-ty, dose, preparation, and route

2 Other medications.Ingestion of agents such as oral glycemics, salicylates, quinine, and pentamidine can lead tohypoglycemia

hypo-3 Ethanol.Consider accidental ingestion of alcohol or otherethanol-containing substances such as mouthwash

B Inborn Errors of Metabolism

1 Carbohydrate metabolism.Examples include galactosemiaand glycogen storage diseases

2 Lipid metabolism.Examples include carnitine deficiencies;very long–, long-, medium-, and short-chain acyl-CoA dehy-drogenase deficiency

3 Amino acid metabolism.Examples include Maple syrup urinedisease and methylmalonic acidemia

C Neonatal Causes

1 Gestational diabetes.These infants, often LGA, are sulinemic at birth and can become hypoglycemic when the pla-cental glucose source is removed

hyperin-2 IUGR or SGA.These infants can have limited glycogen storesand decreased body fat and muscle protein

3 Perinatal stress.Stressors such as fetal hypoxia and turity can lead to hypoglycemia

prema-4 Genetic malformations.Patients with Beckwith-Wiedemannsyndrome may exhibit hypoglycemia

D Ketotic Hypoglycemia.This is the most common form of hood hypoglycemia and is related to prolonged fast, usuallywith intercurrent illness Typical presentation is a child, aged

child-18 months to 5 years, who has missed dinner or breakfast and isfound to be difficult to arouse Can be associated with seizuresand lead to coma

E Sepsis. Hypoglycemia or hyperglycemia can occur in septicshock Usually a sign of late infection

F Severe Liver Failure.Glycogen stores are easily depleted inpatients with advanced liver disease and destruction

G Reactive Hypoglycemia.Can occur post-prandially in a smallpercentage of the population, especially in patients with dumpingsyndrome

H Endocrinopathies. Includes adrenal insufficiency, roidism, and hypopituitarism

hypothy-I Abrupt Discontinuation of TPN.Rare

47.HYPOGLYCEMIA 225

J Factitious Hypoglycemia.Due to laboratory error (unspun bloodthat sits out too long) or as a result of leukocyte metabolism in apatient with markedly increased WBC count

K Insulinoma or Other Neoplasms.

L Other Causes.Severe malnutrition, seizures, vasovagal fainting,narcolepsy, and anxiety attack

IV Database

A Physical Exam Key Points

1.Assess airway, breathing, and circulation (ABCs) and vitalsigns

2.Evaluate for hepatomegaly, pigmentation, short stature, andneurologic signs

B Laboratory Data.Careful history and physical exam usually vide clues to diagnosis Patients with a history of hypoglycemiamay require hospital admission to induce hypoglycemia and toobtain laboratory data during an acute episode

pro-1.Obtain serum glucose, insulin, cortisol, and growth hormonelevels, and urinalysis for ketones If possible, also obtainC-peptide, lactate, ammonia, thyroid-stimulating hormone, andthyroxine levels

2.Serum electrolytes, renal and liver function studies, and CBCmay be helpful in evaluating some of the causes listed underdifferential diagnosis, earlier

C Radiographic and Other Studies.May be indicated to evaluatefor insulinoma, malignancy, and pituitary lesions if suggested byhistory, physical exam, or screening studies

2 Parenteral.In children, give a 2 mL/kg bolus of D25W IV or

IO In infants, give a 2–4 mL/kg bolus of D10W IV or IO Afterthe dextrose bolus, patient should be started on mainte-nance D10W electrolyte solution to provide glucose at a rate of6–8 mg/kg/min

3 Intramuscular or subcutaneous (IM or SQ).If no IV access

is available, give glucagon IM or SQ

a Neonate.Dose is 0.3 mg/kg IM or SQ

b Child or adolescent.Dose is 0.5–1 mg IM or SQ

4 Other agents.Diazoxide, octreotide, and hydrocortisone mayhave a role in treatment of hypoglycemia, depending on thecause

226 I:ON CALL PROBLEMS

B Evaluate for Underlying Cause of Hypoglycemia.If laboratorystudies can be efficiently obtained, this should be accomplishedprior to therapy

VI Problem Case Diagnosis.The 3-year-old child has ketotic glycemia (For further discussion, see Teaching Pearl: Answer,below.)

hypo-VII Teaching Pearl: Question: What is the most common cause ofhypoglycemia in children, and how is it treated?

VIII Teaching Pearl: Answer:Ketotic hypoglycemia is the most commoncause of hypoglycemia in children Immediate treatment consists ofthe administration of glucose (oral glucose if patient can be arousedand airway is intact) Children with this condition are instructed toavoid fasting, especially during times of intercurrent illness, and tohave frequent carbohydrate-rich meals

I Problem.A 6-month-old female infant with a ventricular septal defect

is admitted with a 3-day history of poor feeding, vomiting, anddiarrhea Initial laboratory studies show serum potassium level of2.0 mEq/L (normal for this age: 4.1–5.3 mEq/L)

II Immediate Questions

A Is patient symptomatic?Symptoms of hypokalemia includemuscular weakness, gastric hypomotility, and cardiac distur-bances (arrhythmia, premature atrial contractions [PACs], prema-ture ventricular contractions [PVCs], flattened T waves, STsegment changes, U waves)

B What medication(s) does child take?␤-Agonists, penicillins,loop diuretics, steroids, laxatives, aminoglycosides, and ampho-tericin B may all contribute to hypokalemia Hypokalemia canpotentiate digitalis toxicity

C Is there a history of hypokalemia?A history of hypokalemia inthe patient or a family member may point to associated syn-dromes or tumor

III Differential Diagnosis.To determine the etiology of hypokalemia, onemust first decide which of five primary mechanisms exists: redistribu-tion, renal loss, GI loss, other loss (sweating), or inadequate intake

A Redistribution Hypokalemia.Potassium is primarily an lular ion; hence a small shift of this ion into the cell can cause a

intracel-48.HYPOKALEMIA 227

large change in plasma potassium concentration Extracellularpotassium can shift into the intracellular space in the setting ofalkalosis, ␤-agonist use, catecholamine excess, insulin adminis-tration, hypothermia, and familial periodic paralysis (autosomaldominant)

B Renal Potassium Loss.Can be differentiated based on child’sacid-base status

1 With metabolic acidosis.Includes such disorders as type 1and type 2 renal tubular acidosis, and diabetic ketoacidosis

2 With metabolic alkalosis.Bartter syndrome, Gitelman drome, diuretic therapy, and mineralocorticoid excess (hyperal-dosteronism, Cushing syndrome, adrenal tumor, exogenoussteroid administration)

syn-3 Variable.Renal losses not associated with a specific acid-baseimbalance occur with hypomagnesemia, some penicillins,aminoglycosides, amphotericin B, cisplatin, and osmoticdiuresis

C GI Loss.The major source for extrarenal potassium loss occurs inthe setting of colonic fluid loss, seen with diarrhea and laxativeabuse Severe vomiting can produce hypokalemia in patients withcontraction alkalosis

D Other Loss.Copious sweating is the primary cause of potassiumloss other than from kidney and GI tract

E Inadequate Intake.Produces hypokalemia over time as totalbody stores become depleted

IV Database. Data collection for hypokalemia serves two purposes.First, one must use data to determine the source of potassium deple-tion Second, one must obtain data to assist in diagnosis of relateddisorders and to detect adverse consequences of hypokalemia Most

of the appropriate studies to perform will be based on informationobtained by taking a thorough history Review all medications childmay be taking, including any home remedies administered

A Physical Exam Key Points

1 Overall appearance.Does patient appear severely

dehydrat-ed or cachectic?

