Basic Preoperative Evaluation, Anesthesiological and ... · Basic Preoperative Evaluation, Anesthesiological and Intensive Care Management in the Pediatric Patients Tomohiro Yamamoto

Basic Preoperative Evaluation,Anesthesiological and Intensive CareManagement in the Pediatric Patients

Tomohiro Yamamoto and Ehrenfried Schindler

ContentsIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Cerebral Autoregulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2Perioperative Preparation: Evaluation and Education of Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5Characteristics of the Anesthesia for Neurosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7Practice of the Anesthesia for Neurosurgery: Anesthesia Induction . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8Practice of the Anesthesia for Neurosurgery: Anesthesia Induction in Emergency,Preventing the Aspiration Pneumonitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Practice of the Anesthesia for Neurosurgery: Anesthesia Maintenance Preventingthe Hypothermia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11Practice of the Perioperative Respiration Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13Prevention of the Perioperative Hypoxia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16Hemostasis and Coagulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17Basic Principles of Perioperative Sedation Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17Propofol Infusion Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18Practice of the Perioperative Cardiovascular Management: “Ohm’s Law” . . . . . . . . . . . . . . . . . . . . . 19Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

Introduction

In this section, we describe the general perioperative management of pediatricpatients undergoing the neurosurgical therapies. It is supposed that it is not necessaryto describe the neurosurgical therapies by each disease here, because the readers ofthis textbook are neurosurgeons and experienced concerning neurosurgery. Themanagement of children especially newborns and infants require special care.

T. Yamamoto • E. Schindler (*)Zentrum für Kinderanästhesiologie, Asklepios Klinik Sankt Augustin GmbH, DeutschesKinderherzzentrum (DKHZ), Sankt Augustin, Germanye-mail: [email protected]

# Springer International Publishing AG 2017C. Di Rocco et al. (eds.), Textbook of Pediatric Neurosurgery,DOI 10.1007/978-3-319-31512-6_5-1

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mailto:[email protected]

Therefore, we focus common anesthesia practice, anesthetic drugs, medications usedin perioperative care, and basic principles about maintenance of hemodynamicstability.

Cerebral Autoregulation

Cerebral autoregulation is a mechanism that maintains the cerebral blood flow (CBF)within the normal range despite of changes like increased or decreased arterial bloodpressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and manymore (Paulson et al. 1990). The CBF means a bloodstream necessary for supply ofoxygen and metabolites according for the activity of the brain cells. In adults, theCBF is normally 50 ml/brain tissue 100 g/min and it is equivalent to 15–20% ofcardiac output. Indeed, the oxygen consumption of the brain is equivalent to 20% ofthe total body consumption, although the weight of brain is only about 2–3% of thebody weight. It is supposed that the ratio of CBF and oxygen consumption of brain ishigher in children, because the ratio of the brain weight for the whole body weight ishigher than that in adults. In addition, the brain has extremely few energy storages. Inother words, the brain is an organ having very low tolerance for ischemia.

The factors affecting CBF are as follows:

1. Cerebral perfusion pressure (CPP); the brain perfusion depends on CPP, whichmeans the pressure gradient between the mean cerebral arterial blood pressure(MAP) and the mean cerebral venous pressure. The mean cerebral venouspressure approximates to the more easily measurable intracranial pressure (ICP).CPP = mean arterial blood pressure (MAP) – intracranial pressure (ICP)CPP = CBF � cerebrovascular resistance (CVR)MAP = diastolic blood pressure + 1/3 (systolic blood pressure – diastolic

blood pressure)Actually, CBF is maintained stable by cerebral autoregulation relying on thecerebrovascular reactivity in a wide range of CPP condition. At normotension,CBP remains constant with a MAP of between 50 and 150 mmHg in adults(Paulson et al. 1990). However, the autoregulation curve shifts to the right inpatients with chronic hypertension because of their normal blood pressure (Phil-lips and Whisnant 1992), and it is supposed that the autoregulation curve shifts tothe left in pediatric patients because of their normal lower blood pressure(Vutskits 2014) (Fig. 1). By rise in MAP, cerebral blood vessels dilate in orderto offset its influence, and the tendency to rise in ICP due to increase inbloodstream inhibits the rise in CPP, too. On the other hand, by decrease inMAP, cerebral blood vessels contract in order to keep MAP high. However, bythe lower MAP than the lower limit of autoregulation range, CBF decreasespressure passively, because the cerebral blood vessels have already constrictedmaximally. Similarly, by the higher MAP than the higher limit of autoregulationrange, CBF increases pressure passively, because the cerebral blood vessels havealready dilated maximally. In short, above and below these limits, autoregulation

2 T. Yamamoto and E. Schindler

is lost and CBF becomes dependent on MAP in a linear fashion (Osol et al. 2002).For example, severe hypotension caused by blood loss reduces MAP, and as aresult, reduces CPP (formula above). Therefore, severely shocked patients showthe reduced level of consciousness. On the other hand, intracranial hematoma,tumor, and hydrocephalus increase ICP, and as a result, reduce CPP, too.

2. Arterial blood carbon dioxide partial pressure (PaCO2); PaCO2 alters the cerebralvasomotor tone and thus regulates CBF, too (Meng et al. 2012; Gelb et al. 2008).Hypercapnia increases CBF by its cerebral vasodilatation effect, and on thecontrary, hypocapnia decreases CBF. The relationship between PaCO2 and CBFis almost linear between 20 mmHg and 80 mmHg of PaCO2 (Fig. 2). When PaCO2

changes 1 mmHg, CBF changes 2–4%. It means that CBF is increased approxi-mately doubled at a PaCO2 80 mmHg and is decreased to approximately half at aPaCO2 20 mmHg compared at normocapnia (PaCO2 40 mmHg). CBF does notincrease above PaCO2 80 mmHg any more, because the cerebral vessels are dilatedmaximally at this point. Similarly, CBF does not decrease under 20 mmHg ofPaCO2, because the cerebral vessels have constricted maximally at this point. Inaddition, such extreme hypocapnia should be avoided, because additional cerebralischemic injury can be induced (Curley et al. 2010; Zhou and Liu 2008).The cerebral autoregulation is affected by hypercapnia and hypocapnia. Hyper-capnia makes the plateau phase of CBF higher and shorter than normocapnia dueto its vasodilatation effect (Meng and Gelb 2015). Even 50–60 mmHg of PaCO2

makes the plateau phase of CBF shorter (Meng and Gelb 2015). In contrast,hypocapnia makes the plateau phase of CBF lower and longer than normocapniadue to its vasocontractive effect (Meng and Gelb 2015).

