**Meet the editor**

Dr. Joanne Baerg is an associate professor of Pediatric Surgery at Loma Linda University Children's Hospital. She has a specific interest in clinical research in pediatric surgery and is the director of the Pediatric Surgery Clinical Scholars Research Program. She is a member of the American Pediatric Surgery Association and the Surgical Section of the American Academy of Pediatrics.

## Contents

#### **Preface XI**

## Preface

Neonatal and Pediatric Surgery is a broad field with many challenges. The aim of this short book is to provide the reader with several chapters in the field of neonatal and pediatric surgery. Each chapter provides details on a specific area of this changing field. The scope of this book focuses on a few areas that are rare and challenging. For example, it covers preop‐ erative and postoperative care of neonates. Important anesthesia considerations, including anesthesia for neonates and regional anesthesia, are discussed. A unique chapter on neona‐ tal tumors is presented. The book provides an overview of the recent recommendations for care of infants and children that undergo cardiac surgery. The challenging aspects of caustic ingestion are explained.

Each chapter stands alone as a detailed source of information for the reader. This book brings updated information with structured headings that will allow the reader to remain focused as the material is reviewed. I would like to thank all the authors that contributed their time and expertise to this project.

> **Joanne E. Baerg MD, FACS** Loma Linda University Children's Hospital Loma Linda, CA, USA

**Peri-Operative Care of the Neonate**

**Provisional chapter**

## **Perioperative Care of the Neonate Perioperative Care of the Neonate**

Shelly Haug, Sara Farooqi, Anamika Banerji and Andrew Hopper Shelly Haug, Sara Farooqi, Anamika Banerji and Andrew Hopper Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/67174

#### **Abstract**

Care of the perioperative neonate requires careful consideration of many aspects including the impact of anesthesia and surgery on multiple organ systems. Neonatal care should include close attention to achieving homeostasis and stability in the perioperative period. This chapter will address the critical elements in the management of the surgical neonate.

**Keywords:** neonate, surgical care, Neonatal Intensive Care Unit (NICU)

#### **1. Preoperative care of the neonate**

Care of the preoperative surgical neonate starts with a comprehensive history and physical examination on admission. It is important to focus on airway, respiratory, cardiac, and renal abnormalities which may impact surgery. Preoperative lab studies should include a complete blood count with differential, basic metabolic panel, coagulation studies and cross match blood screening [1, 2].

Preoperative airway management includes consideration of need for intubation and mechanical ventilation and chest radiography to confirm endotracheal tube position, to assess lung volumes and to evaluate cardiomegaly. Endotracheal intubation is often completed by the neonatal intensive care physician though at times pediatric anesthesia may prefer this responsibility; therefore, communication is important.

Additional preoperative goals include optimizing ventilation and oxygenation, correcting abnormal electrolytes and pH and ensuring adequate perfusion. Lab work should forewarn clinicians of anemia and thrombocytopenia which should be corrected with goal neonatal hematocrit of 30–35% and platelet count greater than 100,000 preoperatively. Coagulation studies should be normalized with fresh frozen plasma and cryoprecipitate as needed prior to

surgery. In cases of liver dysfunction, consider vitamin K administration. Disseminated intravascular coagulation should be considered and treated if sepsis is suspected. Ideally, surgery should be deferred if sepsis is suspected.

Adequate intravenous access is necessary prior to surgery. The need for central venous line placement should be determined and discussed with the anesthesiologist and pediatric surgeon in advance. If percutaneous central venous line placement is unsuccessful, central venous line may need to be placed by surgery. Factors that should be weighed in determining the need for central line placement include type of surgery, anticipated recovery time and anticipated length of time to regain bowel function. If the neonate is expected not to tolerate adequate enteral volumes for appropriate nutrition or to be nil per os (NPO) for greater than 2 – 5 days, then central line access should be considered [3].

Length of NPO status should be discussed with the surgeon. For elective procedures requiring anesthesia or sedation, the American Society of Anesthesiologists recommends neonates be NPO for at least 4 hours if fed breast milk and 6 hours if fed formula prior to surgery [4]. NPO status is at times outweighed by the need for emergency surgery in cases of critical illness.

Choice of intravenous fluid replacement is in large part dictated by the disease process, surgery and type of therapy anticipated [5]. Intravenous fluids should include provision for maintenance fluids and, if indicated, fluid and electrolyte replacement to correct deficits and for surgical conditions with anticipated fluid loss (see **Table 1**). Neonates are born with excess total body water in comparison with muscle mass and fat. The more preterm neonates have increased extracellular fluid. After birth, there is a shift of fluid from the extracellular compartment that results in salt and water diuresis by 48 to 72 hours and physiological weight loss in the first week of life. Failure to have adequate diuresis is associated with increased morbidities including pulmonary edema, tissue edema, symptomatic patent ductus arteriosus, necrotizing enterocolitis (NEC) and chronic lung disease [5–8]. Neonates are more sensitive to hypovolemia due to relatively low cardiac contractility. Maintenance fluid replacement should allow for the initial loss of extracellular fluid diuresis over the first week of life while maintaining normal intravascular volume and tonicity reflected by heart rate, urine output, electrolytes and acid/base status [5].

**Table 1.** Maintenance fluid requirements during the first month of life [5].

Careful estimation of ongoing pathogenic fluid losses is important to determine the best volume and composition of fluid replacement. Estimation of fluid and electrolyte losses can be difficult especially in conditions that predispose to third spacing such as sepsis, hypoalbuminemia, intra-abdominal infection, postoperative abdominal surgery or cardiac surgery. Calculating daily gross intake and output along with serial weight can help to estimate fluid loss. Electrolyte losses can be estimated by multiplying the volume of fluid loss by the electrolyte content of the type of body fluid (see **Table 2**) [5].

**Table 2.** Electrolyte content of body fluids [5].

surgery. In cases of liver dysfunction, consider vitamin K administration. Disseminated intravascular coagulation should be considered and treated if sepsis is suspected. Ideally, surgery

Adequate intravenous access is necessary prior to surgery. The need for central venous line placement should be determined and discussed with the anesthesiologist and pediatric surgeon in advance. If percutaneous central venous line placement is unsuccessful, central venous line may need to be placed by surgery. Factors that should be weighed in determining the need for central line placement include type of surgery, anticipated recovery time and anticipated length of time to regain bowel function. If the neonate is expected not to tolerate adequate enteral volumes for appropriate nutrition or to be nil per os (NPO) for greater than

Length of NPO status should be discussed with the surgeon. For elective procedures requiring anesthesia or sedation, the American Society of Anesthesiologists recommends neonates be NPO for at least 4 hours if fed breast milk and 6 hours if fed formula prior to surgery [4]. NPO status is at times outweighed by the need for emergency surgery in cases of critical

Choice of intravenous fluid replacement is in large part dictated by the disease process, surgery and type of therapy anticipated [5]. Intravenous fluids should include provision for maintenance fluids and, if indicated, fluid and electrolyte replacement to correct deficits and for surgical conditions with anticipated fluid loss (see **Table 1**). Neonates are born with excess total body water in comparison with muscle mass and fat. The more preterm neonates have increased extracellular fluid. After birth, there is a shift of fluid from the extracellular compartment that results in salt and water diuresis by 48 to 72 hours and physiological weight loss in the first week of life. Failure to have adequate diuresis is associated with increased morbidities including pulmonary edema, tissue edema, symptomatic patent ductus arteriosus, necrotizing enterocolitis (NEC) and chronic lung disease [5–8]. Neonates are more sensitive to hypovolemia due to relatively low cardiac contractility. Maintenance fluid replacement should allow for the initial loss of extracellular fluid diuresis over the first week of life while maintaining normal intravascular volume and tonicity reflected by heart rate, urine output,

<750 100+ 100–200 120–200 120–180 750–1000 60–70 80–150 100–150 120–180 1001–1500 30–65 60–100 80–150 120–180 >1500 15–30 60–80 100–150 120–180

**Total water requirement by age (mL/kg/day) Day 1–2 Day 3–7 Day 8–30**

should be deferred if sepsis is suspected.

4 Pediatric and Neonatal Surgery

electrolytes and acid/base status [5].

**Birth weight (g) Insensible water loss**

Adapted from Ref. [45].

**(mL/kg/day)**

**Table 1.** Maintenance fluid requirements during the first month of life [5].

illness.

2 – 5 days, then central line access should be considered [3].

Normal saline boluses of 10–20 mL/kg should be given to maintain adequate renal perfusion to ensure normal urine output (2–3 mL/kg/hour). Fluid should also be given to maintain normal blood pressure based on gestational age. Caution should be used when administering greater than 40 mL/kg of fluid boluses to support blood pressure as this should prompt evaluation regarding the cause of hypotension. Fluid boluses must be balanced by the risk of patent ductus arteriosus in at-risk preterm neonates. Need to increase total fluid intake may be better tolerated by gradually increasing overall total daily fluid rate rather than by giving fluid boluses. Metabolic acidosis can be buffered by the administration of sodium acetate in fluids given to maintain central line patency. Hypoproteinemia should be corrected slowly if possible preoperatively to ensure better postoperative wound healing. An early assessment of serum albumin should be considered, as this may be reflective of prognosis for severity of gastroschisis. In most instances, administration of albumin for fluid replacement and to correct hypoalbuminemia should be discouraged as the albumin leaks into the tissues and contributes to tissue edema. Consideration should be given to placement of a Foley catheter for very long procedures or very unstable or chemically paralyzed neonates. Perfusion should be monitored and normalized. Assessment of tissue perfusion includes measuring blood pressure by peripheral cuff or by arterial line placement. Monitoring arterial blood pressure by indwelling arterial line is indicated for critically ill neonates if a period of postoperative instability is expected, if the neonate is requiring vasopressors or for frequent blood sampling.

Significant morbidity and mortality of perioperative neonates are related to hypoxic/ischemic events. Most intensive care units monitor perfusion index as part of skin surface oxygen saturation monitoring [9, 10]. More institutions are using near infrared spectroscopy (NIRS) to assess tissue perfusion. While pulse oximetry provides a measure of arterial oxygen saturation, it may not be particularly useful for determining oxygen delivery to the tissues. NIRS regional oximetry measures the balance between local oxygen delivery and consumption beneath the sensor. NIRS provides an end-organ measure of not only oxygenation, but also perfusion. NIRS can be used as a continuous, real-time, noninvasive bedside monitor using infrared light sensors of regional tissue oxygenation and hemodynamics [11]. It is United States Food and Drug Administration (FDA) approved for use in neonates, including those less than 2.5 kg. Regional tissue oxygen saturation reflects a ratio of arterial and venous blood (25:75%) and the balance between oxygen delivery and tissue consumption. NIRS monitoring usually includes measuring cerebral and somatic, either renal or mesenteric, regional oxygen saturation. There are norms of average NIRS values for cerebral, renal and mesenteric areas of monitoring, providing a noninvasive measure of end-organ oxygenation and perfusion [12]. These norms vary between term and preterm neonates (see **Table 3**).

**Table 3.** Normal ranges of regional oxygen saturation (rSO2) in term [13] and preterm [14] neonates.

Gastric decompression by Replogle sump tube should be discussed with surgeon and must be considered for neonates with intestinal obstruction. Cases to strongly consider gastric decompression include surgical necrotizing enterocolitis, Hirschsprung's disease, intestinal atresias, gastroschisis and omphalocele.

Preoperative labs should be obtained within 24 hours of planned surgery to ensure infection is ruled out. Prophylactic antibiotics should be given within 1 hour of skin entry [1]. At some hospitals, this timing is best achieved if antibiotic such as cefazolin is given in the preoperative surgical area as part of a preoperative checklist. Antibiotic choice should be dependent on disease process. Suspected perforation should be treated with broad-spectrum antibiotics that specifically include Gram-negative and anaerobic coverage. Length of therapy and choice of antibiotics may change depending on the intraoperative findings and culture results.

### **2. Common conditions of the surgical neonate**

Although various conditions require specific management, the initial management of the surgical neonate consists of gastric decompression with placement of a Replogle tube, imaging including abdominal radiographs, and fluid and electrolyte management. The use of antibiotics is dependent upon the suspected pathology. Specialized management considerations are reviewed for the following conditions.

#### **2.1. Gastroschisis**

saturation, it may not be particularly useful for determining oxygen delivery to the tissues. NIRS regional oximetry measures the balance between local oxygen delivery and consumption beneath the sensor. NIRS provides an end-organ measure of not only oxygenation, but also perfusion. NIRS can be used as a continuous, real-time, noninvasive bedside monitor using infrared light sensors of regional tissue oxygenation and hemodynamics [11]. It is United States Food and Drug Administration (FDA) approved for use in neonates, including those less than 2.5 kg. Regional tissue oxygen saturation reflects a ratio of arterial and venous blood (25:75%) and the balance between oxygen delivery and tissue consumption. NIRS monitoring usually includes measuring cerebral and somatic, either renal or mesenteric, regional oxygen saturation. There are norms of average NIRS values for cerebral, renal and mesenteric areas of monitoring, providing a noninvasive measure of end-organ oxygenation and perfu-

Gastric decompression by Replogle sump tube should be discussed with surgeon and must be considered for neonates with intestinal obstruction. Cases to strongly consider gastric decompression include surgical necrotizing enterocolitis, Hirschsprung's disease, intestinal atresias,

Preoperative labs should be obtained within 24 hours of planned surgery to ensure infection is ruled out. Prophylactic antibiotics should be given within 1 hour of skin entry [1]. At some hospitals, this timing is best achieved if antibiotic such as cefazolin is given in the preoperative surgical area as part of a preoperative checklist. Antibiotic choice should be dependent on disease process. Suspected perforation should be treated with broad-spectrum antibiotics that specifically include Gram-negative and anaerobic coverage. Length of therapy and choice of

antibiotics may change depending on the intraoperative findings and culture results.