2 Heart.Is rhythm regular and heart rate adequate?

3 Lungs.Is child making a good respiratory effort?

4 GI.Any evidence of intestinal dysmotility, ileus, or obstruction?

5 Neurologic exam.Is weakness, blunting of reflexes, or thesia present?

pares-B Laboratory Data

1 Serum electrolytes.Identify associated abnormalities thatmay affect treatment (hypomagnesemia) or exacerbate car-diac disturbances (hypocalcemia)

2 ABGs.Remember, alkalosis can cause intracellular shift ofpotassium In addition, many of the renal causes of potassium

228 I:ON CALL PROBLEMS

loss have an associated acid-base disturbance Finally, ananion gap acidosis may be present in the setting of elevatedlactate with severe dehydration, poor cardiac output, or sepsis.Treatment of acidosis produces a “relative alkalosis” and mayexacerbate hypokalemia, so prioritize therapy

3 Urine.Urine sodium, potassium, chloride, and osmolality mayassist in diagnosis Urine drug screening may be useful ifamphetamine or other sympathomimetic drug overdose is sus-pected

4 Other blood testing.Obtain based on history and index ofsuspicion

a Digoxin level.May be critical in treatment of cardiac bances

distur-b Adrenocorticotropic hormone, cortisol, renin, and aldosterone.Assist in determination of underlying adrenaldisorders

C Radiographic and Other Studies

1 Radiographic studies.Rarely helpful in the acute setting butmay help identify underlying abnormalities responsible forhypokalemia Abdominal ultrasound or CT scan may help iden-tify adrenal tumors, and MRI scan of the brain may identify pitu-itary abnormalities associated with increased cortisol release.These studies should be performed based on an index of sus-picion from history and laboratory results

2 ECG.Of paramount importance, especially as serum

potassi-um level drops below 3 mEq/L Rapid recognition of cardiacdisturbances is critical It is also important to monitor cardiacstatus as therapy is instituted (ECG changes, outlined earlier

at II, A, include PACs, PVCs, flattened T waves, ST segmentchanges, and U waves) The classic finding of a U wave ispoorly understood It is believed to represent delayed repo-larization of cardiac muscle The U wave appears after the

T wave As hypokalemia worsens, the T wave flattens andthe U wave becomes more pronounced, producing whatappears to be a prolonged QT interval

V Plan.Treatment is variable, depending on severity of the potassiumdeficit as well as presence of symptoms and associated conditions.Serum potassium level is not a good indication of total body potassi-

um deficit Patients with diabetic ketoacidosis often present with a mal to high serum potassium level, yet have a severe total body deficit

nor-In adult patients (70-kg man) an estimate of total body potassiumdeficit can be approximated as 150 mEq for each 1 mEq/L decrease

in serum potassium from 4 mEq/L No such physiologic studies havebeen performed in children to produce a reliable estimate

A Mild, Asymptomatic Hypokalemia (serum K+3–3.5 mEq/L).

Depending on cause, may resolve without therapy or require oral

49.HYPOMAGNESEMIA 229

supplementation of potassium chloride (KCl) Must considerongoing loss when correcting serum level as well as daily require-ment of 2–3 mEq/kg/day

B Severe or Symptomatic Hypokalemia (serum K+< 3 mEq/L).

Requires more rapid assessment and therapy as well as morestringent cardiac monitoring Typically IV administration of KCl isrequired Usual dose is 0.5 mEq/kg IV, to be given over 1 hour andnot to exceed 40 mEq total Infusion of as much as 1 mEq/kg/hmay be used in severe, life-threatening hypokalemia It is impor-tant to perform all infusions with appropriate cardiac monitoringand to reassess serum potassium level frequently

C Recalcitrant Hypokalemia. Correct serum magnesium andreconsider severity of ongoing potassium loss

VI Problem Case Diagnosis.Hypokalemia in the 6-month-old infantwas secondary to GI loss from severe gastroenteritis Patientresponded well to IV administration of KCl

VII Teaching Pearl: Question.A patient has a serum potassium level of

3 mEq/L and is also anemic; a blood transfusion is ordered Howshould you approach correcting the potassium level?

VIII Teaching Pearl: Answer. Stored blood is often relatively high inpotassium due to red cell hemolysis If the patient is asymptomatic,

it may be wise not to treat a mild hypokalemia when giving blood.Repeating a potassium level after transfusion may show that youhave accomplished your goal

REFERENCES

Barkin R Pediatric Emergency Medicine, 2nd ed Mosby, 1997.

Feld LG, Kaskel FJ, Schoeneman MJ The approach to fluid and electrolyte therapy

in pediatrics Adv Pediatr 1988;35:497–535.

49 HYPOMAGNESEMIA

I Problem. A 15-year-old renal transplant patient develops acutetetany Serum calcium level is 6.5 mg/dL and serum magnesium,0.8 mg/dL (normal: 1.2–2.6 mg/dL)

II Immediate Questions

A Is patient symptomatic?Important and even life-threateningneuromuscular and cardiovascular manifestations may bepresent

B Are there other important electrolyte disturbances?

Hypocalcemia, hypokalemia, and metabolic alkalosis oftenaccompany hypomagnesemia Although these disturbances need

to be recognized and treated, often it is important to correct thehypomagnesemia first (eg, hypocalcemia)

230 I:ON CALL PROBLEMS

C Pertinent Historical Information

1.In infants, is mother diabetic?

2.Has patient undergone procedures that would lead to chronic

GI disorder?

3.What medication(s) does patient take?

III Differential Diagnosis. Hypomagnesemia generally occurs as aresult of GI disorders, renal losses, or dietary deficiency It is animportant contributing factor for tetany in newborns (see Chapter 47,Hypoglycemia, II, F, p 223, for discussion of infants of diabeticmothers)

A GI Disorders.Often due to loss of magnesium-containing tions

secre-1.Acute or chronic diarrhea

2.Malabsorption syndrome

3.Short gut syndrome

4.Prolonged nasogastric suction or vomiting

5.Protein-calorie malnutrition or kwashiorkor

6.Primary intestinal hypomagnesemia (rare X-linked syndromepresenting in neonates)

B Renal Losses.Due to primary and secondary defects

1 Osmotic diuresis, recovery from acute tubular necrosis (ATN), and volume expansion.Nonspecific losses of magne-sium and other electrolytes

2 Diuretics.Loop diuretics (in particular) and thiazides

3 Nephrotoxic agents. Aminoglycosides, amphotericin B,cisplatin, cyclosporine A

4 Hypercalcemia.Competes with magnesium reabsorption

5 Primary renal magnesium wasting. Bartter syndrome,Gitelman syndrome, isolated magnesium wasting WithBartter and Gitelman syndromes, look for hypokalemia andalkalosis

6 Postrenal transplantation.In addition to cyclosporine A

7 Diabetes mellitus.

IV Database

A Physical Exam Key Point

1 Cardiovascular.Irregular heartbeat and hypertension

2 Neuromuscular.Check for neuromuscular excitability withChvostek and Trousseau signs (see Chapter 46,Hypocalcemia, IV, A, 7, p 220) Muscular tremor, weakness,and carpopedal spasm may be present Observe for ataxia,vertigo, nystagmus, and choreiform movements Importantcause of neonatal tetany

B Laboratory Data

1 Serum electrolytes.Concurrent hypokalemia is very common,whether due to GI or renal losses (primary or secondary)

UMg× PCr

FEMg= × 1000.7× PMg× UCr

In which Cr = creatinine; FE = fractional excretion; P = plasma;

U= urine

Fractional excretion in nonrenal disorders should be < 2%; inrenal disorders, it is typically > 5% Magnesium-loading testsdescribed in adults have not been standardized in children

C Radiographic and Other Studies. Perform ECG to look forarrhythmia (prolonged PR interval, wide QRS complex, dimin-ished T wave)

V Plan.Hypomagnesemia, especially if associated with hypocalcemiaand tetany, can be a medical emergency The magnitude of the mag-nesium deficit cannot be determined with accuracy, so empiric for-mulas are used for replacement Acute IV doses of magnesium need

to be followed by longer term enteral or parenteral therapy for fullreplacement

A Severe Hypomagnesemia With Hypocalcemia or Tetany.Goalfor acute therapy is to increase serum magnesium above 1 mg/dL,which should stop seizures or tetany Can give calcium as well(see Chapter 46, Hypocalcemia, p .)