cere

bral

blo

od fl

ow (C

BF)

50mean cerebral arterial blood pressure (MAP)

100 150 2000

pediatric patientsnormotension patientschronic hypertension patients

(mmHg)

Fig. 1 The relationship between the cerebral blood flow (CBF) and the mean cerebral arterial bloodpressure (MAP). At normotension, CBP remains constant with a MAP of between 50 and150 mmHg in adults; however, the autoregulation curve shifts to the right in patients with chronichypertension because of their normal blood pressure, and it is supposed that the autoregulationcurve shifts to the left in pediatric patients because of their normal lower blood pressure

Basic Preoperative Evaluation, Anesthesiological and Intensive Care Management. . . 3

3. Arterial blood oxygen partial pressure (PaO2); PaO2 has little effect on CBF in thenormoxemic range. The cerebral vessels dilate and CBF increases once PaO2 dropsbelow 50 mmHg in order to keep the cerebral oxygen delivery constant (Fig. 3).

4. Cerebral metabolic demand; when the brain cells are activated, the metabolicdemand rises. Cerebral metabolic rate for oxygen (CMRO2) decreases 7% foreach 1 degree fall in body temperature and CBF reduces parallel with reduction ofCMRO2 (Greeley et al. 1991; Baos et al. 2015; Royl et al. 2008). It means,CMRO2 and CBF decrease approximately 50% of normal, when temperaturedecreases 10 degrees from 37 degrees to 27 degrees.CMRO2(=CBF) = normal CMRO2(=normal CBF) � (1–0.07)⊿degree

Vasoconstriction due to hypothermia reduces CBF and ICP. A lot of clinicaltrials have been performed and showed promising findings that hypothermia mayhelp to improve neurological outcomes in cases of cerebral ischemia (Su et al.2015).

cere

bral

blo

od fl

ow (C

BF)

20arterial blood carbon dioxide partial pressure (PaCO2)

40 600 (mmHg)80

Fig. 2 The relationshipbetween the cerebral bloodflow (CBF) and the arterialblood carbon dioxide partialpressure (PaCO2). Therelationship between PaCO2

and CBF is almost linearbetween 20 mmHg and80 mmHg of PaCO2. CBFdoes not increase abovePaCO2 80 mmHg and doesnot decrease under 20 mmHgof PaCO2

cere

bral

blo

od fl

ow (C

BF)

50arterial blood oxygen partial pressure (PaO2)

100 1500 (mmHg)200

Fig. 3 The relationshipbetween the cerebral bloodflow (CBF) and the arterialoxygen dioxide partialpressure (PaO2). PaO2 haslittle effect on CBF in thenormoxemic range. CBFincreases once PaO2 dropsbelow 50 mmHg


Perioperative Preparation: Evaluation and Education of Patients

Generally and traditionally, it is said that height, weight, vital signs, several blood tests(such as cellular evaluation, biochemical analysis, molecular profiles, examination ofinfectious disease), chest X-ray, electrocardiogram, and urinalysis are necessary for apreoperative evaluation by the anesthesiologists. However, all these examinations are notalways necessary in all cases, for example, small scalp injury. In other words, preoper-ative evaluation is not a physical check, but its purpose is to enforce anesthesia safely, forexample, to change the planned anesthesia or intraoperative monitoring, when theexaminations show some abnormalities. Indeed, it is extremely rare that abnormalitiesaffecting the anesthesia management method are discovered by routine examinationsmentioned above by the pediatric patients who seem to be fine and have no especial pastmedical history. On the other hand, these routine examinations include disadvantages ofunnecessary costs and it is sometimes necessary to suppress the crying patient to takeblood samples. And such patients have already a fear of medical workers before seeingthe anesthesiologists, and it is very troublesome for us medical staffs to build a relation-ship of trust with such patients. Therefore, considering the indications of the preoperativeexaminations is very important especially by pediatric patients, and it is also important toconsult the anesthesiologists about essential preoperative examinations, when necessary.

What is of primary importance in the preoperative evaluation is taking the medicalhistory, in particular “SAMPLE history”; signs/symptoms, allergies, medications,past relevant medical history, last oral intake, events leading up to present illness/injury (Table 1). By the children having a slight cold, it is necessary to be judgedwhether the operation can be performed now or it should be postponed, according tophysical findings such as vital signs, state of the respiratory tract, and the evaluation ofthe airway. It should be decided with a consultation to anesthesiologists, because thepediatric patient should undergo for general anesthesia for nearly all of the neurosur-gical procedures in the operating room. In most of the cases no additional invasive ornoninvasive diagnostics are necessary in otherwise healthy children.

The purpose of preoperative fasting is to lower the risk of aspiration-relatedpneumonia by reducing quantity of secretion of the gastric juice and by raising itspH. The guideline by the American Society of Anesthesiologists recommends asfollows: Fasting period for clear liquids such as water, tea, fruit juices without flesh,carbonated drinks is 2 or more hours before procedures requiring general anesthesia,regional anesthesia, or sedation/analgesia. A fasting period for breast milk is 4 ormore hours for both neonates and infants. A fasting period for powdered milk, cow’smilk, and light meal is 6 or more hours for all age (Table 2) (1999). It means that thepatients may drink clear liquids as much as they want, when they get up, even whenthe operation is planned in the morning, and they may have breakfast, when theoperation is planned in the afternoon.

The smooth admission to the operation room or anesthesia induction room is oneof the difficult problems by pediatric patients. The “preparation” is the most impor-tant to solve this problem. It is necessary also for pediatric patients to be informedabout the operation and anesthesia to some extent. In short, they should be informedabout what will happen, even though it is dependent on their age and understanding.


