Chapter 11

Neonatal Emergencies

Christina L. Cochran and Parul P. Soni

Key Points
• Neonatal Resuscitation Program (NRP) guidelines should be employed for
management of a newborn in distress [1].
• Always consider nonaccidental trauma in newborns presenting to the
emergency department (ED).
• Prognosis is often dependent on the underlying aetiology or degree of
illness.
• Overall, early recognition and management will improve long-term
outcome.

Section A: Common Assessment and Treatment Elements

Introduction

Newborns presenting with respiratory illness should be evaluated promptly as

respiratory failure can precipitate quickly. There are many aetiologies of
respiratory illness in the newborn period, of which the most common will be
reviewed.

C.L. Cochran, MD (*) • P.P. Soni, MD, MPH, FAAP

Department of Emergency Medicine, Ann and Robert H. Lurie Children’s
Hospital of Chicago, Northwestern University/Feinberg School of Medicine,
225 E. Chicago Avenue Box #62, Chicago, IL 606011, USA
e-mail: [email protected]; [email protected]

© Springer India 2016 201

S.S. David (ed.), Clinical Pathways in Emergency Medicine: Volume II,
DOI 10.1007/978-81-322-2713-7_11
202 C.L. Cochran and P.P. Soni

Pathophysiology

• Respiratory distress syndrome (RDS) is caused by insufficient surfactant produc-

tion, most commonly in preterm infants.
– Insufficient surfactant causes inappropriate alveolar expansion.
– Decreased alveolar expansion leads to respiratory distress.
• Bronchiolitis is the result of a viral infection affecting the lower respiratory tree.
– Bronchioles become inflamed and increase secretion production.
– Common viral aetiologies include respiratory syncytial virus, human meta-
pneumovirus, rhinovirus, enterovirus, and coronavirus [2].
• Meconium aspiration syndrome (MAS) results from aspiration of meconium at
the time of delivery.

Clinical Features

• Initial signs of respiratory distress include tachypnoea and increased work of

breathing (Table 11.1)
• As distress progresses, newborns are at risk of developing respiratory failure and
apnoea.
• RDS presents in the first days of life (Table 11.2)
• Bronchiolitis is a clinical diagnosis based on physical exam and history [3].
– Newborns will have increased work of breathing with crepitations and rhon-
chi on exam.

Differential Diagnosis

• Consider RDS, bronchiolitis, sepsis, bronchopulmonary dysplasia (BPD), pul-

monary hypertension, pneumonia, MAS, and pertussis.

Table 11.1 Signs of Respiratory Tachypnoea

respiratory distress versus distress Retractions
respiratory failure
Abdominal accessory muscle use
Nasal flaring
Tracheal tugging
Respiratory failure Bradypnoea
Apnoea
Hypoxia/hypoxemia
Carbon dioxide retention
Respiratory acidosis
11 Neonatal Emergencies 203

Table 11.2 Comparison of clinical features and management of RDS and bronchiolitis
RDS Bronchiolitis
Age First 2 days of life First 2 years of life
Aetiology Decreased surfactant Viral infection
Signs/symptoms Tachypnoea, increased work of Tachypnoea, increased work of
breathing, hypoxia breathing, apnoea, hypoxia
Diagnosis CXR, clinical Clinical
Management Supplemental oxygen, surfactant Suctioning, supplemental oxygen

Table 11.3 Chest x-ray Chest x-ray finding

findings in common newborn
Respiratory distress syndrome Ground-glass opacities
respiratory diseases
Decreased lung volumes
Air bronchograms
Pneumonia Focal opacities
Diffuse infiltrates
Foreign body aspiration Air trapping on the side
of the foreign body

• History of meconium presence in amniotic fluids should raise concern for MAS.
• When considering pulmonary hypertension, conduct thorough cardiac evaluation.

Investigations

• Chest radiograph (CXR) should be obtained in patients suspected to have RDS,

pneumonia, and foreign body aspiration (Table 11.3).
• CXR is not indicated in patients with bronchiolitis [3].
• Obtain nasal secretions to confirm pertussis infection.
• If suspected, infectious workup should be completed including blood, urine, and
cerebrospinal fluid studies (CSF).

Treatment

• Intervention can be tailored to a degree of respiratory distress (Table 11.4).