1 Neonates.Give 0.1–0.2 mL/kg per dose of 50% magnesiumsulfate (0.4–0.8 mEq/kg) IV or IM slowly under constant car-diac monitoring May repeat magnesium dose q12–24h

2 Older children and adolescents.Give 0.12 mL/kg per dose

of 50% magnesium sulfate (0.5 mEq/kg) over 1–4 hours by IV;can repeat q12h

3 Adolescents.In case of seizures, can give 0.2 mEq/kg (up to

15 mEq or 180 mg) over 10 minutes Alternative for severehypomagnesemia is 50 mEq magnesium sulfate IV over 8–24hours Use half dose in presence of renal failure

B Moderate Hypomagnesemia or Long-term Therapy.Half of IVdose is excreted in urine, so to fully correct magnesium depletion,slow replacement over 3–5 days may be needed

1 Young children.Dose is elemental calcium, 10–20 mg/kg perdose 4 times daily

2 Older children and adolescents.Oral dose of 300–600 mg/dayelemental magnesium can be given; divide dose to avoiddiarrhea

VII Teaching Pearl: Question. Do all diuretics cause semia?

hypomagne-VIII Teaching Pearl: Answer.No; potassium-sparing diuretics decreaserenal magnesium wasting and are useful in avoiding the hypokalemiaand hypomagnesemia seen with loop diuretics or thiazides

REFERENCES

Agus Z Hypomagnesemia J Am Soc Nephrol 1999;10:1616.

Rude RK Magnesium deficiency: A cause of heterogeneous disease in humans J Bone Miner Res 1998;13:749.

50 HYPONATREMIA

I Problem.A 3-month-old female infant is admitted after several days

of poor oral intake and significant vomiting and diarrhea During aphysical exam, she develops a tonic-clonic seizure Laboratory val-ues show serum sodium concentration of 114 mEq/L (normal:136–146 mEq/L)

II Immediate Questions

A Is patient adequately ventilated, with a safe and patent airway?It is critical to assess the ABCs (airway, breathing, andcirculation) because hyponatremia can be associated with neuro-logic changes and respiratory difficulty Severe neurologic depres-sion is likely to suppress patient’s ability to protect the airway, thusincreasing risk of aspiration

B Does history suggest reasons other than hyponatremia that explain tonic-clonic movements?Gastroenteritis from shigel-losis can be associated with seizures Seizures can also be seenwith drug intoxication, infections (meningitis), and underlying neu-rologic problems

C What factors contributed to patient’s development of tremia?Thorough history that includes clues about the three gen-eral mechanisms (see later discussion at III, B) may expeditedecision about underlying etiology and, therefore, treatment

hypona-D How quickly did hyponatremia develop?Rapid decrease insodium is associated with cerebral edema Acute presentation is

50.HYPONATREMIA 233

more likely to be associated with conditions such as tis and acute renal failure, whereas insidious course is associatedwith conditions such as nephrotic syndrome, adrenal insufficien-

gastroenteri-cy, and cirrhosis

E Is there a laboratory error?Presence of hypernatremia in theabsence of pertinent history and physical findings may suggestlaboratory error It may be prudent to repeat the test

F Pertinent Historical Information.It is important to determinepatient’s fluid intake and output (I&O) over past several days Keyquestions should include volume and types of ingested liquids;amount, volume, and consistency of stools; and patient’s ability toobtain fluid on his or her own

1.If an infant, what type of formula is given, and how is it pared?

pre-2.If a hospitalized child, what are fluid orders? Confirm thatappropriate IV solutions are being administered

3.Does past history include any factors that could influencehomeostatic mechanisms for water and salt balance?Medications (eg, diuretics) and disorders such as renal failure,heart failure, ascites, and intracranial masses may alter thebody’s normal water and salt control mechanisms

III Differential Diagnosis. Hyponatremia signifies an excess ofintravascular free water relative to sodium It is the most commonelectrolyte disturbance; seen in approximately 1.5% of all pediatrichospital admissions The absolute serum sodium number itself indi-cates nothing about the degree of intravascular volume, extracellularfluid volume (ECFV), and total body sodium

A General Mechanisms Producing Hyponatremia.There arethree general mechanisms by which hyponatremia may develop.These mechanisms may occur by themselves or in combinationwith one another

1.Decreased sodium intake

2.Increased sodium excretion

3.Free water retention

B Volume Status. When attempting to identify the cause anddecide treatment for a patient with hyponatremia, clinician mustdetermine patient’s volume status

1.Increased ECFV (hypervolemic hyponatremia)

2.Decreased ECFV (hypovolemic hyponatremia)

3.Pseudohyponatremia and hyponatremia with hypertonicity

C. Figure I–4 outlines the differential diagnosis for hyponatremia

It excludes pseudohyponatremia (increased serum lipids) andhyponatremia with hypertonicity (increased serum glucose)

IV Database.History and physical exams are of paramount importance

in determining proper course of treatment Identifying exact causes

of hyponatremia enables clinician to provide safe and appropriate

234 I:ON CALL PROBLEMS

correction of serum sodium concentration Proper treatment is ofparticular importance due to potential neurologic sequelae of abnor-mal serum sodium Cerebral edema develops when serum sodiumdecreases very rapidly In hyponatremia associated with severeintravascular volume depletion, neurologic sequelae may develop as

a function of hypotension, or the development of a cerebral venoussinus thrombosis

A Physical Exam Key Points

1 Vital signs and general appearance.Mental status changes,weakness, muscular cramps, and hypotension may all beassociated with hyponatremia or decreased intravascularvolume

2 Fluid status.Assess total body water (including both lular and extracellular volume) Assess volume status by check-ing mucous membranes, presence of tears, capillary refill,peripheral edema, ascites, jugular venous distention, tachycar-dia, hypotension, and murmurs

intracel-3 Abdomen.Palpate for masses or organomegaly consistentwith congestive heart failure

B Laboratory Data

1.Electrolytes, including BUN, creatinine, and glucose

2.Serum osmolality as compared with urine osmolality and urinesodium and creatinine

Acute or chronic renal failure SIADH

50.HYPONATREMIA 235

3.Consider serum pH, determination of anion gap, liver functiontests, thyroid function tests, cortisol levels, and aldosteronelevels

4.Plasma triglycerides are useful in identifying tremia Serum glucose dilutes serum sodium because it ishyperosmolar and pulls free water into the intravascular space(hyponatremia with hypertonicity)

pseudohypona-C Radiographic and Other Studies.Radiographic studies typicallyare not helpful unless clinician suspects an underlying malignan-

cy participating in the cause of hyponatremia

1 Chest x-ray.Helps to rule out heart failure, as well as identifyheart size as a factor in determining volume status

2 CT scan of head.May help rule out intracranial mass, rhage, or sinus thrombosis; however MRI is more sensitive formost tumor masses

hemor-3 CT scan or ultrasound of abdomen.May be helpful to mine ascites, portal hypertension, or renal or adrenal masses

deter-V Plan

A Symptomatic Hyponatremia.In patients such as the infant withseizures described in the opening problem, rapid but modest cor-rection of serum sodium concentration is of paramount impor-tance Seizures that develop as a result of hyponatremia aredifficult to treat unless serum sodium is corrected

1 Initial goal.Do not attempt to correct to a normal sodium centration (> 135 mEq/L), but rather to raise serum sodium to

con-a level con-at which seizures mcon-ay be controlled (typiccon-ally > 120mEq/L) This can be performed by administration of 3% saline

2 Rule for 3% saline administration.Administration of 1 mL/kg

of 3% saline will raise serum sodium by approximately1.6 mEq/L

3 Considerations.Keep in mind that seizures may have oped due to rapid decrease in serum sodium and cerebraledema Once seizure activity is controlled, this therapy should

devel-be held and more definitive treatment initiated Administration

of 3% saline is not appropriate for asymptomatic tremia Ideal rate of rise of serum sodium should not exceed

hypona-1 mEq/h once seizures are controlled This managementshould occur in consultation with a pediatric nephrologist andintensivist

B Asymptomatic Hyponatremia

1 Hypovolemic hyponatremia (decreased ECFV)

a. Estimate total fluid deficit

b.Use 0.9% normal saline for maintenance fluids plus deficit

c. Consider ongoing losses when determining fluid rates

2 Hypervolemic hyponatremia (increased ECFV)

a Low urine sodium (edematous states)

236 I:ON CALL PROBLEMS

i. Water and sodium restriction (two-thirds maintenance)

ii.Consider loop diuretics

b High urine sodium.Water restriction (two-thirds tenance)

main-VI Problem Case Diagnosis.The 3-month-old infant had ic-induced seizures as a result of gastroenteritis Urine sodium valuewas < 20 mmol/24 h (normal is 40–120 mmol/24 h) CT scan of thehead was normal Patient showed clinical improvement over the next

hyponatrem-2 days once sodium imbalance was gradually corrected

VI Teaching Pearl: Question.What neurologic condition is associatedwith a rapid increase in serum sodium?

