Summary of different types of VL devices.
\r\n\tThe book will present up to date knowledge on mentioned ADHD topics in order to be implemented in every day clinical practice.
",isbn:"978-1-83962-495-7",printIsbn:"978-1-83962-475-9",pdfIsbn:"978-1-83962-496-4",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"176f5275d9e1e06b24e0ae07b90c424f",bookSignature:"Prof. Hojka Gregoric Kumperscak",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/9499.jpg",keywords:"Clinical Picture, Symptomatology, Symptoms, Clinical Presentation, Comorbidity, Pharmacotherapy, Nonpharmacological, Nutrition and Diet, Genetics, Neuroimaging, Neurotransmitters, Hormones",numberOfDownloads:517,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"June 10th 2020",dateEndSecondStepPublish:"August 6th 2020",dateEndThirdStepPublish:"October 5th 2020",dateEndFourthStepPublish:"December 24th 2020",dateEndFifthStepPublish:"February 22nd 2021",remainingDaysToSecondStep:"7 months",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:"Prof. Kumperscak, MD, PhD graduated from the Faculty of Medicine in Ljubljana, Slovenia. She was trained in child and adolescent psychiatry in Slovenia and abroad. She has held the Chair of the Department of Psychiatry in the University of Maribor in Slovenia (2017) and has been Head of the Child and Adolescent Psychiatry Unit, University Clinical Center in Maribor (2008). She is a President of the Slovenian Association for Child and Adolescent Psychiatry and Adolescent Identity Treatment psychotherapist.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"53417",title:"Prof.",name:"Hojka",middleName:null,surname:"Gregoric Kumperscak",slug:"hojka-gregoric-kumperscak",fullName:"Hojka Gregoric Kumperscak",profilePictureURL:"https://mts.intechopen.com/storage/users/53417/images/system/53417.jpg",biography:"Prof. Hojka Gregoric Kumperscak, MD, PhD was born in Maribor, Slovenia in 1970. She finished Faculty of Medicine in Ljubljana, Slovenia in 1996. She was trained in child and adolescent psychiatry in Slovenia and abroad (Italy, UK, Germany and Switzerland). \r\nShe has held the Chair of the Department of Psychiatry in the Faculty of Medicine, University of Maribor in Slovenia, since January 2017, and has been Head of the Child and Adolescent Psychiatry Unit, University Clinical Center in Maribor since 2008. She is a President of Slovenian Association for Child and Adolescent Psychiatry and Adolescent Identity Treatment psychotherapist. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"55848",title:"Airway Management in ICU Settings",doi:"10.5772/intechopen.69166",slug:"airway-management-in-icu-settings",body:'\nTracheal intubation (TI) is one of daily practiced procedures in the intensive care unit (ICU), especially when the patient has respiratory failure or cardiovascular collapse. It involves highly skilled techniques that require much of training, practice, and expertise. The excellence in airway management in ICU is necessary for intensivist’s every day practice, which when it is lacking does not only compromise the quality of care but also has a potential impact on patient safety.
\nThe optimal intubation condition prevailing in surgical theaters differs a lot in nature than harsh and chaotic scenarios in ICU. The nature of those situations has three factors: the highly skilled anesthesiologists versus the intensivists; the compensated, well‐controlled surgical patient versus the decompensated sick ICU patients; and equipment availability. That is why in ICU settings, the airway instrumentation‐related complications have higher incidence than anesthesia settings. Among the contributory factors for high failure rates are the highly stressful environment, limited expertise level of the providers with different techniques of airway management, the physiological baseline for the patients, inadequate pre‐oxygenation, unfamiliarity with new airway equipment, and the critical time factor in distressed situations in addition to the negative hemodynamic effects for the intubation medications.
Effective pre‐oxygenation is the first step for airway management. If it is done optimally by reaching PEO2 of >90%, it extends the apnea safety time margin for critical ICU patients with already limited oxygen transport and when the intubation for airway control would be time consuming. The apnea time for oxy‐hemoglobin to desaturate below 85% in postoperative period is 23 s in critically ill patients compared to 502 s in healthy adults [1].
\nThe standard pre‐oxygenation used in optimized surgical patients would fail to sustain adequate PaO2 in critically ill patients with hyper‐metabolic profile during apneic period for intubation.
\nThe airway management encountered in a rapidly deteriorating patient with hypoxia from a life‐threatening cardiopulmonary failure is not an uncommon daily ICU scenario. Lack of airway expertise is a high risk for multiple intubation attempts, airway trauma, esophageal intubation, and intubation failure, and consequences were adverse with high percentage of cardiac arrest or brain damage. Moreover, multiple traumatic trials by inexperienced provider could easily convert a simple airway to a difficult one due to airway edema.
Airway evaluation prior to tracheal intubation (TI) is the standard of care in anesthesia settings and should be routinely practiced in ICU before any TI. Many studies about airway evaluation in controlled anesthesia settings showed that combined airway tests are better than each test alone in terms of sensitivity and reliability.
\nAirway tests include Mallampati classification, thyromental distance, neck mobility, inter‐incisor distance, and body mass index (BMI), which are all reliable predictors for difficult airway. Other scores include El Ganzouri test and LEMON test. El Ganzouri test is a numerical score, involves all the abovementioned tests: Mallampati classification, thyromental distance, neck mobility, inter‐incisor distance, and BMI plus under‐bite and previous difficult intubation history. LEMON test involves Look Externally, Mallampati class, Obstruction, and Neck mobility.
Hemodynamic changes during TI are predictable physiological consequences after airway management, which are attributed to three main factors: sympathetic system, cardiac contractility, and mechanical ventilation. Vaso‐dilatory and cardio‐depressive effects of medications, preexisting hypovolemia, and positive‐pressure ventilation are major contributors to any predictable hemodynamic changes. Ketamine and Etomidate are anesthetic agents with a fast onset, short half‐life, and tolerable hemodynamic changes. They are widely used in emergency settings to improve intubation conditions. Etomidate is an anesthetic agent with adrenal inhibition effect. A cardio‐stable agent as Ketamine is preferable in ICU. The critical illness of ICU patients compromises the gastric emptying, making a rapid sequence intubation (RSI) a wise decision. Succinylcholine is a fast acting muscle relaxant with ultra short duration that is commonly used in emergency setting when there are no contraindications to its use. Muscle relaxants have its role in facilitating intubation; however, encountering cannot‐ventilate‐cannot‐intubate (CVCI) scenario after giving muscle relaxants could lead to a fatal airway emergency. Studies found that physicians other than anesthesiologists are reluctant to use muscle relaxants before intubation in the ICU. A large data set found fewer complications, including in patients with difficult airways when muscle relaxants were used. In a prospective multicenter study, Jaber showed that tracheal intubation by muscle relaxants has less complications by 22 versus 37% when muscle relaxants were not used [2]. In another study in emergency department, Li et al. found a significant decrease in esophageal intubation with the use of muscle relaxants (3 vs. 18%) [3]. Succinylcholine should not be used in patients with hyperkalemia, congenital muscle disorders, and burn patients with difficult airway as it could lead to hyperkalemic cardiac arrest. As alternative to Succinylcholine, Rocuronium Bromide (1 mg/kg) can be used for rapid sequence intubation in critical care patients and can be reversed by Sugammadex Sodium.