• Surfactant should be provided to patients with RDS [4].
• Supportive care, including suctioning and supplemental oxygen, is the treatment
of choice for bronchiolitis.
– Salbutamol, normal saline, and hypertonic saline nebulisers have not been
shown to improve outcome in bronchiolitis [3].
• For patients without clear viral aetiology, consider antibiotic coverage.
• If suspicious for pertussis, start prophylactic antibiotics.
204 C.L. Cochran and P.P. Soni

Table 11.4 Recommended Intervention

interventions based on level
Apnoeic Bag-valve-mask ventilation
of respiratory distress
Intubation and mechanical ventilation
Severe distress Continuous positive airway pressure (CPAP)
Intubation and mechanical ventilation
Moderate High-flow nasal cannula
distress Vapotherm
Continuous positive airway pressure (CPAP)
Minimal distress Trial supplemental oxygen via nasal cannula

Prognosis

• Newborns in respiratory distress will require observation and treatment on an

inpatient service.
• Newborns with severe RDS are at risk of requiring long-term supplemental oxy-
gen and developing BPD.
• Bronchiolitis has an overall good prognosis with resolution of symptoms once
the virus infection resolves.

Prevention

• Prevention of bronchiolitis focuses on reducing virus transmission.

• Avoidance of preterm delivery unless clinically indicated will decrease the risk
of RDS.

Section B : Neonatal Cardiac Emergencies

Introduction

Congenital cardiac deformities may present in the first hours to days to weeks of
life. Prompt recognition of a cardiac aetiology is imperative, as management from
cardiogenic shock differs from management of other aetiologies of newborn shock.

Pathophysiology

• Congenital heart defects are a result of abnormal embryogenesis

• Defects can be classified as cyanotic (Table 11.5) and non-cyanotic (Table 11.6).
• Cyanosis is a result of right to left shunting of non-oxygenated blood into sys-
temic circulation.
11 Neonatal Emergencies 205

Table 11.5 Characteristics of cyanotic heart lesions

Total
Transposition anomalous
Truncus of the great Tetralogy of pulmonary
Name arteriosus vessels Tricuspid atresia Fallot venous return
Description Single Pulmonary Absence or Overriding All four
arterial artery underdevelopment aortic arch, pulmonary
trunk supplying of the tricuspid pulmonary veins do not
supplying systemic valve atresia, connect
pulmonary circulation; VSD, right correctly
and aorta ventricular with the left
systemic supplying hypertrophy atrium
circulation pulmonary
circulation
Diagnosis Echo, CT Echo, CXR Echo Echo, CXR CT
angiogram showing “egg showing angiogram,
on a string.” boot-shaped cardiac MRI
CT heart
angiogram
Management CR support, CR support, CR support, Tetralogy CR support,
diuretic PGE1, PGE1, surgical spell: 100 % PGE1,
therapy, surgical intervention oxygen, supplemental
surgical intervention morphine, oxygen, fluid
intervention vasopressor; support,
CR support, surgical
surgical intervention
intervention
VSD ventricular septal defect, Echo echocardiogram, CT computerised tomography, CXR chest
x-ray, CR cardiorespiratory, PGE1 prostaglandin E1

Table 11.6 Non-cyanotic heart defects

Coarctation of the aorta Ventricular septal defect (VSD)
Presentation Cool BLE extremities Time of presentation dependent on the
size of VSD
Decrease pulses in the BLE Signs of heart failure or fluid overload
Decreased blood pressure in the of the lungs
BLE
Diagnosis Echocardiogram Echocardiogram
CT angiogram or MRA of the CXR may demonstrate cardiomegaly
heart/aorta
Management Prostaglandin E1 Haemodynamic support
Haemodynamic support Closure of the defect
Surgical repair
BLE bilateral lower extremities

Clinical Features

• Newborns may present with a variety of findings (Table 11.7).