Although various conditions require specific management, the initial management of the surgical neonate consists of gastric decompression with placement of a Replogle tube, imaging including abdominal radiographs, and fluid and electrolyte management. The use of antibiotics is dependent upon the suspected pathology. Specialized management considerations are

**2. Common conditions of the surgical neonate**

reviewed for the following conditions.

sion [12]. These norms vary between term and preterm neonates (see **Table 3**).

Values differ by sensor type with neonatal sensors reading 10% higher. Adapted from Refs. [13, 14].

**Table 3.** Normal ranges of regional oxygen saturation (rSO2) in term [13] and preterm [14] neonates.

 **rSO2 Term Preterm** Cerebral (%) 66–89 66–83 Renal (%) 75–97 64–87 Mesenteric (%) 63–87 32–66

gastroschisis and omphalocele.

6 Pediatric and Neonatal Surgery

Gastroschisis is a congenital anterior abdominal wall defect that occurs to the right of the umbilical cord insertion that results in herniation of abdominal contents and thereby permitting bowel exposure to amniotic fluid in utero [15]. Abdominal contents generally contain the small intestine; however, larger defects may contain the stomach and colon [16]. Compared to an omphalocele defect, there is no transparent sac to protect the intestine and gastroschisis is not usually associated with other congenital syndromes. However, it may be associated with other gastrointestinal abnormalities such as malrotation, atresia or stenosis. A neonate with a prenatal diagnosis of gastroschisis should preferably be delivered at an institution with multidisciplinary care, influx into maternal-fetal medicine service, neonatal intensive care team and pediatric surgery. At the time of delivery, the neonate should be placed in a bowel bag enclosed to the neonate's axilla. This bag protects the bowel and also helps to retain body heat. Given the location of the defect, the neonate should be placed right side down to avoid tension on the mesenteric vasculature. A Replogle tube should be placed at the time of delivery to allow for abdominal decompression. All neonates should receive empiric broad-spectrum antibiotics, preferably ampicillin and gentamicin. Immediate intubation is not required if the neonate's respiratory status is stable. Some medical experts recommend a controlled, elective intubation to avoid unnecessary airway trauma. Surgical management is dependent on the defect. Surgical options include primary closure, staged reduction with a silo or sutureless umbilical closure [17]. In order to prepare the neonate for surgery, a secure airway should be established as well as adequate intravenous access. Due to the nature of the defect, umbilical lines are contraindicated in gastroschisis. Chemical paralysis is generally dependent on the preference of the surgeon and may be required in neonates with a large defect. When defect size or abdominal pressure issues prevent primary closure, placement of a silo allows for gradual reduction in the intestine into the abdominal cavity. With a silo, abdominal contents are gently "squeezed" into the abdomen daily. Once the contents are reduced, the neonate is taken to the operating room for closure. After the defect is closed, nasogastric decompression is continued until return of bowel function.

Special consideration must be taken in regard to fluid management in gastroschisis due to insensible fluid loss and postoperative third-space fluid shifts. Amount of postoperative fluid administration should generally be less than prior to gastroschisis closure and be balanced with perfusion and urine output [18]. See discussion of preoperative fluid management. Potential complications associated with gastroschisis include ileus, sepsis, intestinal atresias, malabsorption, wound infection and necrotizing enterocolitis [16].

#### **2.2. Omphalocele**

An omphalocele is a congenital ventral abdominal wall defect of the umbilical ring that results in abdominal viscera herniation and is associated with chromosomal, cardiac and/or genitourinary abnormalities [19]. Immediate postnatal management should include protection of the herniated viscera with sterile saline-soaked gauze, and stabilization of viscera to ensure blood supply to the bowel is not kinked by the weight of the bowel. The neonate may be placed right side down or with towels placed under the bowel to help support the externalized intestine. Gastric decompression should be initiated with placement of a Replogle tube on continuous low suction to prevent bowel distention. If volume of gastric drainage exceeds approximately 10 mL/kg per 12 hour shift, gastric fluid should be replaced with 0.9% sodium chloride.

Potential problems with omphalocele include risk of hypothermia due to high heat loss from the exposed bowel as well as risk of vasoconstriction, decreased tissue perfusion and metabolic acidosis [19]. Fluids and electrolyte replacement will need to anticipate additional fluid losses due to the specific disease pathology. Maintenance of intravascular fluid volume is necessary to ensure adequate tissue perfusion and preservation of bowel wall perfusion [19, 20].

Other factors to consider include prevention of sepsis by administering broad-spectrum antibiotic therapy. Due to the association with other anomalies, neonates with omphalocele should be evaluated with chest and abdominal radiography, renal and abdominal ultrasound as well as echocardiogram prior to operation [19]. Repair of the defect will be a primary or a staged closure depending on the size of the defect. Potential postoperative complications include significant increase in intra-abdominal pressures that may compromise venous blood return and hemodynamic and/or respiratory stability due to diaphragmatic elevation [19].

Another important consideration in neonates with omphalocele is the risk of pulmonary hypertension [21]. All neonates with omphalocele should be monitored for evidence of pulmonary hypertension between the second and seventh day after birth as they may not initially present with signs of pulmonary hypertension. Diagnosis should be suspected based on increased oxygen requirement and increased pre- and postductal gradient and confirmed by increased right ventricular pressures (greater than 40 mmHg) on echocardiogram [21].

Short-term postoperative complications include necrotizing enterocolitis, prolonged ileus and respiratory distress. If primary closure is done, the neonate will require assisted ventilation and may require muscle relaxants for a time. It is important to ensure adequate ventilation and oxygenation by adjusting inspiratory and end expiratory pressures to maintain adequate lung volumes as the abdominal distention postoperatively may be aggravated by fluid third spacing due to capillary leak syndrome. Postoperative pain management usually requires continuous infusion of morphine and should be titrated according to appropriate neonatal pain scales (see pain section later in chapter) [22]. Long-term complications include prolonged dependence on parenteral nutrition, gastroesophageal reflux, parenteral nutrition-related liver disease, feeding intolerance and neurodevelopmental delay [19]. When bowel function returns postoperatively, initiation of enteral feeds should be done with breast milk or an elemental formula such as Elecare or Neocate, starting with small volumes and advancing slowly [23, 24]. Neonates with giant omphalocele usually require prolonged time to achieve full enteral feeds, especially if complicated by respiratory insufficiency requiring intubation shortly after delivery or symptoms of gastroesophageal reflux postoperatively [24].

#### **2.3. Obstruction**

See further detail (**Table 4**).

**Table 4.** Neonatal obstruction [25].

Gastric decompression should be initiated with placement of a Replogle tube on continuous low suction to prevent bowel distention. If volume of gastric drainage exceeds approximately 10 mL/kg per 12 hour shift, gastric fluid should be replaced with 0.9% sodium chloride.

Potential problems with omphalocele include risk of hypothermia due to high heat loss from the exposed bowel as well as risk of vasoconstriction, decreased tissue perfusion and metabolic acidosis [19]. Fluids and electrolyte replacement will need to anticipate additional fluid losses due to the specific disease pathology. Maintenance of intravascular fluid volume is necessary to ensure adequate tissue perfusion and preservation of bowel wall perfusion [19, 20].

Other factors to consider include prevention of sepsis by administering broad-spectrum antibiotic therapy. Due to the association with other anomalies, neonates with omphalocele should be evaluated with chest and abdominal radiography, renal and abdominal ultrasound as well as echocardiogram prior to operation [19]. Repair of the defect will be a primary or a staged closure depending on the size of the defect. Potential postoperative complications include significant increase in intra-abdominal pressures that may compromise venous blood return and hemodynamic and/or respiratory stability due to diaphragmatic elevation [19].

Another important consideration in neonates with omphalocele is the risk of pulmonary hypertension [21]. All neonates with omphalocele should be monitored for evidence of pulmonary hypertension between the second and seventh day after birth as they may not initially present with signs of pulmonary hypertension. Diagnosis should be suspected based on increased oxygen requirement and increased pre- and postductal gradient and confirmed by increased right ventricular pressures (greater than 40 mmHg) on echocardio-

Short-term postoperative complications include necrotizing enterocolitis, prolonged ileus and respiratory distress. If primary closure is done, the neonate will require assisted ventilation and may require muscle relaxants for a time. It is important to ensure adequate ventilation and oxygenation by adjusting inspiratory and end expiratory pressures to maintain adequate lung volumes as the abdominal distention postoperatively may be aggravated by fluid third spacing due to capillary leak syndrome. Postoperative pain management usually requires continuous infusion of morphine and should be titrated according to appropriate neonatal pain scales (see pain section later in chapter) [22]. Long-term complications include prolonged dependence on parenteral nutrition, gastroesophageal reflux, parenteral nutrition-related liver disease, feeding intolerance and neurodevelopmental delay [19]. When bowel function returns postoperatively, initiation of enteral feeds should be done with breast milk or an elemental formula such as Elecare or Neocate, starting with small volumes and advancing slowly [23, 24]. Neonates with giant omphalocele usually require prolonged time to achieve full enteral feeds, especially if complicated by respiratory insufficiency requiring intubation shortly after delivery or symptoms of gastroesophageal reflux

gram [21].

8 Pediatric and Neonatal Surgery

postoperatively [24].

See further detail (**Table 4**).

**2.3. Obstruction**

#### **2.4. Necrotizing enterocolitis**

Necrotizing enterocolitis (NEC) is the most common emergent neonatal gastrointestinal diseases among premature neonates [26]. The mortality rate of NEC may range from 20 to 30% with the highest mortality in those neonates who require surgery [27]. Often, an inverse relationship between gestational age and frequency of NEC exists. Therefore, the smaller the neonate, the higher the clinical suspicion for this disease.

Typically, NEC presents with feeding intolerance, hematochezia and abdominal distention. Clinical progression of the disease may ensue rapidly from abdominal discoloration, worsening distention with intestinal perforation leading to clinical deterioration with hypotension, metabolic acidosis and thrombocytopenia requiring intensive medical and surgical support. At the moment of suspicion for NEC, the neonate should be placed NPO and gastric decompression initiated. Intravenous fluid hydration must be provided, along with an urgent surgical consultation. Intravenous antibiotics should be started once NEC is suspected that often include "triple therapy" consisting of Gram-positive, Gram-negative and anaerobic bacteria coverage. Immediate and serial abdominal radiographs should be obtained to assess the presence of pneumatosis intestinalis, one of the hallmarks to diagnose NEC. Laboratory testing should include blood cultures, complete blood count (CBC) to assess for leukocytosis and thrombocytopenia, and C-reactive protein. Serial two-view abdominal radiographs should be obtained to assess for progression. While there are no universally accepted criteria for NEC, Bell's staging system is often used to describe the stages and severity of this disease. The staging is described as follows (see **Table 5**).

**Table 5.** Modified Bell's staging criteria for necrotizing enterocolitis [28].

## **3. Comparison between acute and elective surgical management**

Operative intervention of the acutely ill neonate is less desirable but often unavoidable. In situations of intestinal perforation or a hemodynamically compromised neonate, all efforts should be made to ensure a near stable status of the neonate [1, 2, 5]. If a neonate requires emergent surgical intervention, communication with the surgical team, anesthesiology and neonatology team to discuss diagnosis and planned intervention must be made as soon as possible. Most important in management is establishing a stable airway and adequate intravenous or central line access. Pertinent imaging including radiographs and ultrasound should be readily available for evaluation by the surgical team. The neonatal team should ideally be at bedside to intervene in case of clinical deterioration per Pediatric Advance Life Support (PALS) guidelines. Informed consent for surgery must be obtained with the parents or guardian either in person or via telephone.

One common routine elective operation in neonates is gastrostomy tube placement. A gastrostomy tube or "g-tube" is a small feeding tube that is surgically or percutaneously placed in the stomach for feeding or decompression of air or drainage. Surgical placement is either laparoscopic or open and may be done in association with other procedures [29]. Gastrostomy tubes may be needed for preterm neonates with continued inadequate oral feeding once corrected to term if gastrostomy tube feeding is expected to be needed for greater than 4 weeks. Prior to gastrostomy tube placement, the surgeon may request radiographs to evaluate anatomy of the upper gastrointestinal tract. After gastrostomy tube placement, the neonate may have minor pain at the incision site. Intravenous fluids may be required for the first 24 hour to provide parenteral nutrition to allow the site to heal. Generally, the neonate may be restarted on previous feeds at 25% of the total expected volume, and advanced gradually to full enteral feeds via the g-tube within 24–36 hours as tolerated.. A frequent complication of gastrostomy tubes includes dislodgment, usually within the first 2 weeks after its placement [29]. When this occurs, a physician should replace the tube as soon as possible, so the hole in the stomach does not close. A small amount of leaking is normal and may require protective cream application to the skin. A gastrostomy tube may be left in place permanently or temporarily dependent on the neonate's needs [29].

Another common elective surgical procedure includes inguinal hernia repair. An inguinal hernia repair is an internal opening in the inguinal canal through which fluids and/or intestines may pass through [30]. The neonate may have minor pain at the incision site postoperatively that should be controlled with acetaminophen or small doses of morphine. Neonates should be monitored for postoperative respiratory complications such as apnea and oxygen desaturation. Neonates at risk include those with a history of prematurity, especially if still less than 45 weeks corrected gestational age, and neonates with comorbidities including chronic lung disease, history of necrotizing enterocolitis, anemia, low birth weight or former apnea episodes [31, 32]. Healthy, older neonates may generally be repaired as an outpatient [31].