For example, showing the patients the operation room or anesthesia induction roombeforehand can help them and their parents to understand it and to solve the negativeimaginations. The most important point is “Not to lie the patients.” It is very difficultto restore their confidence, once it is exposed that they were lied. The second mostimportant point is not to let the parents feel uneasiness or to educate the parents notto show their uneasiness as much as possible even when they are feeling uneasy,because the patients feel the uneasiness of parents and become more uneasy.Therefore, the “preparation” includes the parents, too. It is important and helpsthis preparation to show the parents understanding and sympathy that it is a matterof course to feel uneasiness as parents. When the parents nevertheless cannotcooperate with this concept, it may be a case, by which an admission to the operationroom or anesthesia induction room accompanied by the parents is not suitable.

The next question is, whether induction with a mask or intravenous induction isbetter and more comfortable for the pediatric patients, although it is thought thatmask introduction is suitable for the pediatric patients. Some patients hate the smellof the mask, and some patients hate to put a mask on the face because they havealready undergone the general anesthesia several times. In addition, there are dataindicating that the pediatric patients inducted by inhalation anesthesia with forcedmask introduction have more possibility to have unpleasant memory than thepatients induced by intravenous anesthesia (Kotiniemi and Ryhanen 1996). Apremedication can help to solve this point. For example, oral administration ofapproximately 0.5 mg/kg midazolam 15–30 minutes before anesthesia induction isvery easy and useful option, which can make patients cooperative during inductionof anesthesia, and its amnesic effect is also a great advantage. By older patients,7.5 mg up to 15 mg administration of midazolam with tablet/tablets is adequate.Table 3 shows the dose scheme of oral midazolam in our hospital as an example.When the patient hates oral intake of midazolam or is not cooperative, midazolam(0.2 mg/kg) or ketamine (2 mg/kg) can be intranasally administered as an alternative.It should be notice that the nose can ache due to the off-label intranasal

Table 1 “SAMPLE history” for taking the medical history in the preoperative evaluation

S Signs/symptoms

A Allergies

M Medications

P Past relevant medical history

L Last oral intake

E Events leading up to present illness/injury

Table 2 The guideline for fasting periods by the American Society of Anesthesiologists

Clear liquids such as water, tea, fruit juices without flesh,carbonated drinks 2 or more hours (all age)

Breast milk 4 or more hours (both neonatesand infants)

Powdered milk, cow’s milk, and light meal 6 or more hours (all age)


administration of intravenous injection preparation midazolam because of its pH 2.8– 3.8. There are now also midazolam products specially manufactured for intranasaladministration such as midazolam spray. It is reported that 1 μg/kg dexmedetomidineintranasal administration is equal effective, while midazolam is superior in providingsatisfactory conditions during mask induction (Table 4) (Akin et al. 2012; Bhat et al.2016).

Characteristics of the Anesthesia for Neurosurgery

What is characteristic of the neurosurgery, including brain surgery and spinal cordsurgery? Other organs such as liver can compensate the functions of the surgicallyremoved part. However, in the cases of brain or spinal cord surgery, the original functionof a removed part is lost entirely and it leads to postoperative complication directly.

As for the anesthesia of the brain surgery, it is a special characteristic of theneurosurgery that the place of the operation and anesthesia are the same organ, brain.Therefore, it is possible that consciousness of the patient is not given, even if patientscome out of anesthesia, when a brain part controlling consciousness is affected bythe operation. Very interestingly, the brain is an organ bringing about a sense, but itdoes not have the sense by itself. In other words, it does not feel the pain even whenit is cut. However, general anesthesia is necessary for the brain surgery because theskin and the skull feel a pain before the operation arrives at the brain. Once theoperation has arrived at the brain, the deep anesthesia is not necessary and this factenables an awakening craniosurgery. Nevertheless, in general, the patients must beanesthetized by neurosurgery well because they should never move during themaneuver and unexpected body movement of the patient may become fatal. Onthe other hand, the quick awakening of the patients is also demanded by theanesthesia for neurosurgery because it is necessary that the direct postoperativestate of consciousness and complications should be checked. For these elements,

Table 3 Oral dose of midazolam in our hospital

Age (years) Body weight (kg) Dose (mg/kg)

0–1/2 3–7,5 0

1/2–1 7,5–12 0.5

1–2 12–1 5 0.6

2–5 15–20 0.7

5–8 20–28 0.5

8–12 28–50 0.4

>12 >50 0.3 (max 15 mg)

Table 4 Dose of intranasal premedications

Midazolam 0.2 mg/kg

Ketamine 2 mg/kg

Dexmedetomidine 1 μg/kg


the anesthesia for neurosurgery is not as simple or easy as imaged and more stressfulfor anesthesiologists, too.

Practice of the Anesthesia for Neurosurgery: AnesthesiaInduction

In general, the patients need to be intubated, because the head of the patient is locatedremoted from the anesthesiologist and is completely covered under the clean cloth,and therefore, it is impossible to treat it, in case a trouble of respiratory tract occurredduring operation. The reinforced tubes are recommended in order to help reduce riskof kinking because of the same reason.

Propofol bolus of 2–3 mg/kg is reasonable for the intravenous induction becauseof its swift action. Infants or small patients need sometimes more propofol (�5 mg/kg). Barbiturates (thiopental or thiamylal) can also be chosen. Thiopental 3–5 mg isused for a long time and has less influence on breathing and circulation than propofol(Harrison 2004); however, thiopental is contraindicated to use for patients of thebronchial asthma and acute intermittent porphyria. In addition, thiopental can lead tonecrosis when it leaks outside blood vessels because of its extremely strong alka-linity (pH 10.5) (Harrison 2004). Ketamine is another variation for anesthesiainduction, because the intramuscular administration (5–10 mg/kg) as well as intra-venous administration (1–2 mg/kg) is possible in emergency case of uncooperativepatients without venous line. In addition, ketamine decreases intracranial pressure(ICP) without lowering cerebral arterial blood pressure (MAP) or cerebral perfusionpressure (CPP) (Mayberg et al. 1995; Bar-Joseph et al. 2009; Green et al. 2015), andtherefore, it can be chosen for the anesthesia introduction of the patient whosehemodynamics is unstable. However, the single administration of ketamine causesthe nightmare; therefore the combination with 0.1 mg/kg midazolam or 1–2 mg/kgpropofol intravenous administration can be considered.