206 C.L. Cochran and P.P. Soni

Table 11.7 Possible clinical features associated with congenital heart disease
History Vital sign abnormalities Physical exam findings
Abnormal foetal ultrasound Tachycardia (>160 bpm) Shock
Poor/difficult feeding Bradycardia (<80 bpm) Decreased central/peripheral pulses
Cyanosis Hypoxia (<90 % on RA) Poor perfusion
Emesis Tachypnoea Increased work of breathing
Poor weight gain Bradypnoea Pathologic murmur
Maternal diabetes Hypertension Lethargy
Maternal hypertension Hypotension Hepatomegaly
Maternal medication Crackles on lung auscultation
Family cardiac history
bpm beats per minute, RA room air

YES TOF, AVSD, TA, PA, PS

YES MURMUR
NO TGA, PPHN, TAPVR
BL UE FEMORAL PULSES

NO

PIN K FEMORAL PULSES NO COARCT, HLHS, AS

YES VSD, ASD, AS

TOF: Tetralogy of Fallot AVSD: Atrioventricular Septal Defect TA: Truncus Arteriosus PA” Pulmonary Atresia
PS: Pulmonary Stenosis TGA: Transposition of the Great Arteries PPHN: Persistent Pulmonary Hypertension
TAPVR: Total Anomalous Pulmonary Venous Return Coarct: Coarctation HLHN: Hypoplastic Left Heart Syndrome
AS: Aortic Stenosis ASD: Atrial Septal Defect

Fig. 11.1 Assessment of infant colour and central pulses

Differential Diagnosis

• Serious bacterial infection (SBI) should be considered in all neonates presenting

to the ED.
• Metabolic abnormalities, respiratory infections, and feeding difficulties can
present similarly.

Investigations

• Assess colour of the newborn and central/peripheral pulses (Fig. 11.1).

• Measure four extremity blood pressures and pulse oximetry.
– In the setting of coarctation, lower extremity blood pressures and pulse oxim-
etry will be decreased compared to right upper extremity.
• CXR should be obtained to assess the cardiac silhouette.
11 Neonatal Emergencies 207

• Obtain electrocardiogram to assess for rhythm disturbances.

• Echocardiogram is used to assess cardiac anatomy and function.
• Consider blood gas to assess pH and arterial oxygenation.
• Detailed maternal and prenatal history, including ultrasound results, should be
gathered.
– Many maternal conditions and medications can be associated with congenital
heart disease [5].

Treatment

• Supplemental oxygen should be provided.

• Haemodynamic support should be provided with fluids, inotropes, and chrono-
tropes as clinically indicated.
– The degree of fluid resuscitation is dependent on the underlying cardiac
defect.
• Prostaglandins should be initiated to delay closure of the ductus arteriosus in
patients suspected of having a shunt-dependent defect.
– Initial dose – Prostaglandin E1: 0.05 mcg/kg/min
• Initiate inhaled nitric oxide if pulmonary hypertension is suspected.
• Cardiology consult should be obtained as soon as cardiac defect is suspected.

Prevention

• Improved management of maternal diabetes and hypertension may decrease con-

genital heart defects.

Section C: Serious Bacterial Infections (SBI)

Introduction

Any newborn with concern for infectious process should be evaluated and treated
immediately. SBIs in neonates include, but not limited to, urinary tract infections
(UTIs), bacteraemia, sepsis, meningitis, pneumonia, pyelonephritis, and cellulitis.
Neonates with bacterial infection are at high risk for long-term morbidity and mor-
tality [6]. Low threshold for workup of an SBI should be maintained when evaluat-
ing children less than 29 days old.
208 C.L. Cochran and P.P. Soni

Pathophysiology

• Newborns have reduced defence against bacterial infections secondary to an

immature immune system.
• The two most common bacteria responsible for infection in newborns are group
B streptococcus (GBS) and Escherichia coli (E. coli) [7].
• UTIs are the most common bacterial infection in this patient group.
• Necrotising enterocolitis (NEC) is a result of intestinal ischaemia, leading to
bacterial overgrowth and gut necrosis [8].

Clinical Features

• Rectal temperature greater than 38° C is suggestive of infection.

• Infants may present with hypothermia, lethargy, increased sleeping, poor feeding,
jaundice, vomiting, changes in their respiratory pattern, or abnormal vital signs.
• Detailed prenatal and antenatal history should be obtained.
– Risk factors for infection include prolonged rupture of membranes, maternal
fever, maternal infection, and lack of appropriate treatment for maternal GBS.
• Abdominal tenderness, distension, vomiting, bloody stool, and lethargy may
indicate NEC.
• Redness, tenderness, or drainage from the umbilicus is concerning for omphalitis.