## **4. Postoperative care of the neonate**

include "triple therapy" consisting of Gram-positive, Gram-negative and anaerobic bacteria coverage. Immediate and serial abdominal radiographs should be obtained to assess the presence of pneumatosis intestinalis, one of the hallmarks to diagnose NEC. Laboratory testing should include blood cultures, complete blood count (CBC) to assess for leukocytosis and thrombocytopenia, and C-reactive protein. Serial two-view abdominal radiographs should be obtained to assess for progression. While there are no universally accepted criteria for NEC, Bell's staging system is often used to describe the stages and severity of this disease. The stag-

**Stage/classification Systemic signs Abdominal signs Radiographic signs**

IB; suspected Same as above Gross hematochezia Same as above

Gastric residuals, abdominal distention, emesis, heme-positive stool

distention

distention

absent bowel sounds with or without abdominal

Same as above, plus absent bowel sounds, definite tenderness, with or without abdominal cellulitis or right lower quadrant mass

Same as above, plus signs of peritonitis, marked tenderness and abdominal

Same as IIIA Same as IIIA Same as above plus

Normal or intestinal dilation,

Intestinal dilation, ileus, pneumatosis intestinalis

Same as IIA plus ascites

Same as IIA plus ascites

pneumoperitoneum

mild ileus

**3. Comparison between acute and elective surgical management**

Operative intervention of the acutely ill neonate is less desirable but often unavoidable. In situations of intestinal perforation or a hemodynamically compromised neonate, all efforts should be made to ensure a near stable status of the neonate [1, 2, 5]. If a neonate requires emergent surgical intervention, communication with the surgical team, anesthesiology and neonatology team to discuss diagnosis and planned intervention must be made as soon as possible. Most important in management is establishing a stable airway and adequate intravenous or central line access. Pertinent imaging including radiographs and ultrasound should be readily available for evaluation by the surgical team. The neonatal team should ideally be at bedside to intervene in case of clinical deterioration per Pediatric Advance Life Support

ing is described as follows (see **Table 5**).

IA; suspected Temperature instability,

IIB definite, moderately ill Same as above plus mild

IIIA advanced, severely ill,

10 Pediatric and Neonatal Surgery

IIIB advanced, severely ill, perforated bowel

Adapted from Ref. [28].

intact bowel

apnea, bradycardia,

IIA; definite, mildly ill Same as above Same as above with

metabolic acidosis and thrombocytopenia

Same as IIB plus hypotension, bradycardia, severe apnea, combined respiratory and metabolic acidosis, DIC and neutropenia

**Table 5.** Modified Bell's staging criteria for necrotizing enterocolitis [28].

lethargy

Postoperative management should begin with face-to-face communication between the senior clinician caring for the neonate after surgery and the surgeon as well as the anesthesiologist. The neonatologist should be informed of major events that may have occurred during the surgery, the surgery that was performed, the anesthesia the neonate received during the surgery and postoperatively in recovery (especially if paralytic agents were used), as well as the volume and type of fluids or blood products given during the operation.

Temperature homeostasis is important in the postoperative period. Neonates undergoing operative procedures in the operating room are at increased risk of thermal instability. Hypothermia of postoperative neonates leads to an increased risk of adverse respiratory events including increased need for respiratory and cardiac interventions compared to normothermic neonates [33]. Furthermore, hypothermia may cause protein catabolism, hypokalemia and changes in glucose metabolism. Postoperative interventions include applying warm temperature regulating blankets, decreasing skin exposure and warming operative rooms [34].

If the neonate remains intubated postoperatively, obtain a blood gas and chest radiography immediately following return to the ICU to assess oxygenation, ventilation, chest expansion and endotracheal tube position. It is important for clinicians to understand postoperative neonates are prone to apnea and periodic breathing while recovering from anesthesia and in response to pain and pain medications. Neonates are also prone to hypoxemia due to transient decrease in functional residual capacity of the lungs and ventilation/perfusion mismatch. Adequate lung tidal volumes of 6–8 mL/kg expiratory lung volumes should be maintained to prevent atelectasis. Blood gas pH should be maintained at 7.35–7.45 with pCO2 of 40–55 for most neonates. Once the neonate is awake and consistently breathing spontaneously, the clinician should rapidly wean the ventilator and extubate per blood gases if possible. Weaning off mechanical ventilation should be weighed against the need for additional pain control. Surgery should be made aware of neonates requiring nasal continuous positive airway pressure (CPAP) or nasal intermittent mandatory ventilation (IMV) postextubation. Ideally, continuous narcotic infusion for pain control should be at a minimum or discontinued prior to extubation. The clinician should also monitor for the development of pulmonary hypertension by clinical symptoms, pre- and postductal oxygen gradient and confirm by echocardiography [1].

Immediate postoperative labs should include evaluation of hemoglobin/hematocrit. If blood loss is over 15% and not already replaced during the operative period, clinicians should consider replacing with packed red blood cells [35, 36]. Electrolytes should be evaluated in the immediate postoperative period and also monitored every 6 hours for invasive procedures or every 8–12 hours for less intensive procedures for the first 24-hours postoperatively [1].

Surgical neonates may have significant third-space losses depending on the magnitude of the procedure. Phases of fluid resuscitation change with time postoperatively. In the immediate postoperative time period, fluid and blood replacement is often required. Postoperative days 2–4 are often phases of third spacing and vascular leak during which some element of fluid replacement is required in conjunction with diuretics to help mobilize fluids. Avoidance of massive anasarca is important. Abdominal compartment syndrome is especially important to consider in the context of abdominal closures with decreased perfusion and the potential for decreased urine output. Gastroschisis patients are especially prone to large fluid losses. If total parenteral nutrition is not immediately available, D5 lactated ringers should be given. Initial fluids should be given at 150–175 mL/kg/day. Total parenteral nutrition should be optimized to include protein of 3–4 g/kg/day to minimize catabolic state and promote wound healing. Dextrose may need to be adjusted postoperatively due to hyperglycemia secondary to stress and increased fluid administration. Therefore, Accuchecks should be monitored frequently, and glucose infusion rate (GIR) should be adjusted. GIR should be maintained 4–8 µg/kg/min to maintain blood glucose levels of 100–160 mg/dL. Electrolytes should be normalized as much as possible [5]. Consideration of starting enteral nutrition should be discussed when the neonate shows intestinal readiness, presence of bowel sounds and passing gas. Clinicians should monitor for postoperative ileus from the surgery and/or ileus due to pain medications. Antireflux medications should be avoided in the neonate unless for specific surgical cases such as tracheoesophageal fistula where such medications have proven to be necessary. Reflux medications lead to abnormalities of intestinal flora and have been shown to increase neonatal mortality [37].

and changes in glucose metabolism. Postoperative interventions include applying warm temperature regulating blankets, decreasing skin exposure and warming operative rooms [34].

If the neonate remains intubated postoperatively, obtain a blood gas and chest radiography immediately following return to the ICU to assess oxygenation, ventilation, chest expansion and endotracheal tube position. It is important for clinicians to understand postoperative neonates are prone to apnea and periodic breathing while recovering from anesthesia and in response to pain and pain medications. Neonates are also prone to hypoxemia due to transient decrease in functional residual capacity of the lungs and ventilation/perfusion mismatch. Adequate lung tidal volumes of 6–8 mL/kg expiratory lung volumes should be maintained to prevent atelectasis. Blood gas pH should be maintained at 7.35–7.45 with pCO2 of 40–55 for most neonates. Once the neonate is awake and consistently breathing spontaneously, the clinician should rapidly wean the ventilator and extubate per blood gases if possible. Weaning off mechanical ventilation should be weighed against the need for additional pain control. Surgery should be made aware of neonates requiring nasal continuous positive airway pressure (CPAP) or nasal intermittent mandatory ventilation (IMV) postextubation. Ideally, continuous narcotic infusion for pain control should be at a minimum or discontinued prior to extubation. The clinician should also monitor for the development of pulmonary hypertension by clinical symptoms, pre- and postductal oxygen gradient and confirm

Immediate postoperative labs should include evaluation of hemoglobin/hematocrit. If blood loss is over 15% and not already replaced during the operative period, clinicians should consider replacing with packed red blood cells [35, 36]. Electrolytes should be evaluated in the immediate postoperative period and also monitored every 6 hours for invasive procedures or every 8–12 hours for less intensive procedures for the first 24-hours postoperatively [1].

Surgical neonates may have significant third-space losses depending on the magnitude of the procedure. Phases of fluid resuscitation change with time postoperatively. In the immediate postoperative time period, fluid and blood replacement is often required. Postoperative days 2–4 are often phases of third spacing and vascular leak during which some element of fluid replacement is required in conjunction with diuretics to help mobilize fluids. Avoidance of massive anasarca is important. Abdominal compartment syndrome is especially important to consider in the context of abdominal closures with decreased perfusion and the potential for decreased urine output. Gastroschisis patients are especially prone to large fluid losses. If total parenteral nutrition is not immediately available, D5 lactated ringers should be given. Initial fluids should be given at 150–175 mL/kg/day. Total parenteral nutrition should be optimized to include protein of 3–4 g/kg/day to minimize catabolic state and promote wound healing. Dextrose may need to be adjusted postoperatively due to hyperglycemia secondary to stress and increased fluid administration. Therefore, Accuchecks should be monitored frequently, and glucose infusion rate (GIR) should be adjusted. GIR should be maintained 4–8 µg/kg/min to maintain blood glucose levels of 100–160 mg/dL. Electrolytes should be normalized as much as possible [5]. Consideration of starting enteral nutrition should be discussed when the neonate shows intestinal readiness, presence of bowel sounds and passing gas. Clinicians should monitor for postoperative ileus from the surgery and/or ileus due to

by echocardiography [1].

12 Pediatric and Neonatal Surgery

Special fluid consideration must be made for those neonates with gastroschisis that have undergone repair. Once they are repaired, their fluid losses significantly decrease, and thus, parenteral nutrition must be adjusted shortly after surgical closure. Total fluid administration should be decreased to approximately 140–150 mL/kg/day [38], based on the assessment of the neonate's fluid losses. Clinicians should be cautious of fluid volumes as overhydration may lengthen hospital stay and delay enteral feeding [38].

Hypotension secondary to hypovolemia may be treated with 10–20 mL/kg boluses of normal saline or if hypotension is persistent and severe, the clinician should consider fresh frozen plasma. If anemic, packed red blood cells may be used. Albumin should rarely be used and only with great caution as it may worsen third-space fluid losses in neonates. Low albumin is often partially dilutional and when not exacerbated by dilutional effects, is best addressed through maximizing protein delivery through nutrition. Replacement of any gastric output should be considered with 0.45 normal saline with 10 mEq of potassium chloride per liter. If output is large, consider replacing more frequently (i.e., every 4 hours to run over 4 hours versus once a shift over 1 hour if lower output). Replacement of gastric fluid is important to maintain fluid balance but must be balanced with urine output and overall body edema. Vasopressor therapy may be considered for the critically ill postoperative neonate if fluid replacement is already optimized and neonate remains hypotensive with signs of decreased end-organ perfusion. Steroid therapy to aid adrenal stress response may also improve hemodynamic stability; however, it should be used cautiously as steroids may decrease immune response if there is concern for infection.

Fluid status must be monitored closely, and urine output should be maintained at a minimum of 1 mL/kg/hour. The clinician must balance the neonate's overall fluid status as measured by weight, urine output, body wall edema, blood pressure, heart rate and overall clinical status. Edematous neonates may still have low intravascular volumes, and thus, diuretics would possibly exacerbate hypotension.

Blood pressure should be monitored closely, at least hourly if there is no arterial line access. Hypotension in the postoperative period is considered a sign of hypovolemia until proven otherwise. Skin perfusion should be monitored which can be done by NIRS or perfusion index of pulse oximetry monitoring. All tubes and drains should be monitored closely postoperatively for patency, function and how secure they are attached to the patient. Output of sumps, chest tubes, wound drains and Foley catheters should be followed. Pending resolution of ileus and improvement in outputs each should be removed at the earliest time point to prevent infection with persistent foreign bodies.

Prevention of infection is important. White blood cell count, C-reactive protein trend and bandemia should be monitored and blood cultures obtained if concern for infection rises [1]. Be especially cautious of hygienic precautions when handling tubes, drains and any wound dressing changes. The need for postoperative antibiotic coverage should be discussed between the neonatal clinician and surgeon.

## **5. Pain management, sedation and paralysis review**

Pain control should be titrated based on the type of surgery. More invasive surgeries will likely require immediate postoperative pain management including a narcotic drip for the first 24 – 48 hours [39]. Consider morphine 20-50 micrograms/kg/hour or Fentanyl 3 micrograms/kg/hour with as needed (PRN) dosing for breakthrough pain. Pain management should be transitioned to PRN dosing when able. Titration of pain medication should be assessed through reliable and accurate neonatal pain assessment scoring tools such as the "Neonatal Pain, Agitation and Sedation Scale" (N-PASS) [40] or "Crying, Requires increased oxygen administration, Increased vital signs, Expression and Sleeplessness" (CRIES) [41]. A combination of behavioral observations such as facial expression, body posture and tone and physiologic symptoms such as heart rate, blood pressure and oxygen saturation should be taken into consideration by the neonatal pain score used [22].

Nonnarcotic pain management methods should be used such as Sweet-Ease and intravenous Tylenol 20 mg/kg/dose every 6 hours for a 24-48 hour period, unless contraindicated or if there is concern for liver dysfunction. The neonate should be monitored closely for urinary retention if Foley catheter is not in place. The stomach should be decompressed. Nonpharmacological pain management includes protective neonatal positioning if possible with the neonate supported in the flex position. Environmental stimulation should be minimized with decreased lighting, noise and touch.