VII Teaching Pearl: Answer.Central pontine myelinolysis develops inpatients who experience a rapid increase in serum sodium andhence is a risk factor in treatment of hyponatremia

II Immediate Questions

A Does patient have any acute symptoms related to phatemia?Patients with moderate to severe hypophosphatemia(< 1 mg/dL) may have many systemic manifestations and need to

hypophos-be promptly treated Symptoms can include cardiomyopathy withheart failure; muscle weakness that can lead to rhabdomyolysis;hemolysis; and encephalopathy, seizures, and coma

B Are there acute factors that have resulted in severe hypophosphatemia?Most cases of hypophosphatemia resultfrom a shift of phosphate from extracellular to intracellular fluid.Factors causing this shift can be severe and life threatening andinclude refeeding syndromes and treatment of diabetic ketoacidosis(DKA)

C Pertinent Historical Information.Ask about diet, medications,underlying conditions, and relevant family history

III Differential Diagnosis.Hypophosphatemia usually results from one

of the following processes: shift of phosphate into the intracellularcompartment, renal losses, or GI losses Changes can be acute,chronic, or a combination

or those with anorexia nervosa or AIDS.

2 DKA and insulin therapy.Renal losses are also involved

3 Respiratory alkalosis. Increased renal losses are alsopresent

4 Sepsis Especially gram-negative and toxic shock syndrome.

5 Leukemia with blast crisis.

B Increased Urinary Losses

1 Renal tubular defects.Fanconi syndrome (may be primary oracquired), X-linked hypophosphatemic (XLH) rickets, post–renal transplantation status

2 Hyperparathyroidism.Primary (rare in children) or secondary

to vitamin D deficiency or other nonrenal causes

3 Diuretic phase of acute tubular necrosis (ATN).

4 Postobstructive diuresis.

5 Post–renal transplantation status.

C Increased GI Losses

1 Use of oral phosphate-binding antacids.

2 Decreased intake.Starvation, anorexia nervosa, calorie malnutrition At high risk for refeeding syndrome (see III,

protein-A, 1, earlier) Premature infants require phosphate mentation

A Physical Exam Key Points

1 Vital signs and general appearance

a Temperature Severe hyperthermia can cause

hypophos-phatemia through transcellular shift Fever may be a sign ofsepsis or toxic shock

b Respiratory rate May be a sign of respiratory alkalosis.

c Body mass Look for evidence of malnutrition or short

stature, as well as cystinosis or congenital Fanconisyndrome

2 Heart Look for evidence of heart failure as result of severe

depletion

3 Neuromuscular Assess for confusion, coma, and muscleweakness Muscle tenderness may be a sign of rhabdomy-olysis

4 Skeletal Look for bowing, rachitic rosary, and flared growth

plates at wrists and knees as sign of rickets

238 I:ON CALL PROBLEMS

5 Skin Large café au lait spots may point to McCune-Albright

syndrome

B Laboratory Data

1 Basic metabolic panel Low bicarbonate level may point to

acidosis or changes secondary to respiratory alkalosis.Fanconi syndrome may be associated with low bicarbonate,low potassium, and possibly elevated creatinine levels Lowcalcium level points to rickets (not XLH) or hungry bone syn-drome High calcium level may point to hyperparathyroidism,but in children most have secondary hyperparathyroidism withnormal or low calcium

2 ABGs Evaluate acid-base status; look for respiratory alkalosis

or metabolic acidosis

3 CBC with differential Hypophosphatemia may cause

hemol-ysis and thrombocytopeni a Increased WBC with left shift maysuggest sepsis

4 Creatinine phosphokinase Check for rhabdomyolysis if

muscle tenderness is present

5 Uric acid Low in patients with volume overload or Fanconi

syndrome

6 Vitamin D levels 25-Hydroxyvitamin D is diagnostic of vitamin

D deficiency No need to routinely check 1,25-dihydroxyvitamin

D levels

7 Urine studies Spot urine for phosphorus and creatinine

allows measurement of phosphate excretion to see if etiology

is increased renal loss, as in Fanconi syndrome Fanconi drome is characterized by glucosuria, renal tubular acidosis,aminoaciduria, and excretion of small-molecular-weight pro-teins such as ␤2-microglobulin

syn-C Radiographic and Other Studies Consider skeletal survey to

look for changes characteristic of rickets, osteomalacia, or parathyroidism Changes may not point to exact etiology; antacidabuse can lead to osteomalacia

hyper-V Plan.Mild hypophosphatemia is a common finding in hospitalizedpatients, usually due to transcellular shifts of phosphate into intra-cellular fluid, and requires no specific therapy Moderatehypophosphatemia can be treated with oral supplementation, butsevere or symptomatic hypophosphatemia may require careful par-enteral correction

A Moderate Hypophosphatemia (1–2 mg/dL in adolescents; 2–3 mg/dL in infants and young children)

1 Dietary replacement.Milk contains 1 g inorganic phosphateper liter Avoid low-phosphate formulas (Similac PM 60/40) orbreast milk as replacement

2 Enteral supplements.Potassium phosphate can be given as

an oral supplement at a dose of 250–750 mg q6h, depending

on body size Commonly available supplements are Neutra

51.HYPOPHOSPHATEMIA 239

Phos or K-Phos Neutral, which come as 250-mg tablets, sules, or packets Contents can be diluted with 75 mL water ortaken with food Monitor calcium to avoid hypocalcemia Watchfor diarrhea Phosphosoda (Fleet Phosphosoda) can be givenorally or as an enema at a dose of 15–30 mL three to four timesdaily

cap-B Severe Hypophosphatemia (< 1 mg/dL in adolescents; < 2 mg/dL

in children younger than 12 years)

1 Enteral supplements.As listed under moderate phatemia, earlier; use for asymptomatic hypophosphatemia

hypophos-2 Parenteral phosphate. Usually used for symptomatichypophosphatemia Avoid with renal failure Potassium phos-phate can be given IV at a dose of 2.5 mg (0.08 mmol)/kg bodyweight in 1/2normal saline (NS) over 6 hours or, for sympto-matic patients, at 5 mg (0.16 mmol)/kg body weight in 1/2NSover 6 hours Monitor calcium, phosphate, and potassiumevery 6 hours Monitor BP Stop parenteral replacement whenserum phosphate is > 2 mg/dL

C Treatment of Primary Etiology.After emergency treatment,recognition and treatment of primary cause is important Mayrequire vitamin D analogues (see Chapter 46, Hypocalcemia,

p 221)

VI Problem Case Diagnosis.The 10-year-old patient has Fanconi drome, likely due to divalproex sodium administration In addition tolow serum phosphate level, he had low serum potassium level, meta-bolic acidosis, glucosuria, and a very large renal leak of phosphorus

syn-He required large amounts of IV phosphorus and bicarbonate, butthe renal tubular defect improved after stopping divalproex sodium

VII Teaching Pearl: Question.Why is the expression of serum phate as milliequivalents per liter (mEq/L) uniquely confusing ascompared with other ions

phos-VIII Teaching Pearl: Answer. Because the average charge of phate changes at physiologic pH (charge at pH 7.4 is −1.8), thevalency and the value for milliequivalents per liter varies withchanges in serum pH Expression of phosphate in millimoles per liter(mmol/L) and milligrams per deciliter (mg/dL) avoids this problem

phos-REFERENCES

Hruska KA, Lederer ED Hyperphosphatemia and hypophosphatemia In Favus M,

ed Primer on the Metabolic Bone Disorders of Mineral Metabolism, 5th ed.

American Society of Bone and Mineral Research, 2003:286–288.

Rubin MF, Narins RG Hypophosphatemia: Pathologic and practical aspects of its

therapy Semin Nephrol 1990;10:536.

Subramanian R, Khardori R Severe hypophosphatemia: Pathophysiologic

implica-240 I:ON CALL PROBLEMS

52 HYPOTENSION

I Problem.A 2-year-old boy who was admitted earlier in the day withdiarrhea and dehydration now has a BP of 64/33

II Immediate Questions

A What are the vital signs? Is patient adequately perfused? Are airway, breathing, and circulation (ABCs) compromised?