Differential Diagnosis

• Consider hypoglycaemia, metabolic dysfunction, hyperbilirubinemia, congenital

heart conditions, and neurologic dysfunction when assessing a patient with the
above features.

Investigations

• Workup should include CBC, blood culture, urinalysis, urine culture, and CSF
studies including cell count, differential, glucose, protein, and culture.
• Consider obtaining herpes simplex virus (HSV) tests.
• In the setting of omphalitis, send culture of umbilical discharge.
• Obtain cultures prior to antibiotic initiation unless patient is clinically
decompensating.
• For patients with dehydration or concern for metabolic abnormalities, obtain
electrolytes and liver function panel.
11 Neonatal Emergencies 209

• CXR should be considered in newborns with respiratory distress, and hypoxia.

• NEC diagnosis and management is reviewed in Table 11.11 [9].

Treatment

• Prompt antibiotic therapy is essential.

• Initiate broad-spectrum antibiotic coverage with ampicillin and gentamicin and/
or cefotaxime.
– Ampicillin, gentamicin, and cefotaxime dosing is dependent on age and
weight [10].
– Acyclovir covers for possible HSV infection: 20 mg/kg/dose every 8 h [10].
• Continue antibiotics until CSF, blood, and urine cultures have resulted.
• NEC management is reviewed in Table 11.11.

Prevention

• Appropriate treatment of maternal GBS infections reduces the likelihood of

newborn infection [11].

Section D: Newborn Gastrointestinal Emergencies

Introduction

There are a variety of gastrointestinal (GI) emergencies that may present in the
newborn period. The majority of diagnoses can be distinguished based on physical
exam and radiologic evaluation. Omphalocele and gastroschisis are not discussed in
depth, but ED physicians should be aware of these complications.

Hyperbilirubinemia

Pathophysiology

• Most newborns develop clinical hyperbilirubinemia [12].

• Most cases of hyperbilirubinemia are physiologic, or secondary to normal
delayed conjugation and excretion of bilirubin in the newborn, though patho-
logic aetiologies must be considered.
210 C.L. Cochran and P.P. Soni

• Factors contributing to higher bilirubin levels are listed in Table 11.8.

• Patients can be classified into low risk, medium risk, or high risk for complica-
tions of bilirubin (Table 11.9) [12].

Clinical Features

• Newborns with hyperbilirubinemia will appear jaundiced and may have

decreased activity and desire to feed.
• Jaundice occurs in a cranial to caudal progression and presents within the first
week of life, with peak from day 3 to 5.
• Jaundice presenting within the first 24 h of life is likely pathologic.

Differential Diagnosis

• Consider underlying genetic abnormalities, including Gilbert, Crigler-Najjar,

and Dubin-Johnson, when diagnosing unconjugated hyperbilirubinemia.
• Also consider causes of elevated direct/conjugated bilirubin, including biliary
atresia.
• Infection and sepsis can lead to increased bilirubin levels.

Table 11.8 Risk factors for Birth trauma

hyperbilirubinemia
Dehydration
Breast feeding jaundice
Breast milk jaundice (after 1 week of life)
Haemolysis
ABO incompatibility
Polycythaemia
Preterm infant
Infection
Ethnicity (Asian)

Table 11.9 Classifying newborns into risk category based on age and number of risk factors
Gestational age Number of risk factors
Low risk 38 weeks or older with 0
Medium risk 38 weeks or older with 1
35 weeks to less than 38 weeks with 0
High risk 35 weeks to less than 38 weeks with 1 or more
11 Neonatal Emergencies 211

Investigations

• Laboratory workup will demonstrate elevated unconjugated bilirubin levels.

• Consider blood type testing, direct bilirubin level, complete blood count, blood
smear, liver function panel, and infectious workup.

Treatment

• Treatment for hyperbilirubinemia is based on age, risk factors, and level of bili-
rubin (Table 11.10).
• The goal of treatment is to prevent encephalopathy secondary to bilirubin depo-
sition in the brain or kernicterus [12].
• Initial intervention includes oral hydration, intravenous (IV) hydration, and
phototherapy.
• For high-risk cases or concern for kernicterus, exchange transfusion is employed [12].