Pre‐oxygenation before intubation is the standard of care. The standard pre‐oxygenation used in optimized surgical patients could fail to sustain adequate PaO2 in patients with respiratory failure. Randomized control trial (RCT) by Baillard et al. confirmed that pre‐oxygenation done by noninvasive positive‐pressure ventilation (NIPPV) prior to TI is superior to that done classically by a bag‐valve mask device for a 3‐min duration [2]. The patients who have been pre‐oxygenated by NIPPV have higher pulse oximetric saturation (98 ± 2 vs. 93 ± 6%) and higher PaO2 values during TI (203 vs. 97 mmHg) and up to 5 min into the post‐intubation period compared with the bag‐valve mask method. In acute respiratory failure, NIPPV improves oxygenation by delivering high oxygen concentration, by unloading respiratory muscle, recruiting alveoli, and thereby increasing the functional residual capacity in such hypoxemic patients. To confirm the endotracheal tube placement after TI, classically chest inspection for bilateral equal expansion and chest auscultation for equal air entry on both sides have been routinely used. Recently, the American Society for Anesthesiology (ASA) has adopted end tidal CO2 monitor as the standard of care inside the operating room. Confirmation of endotracheal intubation by capnography has 100% sensitivity and specificity. Continuous capnography waveform is recommended as well during chest compression for cardiac arrest victims [4]. Esophageal detector device is an alternative carbon dioxide‐monitoring device. The endobronchial intubation must be ruled out by chest radiograph, as a part of post‐intubation care.
Care bundles are the best evidence‐based therapies that could guarantee the best outcomes when applied together than each therapy alone in the bundle. Intubation bundle has been developed to enhance the quality of intubation procedure by setting a package tool to be followed by any provider in any intubation scenario with every patient. This bundle focuses on standardization of the stepwise process and eliminating the individual preferences and technical variability. The bundle involves maintaining cardiovascular stability, gas exchange, and the neurological status while securing the airway. The proposed ICU intubation management protocol includes 10 elements bundle [2].
\nPresence of two persons.
(Normal saline 500 ml or colloid 250 ml) as fluid loading in the absence of cardiogenic causes of pulmonary edema.
Long‐term sedation ready to start.
Pre‐oxygenation for 3 min by NIPPV with the following parameters:
(FiO2 100%, pressure support ventilation level of 5–15 cm H2O, tidal volume of 6–8 ml/kg, and PEEP of 5 cm H2O).
5. Rapid sequence induction: Anesthetic medications include Etomidate 0.2–0.3 mg/kg or ketamine 1.5–3 mg/kg or Propofol‐Ketamine mixture. Muscle relaxants include Succinylcholine 1–1.5 mg/kg or Rocuronium Bromide 1 mg/kg. Succinylcholine is contraindicated in the following condition, hyperkalemia, severe acidosis, acute or chronic neuromuscular disease, burn patient for more than 48 h and spinal cord trauma, otherwise Rocuronium Bromide is preferred.
\n6. Cricoid pressure or Sellick maneuver should be applied.
7. Immediate confirmation of tube placement by capnography.
\n8. Nor‐adrenaline infusion if diastolic blood pressure still low.
\n9. Start long‐term sedation.
\n10. Initial “protective ventilation”: Tidal volume 6–8 ml/kg of ideal body weight, PEEP 5 cm H2O and respiratory rate between 10 and 20 cycles/min, FiO2 100%, plateau pressure <30 cm H2O.
\nStudies showed that the bundle lowered the life‐threatening complications as severe desaturation, hypotension, or cardiac arrest by 21 versus 34%. Other moderate complications have lowered as well (9 vs. 21%) compared with the non‐bundle group [2].
\nTI in emergency settings in unstable patients could lead to an acute airway emergency. The airway morbidity and mortality increase with unstable hemodynamics and failing oxygenation during emergency intubations. That is why tracheal intubation in the ICU may be lifesaving or life threatening. Airway management in a deteriorating sick patient is a real ICU emergency which cannot be delayed. Rescue airway equipment as THRIVE, NIPPV, and tracheostomy should be ready as a backup when difficult airway is encountered. Fewer complications have been noticed when the TI was done by experienced providers. Familiarity with rescue airway techniques is helpful. The rhythm of ICU environment necessitates precise guidelines that are tailored to ICU settings. Hence, implementation of an intubation care bundle along with a pre‐planned approach to difficult airway is essential for safe TI in the ICU.
Particular issues as the need to re‐intubate following a trial of extubation or accidental extubation are common in ICU. Re‐intubation may be unexpectedly difficult in hypoxic, distressed, or uncooperative patients with multiple risk factors and in patients who have been extubated after prolonged intubation as airway edema is common sequela.
Videolaryngoscopy (VL) is an indirect visualization technique for the larynx mainly for the purpose of airway assessment or airway management especially in ICU area. The images from the video can be displayed, magnified, and recorded on a monitor. Video‐assisted visualization has been evolved in airway practice after the pressing clinical need of difficult airway scenario and lack of new tools other than Macintosh/Miller blades. That was invented in 1940. After many years of clinical practice, the VL techniques have been approved by the American Society of Anesthesia (ASA) and incorporated in their difficult airway algorithms. VL is promoted as a first step to go in anticipated difficult airway scenario.
The first choice of elective oral or nasal intubation in adults, pediatrics, or neonates, in case of anticipated and unanticipated difficult laryngoscopy.
Reduces strain and stress of operator during intubation.
Diagnostic and recording of airway lesions, abnormal anatomy, and pathology.
Can be used for TEE probes [5], naso‐gastric tube [6], double lumen bronchial tube [7], and throat‐pack insertion.
VAFI techniques (video‐assisted fiberoptic intubation).
Good teaching tool for junior staff.
Guide the assistant where to apply external laryngeal manipulation: BURP (Backward Upward Rightward Pressure).
Help presbyopic doctors especially in neonatal intubation.
Awake tracheal intubation [8] and in abnormal intubating position as lateral decubitus [9].
Less traumatic over ordinary laryngoscopy.
Reduce the cervical spine mobility in patients with unstable cervical spine or reduced spinal mobility [10].
Many types have been introduced into the market, which has created many dilemmas for the practitioners which one to choose (Table 1). Each VL device is unique in its size, shape, and profile, which gives specific strength and weakness to each. As a dozen devices are being continuously added to the market, it would be challenging and impractical for the anesthesiologists to obtain and train on all of them. Ideal VL should be intuitive, lightweight, low profile, inexpensive, easily maneuverable, easy to learn and master, remote view screen, with memory storage capacity, and long‐lasting rechargeable batteries. Special features are being added as antifog capabilities by heating of the lens. The device should be easily adaptable to different intubation techniques, for example, nasal and oral.