Use of chemical paralytic agents postoperatively should only be used in cases where there is concern for wound dehiscence, large irreducible gastroschisis or patient instability. Paralytics should be used for shortest time possible, as the use will increase the likelihood of thirdspacing fluids, urinary retention and anasarca [39].

## **6. Follow-up of the surgical neonate**

The care of a neonate following discharge from the ICU is one that requires a multidisciplinary approach. The patient's pediatrician, neonatologist in the High Risk Follow Clinic (when appropriate), various therapists and the primary surgeon will need to see the neonate after discharge [42]. Follow-up visits include neurodevelopment assessment scales using Bayley III and WPPSI-II scores. While there are certain risk factors innate to sick neonates that make them prone to developmental delay such as prematurity and/or congenital defects, there are data to suggest that neonates who require surgical intervention experience initial developmental delays as compared with their healthy counterparts [43]. While there is ample evidence of suboptimal developmental outcomes in neonates requiring cardiac surgery, the data for those undergoing repair of conditions such as gastroschisis suggest that outcomes are similar to those of their healthy cohorts [44]. Those neonates who have had significant surgical intervention and those with severe outcomes such as short gut syndrome require a lifelong close follow-up with the surgical team.

## **Author details**

dressing changes. The need for postoperative antibiotic coverage should be discussed between

Pain control should be titrated based on the type of surgery. More invasive surgeries will likely require immediate postoperative pain management including a narcotic drip for the first 24 – 48 hours [39]. Consider morphine 20-50 micrograms/kg/hour or Fentanyl 3 micrograms/kg/hour with as needed (PRN) dosing for breakthrough pain. Pain management should be transitioned to PRN dosing when able. Titration of pain medication should be assessed through reliable and accurate neonatal pain assessment scoring tools such as the "Neonatal Pain, Agitation and Sedation Scale" (N-PASS) [40] or "Crying, Requires increased oxygen administration, Increased vital signs, Expression and Sleeplessness" (CRIES) [41]. A combination of behavioral observations such as facial expression, body posture and tone and physiologic symptoms such as heart rate, blood pressure and oxygen saturation should be

Nonnarcotic pain management methods should be used such as Sweet-Ease and intravenous Tylenol 20 mg/kg/dose every 6 hours for a 24-48 hour period, unless contraindicated or if there is concern for liver dysfunction. The neonate should be monitored closely for urinary retention if Foley catheter is not in place. The stomach should be decompressed. Nonpharmacological pain management includes protective neonatal positioning if possible with the neonate supported in the flex position. Environmental stimulation should be minimized with decreased

Use of chemical paralytic agents postoperatively should only be used in cases where there is concern for wound dehiscence, large irreducible gastroschisis or patient instability. Paralytics should be used for shortest time possible, as the use will increase the likelihood of third-

The care of a neonate following discharge from the ICU is one that requires a multidisciplinary approach. The patient's pediatrician, neonatologist in the High Risk Follow Clinic (when appropriate), various therapists and the primary surgeon will need to see the neonate after discharge [42]. Follow-up visits include neurodevelopment assessment scales using Bayley III and WPPSI-II scores. While there are certain risk factors innate to sick neonates that make them prone to developmental delay such as prematurity and/or congenital defects, there are data to suggest that neonates who require surgical intervention experience initial developmental delays as compared with their healthy counterparts [43]. While there is ample evidence of suboptimal developmental outcomes in neonates requiring cardiac surgery, the data for those undergoing repair of conditions such as gastroschisis suggest that outcomes are similar to those of their healthy cohorts [44]. Those neonates who have had significant surgical intervention and those with severe outcomes such as short gut syndrome require a lifelong

the neonatal clinician and surgeon.

14 Pediatric and Neonatal Surgery

lighting, noise and touch.

**5. Pain management, sedation and paralysis review**

taken into consideration by the neonatal pain score used [22].

spacing fluids, urinary retention and anasarca [39].

**6. Follow-up of the surgical neonate**

close follow-up with the surgical team.

Shelly Haug\*, Sara Farooqi, Anamika Banerji and Andrew Hopper

\*Address all correspondence to<EMAIL_ADDRESS>
Loma Linda University Children's Hospital, Loma Linda, CA, USA

## **References**

[25] Kimura K, Loening-Baucke V. Bilious vomiting in the newborn: rapid diagnosis of intestinal obstruction. *Am Fam Physician*. 2000;61(9):2791–2798.

[11] Koch HW, Hansen TG. Perioperative use of cerebral and renal near-infrared spectroscopy in neonates: a 24-h observational study. *Pediatr Anesth*. 2016;26(2):190–198.

[12] Alderliesten T, Dix L, Baerts W, et al. Reference values of regional cerebral oxygen saturation during the first 3 days of life in preterm neonates. *Pediatr Res*. 2016;79(1–1):55–64.

[13] Chock V. NIRS Educational Module. November 2016. http://neonatology.stanford.edu/ content/dam/sm/neonatology/documents/NIRS%20Educational%20Module.pdf.

[14] McNeill S, Gatenby JC, McElroy S, Engelhardt B. Normal cerebral, renal and abdominal regional oxygen saturations using near-infrared spectroscopy in preterm infants.

[15] Wilson RD, Johnson MP. Congenital abdominal wall defects: an update. *Fetal Diagn Ther*.

[16] Lund CH, Bauer K, Berrios M. Gastroschisis: incidence, complications, and clinical management in the neonatal intensive care unit. *J Perinat Neonatal Nurs*. 2007;21(1):63–68.

[17] O'Connell RV, Dotters-Katz SK, Kuller JA, Strauss RA. Gastroschisis: a review of management and outcomes. *Obstet Gynecol Surv*. 2016;71(9):537–544. doi:10.1097/

[18] Bonasso PC, Lucke-Wold B, Hobbs GR, Vaughan RA, Shorter NA, Nakayama DK. Excessive postoperative fluid administration in infants with gastroschisis. *Am Surg*.

[19] McNair C, Hawes J, Urquhart H. Caring for the newborn with an omphalocele. *Neonatal*

[20] Philippart AI, Canty TG, Filler RM. Acute fluid volume requirements in infants with anterior abdominal wall defects. *J Pediatr Surg*. 1972;7(5):553–558. doi:10.1016/0022-3468(72)90212-6

[21] Baerg JE, Thorpe DL, Sharp NE, et al. Pulmonary hypertension predicts mortality in infants with omphalocele. *J Neonatal-Perinat Med*. 2015;8(4):333–338. doi:10.3233/

[22] Bhalla T, Shepherd E, Tobias JD. Neonatal pain management. *Saudi J Anaesth*. 2014;8(Suppl

[23] Spatz DL, Schmidt KJ. Breastfeeding success in infants with giant omphalocele. *Adv Neonatal Care Off J Natl Assoc Neonatal Nurses*. 2012;12(6):329–335. doi:10.1097/

[24] Haug S, St Peter S, Ramlogan S, et al. The impact of breast milk, respiratory insufficiency and GERD on enteral feeding in infants with omphalocele. *J Pediatr Gastroenterol Nutr*.

*Netw NN*. 2006;25(5):319–327. doi:10.1891/0730-08<IP_ADDRESS>9

doi:10.1111/pan.12831

16 Pediatric and Neonatal Surgery

doi:10.1038/pr.2015.186

OGX.0000000000000344

2016;82(8):704–706.

NPM-15915011

ANC.0b013e31826150c5

*J Perinatol*. 2011;31(1):51–57. doi:10.1038/jp.2010.71

2004;19(5):385–398. doi:10.1159/000078990

1):S89–S97. doi:10.4103/1658-354X.144085

November 2016. doi:10.1097/MPG.0000000000001463

**Anesthetic Management for Neonates and Children**

[40] Hillman BA, Tabrizi MN, Gauda EB, Carson KA, Aucott SW. The Neonatal Pain, Agitation and Sedation Scale and the bedside nurse's assessment of neonates. *J Perinatol*

[41] Krechel SW, Bildner J. CRIES: a new neonatal postoperative pain measurement score.

[42] Panel SA. Referral to pediatric surgical specialists. *Pediatrics*. 2014;133(2):350–356.

[43] Ludman L, Spitz L, Landsdown R. Developmental progress of newborns undergoing neonatal surgery. *J Pediatr Surg*. 1990;25(5):469–471. doi:10.1016/0022-3468(90)90552-K

[44] Harris EL, Hart SJ, Minutillo C, et al. The long-term neurodevelopmental and psychological outcomes of gastroschisis: A cohort study. *J Pediatr Surg*. 2016;51(4):549–553.

[45] Fanaroff AA, Martin FJ (eds). Neonatal and Perinatal Medicine: Diseases of the Fetus

*Off J Calif Perinat Assoc*. 2015;35(2):128–131. doi:10.1038/jp.2014.154

and Newborn (10th edition). St. Louis: Mosby; 1997, p 672.

doi:10.1542/peds.2013-3820

18 Pediatric and Neonatal Surgery

doi:10.1016/j.jpedsurg.2015.08.062

Initial testing of validity and reliability. *Paediatr Anaesth*. 1995;5(1):53–61.

**Provisional chapter**

## **Anesthetic Management of the Newborn Surgical Patient Patient**

**Anesthetic Management of the Newborn Surgical**

Marissa Vadi, Chelan Nour, Patrick Leiter and

Marissa Vadi, Chelan Nour, Patrick Leiter and Harmony Carter Harmony Carter Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/66932

#### **Abstract**

Providing anesthesia for the newborn requires many considerations beyond what is needed for the older child or adult. This chapter discusses pertinent anesthetic considerations in the care of surgical neonates including preoperative evaluation, intraoperative management and pain management techniques.

**Keywords:** neonatal anesthesia, anesthetic agents, pain management

## **1. Introduction**

Advances in pediatric anesthesiology have contributed to improved outcomes and survival in newborns requiring surgical intervention. Newborn physiology is characterized by a high metabolic rate, limited cardiopulmonary reserve, and decreased renal function. Multisystem organ immaturity underlies the differences in physiologic response to anesthetics in the neonate when compared to the older child or adult. This chapter discusses physiologic considerations, preoperative evaluation and preparation, intraoperative anesthetic management, and pain management techniques unique to the newborn surgical patient.

## **2. Physiologic considerations**

#### **2.1. Cardiovascular**

Fetal cardiac circulation is characterized by two right-to-left shunts: one through the foramen ovale and one through the ductus arteriosus. With the infant's first breaths, the lungs expand,

alveolar fluid is cleared, pulmonary vascular resistance markedly decreases, and left atrial pressure increases [1]. These physiologic changes promote functional closure of the fetal cardiac shunts and mark the beginning of the transition from fetal to newborn circulation.

Anatomic closure of the foramen ovale typically occurs within the first year of life, though some studies indicate over one quarter of foramen ovale remain echocardiography probe patent into adulthood [2]. Functional closure of the ductus arteriosus is achieved between 10 and 15 hours of life, and anatomical closure is usually completed by 2 months of age [3]. Neonatal circulation may revert to fetal circulation if the physiological parameters responsible for cardiac shunt closure are not maintained. As such, it is important to avoid factors that increase pulmonary vascular resistance (physiologic stress, hypoxia, hypercarbia, acidosis, and hypothermia) in newborns. Hypervolemia may also promote reopening of the ductus arteriosus and should be avoided.

Maintenance of heart rate is essential in the neonatal period. Cardiac output is dependent on heart rate, as stroke volume is fixed due to decreased compliance of the immature ventricle [4]. Thus, while maintaining preload is important during anesthetic management, increasing preload provides minimal benefit for improving cardiac output. The sympathetic nervous system is also immature in newborns. Bradycardia may occur after stimulating procedures such as laryngoscopy, oropharyngeal suctioning, or gastric tube placement rather than the expected tachycardia seen in patients with mature sympathetic nervous systems. Treatment with anticholinergics may be required.

#### **2.2. Pulmonary**

Development of the respiratory system begins during fetal organogenesis and continues throughout childhood. Alveolarization starts at 28 weeks of gestational age, and by 40 weeks, alveoli are present at 20–50% of adult values. Type 2 pneumocytes, the main producers of surfactant, appear at approximately 24 weeks of gestational age but are not fully functional until 34–36 weeks of gestational age [5].

Neonates are an increased risk for respiratory fatigue. High chest wall compliance may cause a paradoxical breathing pattern when large breaths are taken [5]. Newborns have a reduced number of fatigue-resistant high-oxidative diaphragmatic muscle fibers; mature levels are not reached until 8 months of age [6]. Neonatal oxygen requirements are 2–3 times the adult requirement, ranging from 6 to 9 mL/kg/min. Increased oxygen demand is met by increased respiratory rate, as there is a minimal inspiratory reserve to increase tidal volume [7].

Neonatal respiratory drive is determined by pO2 via peripheral chemoreceptors in the carotid bodies and by pCO2 influencing central chemoreceptors in the medulla. Respiratory drive is primarily affected by hypoxia, as opposed to hypercarbia in adults. Administration of high oxygen concentrations may depress respiratory drive in the newborn [8].

#### **2.3. Renal**

The kidneys are fully developed anatomically by 34–36 weeks of gestational age but continue to develop functionally after birth. The glomerular filtration rate (GFR) is initially decreased in the neonate due to low systemic arterial pressure and high renal vascular resistance but increases during the first several weeks of extrauterine life [9]. As a result of this initial low GFR, there is a decreased ability of the kidneys to maintain electrolyte balance or clear drugs and excess fluids.

#### **2.4. Neurologic risk**

alveolar fluid is cleared, pulmonary vascular resistance markedly decreases, and left atrial pressure increases [1]. These physiologic changes promote functional closure of the fetal cardiac shunts and mark the beginning of the transition from fetal to newborn circulation.