For the tracheal intubation, the administration of appropriate opioid is necessaryin order to suppress unfavorable reactions such as rise of blood pressure, heart rate,and ICP because of the intubation stress, because propofol or barbiturates has noanalgetic effects. For example, fentanyl (1–3 μg/kg) or remifentanil (1–2 μg/kg)provides appropriate analgesia for intubation (Albertin et al. 2000; Yang et al. 2009).Remifentanil should be administered slowly because it may cause sinus bradycardiathrough the stimulation of the parasympathetic system (Del Blanco Narciso et al.2014; Zaballos et al. 2009); however, it can be usually treated by 0.01 mg/kgatropine administration. It is reported that pretreatment with intravenous atropinecan prevent bradycardia during anesthesia induction with the combination of pro-pofol and remifentanil (Maruyama et al. 2010). In contrast, the effect of routinepretreatment with atropine for vagal reflex bradycardia prior to tracheal intubation inpediatric patients is still controversial (Fastle and Roback 2004; Jones et al. 2012).

Use of the muscle relaxants is usually enough only for the tracheal intubationbecause neurosurgery needs no relaxant by itself. On the contrary, neurosurgicaloperations need sometimes the monitoring of motor evoked potential (MEP). There


are several reports which show that the combination of propofol and appropriateopioids provides adequate conditions for tracheal intubation without muscle relax-ants (Steyn et al. 1994; Erhan et al. 2003a, b). However, the intubation in aninsufficient anesthesia may cause laryngospasm. Every relaxant can be chosen forthe intubation. Suxamethonium (1 mg/kg intravenous administration, 2 mg/kgintramuscular administration) can be used safely without changing ICP, CPP, orelectroencephalogram (EEG) in patients with severe head injuries (Brown et al.1996; Kovarik et al. 1994). Suxamethonium raises intragastric pressure and some-times causes the postoperative muscle pain due to fasciculation. In addition, it can bea trigger for malignant hyperthermia. 1–1.2 mg/kg intravenous administration ofrocuronium provides as quick intubation condition as suxamethonium withoutharmful side effects mentioned above (Tran et al. 2015; Perry et al. 2003, 2008;Sluga et al. 2005). Rocuronium can be neutralized by sugammadex (4 mg/kgintravenous administration) completely, and 16 mg/kg sugammadex can neutralizethe effect of rocuronium direct after 1 mg/kg its administration in emergency (Bomet al. 2002; Shields et al. 2006; Groudine et al. 2007).

Uncuffed tracheal tubes are traditionally used for children younger than 6–7 years,because trachea is narrowest at the cricoid ring level in young children and appropri-ately sided uncuffed tubes seal well. In contrary, an additional cuff increases the riskof airway mucosa injury and a cuff necessitates smaller tubes which increase work ofbreathing because of more airway resistance(Khine et al. 1997).

The uncuffed tracheal tube size is commonly chosen according to Cole’s formula(Cole 1957) among anesthesiologists:

uncuffed tube size: (ID; mm) = (age/4) + 4*ID = internal diameter

The cuffed tracheal tube size should be 0.5–1.0 mm smaller than uncuffedtracheal tubes (Khine et al. 1997):

cuffed tube size: (ID; mm) = (age/4) + 3

Numerous studies investigated appropriate tracheal tube depth in children(Mariano et al. 2005; Kim et al. 2003; Weiss et al. 2005). For example, a methodto withdraw the tube to the carina and further 2 cm after intentional endobronchialintubation (Mariano et al. 2005; Kim et al. 2003). Or a method to place the black linemarker near the tube tip at the vocal cords level (Mariano et al. 2005; Kim et al.2003; Weiss et al. 2005; Weiss et al. 2006). Or there is a formula as follows:

tube depth (oral) (cm) = 3 x tube size (ID; mm) (Mariano et al. 2005)

And the following formulas are traditionally and commonly used amonganesthesiologists:

tube depth (oral) (cm) = (age/2) + 12


tube depth (nasal) (cm) = (age/2) + 14

However, the tubes placed according to these two formulas are sometimes too deepby newborns and small infants (Table 5) (Khine et al. 1997). In addition, the tubedepth can be changed by the change of head position especially in young and smallpediatric patients (Weiss et al. 2006; Jordi Ritz 2008), and the nasal intubation can bea solution for this problem (Olufolabi et al. 2004). Auscultation is the easiest and themost certain method to control the position of tracheal tubes and it is essential not onlyafter the intubation but also after changing head position or converting body postureof the patient. Most recent data showed that special designed “microcuff” tubes forchildren are a good alternative to uncuffed tubes and can be used safely even innewborns (Mhamane et al. 2015; Thomas et al. 2016; Tobias, 2015).

Practice of the Anesthesia for Neurosurgery: AnesthesiaInduction in Emergency, Preventing the Aspiration Pneumonitis

Neurosurgery has not only the elective operations but also emergency operationssuch as cranial trauma, several intracranial hypertension situations because of braintumor, hydrocephalus, acute epidural hematoma, spinal cord injury, and soon. Anesthesia induction in emergency is not so much different from that in electiveanesthesia other than a condition called “full stomach” basically. As mentionedabove, fasting periods for clear liquids and meals are 2 h and 6 h, respectively(1999). However, the stagnation time of the gastric content is prolonged by pain,stress, anxiety, and many more (Ng and Smith 2001). Therefore, all patients foremergency operations must be treated as “full stomach,” even though a long time hasalready passed after the last oral intake. Indeed, the incidence of aspiration aftertrauma is markedly increased because of depression of consciousness and airwayreflex as well as “full stomach” condition (Lockey et al. 1999). It is of importance torecognize that all aspiration patients do not suffer from aspiration pneumonitis. Theaspiration related pneumonitis is well known as Mendelson’s syndrome classicallyand it is reported that the aspiration of gastric contents leads to aspiration relatedpneumonitis (Mendelson 1946). It was reported afterwards that the patients are atrisk of aspiration related pneumonitis if the pH of the gastric contents is<2.5 and the