Rigid blades | Guided channels-Automatically shaped | Video stylets | |||
---|---|---|---|---|---|
Standard blade | Angled blade | Channeled blade | Channeled airway | Rigid stylet | Rigid stylet + Flexing tip |
Storz C-Mac | Coopdech VLP100 | AirTraq | Total track (VLM) Video Laryngeal Mask | Bonfils | RIFL |
Storz DCI | Pentax AWS | Shikani optical stylet | |||
McGrath “AIRCRAFT” | Res-Q-Scope II | ||||
GlideScope | |||||
Storz V-Mac | Storz D-Blade | ||||
King Vision | |||||
Venner A.P. Advance | |||||
MedAn |
Summary of different types of VL devices.
The rigid stylets were in practice for the last 25 years to facilitate retromolar intubation. The bending angle is 40o at the distal end with a view angle of 110°. The video RIFL has a rigid rod with a flexible tip to articulate till 135° by closing the lever by a handgrip.
\nThe stylets are advocated when the mouth opening is limited; however, its applicability is restricted to oral intubation. The video stylets are bulky, requiring space in the room, with no antifogging mechanism. It has the longest intubation time among other video techniques and higher learning curve but is very useful in restricted mouth opening using retromolar space. The Shikani optical stylet is a malleable, stainless steel, J‐shaped endoscope with illumination fibers and a fiberoptic bundle that can be used with a separate camera and monitor system, or on its own with an optical eyepiece. Figure 1 shows Bonfils retromolar videolaryngoscope.
Bonfils retromolar videolaryngoscope (Storz‐Company).
The representatives of the family are Pentax and AirTraq. All channeled devices have been designed mainly for oral intubation; however, the recent version of AirTraq has been studied and used in nasal intubation. The AirTraq is a single‐use optical device with optional video camera attachment. It is available in different sizes and could be used for nasal intubation and double lumen tube insertion; however, it is single use and it requires 30–40 s to reduce fogging. Pentax is similar to AirTraq, with the advantage of the only plastic guide blades which are disposable. The tip is angled by 135o and it cannot be used with an endotracheal tube (ETT) less than 6.5, making it impractical for pediatric population. Both Pentax and AirTraq have been proved to reduce the cervical spine mobility in patients with unstable cervical spine or reduced spinal mobility. Res‐Q‐Scope is a similar device, but the clinical studies are so limited.
Rigid blades are classified into standard blade or angled blade. In general, the standard blades use the various modifications of typical Macintosh blades as C‐Mac (Figure 2). However, the angled blades offer more angulations near the distal tip to widen the view angle. In some equipment, as in Coopdech D-scope, sizes of 0,1 and Miller’s blades are available, etc. C‐scope sizes (sizes 0 and 1) Miller blades are available, but in most of the others Macintosh blades sizes 2, 3, and 4 are the standard.
Videolaryngoscopes.
It was shown that the design familiarity with standard Macintosh blades, side screen, and enhanced view has reduced the learning curve for the inexperienced providers.
\nThe main difference among rigid blades is the blade angulation and the position of the side view screen. In Coopdech VLP100, it has a build‐in screen on top of the device with the view angle of 39–52o, with the option of sizes 2, 3, and 4 Macintosh or size 0, 1 Miller blade. The McGrath “AIRCRAFT” is similar to Coopdech VLP100 in having a build‐in side screen over the handle, but different in having adjustable variable length blades that snaps in place once the length is adjusted. The GlideScope (Figure 3) has an angulation of 60o, with antifogging camera, plastic disposable blades, and separate view screen. GlideScope appeared to be the most intuitive, easy to learn with the steepest learning curve [11] but a little bit bulky in relation to C‐Mac blade; that is why most of clinicians prefer C‐Mac over GlideScope. Venner A.P. Advance and MedAn videolaryngoscopes are also available in the market from these VL types but the clinical studies are so limited.
GlideScope (Verathon Inc., US).
In general, not one device has shown to have a 100% success rate and none has shown to be superior to another. All studies concluded that VL offers better laryngoscopic view if not the same as direct laryngoscopy. Most of the studies have concluded that the intubation time is more with videolaryngoscopy than with the direct laryngoscopy. Relative devices were faster than others by few seconds, DCI Storz Videolaryngoscope is relatively faster by 10 s than GlideScope (34 s) and McGarth (38 s); other study showed that the time for intubation for GlideScope was 33 s, CMAC was 17 s, and McGarth was 41 s [12]. Intubation with the GlideScope has been found to be 99% successful after initial failure of direct laryngoscopy, helping to reduce the incidence of failed intubation. It should be noted that the relative learning curves could affect the performance of GlideScope in some studies, as in the study of Platts‐Mills in emergency department, which showed no difference in intubation failure between GlideScope and Macintosh, and intubation time in GlideScope was longer (12 s) [13] (Figure 3).
\nThe main advantage for the videolaryngoscopy is minimal cervical spine mobility during intubation as the pharyngeal and laryngeal axis should not align together, offering least mobility for cervical instability. Moreover, it is helpful in case of limited accessibility, for example, magnetic resonance imaging (MRI) scanning, beach chair position, or prone position. It also allows sharing the airway view with beyond the operator for teaching or assistance purposes (Figure 2).
\nThe devices of VL have been evaluated and adopted for practice outside the operative room.
The most common disadvantages of VL could be variable learning curve that depends on the level of training and experience, difficult passage of tube despite satisfactory laryngeal view, and loss of the depth perception. The fogging and secretion that could obstruct the camera are among other technical issues. Other disadvantage is the cost that could range from 5000 to 10,000$, which could be a burden in some part of the world; however, the cost could be justifiable in the industrialized part of the world if it could prevent such fatal airway events with its subsequent million dollar lawsuits. One study for VL adoption in Massachusetts emergency departments in 2012 has showed that adoption rate for VL was 43%, a relatively fast rate. The 69% of non‐adopters have attributed that to the cost of the device [14].
It is an airway device used for indirect visualization of the airway either for airway management or for other diagnostic and therapeutic purposes. Traditionally, all old scopes have used the fiberoptic fiber technology; however, the newer scopes, out of reliability issues, do not use the fiberoptic technology anymore and that’s why the nomenclature changed to flexible intubation scope.
Flexible intubation scope is a flexible cord that has fiberoptic fibers (old scopes) or optical fibers with a small camera on the tip of the scope using complementary metal oxide semiconductor (CMOS) technology and the so‐called flexible intubation video endoscope (FIVE) from Storz Company. The proximal handle has a working channel port for oxygen and suction, lever to flex or extend the tip and light source. The diameter of adult scope is of 3.8 and 4.2 mm which can hold ETT of 6.5 mm or more. The diameter of children scope is of 2.2 and 3.1 mm which can hold 3 and 4 mm EET, respectively. Both adult and pediatric scopes have working channel of 1.2 mm. Most of flexible intubation scopes are reusable; however, recently a single‐use flexible intubation scope started to be in the market from Ambu Company.