Hypotension represents a medical emergency and requiresimmediate assessment and treatment To determine lowestacceptable systolic BP for age (represents fifth percentile for age),use the guidelines in Table I–12 If systolic BP falls below theseranges, patient is considered to be hypotensive and metabolicdemands of the body for both oxygen and nutrients may not bemet As treatment is occurring, a simultaneous search for cause

of hypotension should begin

B Is patient tachycardic?Sinus tachycardia is the body’s firstmodality to maintain adequate cardiac output in the face of hypo-volemia and suggests intravascular volume depletion

C How was BP measured?Be sure that cuff size is appropriate.Cuff that is too large may give a falsely low BP Agitation andmovement may alter result and make measurement inaccurate

D What has urine output been?Urine output is the best sive marker of end-organ perfusion and, in the presence of normalrenal function, provides an accurate reflection of intravascularvolume status For pediatric patients, urine output should be atleast 1 mL/kg/h

noninva-E What is patient’s mental status?The body does all it can tomaintain perfusion to heart, brain, and adrenal glands in the face

of hypotension or inadequate cardiac output If mental status isnot normal, assume that cerebral perfusion has been compro-mised This represents an even more urgent medical emergencyand may require immediate attention to airway as fluid resuscita-tion is occurring

F Are invasive monitors in place? If so, measuring centralvenous pressure (CVP) or wedge pressure provides an objective

TABLE I–12 LOWEST ACCEPTABLE SYSTOLIC BLOOD

PRESSURE FOR AGE

Age Lowest Acceptable Systolic BP (mm Hg)

1–10 y 70 + (2 × Age in years)

10 y or older 90

52.HYPOTENSION 241

assessment of intravascular volume status Patients shouldreceive fluid resuscitation until CVP is ≥ 10 cm H2O or wedgepressure is ≥ 15 cm H2O If this is achieved and patient remainshypotensive, consider use of inotropes or vasopressors

G Were any medications recently given?If patient has receivedany sedatives or analgesics that may affect BP, this must be con-sidered as the potential cause of hypotension If so, antidotes may

be given (eg, naloxone for opioids), but patient should still receivefluids Consider an allergic reaction to any medication recentlygiven

III Differential Diagnosis

A Hypovolemia.Gastroenteritis is the most common cause ofhypotension in children Assess patient’s intake and output (I&Os)since admission, but keep in mind that much fluid may still bepresent in the gut, and that third spacing of fluid may be occurring

B Incomplete Resuscitation.Fluid losses may continue Despitewhat may appear to be adequate initial resuscitation, continue toprovide fluid resuscitation if appropriate

C Cardiac Dysfunction.Although uncommon in pediatric patients,myocarditis may present with hypotension and sinus tachycardia.Likewise, pericarditis with pericardial effusion and cardiac tam-ponade may present in a similar fashion Finally, consider otherthings that may impair cardiac output: tension pneumothorax, highpositive end-expiratory pressure if mechanically ventilated (mayimpair venous return), and myocardial ischemia

D Sepsis.Many types of infection in children can be associated withdiarrhea and subsequent hypovolemia If child does not seem to

be responding to initial efforts at resuscitation, a more seriousinfection must be considered Bacterial toxins and subsequentrelease of circulating cytokines can decrease cardiac functionand cause vasodilation, resulting in hypotension (frequently asso-ciated with lactic acidosis)

E Neurogenic Shock.Disturbance of vasomotor tone from injurysuch as trauma to the spinal cord; typically results in hypotensionand tachycardia

F Vasogenic Shock.Inappropriate loss of vasomotor tone can beseen with sepsis, anaphylaxis, adrenal insufficiency, and medica-tions

IV Database

A Physical Exam Key Points

1 Vital signs.High fever by itself may cause vasodilation andhypotension and should be treated with antipyretics and activecooling If present, it should increase suspicion of a more seri-ous infection If patient is tachypneic without evidence of pul-monary disease, consider the presence of metabolic acidosis

242 I:ON CALL PROBLEMS

and an attempt by patient to compensate with respiratory losis See also earlier discussion at II, A, regarding heart rateand BP

alka-2 General appearance.Does patient appear toxic? Is patient indistress? If so, consider serious infections and prepare to bemore aggressive in therapy

3 Skin.Patients in hypovolemic shock have cool, clammy skin.Look for rashes (eg, petechiae or purpura, or a diffuse erythe-matous rash) that may be indicative of more serious infections

4 Neck.Look for jugular venous distention as evidence of rightheart failure, tension pneumothorax, or pericardial tamponade

5 Heart.Listen for heart sounds If sounds are muffled, or a rub

is present, consider pericardial effusion Gallop is indicative ofcardiac dysfunction Examine ECG tracing to be sure tachy-cardia is sinus and that no other rhythm disturbance is present(especially supraventricular tachycardia)

6 Lungs.Unilateral decreased breath sounds may be indicative

of pneumothorax, pleural effusion, or consolidation Listen forcrackles or rales, which are indicative of pneumonia

7 Abdomen.Distention, tenseness, guarding, and hypoactive orabsent bowel sounds may indicate an acute abdomen.Peritonitis with subsequent fluid sequestration may be present

8 Extremities.Assess hands and feet to see if they are cool orwarm Often, if resuscitation is not yet adequate, a line of demar-cation from cool to warm can be noted, and this line travels moredistally until it disappears as patient is resuscitated Assess cap-illary refill If delayed, continue resuscitation Evaluate for pres-ence of edema that may be indicative of third spacing

9 Neurologic exam.Although last in this list, this should be thefirst thing assessed in physical exam Decreased mental statusindicates inadequate cerebral perfusion and requires emer-gent attention and treatment with aggressive fluid resuscitationand consideration of airway protection

B Laboratory Data

1 Hemoglobin and hematocrit.Severe anemia (Hgb < 8 g/dL)has been associated with poor outcomes in patients withshock During fluid resuscitation, hemoglobin is likely to bediluted If hemoglobin is < 8 g/dL and patient does not respond

to aggressive fluid resuscitation, consider transfusion

2 Electrolytes.Hypotensive patients may present with a variety

of electrolyte disturbances (too many to list here) Electrolytesshould be checked initially, and then rechecked frequentlyduring resuscitation Frequent electrolyte assessment will allowappropriate intervention

3 Coagulation studies. If sepsis is suspected, coagulationabnormalities may exist; these may require treatment withfresh frozen plasma, platelets, or cryoprecipitate

52.HYPOTENSION 243

4 ABGs.This evaluation is essential in determining acid-basebalance Metabolic acidosis reflects inadequate perfusion andcardiac output until proven otherwise Compensatory respira-tory alkalosis may also be seen Evaluation of serum lactatelevel may be helpful; level is elevated if perfusion and cardiacoutput are inadequate

C Radiographic and Other Studies

1 Chest x-ray.Allows for determination of pneumothorax, monia, and size of cardiac silhouette Enlarged cardiac silhou-ette may indicate tamponade or failure

pneu-2 Measurement of CVP.If patient is poorly responsive to fluidtherapy alone, therapy with inotropes or vasopressors may benecessary If this occurs, placement of a central venouscatheter should be considered In addition to providing centralaccess for fluid resuscitation, the catheter enables measure-ment of CVP, which will help to direct further therapy If hypoten-sion is refractory or continuous BP monitoring is needed,consider arterial line placement

V Plan

A Immediate Plan

1.Place the largest bore IV possible If unable to obtain rapid IVaccess, an intraosseous (IO) needle should be inserted

2.Immediate action consists of rapid infusion of at least 20 mL/kg

of an isotonic solution (preferably normal saline or lactatedRinger) Aggressive and immediate fluid resuscitation is thecornerstone of management of hypotension This requires atleast 20–40 mL/kg of an isotonic solution that is pushed as rap-idly as possible If there is no response, or inadequateresponse, to initial fluid therapy, continue fluid boluses Somepatients may require as much as 100–120 mL/kg before stabi-lization occurs

3.Administer oxygen to patient, support airway if needed, andplace patient in Trendelenburg position (head 30 degreesbelow feet)

B Specific Plans

1 Hypovolemic shock.Resuscitate with isotonic crystalloids(normal saline or lactated Ringer) Blood products may begiven if hemoglobin is < 8 g/dL or coagulopathy exists Ensureadequate fluid resuscitation before instituting therapy withinotropes or vasopressors Place a Foley catheter to monitorurine output If a central venous catheter is required, measureCVP and provide fluid resuscitation until CVP is at least 10 cm