Table 5 Examples of the sizes of tracheal tubes according to age of patients

Cuffed size (mm ID) Uncuffed size (mm ID) Patient’s age

3.0 4.0 Full-term newborn to 1 year

3.5 4.5 1–3 years

4.0 5.0 3–5 years

4.5 5.5 5–7 years

5.0 6.0 7–9 years


gastric volumes do not necessarily relate to the volume of fluid aspirated into thelungs or the incidence of aspiration related pneumonitis (Ng and Smith 2001;Schreiner 1998; Schwartz et al. 1998; Ingebo et al. 1997). The physiologicalmechanisms preventing regurgitation and aspiration compose of low esophagealsphincter (LES), the upper esophageal sphincter (UES), and the laryngeal reflexes(Ng and Smith 2001). When the patients lose consciousness with anesthesia induc-tion, these functions mentioned above are lost, and as a result, reflux of stomach acidcontents into the esophagus, the larynx, and the mouth may happen. Therefore, the“classical” technique of rapid sequence induction (RSI) has been used for a long timein emergency cases. This RSI technique is composed of pre-oxygenation, intrave-nous anesthesia induction with short-onset relaxants such as suxamethonium, cricoidpressure without ventilation (apneic period) until endotracheal intubation. However,the role of cricoid pressure during RSI is controversial (Algie et al. 2015) and RSIshould not be used transferred directly into pediatric anesthesia practice because ofdanger any more (Engelhardt 2015). In addition, small babies, pediatric patients, orobesity patients has so small functional residual capacity that SpO2 cannot bemaintained for a long time, until endotracheal intubation. Therefore, gentle maskventilation is allowed and moreover recommended in situations such as obesity andcritically ill patients in order to prevent hypoxemia during the apnoeic period(Sajayan et al. 2016). Direct after the intubation, the gastric contents must beabsorbed enough.

Practice of the Anesthesia for Neurosurgery: AnesthesiaMaintenance Preventing the Hypothermia

Pediatric patients are easy to fall into hypothermia during anesthesia. The bodytemperature of the patients under general anesthesia decreases remarkably, because afunction of the temperature center of the hypothalamus is depressed, and in addition,peripheral vessels are expanded and the core body temperature redistributes(Lenhardt 2010; Reynolds et al. 2008). Therefore, it is incorrect to judge that thecore body temperature remains still warm, even if the body surface of the patients isstill warm. The core body temperature decreases rapidly in the first 1 or 2 h after theanesthesia induction and stays stable at around 34 degrees (Fig. 4) (Lenhardt 2010;Reynolds et al. 2008). The perioperative hypothermia causes various harmful phe-nomena and can have influences on the convalescence of the patients (Table 6)(Cheshire 2016). When hypothermia (core temperature of <35 degrees) progresses,the risk of aspiration and the respiratory infectious disease increase from theattenuation of coughing reflection or ciliary function in the respiratory tract (Mallet2002). Shivering is often seen after anesthesia (Just et al. 1992). Shivering increasesoxygen consumptions significantly and causes the oxygenation disorder in theperipheral tissue. In addition, shivering decreases the thoracic compliance and itleads to a drop of tidal volume and respiratory minute volume (Nasiri et al. 2015;Campbell et al. 2015). The slight hypothermia stimulates the sympathetic nerve


system and the cardiac output increases and the blood pressure rises because of theincrease of heart rate and the contraction of the peripheral vessels. However, ashypothermia further progresses, the heart rate and the cardiac contraction decrease.A risk of the ventricular fibrillation increases by 27 degrees temperature, and a riskof the cardiac arrest becomes greater by hypothermia less than 24 degrees. By thestimulation of the sympathetic nerve system by the hypothermia, the secretion ofinsulin decreases and it can lead to hyperglycemia. In the hypothermia, renal bloodflow increases by a shift of the blood from the peripheral tissue by the contraction ofthe peripheral vessels. In addition, the secretion of antidiuretic hormone (ADH)decreases and the reabsorption of primary urine at the distal convoluted tubule inkidney are depressed. Thus, the volume of urine increases by the hypothermia. Inaddition, it can cause not only hypovolemia but also electrolytes abnormality such ashypokalemia, hypomagnesemia, or hypophosphatemia. The intestinal tract peristal-sis is also depressed by hypothermia. And the secretion of gastric acid increasesbecause of the stress from hypothermia and it causes a mucous membrane disorder inthe stomach and duodenum. By hypothermia, the drug metabolic capacity of the

core

bod

y te

mpe

ratu

re

1time after anesthesia induction

2 30 (hour)4 5 6

34.0

35.0

36.0

37.0Fig. 4 The time course of thecore body temperature afteranesthesia induction. The corebody temperature decreasesrapidly in the first 1 or 2 hafter the anesthesia inductionand stays stable at around34 degrees

Table 6 Examples of the harmful phenomena due to perioperative hypothermia

Postoperative respiratory complications due to aspiration and respiratory infectious disease

Shivering increasing oxygen consumptions and causing oxygenation disorder

Cardiopulmonary complications due to the changes of cardiac output and rhythmus

Hyperglycemia through decreasing insulin secretion

Hypovolemia and electrolytes abnormality

Intestinal tract problems and following delay of oral intake

Anesthesia awakening delay due to the rise of blood concentration and the extend of action timeof drugs