Anatomic closure of the foramen ovale typically occurs within the first year of life, though some studies indicate over one quarter of foramen ovale remain echocardiography probe patent into adulthood [2]. Functional closure of the ductus arteriosus is achieved between 10 and 15 hours of life, and anatomical closure is usually completed by 2 months of age [3]. Neonatal circulation may revert to fetal circulation if the physiological parameters responsible for cardiac shunt closure are not maintained. As such, it is important to avoid factors that increase pulmonary vascular resistance (physiologic stress, hypoxia, hypercarbia, acidosis, and hypothermia) in newborns. Hypervolemia may also promote reopening of the ductus arteriosus

Maintenance of heart rate is essential in the neonatal period. Cardiac output is dependent on heart rate, as stroke volume is fixed due to decreased compliance of the immature ventricle [4]. Thus, while maintaining preload is important during anesthetic management, increasing preload provides minimal benefit for improving cardiac output. The sympathetic nervous system is also immature in newborns. Bradycardia may occur after stimulating procedures such as laryngoscopy, oropharyngeal suctioning, or gastric tube placement rather than the expected tachycardia seen in patients with mature sympathetic nervous systems. Treatment

Development of the respiratory system begins during fetal organogenesis and continues throughout childhood. Alveolarization starts at 28 weeks of gestational age, and by 40 weeks, alveoli are present at 20–50% of adult values. Type 2 pneumocytes, the main producers of surfactant, appear at approximately 24 weeks of gestational age but are not fully functional

Neonates are an increased risk for respiratory fatigue. High chest wall compliance may cause a paradoxical breathing pattern when large breaths are taken [5]. Newborns have a reduced number of fatigue-resistant high-oxidative diaphragmatic muscle fibers; mature levels are not reached until 8 months of age [6]. Neonatal oxygen requirements are 2–3 times the adult requirement, ranging from 6 to 9 mL/kg/min. Increased oxygen demand is met by increased

primarily affected by hypoxia, as opposed to hypercarbia in adults. Administration of high

The kidneys are fully developed anatomically by 34–36 weeks of gestational age but continue to develop functionally after birth. The glomerular filtration rate (GFR) is initially decreased

via peripheral chemoreceptors in the carotid

influencing central chemoreceptors in the medulla. Respiratory drive is

respiratory rate, as there is a minimal inspiratory reserve to increase tidal volume [7].

oxygen concentrations may depress respiratory drive in the newborn [8].

and should be avoided.

22 Pediatric and Neonatal Surgery

**2.2. Pulmonary**

bodies and by pCO2

**2.3. Renal**

with anticholinergics may be required.

until 34–36 weeks of gestational age [5].

Neonatal respiratory drive is determined by pO2

The neurologic system is anatomically complete at term, though synaptogenesis and nerve myelination continue throughout childhood. Data from animal studies, as well as retrospective human studies, have raised concern that exposure to anesthetic agents could be detrimental to cognitive development in young children due to effects either on synaptogenesis or apoptosis of the developing brain [10]. The stage of brain development at the time of exposure and the degree of anesthetic exposure, in terms of both exposure frequency and cumulative anesthetic dose, may affect the risk of neurotoxicity.

The SmartTots program, a partnership between the United States Food and Drug Administration and the International Anesthesia Research Society, was established in 2009 to address the growing concern regarding potential adverse consequences of general anesthesia in young children. Two consensus statements, published in 2012 and 2015, counsel that the effect of exposure to anesthetic drugs in young children is unknown. Some, but not all, studies to date have suggested that problems similar to those seen in animals could also occur in infants and toddlers. The benefits of elective procedures must be weighed against the risks associated with anesthesia and surgery [11].

## **3. Preoperative evaluation and preparation**

#### **3.1. History and physical examination**

A thorough preanesthetic history and physical examination must be performed with the goals of identifying potential anesthetic complications due to coexisting disease, determining whether further diagnostic studies are required prior to surgery and anticipating postoperative concerns including pain management and level of cardiorespiratory monitoring required.

Factors that should be addressed in the preanesthetic history are outlined in **Table 1**. A review of all organ systems, including identification of genetic syndromes and associated anomalies, should be completed. Examination of previous anesthetic and surgical records may reveal difficulties with airway management, venous access, or anesthetic emergence and assist in planning future anesthetic management.

Physical examination should assess for evidence of coexisting diseases (e.g., craniofacial abnormalities, congenital heart disease, chronic lung disease). Hydration status may be determined by evaluating skin turgor, mucous membranes, fontanelle fullness, and urine output. Existing intravenous catheters should be examined for patency and hypovolemia treated prior to anesthetic induction. Laboratory studies must be reviewed and significant electrolyte abnormalities and/or anemia corrected preoperatively.

The American Society of Anesthesiologists (ASA) physical status classification system is used as a uniform system for describing the degree of patient morbidity prior to an anesthetic (**Table 2**) [12]. The grading system is not intended for use as a measure to predict operative risk.

**Table 1.** Factors to address in the preanesthetic history.

**Table 2.** American Society of Anesthesiologists physical status classification system.

#### **3.2. Fasting**

Infants are required to fast before procedures requiring sedation and anesthesia in order to minimize the risk of pulmonary aspiration of gastric contents [13]. Fasting times are based on pediatric gastric emptying studies. **Table 3** provides a summary of fasting recommendations by the ASA [14]. Prolonged fasting may lead to hypovolemia and hypoglycemia in infants; glucose-containing intravenous maintenance fluids should be administered prior to the induction of anesthesia.

The majority of pediatric aspiration events occur during anesthetic induction [15]. Risk factors for aspiration in the perianesthetic period include neurologic abnormality, emergency surgery, intestinal obstruction or increased abdominal pressure, light anesthesia, and the skill of the anesthesia provider [16, 17]. Infants and young children are particularly prone to regurgitation and aspiration for a variety of reasons including air swallowing while crying and decreased lower esophageal sphincter incompetence. In one study, almost all cases of pulmonary aspiration occurred in children who gagged or coughed during airway management, either because neuromuscular blockade was not administered or airway manipulation occurred before the child was completely paralyzed [15]. Mortality due to pulmonary aspiration is low, with an estimated incidence between zero and 1:50,000 [15, 16, 18].

**Table 3.** American Society of Anesthesiologists fasting recommendations.

The American Society of Anesthesiologists (ASA) physical status classification system is used as a uniform system for describing the degree of patient morbidity prior to an anesthetic (**Table 2**)

> Diabetes Toxemia Infection

Gestational age and weight Extreme prematurity and/or extremely low birth weight

Medications and medication allergies Type and severity of adverse medication reaction

Drug or alcohol abuse

Neonatal asphyxia Meconium aspiration

Supplemental oxygen requirement

Need for ventilator support

Infants are required to fast before procedures requiring sedation and anesthesia in order to minimize the risk of pulmonary aspiration of gastric contents [13]. Fasting times are based on pediatric gastric emptying studies. **Table 3** provides a summary of fasting recommendations

ASA IV A patient with severe systemic disease that is a constant

ASA VI A declared brain-dead patient whose organs are being

ASA V A moribund patient who is not expected to survive without

threat to life

the operation

removed for donor purposes

**Physical score classification\* Definition**

**Table 1.** Factors to address in the preanesthetic history.

ASA I A normal healthy patient

\*Emergency cases are designated by the addition of "E" to the classification number.

**Table 2.** American Society of Anesthesiologists physical status classification system.

ASA II A patient with mild systemic disease ASA III A patient with severe systemic disease

[12]. The grading system is not intended for use as a measure to predict operative risk.

**Factor Specific concerns** Maternal history during pregnancy Rh-ABO compatibility

24 Pediatric and Neonatal Surgery

Significant birth events Apgar scores

Perinatal course Apneas

**3.2. Fasting**

#### **3.3. Postoperative apnea in former premature infants**

Postoperative apnea is defined as cessation of breathing or no detectable airflow for 15 seconds or longer, or less than 15 seconds with bradycardia. It has been observed in former premature infants after exposure to all forms of anesthetics (intravenous agents, inhalational agents, and regional anesthesia) [19–21]. The incidence of postoperative apnea varies inversely with gestational age at birth and post-conceptual age at the time of surgery. Apnea risk is greater than 1% until 54 weeks of post-conceptual age or 56 weeks of post-conceptual age in infants with a gestational age of 32 or 35 weeks, respectively [22].

Former preterm infants who are less than 60 weeks of post-conceptual age at the time of surgery should be monitored until free of apnea for at least 12 hours. A monitored bed should be arranged for the postoperative period, and family members should be educated regarding the risk of perianesthesia apnea. Children receiving theophylline or caffeine preoperatively should have these medications continued postoperatively [23]. Caffeine administration does not negate the need for postoperative respiratory monitoring. Factors such as anemia, hypothermia, hypoglycemia, hypocalcemia, acidosis, and hypoxemia may increase the risk of apnea and should be avoided.

### **4. Intraoperative management**

#### **4.1. Monitoring and intravenous access**

The ASA's Standards for Basic Anesthetic Monitoring mandates continual evaluation of oxygenation, ventilation, circulation, and temperature during all anesthetics [24]. Placement of both a pre-ductal oxygen saturation monitor on the right upper extremity and a postductal oxygen saturation monitor on a lower extremity should be considered in neonates as a means to detect right-to-left shunting across the ductus arteriosus [25]. A nerve stimulator may be used if neuromuscular blocking agents are administered, though the train-offour response is often diminished in infants less than 2 months old. It is imperative that the operating room be kept warm. Neonates, especially premature infants, are at high risk for heat loss due to an increased surface area to volume ratio when compared to older children and adults [26, 27]. The need for invasive monitoring, including arterial and central venous catheter placement, is determined by the baseline medical condition of the patient and the extensiveness of the planned surgery. Arterial catheters allow for continuous monitoring of heart rate and blood pressure, as well as arterial blood gas sampling [28]. Central venous catheters are utilized when large intravenous access is necessary, central venous pressure monitoring is required, or in hemodynamically unstable conditions likely to require continuous vasopressor infusions. The benefits of placement must always be weighed against the risks associated with use, such as catheter-associated bloodstream infection [29]. A urinary catheter should be considered in surgical cases of prolonged duration or when significant blood loss is expected.

#### **4.2. Anesthetic agents**

Most infants arriving as outpatients for surgery may undergo mask induction of anesthesia with inhaled anesthetic agents. Those patients presenting from inpatient hospital wards or the neonatal intensive care unit (NICU) with intravenous access in situ may undergo intravenous induction of general anesthesia [27].

#### *4.2.1. Inhaled anesthetic agents*

Inhaled halogenated anesthetics (most commonly sevoflurane, isoflurane, and desflurane) are used for both induction and maintenance of general anesthesia. The minimum alveolar concentration (MAC) is the end-tidal concentration of inhaled anesthetic agent at which 50% of patients do not move in response to a noxious stimulus. MAC values are used to compare the relative potencies of anesthetic agents and vary with age for each particular agent (**Table 4**) [30–32]. Of note, MAC values may differ for preterm neonates depending upon the inhalational agent used and the gestational age of the infant.

Sevoflurane is the halogenated agent most commonly chosen for mask induction of anesthesia; its use is associated with a reduced incidence of breath holding, coughing, laryngospasm, and oxygen desaturation when compared with other inhaled anesthetics [30]. Nitrous oxide, a nonhalogenated agent, may be used in conjunction with halogenated

**Table 4.** Minimum alveolar concentration (MAC) values for modern inhalational anesthetics.

inhaled anesthetics to speed inhalational induction ("second-gas effect") or reduce halogenated agent doses during the maintenance phase of anesthesia. Nitrous oxide must be used with caution as it may rapidly diffuse into and expand gas-filled body cavities. Its use should be avoided in laparoscopic surgery and is contraindicated in patients with a pneumothorax [33].

#### *4.2.2. Intravenous anesthetic agents*

**4. Intraoperative management**

26 Pediatric and Neonatal Surgery

**4.1. Monitoring and intravenous access**

blood loss is expected.

**4.2. Anesthetic agents**

*4.2.1. Inhaled anesthetic agents*

nous induction of general anesthesia [27].

tional agent used and the gestational age of the infant.

The ASA's Standards for Basic Anesthetic Monitoring mandates continual evaluation of oxygenation, ventilation, circulation, and temperature during all anesthetics [24]. Placement of both a pre-ductal oxygen saturation monitor on the right upper extremity and a postductal oxygen saturation monitor on a lower extremity should be considered in neonates as a means to detect right-to-left shunting across the ductus arteriosus [25]. A nerve stimulator may be used if neuromuscular blocking agents are administered, though the train-offour response is often diminished in infants less than 2 months old. It is imperative that the operating room be kept warm. Neonates, especially premature infants, are at high risk for heat loss due to an increased surface area to volume ratio when compared to older children and adults [26, 27]. The need for invasive monitoring, including arterial and central venous catheter placement, is determined by the baseline medical condition of the patient and the extensiveness of the planned surgery. Arterial catheters allow for continuous monitoring of heart rate and blood pressure, as well as arterial blood gas sampling [28]. Central venous catheters are utilized when large intravenous access is necessary, central venous pressure monitoring is required, or in hemodynamically unstable conditions likely to require continuous vasopressor infusions. The benefits of placement must always be weighed against the risks associated with use, such as catheter-associated bloodstream infection [29]. A urinary catheter should be considered in surgical cases of prolonged duration or when significant

Most infants arriving as outpatients for surgery may undergo mask induction of anesthesia with inhaled anesthetic agents. Those patients presenting from inpatient hospital wards or the neonatal intensive care unit (NICU) with intravenous access in situ may undergo intrave-

Inhaled halogenated anesthetics (most commonly sevoflurane, isoflurane, and desflurane) are used for both induction and maintenance of general anesthesia. The minimum alveolar concentration (MAC) is the end-tidal concentration of inhaled anesthetic agent at which 50% of patients do not move in response to a noxious stimulus. MAC values are used to compare the relative potencies of anesthetic agents and vary with age for each particular agent (**Table 4**) [30–32]. Of note, MAC values may differ for preterm neonates depending upon the inhala-

Sevoflurane is the halogenated agent most commonly chosen for mask induction of anesthesia; its use is associated with a reduced incidence of breath holding, coughing, laryngospasm, and oxygen desaturation when compared with other inhaled anesthetics [30]. Nitrous oxide, a nonhalogenated agent, may be used in conjunction with halogenated Similar to inhaled halogenated anesthetics, intravenous anesthetic agents may be utilized for both induction and maintenance of anesthesia. Agent choice is commonly based upon the following drug properties: speed of onset, duration of action, cardiovascular stability, and side-effect profile [34].