The main indication of flexible scope intubation (FSI) in anesthesia care and ICU settings is to secure the placement of endotracheal tube when there is anticipated airway difficulty and confirmation of tube position after intubation if necessary. It can be used as well in the management of abnormal airway anatomy, obstructive upper airway lesion, and unstable cervical spine to limit the cervical mobility, and the evaluation of airway obstruction is another anesthetic indication as a preoperative assessment (preoperative naso‐endoscopy in pre‐assessment anesthesia clinic) or directly prior to intubation for the patients with known anatomical abnormalities in the upper airway. The choice of the route has its indications as well, as nasal route is used in a case of limited mouth opening or a strong gag reflex, or if the surgery needs nasal intubation. Other indications other than primary anesthetic care involve diagnostic and therapeutic purposes, see Table 2.
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Indications of flexible scope intubation (FSI).
There are no absolute contraindications for the FSI, but in the following situations difficult to impossible scenarios could be encountered. Large airway bleeding and secretions could make the view impossible. The limited clinical experience of the operator, the necessities for rapid airway control, the need to insert the tube under vision to minimize further trauma to the upper airway, and uncooperative patient are other contraindications. However, it is not absolute, as uncooperative patient can be intubated as sleep FSI and the visualization for ETT insertion could be achieved by adjuvant airway as in fiberoptic‐assisted videoscopic intubation (FAVI), a technique, when other indirect visualization technique, as C‐Mac VL (Figure 2), is used to facilitate the insertion of ETT under vision. Nasal route is contraindicated in case of severe craniofacial deformity and skull base fracture.
The preparation step for FSI is the most important step for a successful procedure. It involves patient selection and preparation, airway anesthesia and equipment preparation. The patient selection will determine whether the FSI will be through the oral or nasal route and whether it will be awake or sleep FSI. Generally, the awake has better visualization than the deep, due to loss of muscle tone and pharyngeal collapse after induction of anesthesia.
\nIt starts by good communication with the patient and proper assessment of the underlying condition. Anti‐sialagogues should be applied for all patients whether it is oral or nasal, as secretions do not only affect the view but also limit the action of the local anesthetics. Commonly, it is recommended to use intravenous 0.2 mg glycopyrrolate, 15 min before the procedure. For patients with high risk for aspiration, risk and benefit should be analyzed as airway anesthesia and long intubation time could compromise the airway reflexes and increase aspiration risk. Certain measures have been recommended to minimize that risk: as intubation in head‐up position, administration of 0.3 M sodium citrate 30 ml and Metoclopramide 10 mg or Ranitidine 50 mg within 1 h before the start of the procedure. Patient positioning depends on the technique and patient and operator’s preference as well. Positions could be sitting (beach‐chair), lateral decubitus for awake FSI or supine positions for sleep FSI and prone position as a rescue technique.
\nAirway anesthesia is a critical step in the procedure. It can be done by applying the local anesthetic solutions, gel, or ointment by atomizer, nebulizer, or “spray as you go technique.” Airway anesthesia equipment includes atomizing devices, nebulizers, syringes and needles, and cotton swabs.
\nCombined techniques are always recommended to optimize the outcome. Combination of 4% lidocaine nebulization, atomization spray to tongue, and oropharynx followed by “spray as you go” through the working channel of the scope using epidural catheter are commonly applied together.
\nCautions should be taken not to exceed with the lidocaine dosage above 6 mg/kg to avoid systemic toxicity. Trans‐tracheal local anesthetic infiltration and nerve blocks could be used with a skilled operator but it is not commonly done. Glossopharyngeal nerve block, superior laryngeal nerve block, sphenopalatine nerve block, and anterior ethmoidal nerve block are among the nerves that could be blocked; however, the discussion of each nerve technique will be beyond the scope of this chapter. For nasal anesthesia, vasoconstrictors as 1% phenylephrine or 0.05% oxymetazoline are added to the local anesthetics to minimize nasal bleeding.
\nAirway equipment includes flexible intubating scope, face mask, specialized oral airway, and endotracheal tube, antifogging agent, lubricating agent, nasopharyngeal airway, oral or nasal mucosal atomization device (MAD) and video monitor. All equipment should be checked for functionality before any operation.
Oral intubation is the most common route. Stepwise approach should be followed: as ETT is loaded first to the scope, then oropharyngeal suction before insertion of scope, then applying of bite blocker or fiberoptic plastic airway (e.g., Ovassapian, Williams, or Berman). FSI should always be in the midline till satisfactory view is achieved. The working channel offers a source for suction, oxygen insufflation, or channel for epidural catheter during the procedure.
\nNasal intubation has its advantage in avoiding the gag reflex; however, the chance of epistaxis is high. Topical nasal decongestant such as 0.05% oxymetazoline and 1% phenylephrine should be used to decrease the nasal mucosal irritation and bleeding.
\nAwake intubation necessitates patient cooperation, adequate airway anesthesia; however, sedation may be required. The patient is asked to swallow or breathe deeply and smoothly. Sedation could be titrated on individual basis, based on the underlying comorbidities. Commonly used sedation is Remifentanil infusion starting with 0.05 µg/kg/min or Remifentanil target‐controlled infusion (TCI) mode with or without 1–2 mg Midazolam or Dexmedetomidine 0.3 µg/kg/h with or without Midazolam 1–2 mg or incremental doses of Midazolam 1 mg alone. Propofol TCI is another alternative to Midazolam as a sedative agent.
\nSleep intubation could be done after induction of anesthesia in certain circumstances.
It is important to keep in mind that FSI is a complex clinical procedure with requirements of special skills, which make even good preparation not enough to guarantee the success. Practicing certain adjuvant measures as strategies for enhancing the laryngoscopic view and facilitated ETT insertion could decrease the failure rate. Enhancing the view could be achieved by keeping airway patent by one or more of the following: jaw thrust, pulling tongue out by a gauze, fiberoptic oral airway placement, external laryngeal manipulation, insertion of laryngoscopic blade with lifting the epiglottis away from the pharyngeal wall (VAFI technique), and clearing the lens fogging by gentle touch of mucus membrane. Facilitated ETT insertion aims to minimize a possible trauma from the blind insertion of the tube after the FIS has reached the carina. The facilitation could be done by a 90o anticlockwise rotation of the tube to avoid getting caught at right arytenoid, warming the tube, flexible tube and combination of direct and indirect laryngoscopic technique or using video‐assisted fiberoptic intubation (VAFI) technique.
Flexible intubation scope is unique airway visualization equipment that offers great clinical help, not only in the management of difficult airway scenarios but also in the diagnosis and treatment as well. More details are described under bronchoscopy section.