Infection of the operation wound

Increase in amount of bleeding and transfusion


liver decreases, too. As a result, the blood concentration of the drugs rises andextends the action time, and it leads to anesthesia awakening delay combined withhypnosis and amnesia by hypothermia, or increase of postoperative respiratorycomplications because of the remaining muscle relaxant. The risk of infection ofthe operation wound can also increase, because migration and phagocytic ability ofwhite blood cells and monocytes is suppressed by hypothermia (Kurz et al. 1996;Melling et al. 2001), and because the oxygen supply to the operation wound part isdecreased by the vasoconstriction in hypothermia, while a review reports that thehypothermia does not increase in the overall risk of infection, whereas it associateswith the risk of postoperative pneumonia and sepsis (Geurts et al. 2014). Increase inamount of bleeding due to the hypothermia is a big problem, too. It is an establishedtheory for a long time that hypothermia impairs platelet function (Valeri et al. 1992)and coagulation cascade (Rohrer and Natale 1992), and it is also reported that evendecrease of body temperature less than 1 degree increases blood loss by 16% and therisk for transfusion by 22% (Rajagopalan et al. 2008). However, a recent studyreports that the treatment using intentional hypothermia does not impair coagulation(Nielsen et al. 2016). As described above, the perioperative temperature manage-ment is a very important theme because hypothermia leads to several complicationswhich can concern the morbidity and mortality of the patients (Lenhardt 2010;Reynolds et al. 2008; Cheshire 2016; Mallet 2002; Just et al. 1992; Nasiri et al.2015; Campbell et al. 2015; Kurz et al. 1996; Melling et al. 2001; Valeri et al. 1992;Rohrer and Natale 1992; Rajagopalan et al. 2008), although there are several reportsrecently contradicting these established theories (Geurts et al. 2014; Nielsen et al.2016).

Practice of the Perioperative Respiration Management

The simple knowledge about the mechanical ventilation is necessary because somepatients need postoperative artificial respiratory management. The mainly used respira-tory mode settings are following three: volume control ventilation (VCV), pressurecontrol ventilation (PCV), and pressure support ventilation (PSV). By the artificialrespiration, mechanical forced ventilation with positive pressure is carried out in theinspiratory phase and the expiration is carried out by the thoracic elasticity of the patientpassively. In VCV, an amount of the tidal volume is set. The ventilator provides a fixedtidal volume in constant speed in a set inspiratory time. Therefore, the airway pressureand the ventilation volume rise gradually in the inspiratory phase (Fig. 5). When anamount of ventilation reaches the set tidal volume, the ventilator stops ventilation. Thus,the amount of pulmonary ventilation decreases, in case that the respiratory circuit has aleak somewhere, for example because of too small tracheal tube. In short, the set tidalvolume is not guaranteed at all, although it is called “volume control” ventilation. InPCV, a peak airway pressure is set. The ventilator gives the airway a fixed pressure andkeeps it during a set inspiratory time (Fig. 5). Therefore, the tidal volume can be kepteven when the respiratory circuit has small leak because the ventilator sends ventilation


volume during the inspiratory phase until the airway pressure reaches the set airwaypressure.However, the tidal volume varies among patients and should be titrated becauseeach patient has different thorax compliance. The tidal volume decreases when thetracheal tube bends or it is clogged with sputum in PCV mode. Pressure supportventilation (PSV) senses the spontaneous breathing of the patient and assists it to theset airway pressure. PSV is used mainly for weaning from mechanical ventilation. Inaddition, PaCO2 or the breathing frequency can be used as good indexes to evaluate thestate of patients. For example, when the patient has tachypnea and very low PaCO2, itmay indicate that the intracranial pressure is elevated extremely and the patient managesto decrease the intracranial pressure by hyperventilation, if the ventilation setting is notwrong. Nevertheless, it is necessary to be careful about that PaCO2 rises when acondition of the parents gets worse and the respiratory centers located in the brainstem are impaired.

time

airw

ay p

ress

ure

time

time

flow

volu

me

Pressure-time(VCV)

flow-time(VCV)

volume-time(VCV)

time

airw

ay p

ress

ure

time

time

flow

volu

me

Pressure-time(PCV)

flow-time(PCV)

volume-time(PCV)

Fig. 5 Pressure-time diagrams (schema without PEEP), flow-time diagrams, and volume-timediagrams in volume control ventilation (VCV) and pressure control ventilation (PCV). The airwaypressure and the ventilation volume rise gradually in the inspiratory phase in VCV because theventilator provides a fixed tidal volume in constant speed. The peak airway pressure is set in PCVand the ventilator keeps it during the inspiratory time. Area under the curve (AUC) of the volume-time diagram is equivalent to the tidal volume. The height of the airway pressure curve of PCV islower than that of VCV for the same tidal volume


The superiority and inferiority of PCVand VCVare still controversial (Campbelland Davis 2002). However, PCV may have more advantages the VCV because eachalveolus has different compliance and all alveoli do not swell out uniformly when afixed tidal volume is provided in constant speed in the inspiratory phase in VCV. Inother words, only alveoli with high compliance are ventilated and the alveoli with lowcompliance are not ventilated and it causes atelectasis. In contrast, in PCV, the alveoliwith low compliance can be ventilated because the ventilator sends gas in theinspiratory phase until the airway pressure reaches the set airway pressure. Areaunder the curve (AUC) of the volume-time diagram is equivalent to the tidal volume(Fig. 5) and the height of the airway pressure curve of PCV is lower than that of VCVfor the same tidal volumewith the same length of the base (=with the same ventilationfrequency and inspiratory time), because the pressure-time diagrams in the inspiratoryphase of PCVand VCVare quadrangle and triangle, respectively. The pressure-timediagram in the inspiratory phase of PCVis quadrangle because the ventilator providesand keeps the set peak airway pressure during the inspiratory phase. In contrast, thepressure-time diagram in the inspiratory phase of VCV is triangle because theventilator provides the fixed tidal volume in constant speed in a set inspiratory time.

The tidal volume of 6–8 ml/kg is recommended because it is reported that suchtidal volume improves the oxygenation, thorax compliance, recovery rate fromartificial respiratory management and mortality rather than 10–12 ml/kg of tidalvolume (Amato et al. 1995; Amato et al. 1998; Brower et al. 2000).