Propofol is an intravenous agent with sedative-hypnotic properties resulting from gammaaminobutyric acid (GABA)-mediated inhibitory neurotransmission. Systolic blood pressure falls approximately 15% after propofol administration due to decreases in preload, cardiac contractility, and systemic vascular resistance. Propofol is a potent respiratory depressant, and apnea may occur transiently after bolus administration. Pain on injection may be attenuated with intravenous lidocaine administration.

Ketamine is a phencyclidine derivative that antagonizes N-methyl-D-aspartate (NMDA) receptors. This results in a "dissociative"-type anesthesia and a potential for disturbing dreams or delirium. Ketamine possesses excellent amnestic, analgesic, and bronchodilation properties. Administration is associated with favorable hemodynamic parameters except in catecholamine-depleted patients. The use is limited in patients with a history of seizure disorder and in those in whom increases in intracranial and/or intraocular pressures would be detrimental. Nystagmus, myoclonus, and copious oral secretions are frequent side effects of ketamine use.

Etomidate depresses the reticular activating system and mimics the inhibitory effects of GABA. It possesses minimal effects on the hemodynamic system but can decrease ventilatory drive. Induction doses are known to transiently inhibit enzymes involved in cortisol and aldosterone synthesis with the potential for adrenocortical suppression.

Thiopental is a barbiturate that acts by prolonging the duration of GABA-mediated chloride channel opening. Administration can cause cardiovascular depression that is accentuated in the hypovolemic patient. Compared to other induction agents, acute tolerance to thiopental may develop, and prolonged sedation can be noted after induction doses [35].

#### *4.2.3. Neuromuscular blocking agents*

Neuromuscular blocking drugs allow for patient immobility, smooth endotracheal intubation, increased tolerance of mechanical ventilation, and optimal surgical relaxation. They are classified into two groups, depolarizing and non-depolarizing agents, based on activity at the neuromuscular junction [36]. The choice of drug depends on the desired speed of onset, duration of action, route of elimination, and side-effect profile.

Succinylcholine is the only depolarizing agent currently available for clinical use. An increased dose of succinylcholine is necessary in infants due to relative effect resistance at the neuromuscular junction and the larger volume of distribution in the neonate. Succinylcholine is metabolized by circulating pseudocholinesterase. It has a very rapid onset (60 seconds) and short duration of action (5 minutes). Succinylcholine carries an FDA "black box warning" against routine use in children due to risk of hyperkalemic cardiac arrest in patients with undiagnosed neuromuscular disorders [37]. Thus, it is recommended that the use of succinylcholine in children be reserved for emergency intubation or instances where immediate securing of the airway is necessary (e.g., laryngospasm, difficulty airway, full stomach) [38].

Non-depolarizing neuromuscular blocking agents are divided into intermediate (atracurium, cisatracurium, rocuronium, and vecuronium) and long-acting (pancuronium) varieties [26]. Neuromuscular blocking drugs are responsible for over 35% of anesthetic-related hypersensitivity reactions and should be considered as potential causes if anaphylaxis is suspected in the perianesthetic period. The effects of non-depolarizing muscle relaxants may be antagonized by an anticholinesterase (neostigmine or edrophonium) administered in conjunction with an anticholinergic agent (glycopyrrolate or atropine) to minimize parasympathetic side effects. Successful reversal of neuromuscular blockade in infants is demonstrated by adequate return of strong hip and/or arm flexion, abdominal muscle contraction, and return of the train-offour twitch response to four equal twitches.

Historically, neuromuscular blocking drugs could only be reversed after adequate time had elapsed to demonstrate some natural return of neuromuscular function. Sugammadex, a cyclodextrin oligosaccharide, is a new reversal agent that inactivates steroidal neuromuscular blocking agents such as vecuronium and rocuronium via direct encapsulation. This mechanism allows for rapid and complete reversal of neuromuscular blockade within minutes of administration of a neuromuscular blocking agent. Studies examining sugammadex use in children aged 2–18 years suggest no evidence of higher incidence of adverse effects with sugammadex compared to that with neostigmine or placebo [39]. Data regarding the safety of sugammadex in infants are currently limited.

#### **4.3. Fluid and blood product management**

Calculating total intraoperative fluid requirements necessitates considering fluid type, maintenance fluid requirements, evaporative fluid losses, and replacement of intraoperative blood loss.

#### *4.3.1. Glucose requirements*

Healthy infants and children can remain euglycemic for up to 17hours despite fasting. Infants receiving total parenteral nutrition or 10% dextrose in water (D10W) preoperatively require continued glucose replacement intraoperatively [27, 40]. Glucose levels naturally increase intraoperatively secondary to decreased insulin sensitivity from release of surgery-related stress hormones.

#### *4.3.2. Maintenance fluid requirements*

*4.2.3. Neuromuscular blocking agents*

28 Pediatric and Neonatal Surgery

tion of action, route of elimination, and side-effect profile.

four twitch response to four equal twitches.

sugammadex in infants are currently limited.

**4.3. Fluid and blood product management**

*4.3.1. Glucose requirements*

Neuromuscular blocking drugs allow for patient immobility, smooth endotracheal intubation, increased tolerance of mechanical ventilation, and optimal surgical relaxation. They are classified into two groups, depolarizing and non-depolarizing agents, based on activity at the neuromuscular junction [36]. The choice of drug depends on the desired speed of onset, dura-

Succinylcholine is the only depolarizing agent currently available for clinical use. An increased dose of succinylcholine is necessary in infants due to relative effect resistance at the neuromuscular junction and the larger volume of distribution in the neonate. Succinylcholine is metabolized by circulating pseudocholinesterase. It has a very rapid onset (60 seconds) and short duration of action (5 minutes). Succinylcholine carries an FDA "black box warning" against routine use in children due to risk of hyperkalemic cardiac arrest in patients with undiagnosed neuromuscular disorders [37]. Thus, it is recommended that the use of succinylcholine in children be reserved for emergency intubation or instances where immediate securing of the airway is necessary (e.g., laryngospasm, difficulty airway, full stomach) [38]. Non-depolarizing neuromuscular blocking agents are divided into intermediate (atracurium, cisatracurium, rocuronium, and vecuronium) and long-acting (pancuronium) varieties [26]. Neuromuscular blocking drugs are responsible for over 35% of anesthetic-related hypersensitivity reactions and should be considered as potential causes if anaphylaxis is suspected in the perianesthetic period. The effects of non-depolarizing muscle relaxants may be antagonized by an anticholinesterase (neostigmine or edrophonium) administered in conjunction with an anticholinergic agent (glycopyrrolate or atropine) to minimize parasympathetic side effects. Successful reversal of neuromuscular blockade in infants is demonstrated by adequate return of strong hip and/or arm flexion, abdominal muscle contraction, and return of the train-of-

Historically, neuromuscular blocking drugs could only be reversed after adequate time had elapsed to demonstrate some natural return of neuromuscular function. Sugammadex, a cyclodextrin oligosaccharide, is a new reversal agent that inactivates steroidal neuromuscular blocking agents such as vecuronium and rocuronium via direct encapsulation. This mechanism allows for rapid and complete reversal of neuromuscular blockade within minutes of administration of a neuromuscular blocking agent. Studies examining sugammadex use in children aged 2–18 years suggest no evidence of higher incidence of adverse effects with sugammadex compared to that with neostigmine or placebo [39]. Data regarding the safety of

Calculating total intraoperative fluid requirements necessitates considering fluid type, maintenance fluid requirements, evaporative fluid losses, and replacement of intraoperative blood loss.

Healthy infants and children can remain euglycemic for up to 17hours despite fasting. Infants receiving total parenteral nutrition or 10% dextrose in water (D10W) preoperatively require continued Maintenance fluid requirements are determined by accounting for water losses from the renal, pulmonary, and gastrointestinal systems in addition to calculating baseline body weight and calorie usage [40]. While a variety of formulas exist to determine the maintenance fluid requirements of an infant or child, the simplest is the "4-2-1" rule shown in **Table 5** [40, 41].

D5 0.25% normal saline (NS) and D5 0.45% NS are commonly chosen maintenance fluids for children, as they closely accomplish the goal of delivering 3 mEq of sodium, 2 mEq of potassium, 2 mEq of chloride, and 5 g of glucose for every 100 mL of water administered. *Nil per os* (NPO) fluid deficit is calculated by multiplying the hourly maintenance fluid requirement by the number of hours the patient has been NPO. The NPO deficit is typically replaced intraoperatively as follows: half the total volume deficit is administered in the first hour, one quarter in the second hour, and the remaining quarter in the third hour.

Intraoperative evaporative fluid losses may be replenished with isotonic crystalloid or colloid fluids according to the following formula based on the invasiveness of surgery: superficial 1–2 mL/kg/h, moderate/intrathoracic 4–7 mL/kg/h, open intra-abdominal 6–10 mL/kg/h, and neonates with necrotizing enterocolitis >50 mL/kg/h. Current data are limited but do not support specific benefits of human albumin usage over other colloids or crystalloids in neonates [42, 43]. Favored colloid usage is institutional and region specific; many centers in the United States utilize albumin, while institutions in other nations favor hydroxyethyl starches or gelatins [44].

**Table 5.** Maintenance fluid requirements by weight.

#### *4.3.3. Blood products*

Estimated blood volume is calculated based on the age and weight of the patient (**Table 6**) [45]. Prior to surgery, one may calculate the maximum allowable blood loss (MABL) that would necessitate blood transfusion using the following equation:

MABL <sup>=</sup> *EBV* <sup>×</sup> (*Hct* current - *Hct* min) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ (*Hct* current) (1)

where *Hct current* is the current hematocrit and *Hct min* is the minimum acceptable hematocrit.

**Table 6.** Calculating estimated blood volume.

Recommended doses for replacement of blood products are outlined in **Table 7** [46].

Packed red blood cells (PRBCs) have a hematocrit of approximately 55–70%. Fresh frozen plasma (FFP) administration is indicated when there is laboratory evidence of coagulopathy or significant blood loss approaching one blood volume [47]. Intraoperative platelet transfusion is more likely to be necessary with preoperative platelet counts <150,000 per mm<sup>3</sup> or after the loss of two to three blood volumes [41, 48]. Massive blood loss has historically been replaced in a 1:1:1 fashion with PRBCs, FFP, and platelets. Currently, it is recommended that FFP administration begins after one blood volume has been lost or at the first sign of clinical coagulopathy [49]. It is imperative for the surgeon and the anesthesiologist to maintain excellent communication regarding expectations for blood loss and proper preparation of the patient including any necessary laboratory screening tests for blood typing, antibodies, and cross matching.

**Table 7.** Recommended doses for replacement of blood products.

#### **5. Neonatal pain management**

Pain has been defined as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage" [50]. Accurately defining and quantifying pain in the neonate has challenged the medical community for decades.  Because neonates and infants cannot verbally communicate pain, regrettably their pain may go unrecognized and undertreated.

Historically, it was believed that neonates did not have the same pain perception as older infants and adults. Opioids were known to cause respiratory depression and were considered harmful; thus, postoperative analgesia with opioids was discouraged. This remained the predominant view until as late as in 1987, when research by Anand and colleagues challenged this long-standing tradition by demonstrating that unattenuated noxious or painful stimuli during neonatal cardiac surgery caused a deleterious stress response and increased morbidity. Anand published two landmark papers presenting scientific evidence that neonates experience pain and the medical necessity for treating such pain. Change in practice soon followed, accompanied by a rapid expansion of literature in this area [51–53].

Neonates in the intensive care unit are estimated to undergo as many as 14 invasive procedures associated with pain each day, with analgesia inconsistently provided for many of these procedures (**Table 8**) [54]. This is concerning as research has correlated undertreated pain in the neonatal period with long-term detrimental effects, including behavioral disorders and altered sensitivity to pain later in life [55–59].

#### **5.1. Pain assessment**

or

Recommended doses for replacement of blood products are outlined in **Table 7** [46].

 Calculating estimated blood volume.

30 Pediatric and Neonatal Surgery

cross matching.

**5. Neonatal pain management**

**Table 7.** Recommended doses for replacement of blood products.

ognized and undertreated.

Packed red blood cells (PRBCs) have a hematocrit of approximately 55–70%. Fresh frozen plasma (FFP) administration is indicated when there is laboratory evidence of coagulopathy or significant blood loss approaching one blood volume [47]. Intraoperative platelet transfusion is more likely to be necessary with preoperative platelet counts <150,000 per mm<sup>3</sup>

after the loss of two to three blood volumes [41, 48]. Massive blood loss has historically been replaced in a 1:1:1 fashion with PRBCs, FFP, and platelets. Currently, it is recommended that FFP administration begins after one blood volume has been lost or at the first sign of clinical coagulopathy [49]. It is imperative for the surgeon and the anesthesiologist to maintain excellent communication regarding expectations for blood loss and proper preparation of the patient including any necessary laboratory screening tests for blood typing, antibodies, and

Pain has been defined as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage" [50]. Accurately defining and quantifying pain in the neonate has challenged the medical community for decades.  Because neonates and infants cannot verbally communicate pain, regrettably their pain may go unrecAn ongoing challenge involves appropriately assessing and effectively treating pain in the neonate. The immature dorsal horn circuits predominantly exhibit excitatory tone, with weaker inhibitory GABA and glycine signaling. It is uncertain whether or not this lack of inhibitory processing increases the neonate's perception of pain. Flexion reflexes may be elicited with either tactile or nociceptive touch; conversely, neonates with no behavioral reaction to heel lance showed a strongly activated cortex on EEG in one study, demonstrating the inadequacy of behavioral indicators to reliably detect pain [60].