FSI is a complex procedure with no straightforward steps. To master the technique, it requires a lot of practice with high learning curve. Extra equipments are always necessary; moreover, it requires time for preparation and cannot help in emergency situation. Nasal epistaxis, minor airway trauma as erythema, and vocal cord injury could occur.
Flexible fiberoptic bronchoscopy is frequently used for diagnosis and therapy, performed in ventilated patients via an endo‐tracheal tube or tracheostomy tube in ICU and other critical areas. Indication may be diagnostic or therapeutic (Table 2). The most common indications include clearance of retained secretion, mucous plug, lung collapse, endobronchial brush, removal of blood clot, diagnosis of ventilator‐associated pneumonia by broncho‐alveolar lavage (BAL), trans‐bronchial biopsy, detection of airway lesions (e.g., neoplastic), endobronchial ultrasound (US), and visualization of instruments during percutaneous tracheostomy. Contraindications are relative so each patient should be carefully assessed for risk benefits. Contraindications include uncooperative patient, unstable patient as severe hypoxemia, hypercarbia, unstable asthma, recent myocardial infarction, or any situation of possible serious hemorrhage after biopsy as uremia, tracheal obstruction or stenosis and pulmonary hypertension.
Separate operator should manage airway and ventilation. The bronchoscopist should be prepared to interrupt the procedure immediately if there is destabilization. Patients are pre‐oxygenated, anesthetized, paralyzed, and ventilated on 100% O2. Positive end expiratory pressure (PEEP) should be maintained. Impairment of gas exchange is common due to tube obstruction and when suction is applied through the scope.
\nEndotracheal tubes smaller than 8‐mm internal diameter may be significantly occluded by flexible fiberoptic bronchoscopy and this could impair ventilation and oxygenation. A lubricated swivel (or elbow) connector with a fitted rubber cap prevents loss of ventilation. If pressure‐controlled ventilation is used, peak pressure setting should be increased to compensate for the loss of tidal volume. Suction periods should be limited to 5 s or less. Thick secretions often require instillation of saline (10–20 ml) down the injection port to dissolve them. During broncho‐alveolar lavage (BAL), a sputum trap should be used between bronchoscope and wall suction.
Bleeding dyscrasias: Coagulation studies, platelet counts, and hemoglobin concentration are necessary before the procedure especially when there are clinical risk factors for abnormal coagulation. Bronchoscopy with lavage can be performed with platelet counts of >20,000 per/μl.
Pneumothorax: A chest radiograph should be obtained if a patient is symptomatic or if there is a clinical suspicion of possible pneumothorax after trans‐bronchial biopsy. Patients should be advised of the potential for delayed complications following trans‐bronchial biopsy.
Fever and infection: Antibiotic prophylaxis is not warranted before bronchoscopy for the prevention of endocarditis, fever, or pneumonia.
Ischemic heart disease: flexible fiberoptic bronchoscopy should ideally be delayed for 4 weeks after MI.
Mechanical ventilation can be delivered to the patient who requires ventilatory support either initially through endotracheal tube (ETT) for short‐term period or through tracheostomy tube, in cases where the respiratory support will be prolonged due to underlying medical reasons [15].
\nTracheostomy versus intubation: The relative advantages and disadvantages of tracheostomy and endotracheal intubation are outlined in Table 3 [16–20].
Intubation | Tracheostomy | |
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Advantage |
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Advantage and disadvantage tracheostomy versus intubation.
Tracheostomy techniques: Bedside percutaneous tracheostomy is an alternative to operative (open) tracheostomy, as it could be done either at the bedside or in the operating room. Successful performance of the bedside percutaneous procedure is related to the expertise of the operator and supportive personnel. Surgeons or well‐trained critical care clinicians could do with fewer complications. Choosing between open or percutaneous tracheostomy depends upon the availability of each procedure and institutional expertise.
\nPercutaneous versus operative: Percutaneous tracheostomy offers numerous advantages compared to operative tracheostomy: it requires less time to perform, it is less expensive, and it is typically performed sooner (because an operating room doesn’t have to be scheduled). In addition, overall complications may be less frequent with percutaneous tracheostomy than surgical tracheostomy, even though percutaneous tracheostomy has an increased risk of anterior tracheal injury and posterior tracheal wall perforation.
\nData describing outcomes comparing both techniques are conflicting, which may reflect the different techniques used to perform percutaneous tracheostomy (e.g., ultrasound‐guided, bronchoscopy‐guided, dilatational, other).
Infection: In two meta‐analyses of randomized controlled trials, percutaneous dilatational tracheostomy reduced wound infections (e.g., odds ratio: 0.28, 95% CI: 0.16–0.49) compared to both surgical tracheostomy performed in the ICU and surgical tracheostomy performed in the operating room. A separate meta‐analysis of 29 randomized and non‐randomized studies reported a similar reduction in the rate of wound infection with percutaneous tracheostomy [21].
\nBleeding and mortality: When compared to surgical tracheostomy performed in the operating room, only percutaneous dilatational tracheostomy has also been associated with reduced bleeding (odds ratio: 0.29, 95% CI: 0.12–0.75) and mortality (odds ratio: 0.71, 95% CI: 0.50–1.0). A similar reduction in overall mortality was reported in another 10‐year review of 616 trauma patients that compared those who underwent percutaneous tracheostomy with those who underwent open tracheostomy (10 vs. 15%) [17].
\nBy contrast, another meta‐analysis of 20 trials reported no difference in mortality or major bleeding [18]. In a separate meta‐analysis, perioperative complications (including death, serious cardiorespiratory events, and minor complications) were rare, but more common with percutaneous tracheostomy than with surgical tracheostomy. In another meta‐analysis of 29 studies, no significant difference in bleeding or tracheal stenosis was reported [20].
\nScarring: While one meta‐analysis reported no difference in the rate of tracheal stenosis or scarring, another reported significant reduction on the rate of scarring.
\nTaken together, the data suggest that percutaneous dilatational tracheostomy offers numerous advantages compared to surgical tracheostomy. However, the benefit of percutaneous tracheostomy may be substantially less dependent upon the technique employed.
Relative contraindications to percutaneous tracheostomy include age under 15 years of age; uncorrectable bleeding diathesis; gross distortion of the neck from hematoma, tumor, thyroid gland enlargement, or scarring from previous neck surgery; documented or clinically suspected tracheomalacia; evidence of infection in the soft tissues of the neck; obese and/or short neck which obscures landmarks; and inability to extend the neck because of cervical fusion, rheumatoid arthritis, or other causes of cervical spine instability.
\nIt should be reiterated that these contraindications are relative. Percutaneous dilatational tracheostomy has been performed successfully by skilled operators in patients who were very old, were morbidly obese, had a history of previous tracheostomy, or had thrombocytopenia (the patients received pre‐procedure platelet transfusions). It has also been performed successfully in patients receiving high‐frequency oscillation ventilation or positive end expiratory pressure (PEEP) at a level of >10 cm H2O.