H2O If BP, perfusion, or urine output remains inadequate, sider vasopressors or inotropes

con-2 Cardiogenic shock. A central venous catheter will berequired Consider a pulmonary artery catheter If pericardial

244 I:ON CALL PROBLEMS

tamponade is present, drainage of pericardial fluid is required

If there is evidence of myocarditis, cardiology colleaguesshould be consulted Generally, medications that are bothinotropes and afterload reducers are best in these situations.Consider dobutamine, milrinone, or amrinone Dopamine mayalso be helpful If patient is still poorly responsive, then norepi-nephrine or epinephrine may be useful

3 Neurogenic shock.Initial therapy includes aggressive volumeresuscitation If hypotension persists, therapy with vasopres-sors or inotropes is indicated

4 Vasogenic shock (includes septic shock and anaphylactic shock).Initial therapy consists of aggressive volume resusci-tation; be prepared to give very large volumes of fluid Therapywith vasopressors or inotropes may be required, but shouldnot be started until adequate fluid resuscitation has occurred(CVP> 10 cm H2O) If patient is poorly responsive to resusci-tation with crystalloids, blood products should be considered,especially if anemia, thrombocytopenia, or coagulopathy ispresent Treatment of underlying infection with appropriateantibiotics is essential If patient is in anaphylactic shock, treatimmediately with isotonic fluids and epinephrine (0.01 mL/kg of1:1000 SQ to a maximum dose of 0.3 mL) Diphenhydramineand ranitidine may be useful adjuncts to therapy Vasogenicshock can also be seen with an addisonian crisis, which should

be treated with hydrocortisone

VI Problem Case Diagnosis.The 2-year-old patient was diagnosedwith hypovolemic shock secondary to gastroenteritis Despite initialresuscitation, he continued to have ongoing fluid losses and theneed for further aggressive fluid resuscitation He was given an addi-tional 20 mL/kg of normal saline, which was repeated twice until thesystolic BP remained adequate (> 75 mm Hg)

VII Teaching Pearl: Question.Is presence of hypotension necessary tomake the diagnosis of shock?

VIII Teaching Pearl: Answer.No; shock is an acute syndrome terized by inadequate circulatory perfusion of tissue to meet themetabolic demands of vital organs It is a misconception that shockoccurs only with low BP (hypotension) Through various compensa-tory mechanisms, hypotension may be a late finding in shock

charac-REFERENCES

Frankel LR, Mathers LH Shock In: Behrman RE, Kliegman RM, Jenson HB, eds.

Nelson Textbook of Pediatrics, 17th ed Saunders, 2000:296–301.

Hazinski MF, Barkin RM In: Barkin et al, eds Pediatric Emergency Medicine:

53.HYPOTHERMIA 245

53 HYPOTHERMIA

I Problem.A 4-year-old boy is brought to the emergency department

by EMS personnel after falling through the ice into a frozen pond Hewas immersed in the water for less than 5 minutes, and his head wassubmerged for less than 1 minute He is lethargic, with a rectal tem-perature of 32°C (89.6°F)

II Immediate Questions

A What are the vital signs? Is patient breathing?Is there apulse? Does patient have a cardiac arrhythmia?

B What is patient’s core temperature?Hypothermia is defined as

a core temperature of 35°C (95°F) or less It occurs when the body

is no longer able to sustain normal temperature Onset ofhypothermia depends on the imbalance between increased heatloss and decreased heat production Core temperature will helpdetermine medical therapies: passive or active rewarming, car-dioversion, or drug therapy

C What is the clinical setting?Very young children are susceptible

to hypothermia as a result of environmental exposure Alcoholingestion also predisposes humans to environmentally inducedhypothermia

D Is there a history of other medical problems?Patients withhypoglycemia, hypopituitarism, and hypoadrenalism may presentwith hypothermia

E Does patient have any possible source of infection?Septicpatients may be hypothermic

III Differential Diagnosis

A Contributing Factors for Hypothermia.Children have a highersurface area to mass ratio than adults and therefore cool fasterand become hypothermic at an increased rate Environmental fac-tors such as cold, wind, and inadequate clothing can increaseheat loss Heat production can be affected by such factors as age,trauma, medical illness, and alcohol ingestion

B Physiologic Stages of Hypothermia

1 Mild hypothermia: Core temperature of 32–35 °C (89.6–95°F).

Increased metabolic rate and tachypnea occur; shiveringmechanism is usually preserved; BP is maintained; dysarthria,ataxia, and apathy can develop

2 Moderate hypothermia: Core temperature of 28–32 °C (82.4 °F) Cardiac output, respiration, and level of conscious-

ness all decrease; shivering mechanism diminishes; atrial rillation and other dysrhythmias occur

fib-3 Severe hypothermia: Core temperature < 28 °C (82.4°F).

Shivering is absent; loss of consciousness occurs; cerebralblood flow is decreased; acid-base balance is disrupted; there

is increased susceptibility to ventricular fibrillation or asystole;significant hypotension can occur

246 I:ON CALL PROBLEMS

C ICU Patient.Hypothermia typically results from thermoregulatoryimpairment, such as drug or alcohol intoxication, massive CNSinjury, burns, sepsis, or endocrinopathies

IV Database

A Physical Exam Key Points

1 Vital signs.Core temperature, BP, and volume status should

be continuously monitored Look for shivering as a mechanism

of heat production Hypothermic patients may be stricted peripherally and have distal pulses that are difficult topalpate Severely hypothermic patients will have paradoxicalvasodilation and cutaneous erythema

vasocon-2 Neurologic exam.Check mental status and perform a plete neurologic exam if patient is not comatose Assign a mod-ified Glasgow Coma Scale score (see Appendix F, p 765).Observe for signs of increased intracranial pressure

com-3 Secondary survey.Observe for signs of trauma or continuingblood loss Hemostasis and volume resuscitation may be nec-essary before correction of hypothermia can succeed

3 Urinalysis.Rule out rhabdomyolysis and myoglobinuria ing from excessive shivering and cell breakdown

result-4 ABGs.Provide acid-base, ventilation, and oxygenation status

C Radiographic and Other Studies

1 Chest x-ray.Look for pulmonary edema or aspiration

2 Continuous ECG monitoring.Rule out cardiac dysrhythmia

3 CT scan. Used to rule out intracranial or intra-abdominalprocess, especially in suspected trauma patients

4 Neck x-rays.Often needed in patients with suspected head orneck trauma to evaluate the cervical spine

V Plan.Management must address the underlying condition impairingthermoregulation that led to hypothermia Hypothermic patients are

at increased risk of refractory ventricular fibrillation, which may beprovoked by rough handling, including chest compressions and elec-trical defibrillation Aggressive volume resuscitation with isotonic flu-ids is a mainstay in treating hypothermia Method chosen to rewarmpatient must be tailored to the individual, and presence or absence

of circulation is at least as important as patient’s temperature Mosttextbooks mandate active rewarming for core temperature < 28°C

B Passive Rewarming (Patients Who Are Shivering).Shiveringmechanism is usually preserved if core temperature exceeds

30°C (86°F) As long as patient is shivering, passive rewarmingtechniques may be utilized These include removing cold or wetclothing, transporting to a warm environment, and covering withdry blankets Passive rewarming requires that patient have spon-taneous heat production, which makes it useful only in mild cases

of hypothermia

C Active Rewarming (Patients Who Are Not Shivering).Patientswho are not shivering have lost their thermoregulatory drive andrequire active rewarming Controversy exists over exact tempera-ture at which to begin internal active rewarming Decision should

be made based on individual patient and institutional expertise

1 External active rewarming.Includes techniques such as hotpacks, heating lamps, and warm water baths These techniquesare familiar, inexpensive, and readily available External activerewarming may result in rewarming shock, decreased core tem-perature (afterdrop), and ventricular fibrillation Severe hypov-olemia is common in hypothermic patients due to vascular leakand a profound cold diuresis Heat applied externally restorescirculation to the coldest part of the body, which dumps cold andstagnant blood into the core This, combined with an alreadydepressed myocardium, dilated vascular beds, and hypov-olemia, can lead to vascular collapse and a drop in core tem-perature External active rewarming is unlikely to be effective inpatients who do not have adequate spontaneous circulation

2 Internal active rewarming (core rewarming).Preferred forsevere hypothermia or patients with absent or ineffective circula-tion Common techniques include warm humidified oxygen,heated intravascular fluids, closed thoracic or pleural lavage withwarm saline, and heated lavage of bladder, stomach, colon, orperitoneum Open thoracotomy with mediastinal irrigation andextracorporal circulation with heating elements are also effective.Core rewarming requires invasive devices not always available atrural or community hospitals These methods are advantageous

in that they are very effective and they lessen the chance ofrewarming shock, core cooling, and cardiac arrhythmias

VI Problem Case Diagnosis.The 4-year-old boy had mild hypothermiafrom environmental exposure He maintained his ability to shiver andresponded well to passive rewarming

II Immediate Questions

A Is patient experiencing impending respiratory failure?