PEEP (positive end-expiratory pressure) is also an important factor for theartificial respiratory management and adequate oxygenation. At first, begin amechanical ventilation with around 5 cmH2O PEEP. Then raise the PEEP graduallykeeping the respiratory pressure.

peak airway pressure = respiratory pressure + PEEP

The tidal volume increases gradually as PEEP is set higher, though the respiratorypressure is not changed. It is because the collapsed alveoli swell out consequentlywith increasing PEEP. This increase of tidal volume stops at a certain PEEP level,where all collapsed alveoli are swollen out (Fig. 6). However, there is no clearguidance, despite several clinical trials to define the optimal PEEP level (Broweret al. 2004; Mercat et al. 2008; Hubmayr and Malhotra 2014). It is supposed thatPEEP level of between 5 and 10 cmH2O is enough and a limitation considering theinfluence on cardiovascular system or intracranial pressure (ICP) practically. Whenthe collapsed alveoli swell out again, it causes “shear stress” in the alveolar stromabetween the alveoli which are already swollen out and it leads to ventilator-inducedlung injury (VILI). Therefore, it is a very important strategy to keep the alveoli notcollapsed (“open lung approach”) in order to not only to prevent VILI but also toimprove the oxygenation and lung mechanics in patients (Cinnella et al. 2015; Spiethet al. 2011). The maneuver to try to get an effective tidal volume in low pressure bypuffing out the lungs enough once in while with high respiratory pressure around


20 cmH2O and high PEEP around 20 cmH2O for 15–30 seconds, as far as acardiovascular system permits it, is called “recruitment maneuver” (Barbas et al.2005; Valente Barbas 2003). This concept is based on the mechanics that it does notneed high ventilation pressure, once the alveoli are swollen out.

Prevention of the Perioperative Hypoxia

As a part of perioperative care management, it is necessary to pay attention topossibility of the postoperative hypoxia after the anesthesia or extubation. It isreported that hypoxemia occurs more often and commonly than expected after thegeneral anesthesia and it can occur already in the postanesthesia care unit (PACU),and that it is difficult to detect clinically and associated with ASA class, surgicalduration and preoperative mean SpO2 (Aust et al. 2015; Daley et al. 1991; Laycockand McNicol 1988; Moller et al. 1990). Therefore, certain monitorings such as SpO2

are necessary for the early detection of hypoxemia and oxygen dosage in anappropriate timing. What should be regarded in the choice of the oxygen dosagemethod is the required inhalational oxygen density. For the slight hypoxemia, thelow flow dosage of oxygen via nasal cannula or face mask is enough. However, forthe moderate or severe hypoxemia, the high flow dosage of oxygen via venture maskor reservoir mask is necessary. Especially in the pediatric patients, it is necessary toconsider the comfort of the oxygen dosage method because the compliance andcooperation are sometimes more difficult than the adult patients.

tidal

vol

ume

2

positive end-expiratory pressure

4 60(cm H2O)

8 10 121 3 5 7 9 11

Fig. 6 The relationship between the increase of tidal volume and positive end-expiratory pressure(PEEP). The tidal volume increases gradually as PEEP is set higher because the collapsed alveoliswell out consequently with increasing PEEP. The arrow (") shows the point, where the tidalvolume does not increase any more. It is because all collapsed alveoli are swollen out at this PEEPlevel (in this schema at 9 cm H2O as an example)


Hemostasis and Coagulation

It is reported that the coagulation system of children is different from adult (“devel-opmental hemostasis”) and that the blood concentration of coagulation factors andalso the fibrinolytic system are age-dependent, and therefore, the reference limitsfrom adult practice cannot be transferred to children one to one (Andrew 1995a, b,1997). Another important fact is that absolute values of reference ranges for coag-ulation assays in neonates, infants, and children vary with different analyzer andreagent systems. That means that each laboratory should define specific ranges forchildren tested there (Male et al. 1999; Monagle et al. 2006).

As the transfusions of homologous blood components is associated not only withinfectiologic and immunologic risks (Brand 2016) but also with increased mortality(Wang et al. 2016; Goobie et al. 2016), blood-saving strategies to decrease the amount ofhomologous blood used are of fundamental importance also in pediatric neurosurgery.

Tranexamic acid (TXA) is reported to decrease intraoperative blood loss (Sethnaet al. 2005; McCormack 2012) and used more as an antifibriniolytic agent (Mayeuxet al. 2016; Cheriyan et al. 2015; Van Aelbrouck et al. 2016). One big issue with theuse of TXA in neurosurgical patient is the fact that TXA may cause seizures orconvulsion. The mechanism by which TXA can evoke epileptic seizures is reportedto be binding to the GABA (γ-aminobutyric acid) A receptors (Furtmuller et al.2002). These convulsive effects are dose dependent (Lin and Xiaoyi 2016; Leckeret al. 2016). According to published data and our experience, we would recommendthe following dosage regimen: TXA bolus of 10 mg/kg as infusion for 10–15minutes before skin incision followed by a continuous administration of 3 mg/kg/huntil the end of operation (McCormack 2012; Dunn and Goa 1999). In case ofpersistent coagulation disorder, TXA can be infused at the PICU continuously.

Basic Principles of Perioperative Sedation Management

Some patients need perioperative sedation for following indications: reduction ofpain, anxiety, and psychological stress, prevention of actions accompanied bydanger of patients themselves such as self-removal of drains and catheters or fallingfrom the bed, hemodynamic stability, synchronizing to artificial respiration manage-ment, keep of the normal circadian rhythm, and more.

A combination of medications of varying actions with appropriate doses such asopioids, analgetics, and hypnotics is adequate and important to prevent their sideeffects, too. A combination of more than three medications should be avoidedbecause of the increase in delirium risk and side effects.