\nA study that evaluated the rates of bleeding complications during percutaneous tracheostomy showed that bleeding complications could be predicted by a platelet count less than 50,000/μl, an activated partial thromboplastin time longer than 50 s, or the presence of two or more coagulation disorders. Administration of prophylactic subcutaneous heparin did not increase the risk of bleeding [18].
\nFor patients undergoing a bronchoscopic‐guided percutaneous tracheostomy, a bedside checklist, similar to that performed for open tracheostomy performed in the operating room, may be associated with reduced procedural complications.
Acute: The most common acute (e.g., first few days) complications include obstruction and pneumothorax as well as postoperative hemorrhage and infection.
\nObstruction: Percutaneous tracheostomy tubes can become partially obstructed by the posterior membranous trachea following initial placement, although symptomatic obstruction is uncommon. This complication appears to be related to the experience of the clinician performing the procedure. However, the swelling of the posterior tracheal wall could cause symptomatic compression of the tube up to 1 week after placement.
\nSubcutaneous emphysema and pneumothorax: The incidence of subcutaneous emphysema and pneumothorax is 1.4 and 0.8%, respectively [19]. Cadaver models revealed that imperfect positioning of fenestrated cannula and posterior wall perforation are possible mechanisms for these complications [19].
\nChronic complications of tracheostomy (i.e., weeks and months) that are specific to tracheostomy include the following:
\nTracheal stenosis: Granulation tissue is the main reason for tracheal obstruction in patients under long mechanical ventilation by tracheostomy, which differs from the stenosis that develops in endotracheal tube that will be appearing earlier and be web‐like. Stenosis of the trachea is not only below the tracheostomy tube, but it may occur above the tracheal stoma but below the glottis. That could contribute to high‐peak airway pressures and difficulty in weaning. Treatment includes the placement of a longer tracheostomy tube, surgical intervention, or the placement of a tracheal stent [20].
Tracheoarterial fistula: Massive hemorrhage due to a tracheoarterial fistula is the most devastating complication. Tracheoarterial fistula (most often a tracheoinnominate artery fistula) was more common in the past from low‐positioned tracheostomy tubes and is now rarely encountered with several studies reporting an incidence of <1% in both short‐term and long‐term tracheostomies [21]. The development of a tracheoarterial fistula is a life‐threatening complication with a reported survival of 14%. Tracheoarterial fistulas are due to erosion from the tube tip or cuff into the anterior wall of the trachea resulting in a fistulous communication with the innominate artery as it passes anteriorly across the trachea. Patients may develop a “sentinel” bleeding followed by massive hemoptysis. Diagnosis is dependent upon a high index of suspicion, and when suspected, immediate action should be undertaken to stop the bleeding since diagnostic modalities such as angiography or bronchoscopy may lead to delay and death.
The following temporizing maneuvers may be performed while waiting for definitive therapy, which is surgical repair [22].
\nIn an attempt to compress the innominate artery, the tracheostomy or endotracheal tube cuff may be overinflated.
If the above fails, an ETT may be placed orally, the tracheostomy removed, and the cuff inflated distal to the tracheostomy site.
If that fails, a finger can be placed through the tracheostomy stoma and positioned distally into the trachea (“The little Dutch boy maneuver”); the finger is then pulled anteriorly to compress the artery against the sternum (pressure should be sufficient to lift the torso anteriorly). Pressure should be maintained during transport to the operating room. Ventilation and oxygenation need to be preserved with a bag‐valve mask or intubation with an ETT orally.
Reduced phonation: Following tracheostomy, many patients experience a reduction in or loss of phonation, the duration of which may be prolonged or indefinite, and the effect of which can be devastating to some patients. Traditionally, speech valves are used in tracheostomized patients (with the cuff deflated) who successfully wean from mechanical ventilation and are able to self‐ventilate. Preliminary data suggest that early phonation is feasible and may be beneficial when instituted during mechanical ventilation in tracheostomized patients. As an example, one randomized trial of 30 ventilated tracheostomized patients reported that early intervention with cuff deflation plus an in‐line speaking valve during mechanical ventilation shortened the time to phonation by 11 days, when compared with late intervention using the standard approach. Further research is needed before in‐line speaking valves can become routine for this population [22].
\nOthers: Tracheoesophageal fistula is more commonly encountered with prolonged endotracheal intubation and is discussed separately.
\nAlthough not studied in a randomized trial, the complication rate associated with tracheostomy may be increased in obese patients with a body mass index of ≥35 [22].
\nChanging a tracheostomy tube: There are no universally accepted indications for changing a tracheostomy tube. Therefore, the following indications are based on clinical experience rather than on empirical evidence:
\nRoutine changes: Tracheostomy tubes are routinely changed from 7 to 14 days after initial insertion and then every 60 to 90 days. Observational data suggest that changing the tracheostomy tube before 7 days may be associated with earlier use of a speaking valve and earlier ability to tolerate oral intake. A consensus statement recommends changing the tracheostomy tube at 3–7 days if inserted operatively but 10–14 days if placed via the percutaneous dilatational method.
\nPatient discomfort: Patient discomfort may respond to a reduction in the size of the tracheostomy tube.
\nMalposition: Tracheostomy tube malposition may respond to a change in the length or size of the tracheostomy tube.
\nPatient‐ventilator asynchrony: Patient‐ventilator asynchrony that is related to the tracheostomy tube may respond to changing the tube.
\nCuff leak: A cuff leak may be due to malposition of the tracheostomy tube (particularly in the setting of tracheomalacia) and may respond to changing the tube.
\nFracture: Fracture of the tracheostomy tube or flange is an indication for a new tracheostomy tube.
\nType change: Changing a tracheostomy tube from one type to another may be indicated by the clinical circumstances; as an example, changing from a balloon cuff to either a foam cuff or a cuff‐less tracheostomy tube.
\nBronchoscopy: Flexible bronchoscopy generally requires a tracheostomy tube with an inner diameter of at least 7.5 mm; thus, the tracheostomy tube may need to be changed to one with a larger inner diameter to facilitate bronchoscopy.
\nDecannulation: Appropriate candidates for tracheal decannulation after weaning from mechanical ventilation include patients who fulfill all the following criteria:
\nNo upper airway obstruction, ability to clear secretions that are neither too copious nor too thick, and presence of an effective cough. In patients with neuromuscular disease, a peak cough flow greater than 160 ml/min generally predicts successful decannulation. The value of this measurement in patients without neuromuscular disease is unknown.
\nFailed decannulation has been associated with age, greater severity of illness, the presence of renal failure, and a shorter duration of spontaneous breathing prior to decannulation or the insertion of a tracheostomy plug.
The removal of endotracheal tube (ETT) termed as extubation is the last step of ventilatory weaning. Extubation step necessitates consideration of patient condition, experience with extubation techniques, and post‐extubation management.
\nBefore extubation: Successful weaning from mechanical support is not the only prerequisite for safe extubation. Extubation is carried on patent airway with adequate airway reflex after independence from ventilatory support.