Prognosis

• Overall prognosis of hyperbilirubinemia is very good [12].

• The incidence of kernicterus is declining with the advent of phototherapy and
exchange transfusion, though patients with kernicterus continue to have long-
term neurologic morbidities [12, 13].

Table 11.10 Trigger levels of total serum bilirubin for phototherapy and exchange transfusion in
infants 35 weeks or greater [12]
Phototherapy level Exchange transfusion
Age of newborn Risk level (μmol/L) level (μmol/L)
24 h Low 196 324
Medium 162 282
High 128 256
48 h Low 258 376
Medium 222 324
High 192 290
72 h Low 299 410
Medium 265 360
High 230 316
96 h Low 336 428
Medium 294 384
High 247 324
5 days and older Low 359 428
Medium 307 384
High 256 324
212 C.L. Cochran and P.P. Soni

Prevention

• Prevention of hyperbilirubinemia focuses on appropriate hydration of the new-

born and appropriate treatment of maternal infections at the time of delivery.
• Awareness of risk factors will assist in early recognition and intervention.
• Kernicterus is an entirely preventable disease though not reversible [12].

Duodenal Atresia

Pathophysiology

• Duodenal atresia occurs when there is an occlusion of the duodenum, restricting

passage of materials through the small bowel.
• Overall incidence is reported at 1 in 6,000 births [14]
• This diagnosis is highly associated with trisomy 21.

Clinical Features

• Patients will present in the first days of life with bilious vomiting.
• Physical exam may reveal a scaphoid abdomen.
• Newborn may pass meconium but is unlikely to have any bowel movements.
• Prenatal history is often positive for polyhydramnios.

Differential Diagnosis

• Infection, oesophageal atresia, tracheaoesophageal fistula, pyloric stenosis, and

reflux should be considered.
• Vomiting in the setting of duodenal atresia is bilious in nature, distinguishing this
diagnosis from many others.

Investigations

• Abdominal x-ray will reveal a double bubble sign indicating trapped air in the
stomach and proximal duodenum.
• Electrolytes, including glucose, should be obtained to assess hydration and nutri-
tional status.
11 Neonatal Emergencies 213

Treatment

• Management of duodenal atresia is reviewed in Table 11.11.

Prognosis

• Complications may include dependence of parenteral nutrition, poor growth,

perforation of the duodenum, and stricture at the site of anastomosis [15].

Hirschsprung’s Disease

Pathophysiology

• Hirschsprung’s disease is the result of failed migration of neural crest cells lead-
ing to a lack of innervation in a section of the colon.
• The aganglionic colon is unable to relax, leading to constriction of that
segment.
• Hirschsprung’s disease is more common in males with a 4:1 male to female pre-
dominance [16].

Clinical Features

• Most newborns present with delayed passage of meconium and stool.

– Ninety-eight percent of normal newborns pass meconium within 48 h.
• Newborns may present with abdominal distension, vomiting, or stringy stools
• Physical exam reveals a tight anal sphincter and explosive stooling with rectal
exam.
• Patients may present with toxic megacolon – extreme dilation of the colon lead-
ing to distension, pain, perforation, and shock.

Differential Diagnosis

• Consider constipation, meconium ileus, duodenal atresia, or other intestinal

obstruction.
214 C.L. Cochran and P.P. Soni

Table 11.11 Characteristics of duodenal atresia, Hirschsprung’s disease, and necrotizing

enterocolitis
Duodenal atresia Hirschsprung’s disease NEC
Age First days of life First days of life First months of life
Gender None Male > female None
dominance
Emesis Bilious Bilious, Non-bilious or bilious
stool – coloured
Abdominal x-ray Double bubble sign Dilation of the Pneumatosis, abdominal
findings proximal colon, lack free air, portal venous gas
of air in the rectum
Diagnosis Abdominal x-ray Rectal suction biopsy Clinical with x-ray findings
Management NPO, nasogastric NPO, nasogastric tube NPO, nasogastric tube
tube placement, IV placement, IV placement, IV hydration,
hydration, surgical hydration, surgical initiate antibiotics, surgical
repair repair consult

Investigations

• Rectal suction biopsy of the narrowed section of the colon is gold standard for
diagnosis [17].
• Anal manometry and barium enema can assist with diagnosis.
• If toxic megacolon is suspected, obtain abdominal x-ray, electrolytes, complete
blood count, and blood culture.