It is supposed that morphine is the most popular opioid used in perioperativemanagement. For the continuous dosage of morphine, around 10 μg/kg/h is adequatefor babies and small pediatric patients; however, they need sometimes higher doses(10–30 μg/kg/h). 2–5 μg/kg/h is enough for most of the patients elder than the pupilperiod. Fentanyl or sufentanil is required in case that sedation with morphine isinsufficient. Midozolam is used most commonly as a hypnotic within the


perioperative management. Barbiturates have a great advantage to decrease theintracranial pressure (ICP) for neurosurgical patients (Majdan et al. 2013; Brattonet al. 2007). However, barbiturates are sometimes not appropriate for the postoper-ative patients, because it causes hyperalgesia. Ketamine can be a good option for thesedation of the patients with severe pain after injury or operation because of itsanalgesic effect as well as its effect decreasing the intracranial pressure (Mayberget al. 1995; Bar-Joseph et al. 2009; Green et al. 2015). However, monotherapeuticuse of ketamine should be avoided, because it causes the nightmare as mentionedabove. Clonidin is also an option, when using careful about its possibility to causebradycardia or atrioventricular block. Dexmedetomidine might be a very goodalternative for sedation also of pediatric patients (Sulton et al. 2016). Effectivenessof intranasal administration of dexmedetomidine (1 μg/kg) instead of midazolam forpediatric patients is also reported (Malhotra et al. 2016; Sheta et al. 2014; Yuen et al.2008). The doses mentioned here are only examples, and they should be regulated bythe need and reaction of the patient (Table 7).

Propofol Infusion Syndrome

Propofol is very commonly used for sedation in the intensive care unit as well as forintraoperative sedation and general anesthesia with very useful profiles. However, itis necessary to keep the possibility of a serious side effect with very high mortality“propofol infusion syndrome” into mind. The use of propofol was approved by theFood and Drug Administration (FDA) in November 1989. The first case concerningdeath of 3-year-old child associated with propofol infusion was reported in 1990(Adverse effects of propofol (Diprivan) 1990). After that similar cases about pedi-atric patients were reported and they developed high anion gap lactic acidosis,cardiovascular collapse, multiple organ failure, rhabdomyolysis, hepatomegaly,and lipemia (Parke et al. 1992; Bray 1998). Many physicians may believe thatpropofol infusion syndrome happens only in young pediatric patients; however, itis also reported in adolescent (Hanna and Ramundo 1998) and adult patients(Marinella 1996).

Table 7 Dose of medications for perioperative sedation management

Perfusion Additional intravenous bolus

Morphine 10–30 μg/kg/h 50–100 μg/kgFentanyl 0.5–5 μg/kg/h 1–10 μg/kgSufentanil 1–5 μg/kg/h 2–3 μg/kgMidazolam 0.1–0.2 mg/kg/h 0.1–0.2 mg/kg

Phenobarbital 2.5–5 mg/kg every 12 h

Ketamine 0.5–2 mg/kg/h 0.5–1 mg/kg

Clonidin 1–2 μg/kg/h 1 μg/kgDexmedetomidine 0.2–0.7 μg/kg/h


Recent reports and reviews recommend that propofol should be used limited theduration of propofol infusion to 24 h (or maximal 48 h) at a dose of less than or equalto 4 mg/kg/h and carefully about the symptoms such as high anion gap acidosis withelevated lactic acid, cardiovascular collapse including ECG changes or arrhythmia,multiple organ failure including renal or hepatic dysfunction, skeletal muscle man-ifestation such as myopathy or rhabdomyolysis, hypertriglyceridemia, hyper-kalemia, myoglobinuria, fever, and so on (Mirrakhimov et al. 2015; Felmet et al.2003; Krajcova et al. 2015). In case of suspected propofol infusion syndrome, theadministration of propofol must be immediately discontinued and the managementof metabolic acidosis and following multiple organ failure should be considered andbegun as early as possible, including administration of vigorous fluid, sodiumbicarbonate, calcium, insulin, and so on (Mirrakhimov et al. 2015; Zimmermanand Shen 2013; Maxwell et al. 2013).

Practice of the Perioperative Cardiovascular Management:“Ohm’s Law”

The “Ohm’s law” can be applied to understand the cardiovascular status of thepatients and to decide the adequate choice of the therapy and medications inperioperative management.

V ¼ R� I

V means the voltage, R means the resistance, and I means the current. In order toapply this “Ohm’s law” to the hemodynamics in the human body, V is equal to theblood pressure (BP), I is equal to the cardiac output (CO), and R means the systemicvascular resistance (SVR). The cardiac output consists of the systolic volume of theleft ventricle (SV) and the heart rate (HR). Therefore, the “Ohm’s law for thehemodynamics in the human body” can be expressed in the following expression:

BP ¼ AVR� SV � HR

This expression shows that the change of the blood pressure (BP) is a result of thechanges of the right side of the expression. By a massive bleeding for example, thesystolic volume (SV) is reduced because of reduction of filling of the left ventricle,and it will be compensated by increase of heart rate (HR) and systemic vascularresistance (SVR) for a while in order to keep the left side of the expression (=BP),which is a result of the changes of the right side of the expression. Considering this“Ohm’s law for the hemodynamics in the human body”, it can be easily understoodthat the compensation of the preload by the infusion or transfusion is the adequatetherapy in such situations. As another example in small pediatric patients or babies,the BP cannot be compensated so much by the rise of SV due to the small capacity ofthe left ventricle. Therefore, the rise of HR with administration of atropine forexample is an adequate therapy when the HR is extremely decreased. The


pathophysiology of Cushing reaction (=hypertension with bradycardia) is aresponse to increased intracranial pressure (ICP). The SVR increases in order toincrease the BP, and in contrary, the HR decreases as a reaction to keep the left sideof the expression (=BP) unchanged.

In this matter, the “Ohm’s law for the hemodynamics in the human body” is verysimple but very helpful in thinking about the causes of the change in blood pressureand the adequate choice of therapy and medications such as ephedrine, atropine, andcatecholamines.

Conclusion

In this chapter, we described the basic perioperative evaluation, anesthesiologicaland intensive care management by the pediatric patients undergoing neurosurgeryfrom the standpoint of the cardioanesthesiologists. Anesthesia is not an end in itself,but perioperative management for the neurosurgical patient must always be one partof a continuous process of patient care. Internal guidelines have to be agreed byneurosurgeons, anesthesiologists, and intensivists to ensure continuity in the wholepatient care.

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