\nAirway protection: Airway protection requires a conscious patient with a strong cough reflex and minimal secretions.
\nTypical criteria for successful weaning: Fully awake and cooperative, good muscle tone and function, intact bulbar function, stable hemodynamic, no dysrhythmias, Hb greater than 8.0 gm%, minimal inotropic requirements, optimal fluid balance, respiratory FiO2 < 0.4, PEEP < 10 cm H2O, no significant respiratory acidosis (PH > 7.3 or PaCO2 <6.5 kPa), good cough, normal metabolic pH, normal electrolyte balance, non‐distended abdomen, adequate nutritional status, normal CO2 production, and normal oxygen demands [23].
\nSome patients will be extubated without difficulty and others will rapidly deteriorate as a result of inadequate respiratory effort or clearance of secretions. Those patients will require re‐intubation, ventilation, and another period of optimization and consideration for tracheostomy. Some patients will benefit from weaning straight onto mask CPAP or NIV [23].
\nDifficult extubation: Extubation of a patient with a known difficult airway requires careful planning in anticipation for potential re‐intubation. If there are doubts about airway patency prior to extubation, then direct laryngoscopy, fiberoptic bronchoscopy, and assessment of leak upon cuff deflation are useful checks. Patients who are considered likely to be difficult to re‐intubate can be extubated with an airway exchange catheter in situ, to allow rapid re‐intubation. Intravenous dexamethasone, nebulized adrenaline, and Heliox have been used with variable success in such circumstances.
\nRisk factors for extubation failure are peak expiratory flow rate (PEFR) of ≤ 60 L/min, sputum volume production of > 2.5 ml/h, and compromised neurological status. Combination of three risk factors reliably predicts extubation failure by 100% compared to 3% if no risk factor mentioned above is present [24].
\nPost‐extubation management: Post‐extubation care includes suctioning, bronchodilator therapy, diuresis, or noninvasive ventilation (NIV). Those measures could aid to prevent re‐intubation by improving the oxygenation and airway clearance.
\nOxygen (including high‐flow nasal cannula (HFNC)): Every patient should be oxygenated post‐extubation. We prefer using devices that provide adequate oxygenation and comfort for the patient. For most patients, this goal is achieved with low‐flow devices (nasal prongs, simple, or venturi face masks). When higher flows of oxygen are required, high‐flow nasal cannula (HFNC) may offer improved oxygenation, provide a small amount of positive end expiratory pressure (PEEP), and is better tolerated when compared with oxygen delivered through low‐ or high‐flow face masks.
\nThe efficacy of HFNC in the post‐extubation setting was best illustrated in a trial of 527 patients who were mechanically ventilated for an average of only 1–2 days and considered to be at low risk for re‐intubation following extubation. Compared to conventional low‐flow oxygen therapy, HFNC reduced the rate of re‐intubation at 72 h (5 vs. 12%) as well as the rate of respiratory failure (14 vs. 8%). However, methodologic flaws such as imperfect blinding and the high proportion of postsurgical and neurologic patients, where HFNC may have improved secretion clearance, may have biased results in favor of HFNC. Although encouraging, this trial does not support the routine use of HFNC following extubation [25].
\nIn addition, while further studies are required to clarify who benefits the most from HFNC after extubation, its use in those who are severely hypoxemic is appropriate (e.g., partial arterial pressure of oxygen/fraction of inspired oxygen ratio <300). Further details regarding HNFC in other medical and postoperative populations and efficacy compared with NIV in post‐extubation patients are discussed separately.
Different names and descriptions of this therapy:
\nHFNC: High‐Flow Nasal Cannula.
\nTHRIVE: Transnasal Humidified Rapid Insufflation Ventilatory Exchange.
\nPOINT: Perioperative Oxygenation Insufflatory Nasal Therapy (Figure 4).
High‐flow nasal cannula (HFNC) (Aqua VENT FD 140® from Armstrong Medical Company, Northern Ireland).
Or transnasal insufflation or nasal high‐flow or nasal high‐flow ventilation or high‐flow therapy or high‐flow nasal cannula oxygen therapy.
\nHFNC oxygen delivery system involves a mixture of oxygen/air, an active humidified, heated circuit, and nasal cannula. The active heater and humidifier are able to deliver heated and humidified high flow reaching 60 L/min than has many physiological advantages. High flow is able to reduce dead space by maintaining PEEP inside the airway and supplying constant fraction of oxygen. In spite of limited evidence in literature in ICU, it has gained popularity among physicians in various critical conditions. The existing evidence in neonates proves that HFNC decreases the work of breathing by reducing the respiratory rate and sufficiently supports the patient ventilation, reducing the escalation of ventilator support [26].
\nAs the evidence is still evolving, still the indications and contraindications should be considered for each case individually.
Hypercapnic respiratory failure.
Hypoxemic respiratory failure.
Post‐extubation.
Pre‐intubation oxygenation.
Sleep apnea.
Acute heart failure.
Bilateral nasal blockade as postnasal operations.
Nasal bleeding.
Nasal tumors.
Nasal infection.
It is also unlikely that HFNC can readily rescue those patients who have total airway obstruction and its use in the presence of a known or suspected cranial base fracture is also not advised.
Better tolerated in some patients than face masks.
Fixed performance, permitting accurate delivery of up to 100% oxygen in most clinical situations.
Gas is warmed and humidified.
Low‐level positive airways pressure is possible.
An additional benefit is that nasal high‐flow devices have been shown to produce positive airway pressures of over 5 cm H2O, thus permitting their use in place of low‐level CPAP [26].
It is an open system and we do not have to care about the tight contact of interfaces, and HFNC can be applicable to patients with claustrophobia.
Results of large‐scale clinical trials are still awaited.
More expensive than standard oxygen delivery devices.
Not yet available in all hospitals, and rarely outside of critical care.
Airway management in the critical care is challenging and differs from the operating theatre. The supra‐glottic airway devices (SGADs), especially the laryngeal mask airway (LMA), provide a fast and lifesaving way in the critical events.
Can solve “Cannot Intubate, Cannot Ventilate” (CICV) scenario.
Passing a Bougie through it, then intubation over a Bougie or using an Aintree Intubating Catheter (Cook Critical Care, Bloomington, IN, USA).
Bronchoscopy through LMA.
Used as an airway while performing a tracheostomy.
Ventilation during cardiac arrest instead of an ETT, if no skilled staffs are available.
Minimal skills requirements to use an LMA.
No muscle relaxant is required.
No contact with vocal cords, less irritating than ETT.
No guarantee for a good airway, as the tip may fold on itself blocking the airway.
No good seal with no protection from aspiration.
Intubating through the LMA could be problematic. As it has shown that the LMA opening sits perfectly above the cords only in 45–60% of the time [27]. This means almost half of the time the LMA is directing the ETT away from the cords. The situation is worse in difficult airway as the provider was perfectly capable of shoving the tube the wrong way without any help.