Hypotonia, especially when associated with muscle weakness,may result in respiratory compromise Evaluate airway patency,protection, and efficacy of respiratory effort

B Is inability to sit due to muscle weakness, hypotonia, or both?Answer helps narrow differential diagnosis and guideimmediate approach In patients who have CNS causes of hypo-tonia, muscle weakness is not present; these patients have pre-served deep tendon reflexes or hyperreflexia Patients who havediseases affecting the lower motor neuron usually have bothweakness and hypotonia and, if the anterior horn cell or peripher-

al motor neuron is involved, have diminished or absent reflexes

C Is there abnormal phasic tone, postural tone, or both?

1.Phasic tone is the rapid contraction of a muscle Examiningdeep tendon reflexes best tests this Determine if reflexes arepresent or absent If present, determine if they are symmetric,diminished, or brisk

2.Postural tone is sustained or prolonged contraction againstgravity Examining child’s traction response, horizontal suspen-sion, and vertical suspension can assess postural tone.Traction response is elicited by pulling child to a sitting positionfrom a supine position Examiner should feel child resistingagainst the traction Child should initiate lifting the head asbody is raised and should attempt to keep the head erect whensitting Significant head lag and failure to flex limbs in response

to traction is indicative of hypotonia In horizontal suspension,infant with normal tone should maintain head at midline; flexhips, knees, and elbows; and keep back straight In verticalsuspension with examiner’s hands under the axilla, infant with

54.HYPOTONIA 249

normal tone should allow for suspension without compressingthe thorax, given normal shoulder strength In addition, infantshould hold the head erect and flex at the knees, hips, andankles

D Is process acute, subacute, or chronic?This may or may not

be an easy classification, because sometimes an acute event canexacerbate an underlying condition It is one way to stratify thediagnostic possibilities Botulism, spinal cord trauma, sepsis,intestinal obstruction, Reye syndrome, toxic encephalopathy, con-cussion, intracranial hemorrhage, tumors of the posterior fossa,Guillain-Barré syndrome, myasthenia gravis, and collagen vascu-lar disease can all present with acute or subacute onset of hypo-tonia

E Does underlying process involve brain, spine, or motor unit?

For normal tone to be present, patient must have intact centralnervous and peripheral nervous systems

F What is child’s developmental history? Are milestones delayed?Is the delay in motor milestones, only, or also in speechand cognitive development? Children with hypotonia from a CNSsource usually present with more global developmental delay

G What is child’s birth history?Is there a history of decreasedintrauterine movement, distress, hypoxia, apnea, infection, hyper-bilirubinemia, and neonatal seizures? In addition to identifyingpossible causes, this information helps to identify time of onset.Presence of decreased intrauterine movement, fetal distress,polyhydramnios, joint contractures, arthrogryposis, or dislocation

of hips noted at birth all provide evidence of probable prenatalonset

H What is patient’s immunization status?Was child vaccinatedagainst polio? Is there a history of travel with possible polioexposure?

I Are any family members nonambulatory? Is there a family history of childhood deaths?Family history helps to determinepossible congenital causes (eg, glycogen storage disease, hered-itary neuromyopathies, spinal muscle atrophy, Ehlers-Danlos syn-drome, Tay-Sachs disease, congenital myasthenia gravis, orbenign congenital hypotonia)

J Any history of trauma?Newborn infants with spinal cord injuriescan present with hypotonia This is more common with breechvaginal deliveries but can be seen with cephalic presentations.Abnormal rectal tone, a distended bladder, lack of deep tendonreflexes with no spontaneous movement in the lower extremities,

or loss of sensation below the nipple line should alert clinician tospinal cord insult

K Any possible exposure to Clostridium botulinum spores?

Spores can be found in soil and honey Exposure to soil disruptionsuch as excavation sites or ingestion of honey would both be

250 I:ON CALL PROBLEMSsignificant risk factors In cases of infantile botulism, constipationusually precedes the onset of ascending hypotonia A careful his-tory of stooling pattern should be included.

III Differential Diagnosis

A Brain Disorders.Consider toxicity, metabolic encephalopathy,chromosomal disorder (eg, Prader-Willi syndrome, trisomy 21),infection, periventricular leukomalacia, cerebrovascular accident,hypoxic ischemic encephalopathy, trauma (intracranial hemor-rhage), cerebral palsy, benign congenital hypotonia, mass (tumor,cyst)

B Spinal Cord Disorders.Trauma and hypoxic ischemic insult

C Anterior Horn Cell Disorders.Poliomyelitis and spinal muscleatrophy

D Peripheral Nerve Disorders. Polyneuropathy, Guillain-Barrésyndrome, trauma

E Neuromuscular Junction Disorders.Infantile botulism, thenia gravis, transitory neonatal myasthenia gravis, aminoglyco-side antibiotic, hypermagnesemia

myas-F Muscle Disorders.Hypothyroidism, metabolic myopathies (eg,acid maltase deficiency, phosphorylase deficiency, glycogen stor-age disease), muscular dystrophies, polymyositis

G Systemic Diseases.Malnutrition, sepsis, intestinal obstruction,cyanotic heart disease, collagen vascular disease

b.Any signs of sepsis? Check for decreased skin perfusion,tachycardia, and prolonged capillary refill

2 Vital signs and respirations.Is the airway protected? Checkgag reflex What is the respiratory effort, and is it effective?Check for grunting, flaring retractions, paradoxical respiratorymovements, and overall aeration Confirm with pulse oximetry

hyper-54.HYPOTONIA 251

d Sensation.Loss of sensation raises concern of spinal cordinjury However, inability to withdraw from a noxious stimulusmay indicate severe muscle weakness To assess thisparameter more carefully, examine infant’s ability to resistgravitational forces when an extremity is raised Childrenwith lower motor neuron disease should have preservedmental status

e Tongue fasciculation.Given the generous subcutaneoustissue mass usually present on most infants, muscle fascic-ulation or wasting may be difficult to assess elsewhere

4 Musculoskeletal findings.Any arthrogryposis, contractures,

or dislocations? Presence of these findings during infancypoints to a prenatal onset

B Laboratory Data.Initial studies are guided by history and cal exam but will likely include the following:

physi-1.CBC with differential

2.Infectious workup (eg, blood culture, urinalysis, urine culture,lumbar puncture) Consider if infection is suggested by history

or physical exam

3.Electrolytes (including glucose, calcium, potassium)

4.BUN and creatinine

5.Thyroid function tests

6.Urine for organic acids

7.Creatine phosphokinase

8.Other tests (as appropriate)

a. Stool studies for Clostridium botulinum.

b.DNA test for spinal muscle atrophy (SMA) or myotonicdystrophy

C Radiographic and Other Studies

1 CT or MRI scan of spine.Obtain acutely if there is concern ofpossible spinal cord injury in an infant

2 Electromyogram.Obtain if muscle weakness is present

3 MRI scan of head.Consider if laboratory studies do not port diagnosis of myopathy and there is concern of a centralCNS process, including tumor, cyst, enlarged ventricles, cere-bral atrophy, or congenital malformation

sup-4 Chest x-ray.If respiratory symptoms are present

V Plan.Most children with hypotonia have a chronic or subacute entation It is critical to recognize an acute presentation of hypotonia.Thorough history and physical exam allow clinician to narrow the dif-ferential diagnosis based on its chronicity and anatomic classifica-tion This in turn allows for systematic and focused evaluation ofchild

pres-A Initial Management

1.If child’s presentation is acute or if child is experiencing anacute exacerbation of a subacute or chronic problem, it is

malnu-3.Most commonly, hypotonia is related to a known CNS insult Ifchild has central hypotonia and no identifiable preceding insult,the hypotonia is often benign Children with central hypotoniaare also treated with supportive therapy, including physicaltherapy A swallowing evaluation may be required, and feedingsupport such as nasogastric tube feedings may be required ifchildren have significant sucking or swallowing difficulties.