Distinguishing between pain and agitation is also difficult as there are overlapping behavioral and physiologic manifestations [61]. Facial expression (total facial activity with specific features including brow lowering, eye squeeze, nasolabial furrow, and open mouth) is considered the most sensitive behavioral indicator of acute pain. Other behavior pain indicators include body posture, limb movements, cry, consolability, and sleep/wakefulness. Physiological parameters include heart rate, respiratory rate and pattern, oxygen saturation,

**Table 8.** Commonly performed painful procedures in the neonatal intensive care unit.

and blood pressure. These parameters are also important, but less specific, as alterations may be the result of the underlying disease process rather than pain. In the mechanically ventilated neonate with neuromuscular blocking therapy, pain must be evaluated based on changes in heart rate or blood pressure. Biological markers for pain such as emotional sweating (palm or sole, measured by skin conductance or galvanic skin response) or increased stress hormones (serum or saliva cortisol) are used in research but have limited clinical utility. Among the validated neonatal pain scales, premature infant pain profile (PIPP) assesses procedural pain, and neonatal pain, agitation, and sedation scale (N-PASS) assesses ongoing pain and sedation in both term and preterm neonates, providing an advantage over other available neonatal pain assessment tools (**Table 9**) [62–65].

#### **5.2. Therapeutic approach**

Neonatal pain is best managed using a tiered approach. Painful procedures should be avoided when possible through the use of noninvasive monitoring and bundling of laboratory blood draws. Non-pharmacological therapy, such as nonnutritive sucking, oral sucrose, breast or bottle feeding, and swaddling, can be used during mildly painful events (i.e., lab draws, line insertion, removal of adhesives, wound treatment, bladder catheterization). Topical anesthetics may be used prior to skin-breaking procedures, though caution must be exercised in the preterm neonate as the epidermis is structurally and functionally immature, increasing the risk of toxicity. Acetaminophen is effective for mild pain and as an adjuvant for moderate to severe pain. Ketamine is a potent analgesic and NMDA antagonist that can be utilized during moderate to severe painful procedures of short duration or as an adjuvant to prevent opioid tolerance. Systemic opioid analgesics are utilized to treat moderate to severe pain in conjunction with the above therapies (**Table 10**) [66, 67]. Analgesic medications are most reliable when given intravenously, as oral absorption is unpredictable in the neonate [64, 68].

**Table 9.** Summary of validated neonatal pain scales.

#### Anesthetic Management of the Newborn Surgical Patient http://dx.doi.org/10.5772/66932 33

**Table 10.** Recommended analgesic dosing for neonates.

and blood pressure. These parameters are also important, but less specific, as alterations may be the result of the underlying disease process rather than pain. In the mechanically ventilated neonate with neuromuscular blocking therapy, pain must be evaluated based on changes in heart rate or blood pressure. Biological markers for pain such as emotional sweating (palm or sole, measured by skin conductance or galvanic skin response) or increased stress hormones (serum or saliva cortisol) are used in research but have limited clinical utility. Among the validated neonatal pain scales, premature infant pain profile (PIPP) assesses procedural pain, and neonatal pain, agitation, and sedation scale (N-PASS) assesses ongoing pain and sedation in both term and preterm neonates, providing an advantage over other available neonatal pain

Neonatal pain is best managed using a tiered approach. Painful procedures should be avoided when possible through the use of noninvasive monitoring and bundling of laboratory blood draws. Non-pharmacological therapy, such as nonnutritive sucking, oral sucrose, breast or bottle feeding, and swaddling, can be used during mildly painful events (i.e., lab draws, line insertion, removal of adhesives, wound treatment, bladder catheterization). Topical anesthetics may be used prior to skin-breaking procedures, though caution must be exercised in the preterm neonate as the epidermis is structurally and functionally immature, increasing the risk of toxicity. Acetaminophen is effective for mild pain and as an adjuvant for moderate to severe pain. Ketamine is a potent analgesic and NMDA antagonist that can be utilized during moderate to severe painful procedures of short duration or as an adjuvant to prevent opioid tolerance. Systemic opioid analgesics are utilized to treat moderate to severe pain in conjunction with the above therapies (**Table 10**) [66, 67]. Analgesic medications are most reliable

when given intravenously, as oral absorption is unpredictable in the neonate [64, 68].

 Therapeutic approach**

32 Pediatric and Neonatal Surgery

Neonatal pain, agitation, and sedation

Cry, requires oxygen, increased vital signs, expression, sleeplessness (CRIES)

**Table 9.** Summary of validated neonatal pain scales.

scale (N-PASS)

Postsurgical pain should be anticipated and preemptively treated to mitigate the pain and stress response. In conjunction with analgesic medications, local anesthetics may be administered as a field block, as a targeted nerve block, or as an epidural block (**Table 11**) to effectively treat procedural and surgical pain. Care must be taken during the placement of

**Table 11.** Neuraxial and peripheral nerve block indications.

present to minimize infectious risks.

local anesthetics, as unintended intravascular delivery can lead to systemic toxicity manifesting as altered consciousness, seizures, hemodynamic instability, and ultimately cardiovascular collapse. Safe practice includes aspiration prior to injection, slow incremental dosing, adherence to maximum dosing guidelines, and appropriate dose reductions for the neonate (**Table 12**) [69]. Local anesthetic toxicity must be promptly recognized and treated (**Table 13**) [70].

\*Maximum doses are additive and not independent of each other; *local anesthetic dosing should be decreased by 50*% *in neonates*.

**Table 12.** Commonly used local anesthetics.

#### **Local anesthetic toxicity (LAST) management**

**Table 13.** Treatment of local anesthetic toxicity.

## **Author details**

Marissa Vadi\*, Chelan Nour, Patrick Leiter and Harmony Carter

\*Address all correspondence to<EMAIL_ADDRESS>
Loma Linda University School of Medicine, Loma Linda, CA, USA

## **References**

**Local anesthetic toxicity (LAST) management**

**Table 12.** Commonly used local anesthetics.

• Managing the airway, administering 100% oxygen • Treat seizure activity (benzodiazepines preferred) • Alert nearest facility capable of cardiopulmonary bypass

• Institute 20% lipid emulsion therapy (lipidrescue.org)

**Table 13.** Treatment of local anesthetic toxicity.

• Support cardiovascular function (prolonged CPR, reduced epinephrine doses)

local anesthetics, as unintended intravascular delivery can lead to systemic toxicity manifesting as altered consciousness, seizures, hemodynamic instability, and ultimately cardiovascular collapse. Safe practice includes aspiration prior to injection, slow incremental dosing, adherence to maximum dosing guidelines, and appropriate dose reductions for the neonate (**Table 12**) [69]. Local anesthetic toxicity must be promptly recognized and treated

**dose**

Bupivacaine 2.5 mg/kg 1 mg/kg Commonly used for field

Ropivacaine 3 mg/kg 1.5 mg/kg Decreased motor block and

Chloroprocaine 14 mg/kg 7 mg/kg No plasma accumulation due

\*Maximum doses are additive and not independent of each other; *local anesthetic dosing should be decreased by 50*% *in*

1 g/5 kg 1 g Equal parts lidocaine and

Prilocaine Not recommended Not recommended Concern for

**Topical anesthetic Maximum dose Comments**

**Comments**

bupivacaine

blocks)

blocks and wound infiltration

cardiotoxicity compared with

Vasoconstrictor effects (avoid using for digital and penile

methemoglobinemia

Maximum skin contact

Risk of methemoglobinemia increased in premature

to short half life

prilocaine

1 hour

neonates

**Local anesthetic Standard maximum dose \* Recommended neonatal**

Lidocaine 5 mg/kg 2.5 mg/kg

• Obtain help

*neonates*.

Eutectic mixture of local anesthetics (EMLA)

(**Table 13**) [70].

34 Pediatric and Neonatal Surgery

[24] American Society of Anesthesiologists. Standards for Basic Anesthetic Monitoring [Internet]. 2015. Available from: http://www.asahq.org/~/media/sites/asahq/files/public/resources/standards-guidelines/standards-for-basic-anesthetic-monitoring.pdf [Accessed 2016-08-01].

[12] American Society of Anesthesiologists. ASA Physical Status Classification System [Internet]. 2014. Available from: https://www.asahq.org/resources/clinical-information/

[13] Cote CJ, Goudsouzian NG, Liu LM, Dedrick DF, Szyfelbein SK. Assessment of risk factors related to the acid aspiration syndrome in pediatric patients – gastric ph and resid-

[14] Apfelbaum JL, Caplan RA, Connis RT, Epstein BS, Nickinovich DG, Warner MA. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: Application to healthy patients undergoing elective procedures: An updated report by the American Society of Anesthesiologists Committee on Standards and Practice Parameters. Anesthesiology. 2011;**114**:494–511. DOI: 10.1097/

[15] Warner MA, Warner ME, Warner DO, Warner LO, Warner EJ. Perioperative pulmonary

[16] Olsson GL, Hallen B, Hambraeus-Jonzon K. Aspiration during anaesthesia: A computeraided study of 185,358 anaesthetics. Acta Anaesthesiol Scand. 1986;**30**:84–92.

[17] Walker RW. Pulmonary aspiration in pediatric anesthetic practice in the UK: A prospective survey of specialist pediatric centers over a one-year period. Paediatr Anaesth.

[18] Borland LM, Sereika SM, Woelfel SK, Saitz EW, Carrillo PA, Lupin JL, Motoyama EK. Pulmonary aspiration in pediatric patients during general anesthesia: Incidence and

[19] Krane EJ, Haberkern CM, Jacobson LE. Postoperative apnea, bradycardia, and oxygen desaturation in formerly premature infants: Prospective comparison of spinal and gen-

[20] Sale SM, Read JA, Stoddart PA, Wolf AR. Prospective comparison of sevoflurane and desflurane in formerly premature infants undergoing inguinal herniotomy. Br J Anaesth.

[21] Davidson AJ, Morton NS Arnup SJ, de Graaff JC, Disma N, Withington DE, Frawley G, Hunt RW, Hardy P, Khotcholava M, von Ungern Sternberg BS, Wilton N, Tuo P, Salvo I, Ormond G, Stargatt R, Locatelli BG, McCann ME. Apnea after awake regional and general anesthesia in infants: The general anesthesia compared to spinal anesthesia study–comparing apnea and neurodevelopmental outcomes, a randomized controlled

[22] Cote CJ, Zaslavsky A, Downes JJ, Kurth CD, Welborn LG, Warner LO, Malviya SV. Postoperative apnea in former preterm infants after inguinal herniorrhaphy. A com-

[23] Kelly DH, Shannon DC. Treatment of apnea and excessive periodic breathing in the full-

trial. Anesthesiology. 2015;**123**:38–54. DOI: 10.1097/ALN.0000000000000709

asa-physical-status-classification-system [Accessed 2016-10-30].

aspiration in infants and children. Anesthesiology. 1999;**90**:66–71.

ual volume. Anesthesiology. 1982;**56**:70–72.

outcome. J Clin Anesth. 1998;**10**:95–102.

eral anesthesia. Anesth Analg. 1995;**80**:7–13.

2006;**96**:774–778. DOI: 10.1093/bja/ael100

bined analysis. Anesthesiology. 1995;**82**:809–822.

term infant. Pediatrics. 1981;**68**:183–186.

ALN.0b013e3181fcbfd9

36 Pediatric and Neonatal Surgery

2013;**23**:702–711.

[54] Anand KJ, International Evidence-Based Group for Neonatal Pain. Consensus statement for the prevention and management of pain in the newborn. Arch Pediatr Adolesc Med. 2001;**155**:173–180. DOI: 10.1001/archpedi.155.2.173

[38] Engelhardt T. Rapid sequence induction has no use in pediatric anesthesia. Paediatr

[39] Won YJ, Lim BG, Lee DK, Kim H, Kong MH, Lee IO. Sugammadex for reversal of rocuroniuminduced neuromuscular blockade in pediatric patients: A systematic review and metaanalysis. Medicine (Baltimore). 2016;**95**:e4678. DOI: 10.1097/MD.0000000000004678

[40] Bailey AG, McNaull PP, Jooste E, Tuchman JB. Perioperative crystalloid and colloid fluid management in children: Where are we and how did we get here? Anesth Analg.

[41] Arya VK. Basics of fluid and blood transfusion therapy in paediatric surgical patients.

[42] Boldt J. Use of albumin: An update. Br J Anaesth. 2010;**104**:276–284. DOI: 10.1093/bja/aep393

[44] Gray R. Which colloid to choose for neonates, infants and children. South Afr J Anaesth

[45] Cote CJ, Lerman J, Anderson BJ, editors. A Practice of Anesthesia for Infants and Children. 5th ed. Philadephia: Elsevier Saunders; 2013. 198 p. DOI: 10.1213/ane.0b013e3182a00428

[46] Davies P, Robertson S, Hegde S, Greenwood R, Massey E, Davis P. Calculating the

[47] Keir AK, Stanworth SJ. Neonatal plasma transfusion: An evidence-based review.