Treatment

• Management of Hirschsprung’s Disease is reviewed in Table 11.11

• In the case of toxic megacolon, provide resuscitation as clinically indicated and
IV antibiotics

Prognosis

• Long-term complications of Hirschsprung’s disease include constipation, bowel

dysfunction, and toxic megacolon [17].

Section E: Metabolic Emergencies

Introduction

Metabolic disorders can masquerade as many different diagnoses on initial presen-

tation. In newborns, always consider underlying metabolic disorders such as
11 Neonatal Emergencies 215

congenital adrenal hyperplasia (CAH), thyroid dysfunction, fatty acid disorders,

amino acid disorders, urea cycle disorders, organic acid disorders, and glycogen
storage disease.

Pathophysiology

• Metabolic emergencies in a newborn result from a range of disorders and

deficiencies.
• Pathophysiology is entirely dependent on the underlying disorder.

Clinical Features

• Newborns may present with poor weight gain, feeding difficulties, lethargy, eme-
sis, diarrhoea, and decreased movement.
• Female and male infants with CAH present with slight variation [18].
– Females will likely have ambiguous genitalia with enlarged clitoris.
– Males tend to present with salt wasting and electrolyte abnormalities includ-
ing hyponatremia and hypokalaemia.

Differential Diagnosis

• Consider sepsis, genetic disorders, and cardiac abnormalities in these patients.

Investigations

• Newborn screening results should be reviewed.

• Glucose levels should be obtained immediately.
• Blood gas should be obtained to assess for signs of metabolic acidosis or
alkalosis.
• Multiple metabolic disorders can present with electrolyte derangement.
• Obtain ACTH, cortisol, and 17-hydroxyprogesterone levels if concerned for
CAH [18].
• Consider urine organic acids, serum amino acids, acylcarnitine profile, lactate,
and pyruvate in non-emergent phase.
• Consider thyroid studies in patients with clinical signs or maternal history of
antithyroid antibodies.
216 C.L. Cochran and P.P. Soni

Treatment

• Provide dextrose for patients with hypoglycaemia defined as less than 2.6 mmol/L
or symptomatic.
– Oral feeds with dextrose (milk, formula) if patient tolerates.
– IV dextrose 10 % bolus of 2 ml/kg.
– If blood sugar remains low, consider an IV infusion of 10 % dextrose.
• Consider stress-dose steroids if CAH and adrenal crisis are suspected [10].
– Hydrocortisone IV: 50–100 mg/m2
• Correct electrolyte abnormalities as indicated.
– CAH patients may require sodium chloride supplementation [18].
– Consider sodium benzoate for sodium replacement after discussion with an
endocrinologist.

Prognosis

• Many metabolic disorders require long-term dietary supplementation or

restriction.

Prevention

• Newborn screening should be administered on all newborns in the first 3 days of life.

Section F: Haematologic Emergencies

Introduction

Bruising, bleeding, and petechiae are not common presenting issues in newborns,
though when present, should raise concern. Broad differentials should be main-
tained for these clinical features.

Pathophysiology

• In neonatal alloimmune thrombocytopenia, maternal antibodies cross the pla-

centa and target paternally derived antigens, causing destruction of the platelet.
• Autoimmune thrombocytopenia occurs when maternal antibodies target mater-
nal and neonatal platelets.
11 Neonatal Emergencies 217

Clinical Features

• Patients may present with easy bleeding, petechiae, and purpura.

– Assess if males experienced prolonged bleeding with circumcision.
• Mental status changes could be indicative of intracranial haemorrhage.

Differential Diagnosis

• Consider vitamin K deficiency, neonatal alloimmune thrombocytopenia, and

autoimmune thrombocytopenia.
• Also consider nonaccidental trauma, infection, underlying coagulopathy, necro-
tizing enterocolitis, haemophagocytic lymphohistiocytosis, and leukaemia.

Investigations

• Gather thorough history including maternal medications, illnesses, birth history,

and vitamin K administration.
• Obtain complete blood count, coagulation panel.
• Maintain a low threshold for infectious workup
• Cranial computerised tomography (CT) scan or ultrasound should be completed
if concerned for intracranial bleed.
• Consider haematology/oncology consult.