B Congenital Myopathies.Treatment of most patients with genital myopathies is supportive Diagnosis of spinal muscularatrophy is important to help guide future decisions regardingappropriate level of intervention, including intubation In general,the younger the child at diagnosis, the worse will be the progno-sis

con-VI Problem Case Diagnosis.The 8-month-old girl was diagnosed withspinal muscular atrophy, based on a DNA test demonstrating pres-

ence of SMN gene Of interest, an infection with respiratory syncytial

virus caused bronchiolitis, which led to the acute presentation

VII Teaching Pearl: Question.If a patient presents with hypotonia yetwith vibrant facial expressions, what does this suggest?

VIII Teaching Pearl: Answer. Children with neuromuscular diseaseoften have preserved facial expressions and appear vibrant despitesignificant hypotonia and weakness

55 INABILITY TO VOID (URINARY RETENTION)

I Problem.A 3-year-old boy is brought to the emergency department

by his parents with a complaint of no urination in the past 24 hours

He appears uncomfortable

55.INABILITY TO VOID (URINARY RETENTION) 253

II Immediate Questions

A Is patient toilet trained?Has patient attained dryness at nightand at daytime, or is patient in transition phase, still wearing pull-ups? Has the urinary stream been straight and strong or weak-ened and interrupted?

B Is patient constipated?Are bowel habits regular?

C Is there pain on urination or fever?Pain with fever suggestsUTI

D History of trauma?Urethral rupture is an emergency

E What medication(s) does patient currently take?

Anticholinergics (eg, imipramine) can cause urinary retention

F What is the prenatal history?Was a prenatal ultrasound formed and, if so, were findings normal? Abnormal urinary flowcan be seen with renal dysplasia or GU obstruction

per-G Is there a past medical history of UTI?Children with GU refluxcommonly present with recurrent UTIs

H What is the social situation?Is there a history suggestive ofsexual abuse? See Chapter 15, Child Abuse: Sexual, p 75

I Are there other associated signs or symptoms?Loss of weight,leg pain, and neurologic symptoms provide clues to other underlyingconditions

III Differential Diagnosis

A Transitional Voiding or Dysfunctional Voiding Syndromes.

Intermediate stage of toilet training, fright of bathrooms

B Constipation.Large amounts of stool in the colon can impinge

E Neurogenic Bladder.Occult spinal dysraphism

F Pelvic Malignancy.Rhabdomyosarcoma

G Sexual Abuse or Other Psychological Stressors.

IV Database

A Physical Exam Key Points

1 General appearance.Does child appear well or ill, able or uncomfortable, playful or timid?

comfort-2 Abdomen.Tender, tense, smooth suprapubic mass usuallyindicates a distended bladder Prominence in left lower quad-rant often indicates that sigmoid colon is distended with stool

3 Back.Observe for lumbosacral skin abnormalities (café au laitspots, hemangiomas, fatty appearance, skin dimple or skin tag,tuft of hair, dermal vascular malformation, or subcutaneouslipomas)

254 I:ON CALL PROBLEMS

4 Genitalia.Phimosis (if uncircumcised), meatal stenosis, anderythema of prepuce or glans may represent acute bal-anoposthitis; ecchymotic areas may represent physical orsexual abuse

5 Rectal exam. Perform gently with a well-lubricated smallfinger Position patient on side, with legs drawn into chest.Assess anal tone and rectal vault content for the following:loose or impacted stool; indurated mass in area of prostate andbladder neck, which could represent pelvic malignancy (rhab-domyosarcoma)

6 Neurologic exam.Check for sensation in perineum Examineextremities for high arched foot, discrepancy in muscle size

B Laboratory Data.Obtain basic metabolic panel, CBC with ential, urine for analysis and culture

differ-C Radiographic and Other Studies

1 KUB.Useful in general assessment of bowel pattern, occultspinal dysraphism, abdominal masses, stool impaction

2 Renal and bladder ultrasound.Evaluate appearance of der and kidneys for acute changes (bladder distention, ureteral

blad-or renal pelvis dilation) blad-or chronic changes (bladder wall ening and hydroureteronephrosis with parenchymal thinningand ureteral tortuosity)

thick-3 Voiding cystourethrogram (VCUG).Can be performed tively if ultrasound shows hydronephrosis or bladder wall thick-ening to rule out bladder outlet obstruction secondary toposterior urethral valves

elec-4 Urodynamic studies.May be necessary if neurologic or tional cause is suspected

func-5 MRI scan of abdomen and lumbosacral spine.To excludetethered cord or bladder abnormalities

V Plan.Determine if patient needs medical intervention (eg, zation) or simply assistance with elimination If patient has signs andsymptoms of UTI, a neurologic disorder, or abnormalities on ultra-sound, intervention is more likely to be necessary

catheteri-A Constipation.Give an enema and begin bowel program (ie,mineral oil or stool softeners) See Chapter 18, Constipation,

V, C, p 91

B Voiding Problems Secondary to Toilet Training Imbalance

1.Avoid catheterization if possible Give midazolam (nasally or

orally, 1–5 mg/kg PO as 1 dose to a maximum of 20 mg; time

of onset, 10–30 minutes) to relax patient and perform bladdermassage (gently massage suprapubic area until distendedbladder becomes tense, representing impending urination).Midazolam will relax external urinary sphincter, facilitating uri-nation Avoid ambulation, because balance may be affected

2.If patient is still unable to void, instill 2% lidocaine solution intourethra and catheterize while still under midazolam effect, to

56.INCREASED INTRACRANIAL PRESSURE 255

minimize recollection of catheterization Remove catheter afterdraining bladder Give ibuprofen, 10 mg/kg every 6 hours, tocontrol dysuria associated with catheterization

C Organic Urinary Retention.Catheterize urethra to drain bladder.Try a 10 or 12 Fr Foley catheter or a 10 Fr straight catheter (smaller

in younger children); a straight catheter may be more easilyadvanced, but it needs to be taped to the penis with clear adhesivetape (Tegaderm) Leave catheter in place and consult urologycolleagues

D Cystoscopy and Endoscopic Valve Ablation.Consult urologycolleagues if posterior urethral valves are demonstrated byVCUG

VI Problem Case Diagnosis.The 3-year-old boy has dysfunctionalelimination syndrome with constipation and dysfunctional voiding Heresponded to a bowel program of mineral oil and stool softeners

VII Teaching Pearl: Question.What is the bladder capacity of a old child?

3-year-VIII Teaching Pearl: Answer.Approximately 150 mL; a normal bladder

at birth holds 30–60 mL and increases its capacity by approximately

30 mL per year until puberty Bladder capacity can be calculatedusing the following formula: Volume in ounces = age in years + 2

REFERENCES

Baskin LS, Kogan BA, Duckett JW Handbook of Pediatric Urology Lippincott-Raven,

1997.

Bauer SB Neuropathology of the lower urinary tract In: Belman AB, King LR, Kramer

SA, eds Clinical Pediatric Urology, 4th ed Martin Dunitz, 2002:371–408.

Koff SA, Jayanthi VR Dysfunctional elimination syndromes of childhood In: Walsh

PC, Retik AB, Vaughn ED, Wein AJ, eds Campbell’s Urology, 8th ed Elsevier,

2002:2262–2280.

Wein AJ Drug therapy for neurogenic and non-neurogenic bladder dysfunction In:

Seidmon EJ, Hanno PM, eds Current Urologic Therapy, 3rd ed Saunders,

1994:291–298.

56 INCREASED INTRACRANIAL PRESSURE

I Problem.A 7-year-old girl with a 1-week history of headaches andvomiting presents with depressed mental status CT scan of thehead demonstrates a large mass in the posterior fossa and dilatedcerebral ventricles

II Immediate Questions

A Is patient maintaining a safe and patent airway?Severe rologic depression is likely to suppress a patient’s ability to protectthe airway, thus increasing the risk of aspiration

neu-B What are the vital signs?Patients with increased intracranialpressure (ICP) often become hypertensive If there is significant