[48] Sloan SR, Parker RI. Current status of platelet transfusion in pediatric patients. Transfus

[49] Goel R, Cushing MM, Tobian AA. Pediatric patient blood management programs: Not just transfusing little adults. Transfus Med Rev. 2016;**30**:235–241. DOI: 10.1016/j.

[50] International Association for the Study of Pain. IASP Taxonomy [Internet]. 2012. Available from: http://www.iasp-pain.org/Taxonomy#Pain [Accessed: 2016-09-07].

[51] Anand KJ, Sippell WG, Aynsley-Green A. Randomised trial of fentanyl anaesthesia in preterm babies undergoing surgery: Effects on the stress response. Lancet. 1987;**1**:62–66.

[52] Anand KJ, Hickey PR. Pain and its effects in the human neonate and fetus. N Engl J Med.

[53] Rutter N, Doyal D. Neonatal care and management of pain: Historical and ethical issues.

Semin Neonatol. 1998;**3**:297–302. DOI: 10.1016/S1084-2756(98)80084-5

required transfusion volume in children. Transfusion. 2007;**47**:212–216.

Transfus Med Rev. 2016;**30**:174–182. DOI: 10.1016/j.tmrv.2016.07.001

Med Rev. 2016;**30**:230–234. DOI: 10.1016/j.tmrv.2016.07.006

1987;**317**:1321–1329. DOI: 10.1056/NEJM198711193172105

Anaesth. 2015;**25**:5–8. DOI: 10.1111/pan.12544

Analg. 2015;**21**:56–58.

38 Pediatric and Neonatal Surgery

tmrv.2016.07.004

DOI: 10.1016/S0140-6736(87)90065-1

2010;**110**:375–390. DOI: 10.1213/ANE.0b013e3181b6b3b5

Indian J Anaesth. 2012;**56**:454–462. DOI: 10.4103/0019-5049.103960

[43] Uhing MR. The albumin controversy. Clin Perinatol. 2004;**31**:475–488.

#### **Spinal Anaesthetic Management in Paediatric Surgery Spinal Anaesthetic Management in Paediatric Surgery**

#### Esra Caliskan Esra Caliskan

[68] Anand KJ, Aranda JV, Berde CB, Buckman S, Capparelli EV, Carlo WA, Hummel P, Lantos J, Johnston CC, Lehr VT, Lynn AM, Maxwell LG, Oberlander TF, Raju TN, Soriano SG, Walco GA. Analgesia and anesthesia for neonates: Study design and ethical

[69] Gunter JB. Benefit and risks of local anesthetics in infants and children. Paediatr Drugs.

[70] American Society of Regional Anesthesia and Pain Medicine. Checklist for Treatment of Local Anesthetic Systemic Toxicity [Internet]. 2016. Available from: https://www.asra. com/advisory-guidelines/article/3/checklist-for-treatment-of-local-anesthetic-systemic-

issues. Clin Ther. 2005;**27**:814–843. DOI: 10.1016/j.clinthera.2005.06.021

2002;**4**:649–672.

40 Pediatric and Neonatal Surgery

toxicity [Accessed: 2016-10-30].

Additional information is available at the end of the chapter Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/67409

#### **Abstract**

The first paediatric cases involving the use of spinal anaesthesia were published at the end of the nineteenth century. However, the technique did not receive much interest in paediatric anaesthesia until the 1980s. In the last three decades, paediatric spinal anaesthesia has received widespread approval as an alternative technique to general anaesthesia in school-/preschool-aged children, particularly in term and preterm neonates with high risk associated with general anaesthesia. The development of new and safer local anaesthetics mainly through better understanding of the pharmacokinetics and dynamics and dedicated paediatric tools are the keys to this success. Paediatric spinal anaesthesia is an easy and effective technique, and its high efficiency and safety are supported by the presence of numerous publications from the medical literature. However, it remains limited to situations in which general anaesthesia poses a major risk. Despite these advances, it is important to understand the correct technique and the anatomy of children at different ages. Also, the appropriate equipment, the pharmacokinetics and toxicities of local anaesthetics and the indications and complications of paediatric regional blocks should be well known. The goal of this chapter is to review and discuss some of these topics of paediatric spinal anaesthesia for paediatric surgery.

**Keywords:** paediatrics, anaesthetic techniques, regional anaesthesia, paediatric spinal anaesthesia, complications, anaesthetic management

## **1. Introduction**

#### **1.1. History of paediatric spinal anaesthesia**

The use of paediatric regional anaesthesia began in the first half of the 1900s. In 1898, Bier [1] performed the first spinal anaesthetic, and two of his patients were children. Bier's publications were followed by reports by Donitz in Europe [2]. In addition, in 1909–1910, two detailed articles about more than 100 children with spinal anaesthesia were published by Gray [3, 4] in the Lancet.

and reproduction in any medium, provided the original work is properly cited.

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

With the development of general anaesthesia, there was little interest in paediatric spinal anaesthesia until the 1950s. Since then, paediatric spinal anaesthesia has become a more popular technique for the anaesthesiologist, and during the last three decades, the spinal anaesthetic approach has increased dramatically in children. This technique has been used safely in premature and ex-premature infants with a high risk of apnoea associated with general anaesthesia [5–8]. Also, spinal anaesthesia is an uncomplicated and effective technique that provides a rapid onset and exceedingly effective analgesia, sympathetic and motor block in the lower part of the body [9].

Despite the increased prevalence of spinal anaesthesia in children, it is still not practised everywhere owing to the use of conventional general anaesthesia.

## **2. Spinal anaesthetic approach: anatomical and physiological differences in paediatric patients**

#### **2.1. Anatomical structure of and differences in vertebral column**

The anatomical structure of the spinal column in children differs from that of adults. In premature infants (approximately 90%), the spinal cord terminates between the L2–L3 vertebra [10]. In newborns, the spinal cord extends down to the level of the L3 lumbar vertebra, compared with the L1 lumbar vertebra in adults (**Figure 1**) [11–13].

**Figure 1.** Anatomical structure and differences between paediatric and adult invertebral column (Remodified from Frawley and Ingelmo [13]).

The dural sac ends at the L4 vertebra at birth but reaches S2 by the end of the first year of life (**Figure 1**) [13]. Shin et al. confirmed that the end of the dural sac was at a median level of the upper S2 in children aged less than 36 months of age [14].

The iliac crest (intercristal line—Tuffier's line) can be used to determine safe puncture levels for children in the same way as in adults. In infants, the intercristal line passes through the vertebral column at the L4–5 or L5–S1 interspace, well below the termination of the spinal cord [13]. Therefore, the L4–5 or L5–S1 intervertebral space should be used for needle placement in children.

Studies related to vertebral anatomy in children demonstrated that the distance between the skin and the subarachnoid space at the level of the L4–5 interspace is 6 mm at birth and 10–12 mm at 1 year of age [15]. Ecoffey et al. [16] reported that the distance between the skin and the subarachnoid space was 10–18 mm in the lumbar region and 7–14 mm in the thoracic region in children less than 3 years of age.

The pelvis has a more rounded structure in infants, and the iliac crest is lower than in adults. Another anatomical difference in paediatric patients is the flexibility of a child's spine and intervertebral spaces, which are easily palpated [13]. In addition to these characteristics, ossification of the vertebral lamina is incomplete, and the spinal needle can readily enter the bone. The lumbar spinal canal differs in the paediatric age group too; the interpedicular diameter of the spinal canal at the lumbar level is quite wide and is 70% of the adult size at birth [9, 17].

All these anatomical differences between children and adult scan facilitate dural puncture in children, but paediatric spinal anaesthesia is a specialised technique, and these anatomical characteristics must be taken into consideration in order not to cause complications when performing the spinal technique.

#### **2.2. Physiological differences between adult and paediatric patients**

In neonates, insufficient myelinisation and a weak endoneurium provide an ineffective barrier to drug diffusion. These anatomical and physiological characteristics mean the rapid onset and offset of block [12, 18].

Vascularisation of the pia mater is relatively high in neonates. Cardiac output is also higher in children than in adults. Because of these two factors, local anaesthetic reabsorption is rapid, and the duration of block is shorter. Compared to adults, the total cerebrospinal fluid (CSF) volume is higher in children (neonates, 10 ml kg−1; infants and toddlers, 4 ml kg−1), and because the ligament density is low, the feeling of loss of resistance is less marked than in adults.

In infants, the lack of lumbar lordosis and increased limits of spinal flexibility can predispose to high spinal blockade with differences in positioning compared with older children [12, 13].

## **3. Benefits of spinal anaesthesia in children**

#### **3.1. Effective pain control**

With the development of general anaesthesia, there was little interest in paediatric spinal anaesthesia until the 1950s. Since then, paediatric spinal anaesthesia has become a more popular technique for the anaesthesiologist, and during the last three decades, the spinal anaesthetic approach has increased dramatically in children. This technique has been used safely in premature and ex-premature infants with a high risk of apnoea associated with general anaesthesia [5–8]. Also, spinal anaesthesia is an uncomplicated and effective technique that provides a rapid onset and exceedingly effective analgesia, sympathetic and motor block in

Despite the increased prevalence of spinal anaesthesia in children, it is still not practised

**2. Spinal anaesthetic approach: anatomical and physiological differences**

The anatomical structure of the spinal column in children differs from that of adults. In premature infants (approximately 90%), the spinal cord terminates between the L2–L3 vertebra [10]. In newborns, the spinal cord extends down to the level of the L3 lumbar vertebra, com-

The dural sac ends at the L4 vertebra at birth but reaches S2 by the end of the first year of life (**Figure 1**) [13]. Shin et al. confirmed that the end of the dural sac was at a median level of the

**Figure 1.** Anatomical structure and differences between paediatric and adult invertebral column (Remodified from

The iliac crest (intercristal line—Tuffier's line) can be used to determine safe puncture levels for children in the same way as in adults. In infants, the intercristal line passes through the

everywhere owing to the use of conventional general anaesthesia.

**2.1. Anatomical structure of and differences in vertebral column**

pared with the L1 lumbar vertebra in adults (**Figure 1**) [11–13].

upper S2 in children aged less than 36 months of age [14].

the lower part of the body [9].

42 Pediatric and Neonatal Surgery

**in paediatric patients**

Frawley and Ingelmo [13]).

Spinal anaesthesia provides effective analgesia with minimal physiological changes or adverse effects and is an alternative to systemic analgesics (such as opioid and non-opioid analgesics) [19]. This feature provides a significant advantage in cases where systemic opioid use is contraindicated, especially in children at risk of opioid-induced adverse effects.

Effective analgesia also creates ideal physiological conditions for the recovery period for children and their families. An awake, cooperative and painless child adjusts more easily to the postoperative period. Additionally, efficient pain control reduces adverse effects due to the neuroendocrine stress response.

#### **3.2. The effects of anaesthetics on neuronal development**

In recent years, many important studies and preclinical data have been reported that describe how general anaesthesia affects neurodevelopmental outcome in young animals [20]. Changes in brain development include dose-dependent neuronal apoptosis, impairment of neuronal differentiation, synaptogenesis and changes to dendritic morphology [21].

The neurodegenerative effect seems to be both time and dose dependent. In animal studies, anaesthetic drugs (these act through the NMDA and GABA receptors) played a role in neurodegeneration.

In young animals, long-term cognitive and behavioural changes associated with general anaesthetics have been shown in several studies, but these findings must be supported by human studies and clinical data.

In recent years, various reviews, cohort studies and two meta-analyses have established that there is an association between anaesthesia in childhood and neurodevelopmental outcome [22].

In a randomised clinical trial, Davidson et al. compared the neurodevelopmental outcome in children who received either awake regional anaesthesia or sevorane-based general anaesthesia for inguinal herniorrhaphy in early infancy (the general anaesthesia compared to spinal anaesthesia (GAS) trial) [23]. The authors found that exposure to just less than 1 h sevoflurane general anaesthesia in infancy did not increase the risk of adverse neurodevelopmental outcome at 2 years of age. Nonetheless, reducing exposure to general anaesthesia especially in premature infants is important so as to reduce the deleterious effects of inhalational anaesthesia.

## **4. Physiological effects and advantages of spinal anaesthesia**

#### **4.1. Respiratory effects**

Spinal anaesthesia has been correlated with minimal respiratory changes and ensures continuity of spontaneous breathing during surgery. This advantage is important in high-risk children in whom the anaesthetist wishes to avoid tracheal intubation and mechanical ventilation.

In summary, the respiratory benefits of spinal anaesthesia are as follows: effective analgesia without respiratory depression, improved respiratory performance and enhanced ventilatory response to hypercapnia with bupivacaine (possible mechanism is a direct stimulating effect of bupivacaine on the respiratory centre) [24].

In the neonatal period, the risk of opioid-related respiratory depression and sensitivity to muscle relaxant is more pronounced. However, spinal anaesthesia decreases the requirement for anaesthetic agents, muscle relaxants and opioids during surgery. These effects are especially important for reducing the risk of postoperative apnoea in high-risk infants that require surgery in this period [25].

#### **4.2. Haemodynamic properties**

Effective analgesia also creates ideal physiological conditions for the recovery period for children and their families. An awake, cooperative and painless child adjusts more easily to the postoperative period. Additionally, efficient pain control reduces adverse effects due to the

In recent years, many important studies and preclinical data have been reported that describe how general anaesthesia affects neurodevelopmental outcome in young animals [20]. Changes in brain development include dose-dependent neuronal apoptosis, impairment of neuronal

The neurodegenerative effect seems to be both time and dose dependent. In animal studies, anaesthetic drugs (these act through the NMDA and GABA receptors) played a role in

In young animals, long-term cognitive and behavioural changes associated with general anaesthetics have been shown in several studies, but these findings must be supported by