Treatment

• Immediately administer vitamin K if not previously given or coagulopathy is

suspected.
– Vitamin K: 0.5–1 mg intramuscularly, subcutaneously, or intravenously [10]
• Provide platelet transfusion if patient is thrombocytopenic and actively bleeding
(Table 11.12).
• Consider fresh frozen plasma in setting of moderate to severe bleeding.
• If concerned for an antibody-mediated process, consider intravenous immuno-
globulin (IVIg) and/or platelet transfusion [19, 20].
– IVIg: 0.4–1 g/kg/day [19, 20].
– Steroid infusion can be considered as adjunct therapy [19, 20].
• Antibiotic therapy for infants with suspected bacterial infection
218 C.L. Cochran and P.P. Soni

Table 11.12 Potential Platelet level Clinical condition

triggers for platelet
Normal Platelet function disorder with bleeding
transfusion
Platelet count Major bleeding
<100 Disseminated intravascular coagulopathy
Preoperative
Sepsis
Platelet count <50 Minor bleeding
Exchange transfusion
Preterm infant
Platelet count <30 Asymptomatic term infant

Prognosis

• Intracranial haemorrhage and lower platelet levels are associated with increased
risk of morbidity and mortality [21].
• Majority of newborns with thrombocytopenia have good outcomes [21].

Prevention

• Administration of vitamin K immediately following birth

• Close monitoring of infants born to moms with idiopathic thrombocytopenia

Section G: Neurologic Emergencies

Introduction

Seizures may present in the neonatal period as a secondary process or as a primary

seizure disorder. The primary goal after stabilisation of the patient should be to
uncover and manage the underlying aetiology of the seizure.

Pathophysiology

• Seizures are more frequent in preterm infants and infants with hypoxic ischemic
encephalopathy (HIE) [22].
• Abnormal movements occur secondary to withdrawal from maternal drug expo-
sure, commonly opioids.
11 Neonatal Emergencies 219

Clinical Features

• Seizures may manifest with abnormal extremity or eye movements.

• Withdrawal symptoms are listed in Table 11.13 [23].
– Neonatal abstinence scoring may be utilised to assess for risk of neonatal
withdrawal.

Differential Diagnosis

• Aetiologies of seizure range from encephalopathy, stroke, HIE, metabolic disor-

ders, infection, to genetic disorders [24].
• Electrolyte abnormality can present abnormal movements or behaviour.
• Nonaccidental trauma should always be considered.

Investigations

• Obtain glucose and electrolytes in infants with abnormal movements.

• Gather thorough history, including maternal history, maternal medications,
maternal infections, and birth history [24].
• Obtain head imaging
• Complete infectious workup, including CSF studies, should be performed.
• Send urine and meconium toxicology screens to assess for withdrawal
syndrome.

Table 11.13 Comparison of neonatal seizures and withdrawal syndrome

Neonatal seizure Withdrawal syndrome
Clinical – Abnormal focal or generalised – Inconsolable, high-pitched crying
features movements – Diarrhoea, vomiting
– Decreased responsiveness – Poor feeding
– Yawning, sneezing
– Sleep disturbance
Diagnosis – Clinical/history – Neonatal abstinence scoring
– EEG – Maternal drug history
– Infectious workup – Urine drug screen
– CT or ultrasound of the head – Meconium drug screen
Management – Phenobarbital 20 mg/kg IV10 – Supportive care
– Fosphenytoin 20 mg PE/kg IV10 – Methadone
– Lorazepam 0.05 mg/kg IV10 – Second line agents: phenobarbital,
clonidine, lorazepam
220 C.L. Cochran and P.P. Soni

Treatment

• If hypoglycaemia is present, correct with IV dextrose.

• Consider treating a seizing neonate with phenobarbital or phenytoin [24].
• If seizures are nonresponsive to the above medications, please consider loraze-
pam or levetiracetam.
• In cases of neonatal withdrawal, provide supportive care and tailor medical man-
agement based on maternally abused drug (Table 11.13).

Prognosis

• Prognosis depends on the underlying aetiology and duration of symptoms

[24, 25].

Prevention

• Maternal education on the harms of drug use

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