Experts have recommended the use of LMA in a “Cannot Intubate, Cannot Ventilate” (CICV) scenario while waiting for a better airway. It has shown that LMAs have saved lives in such situations [28].
The dilemma of LMAs not offering a good seal has no effect on clinical outcomes. Risk of aspiration has never been demonstrated, even with the old generations of LMA [29].
No difference between the LMA and routine bag‐mask and ETT anesthesia [29]
Using the LMA as an airway while performing a tracheostomy has no sufficient evidence in the literature. There is no difference in the rate of complications, but the tracheostomies involving LMAs seemed to be quicker, may be due to less time to adjust the ETT cuff above the cords [30].
Mostly due to a cuff leak.
The need for a different endotracheal tube (ETT) size as when smaller one is needed in patients with vocal cord edema or larger ETT for flexible bronchoscopy procedure.
Change of special types of ETT like reinforced or double lumen to ordinary ETT.
However, exchanging the ETT may be life‐threatening and lead to
\nEsophageal intubation.
Loss of the airway.
Severe hypoxia.
Cardiac arrest.
The risk may be more in those with a difficult airway or those with poor cardiopulmonary reserve.
The ideal way for ETT exchange has not yet been studied. Experienced team with advanced airway skills should be consulted priorv to ETT replacement.
\nThe ETT placement can be done under direct laryngoscopy or indirect laryngoscopy with or without a Bougie guide. The initial airway assessment by direct laryngoscopy will determine which tool should be used. When a good laryngeal view is obtained by direct laryngoscopy, ETT can be introduced safely; however, in difficult laryngeal view, video laryngoscopy should be sought. Intubation medications are recommended to be used as well in tube exchange. Video laryngoscopy has been shown, compared with historical controls, to reduce the number of attempts at ETT exchange, with fewer complications including hypoxemia, esophageal intubation, bradycardia, and need for rescue airway device intervention [31].
Virtual endoscopy (VE) (Figure 5) is a noninvasive technology by which two‐dimensional (2D) or three‐dimensional (3D) images are reconstructed by computer software from high‐resolution computed tomography (CT) scan (Figure 6). Virtual bronchoscopy was initially reported in 1993, but it was modified in 1996 to be used in virtual laryngoscopy. The virtual images reconstructed by software have comparable quality of fiberoptic views with sensitivity of 100% to detect upper airway lesions [32, 33]. The novel application of virtual laryngoscopy is eminent in the assessment and staging of upper airway lesion, comprehensive preoperative airway assessment, and planning of complex reconstructive upper airway surgeries. The “fly‐through” reconstructions provided accurate and comparable images to fiberoptic bronchoscopy, which provided valuable information for the evaluation of the airway passages in a step forward prior to going to the difficult airway management (Figure 5). The utilization of the 3D imaging package is now commercially available within the workstation delivered by the different vendors worldwide, to obtain 3D models of the airway. This approach will be the added value and advantage that most anesthetists and intensive care physician would be able to use this technology to construct VE images of the airway from existing CT images and find them easy to interpret (Figure 7).
Virtual endoscopic evaluation of the air way. The vocal cords are well demonstrated. The accompanied reference images in axial, coronal, and sagittal planes with the virtual endoscope are noted, and its apex represents the eyepiece while the base represents the virtual lens.
Curved MPR multi‐planar reconstruction of the airway showing the entire airway in single plane from the nares down to the trachea allowing accurate measurement and orientation of the airway caliber at the different levels.
Lateral projections of the SSD‐shaded surface display using volume‐rendering techniques for the airway. SP: sphenoid sinus; NS: nasopharynx; VC: vocal cord.
This state‐of‐the‐art technology has a promising future value in airway management for both anesthesiologists and intensivists as they will be able to easily interpret the airway images by noninvasive way (Figure 8).
Antero‐posterior (AP) curved MPR multi‐planar reconstruction of the airway showing the entire airway in single plane from the nares down to the trachea allowing accurate measurement and orientation of the airway caliber at the different levels. MS: maxillary sinus; V: vallecula; PS: piriform sinus.
Ultrasound (US) examination of the upper airway in critically ill patients supplies a number of attractive advantages compared with competitive traditional imaging techniques or endoscopy. It is widely available, portable, repeatable, relatively cheap, pain‐free, safe, and bedside machine in every operating theater and ICU suite.
Locate the anatomy of major vessels and the thyroid gland in relation to tracheostomy site [34].
Localize tracheal rings and cricothyroid membrane (Figure 9).
Identify midline, puncture site for percutaneous tracheostomy.
Checking of endotracheal intubation and detection of esophageal intubation [34].
Estimation of gastric content [35].
Recognize the air‐tissue border from tongue to mid‐trachea and at the pleural level [36].
Localize the trachea by combining palpation of the sternal bone with US.
Identify the “string of‐pearls” sign that identifies the tracheal rings and mark the cricothyroid membrane as part of difficult airway management skills [34].
Recognize sonographic evidence of lung movement during respiration and exclude a pneumothorax [34].
Recognize endobronchial intubation and one‐lung ventilation [36].
Ultrasound images of larynx and trachea rings.
The airway competence in ICU should be coping with the rapidly evolving advances in airway management. Therefore, efforts should be focused on the three pillars of airway mastery: airway providers as intensivists or critical care physicians, equipment, and operational plans. Not all institutions can afford all airway equipment in the market; however, they should make sure that critical care providers have a full access to the available tools and they are comfortable using it. Educational sessions and refresher courses should be tailored to meet the competence level of the ICU providers and equipment availability. Operational plan includes developing institutional airway protocols and implementing difficult airway guidelines. The protocols should consider different staffing models of ICU and make sure all the time at least one member of the team with the highest experience in airway should be always available.
Airway management in intensive care patients may be lifesaving or life threatening.
Maintenance of patent airway, adequate ventilation, and pulmonary gas exchange are very important in critically ill patients. Airway management in intensive care patients differs significantly from routine surgical procedures in the operating room.
Critical care physicians should be familiar with the equipment and the techniques to maintain and secure the airway.
Maternal infections during pregnancy can have a direct impact on the developing fetus and in some infections can result in fetal demise. It is extremely important to screen women for infections when it is available and practical and to treat when necessary. The current screening tests recommended by the American College of Obstetricians and Gynecologists include rubella, hepatitis B, hepatitis C, human immunodeficiency virus (HIV), Group B streptococcus (GBS), tuberculosis and sexually transmitted infections including syphilis, chlamydia, and gonorrhea if risk factors are present [1]. The incidence of congenital infections in infants varies, with syphilis increasing dramatically from 639 cases in 2016 to over 1300 cases in 2018 in the United States [2]. Additionally, congenital cytomegalovirus, varicella zoster virus and herpes simplex virus diagnoses have increased over the last five decades [3]. Rubella has decreased since the introduction of Rubella immunization; prior to utilization of the immunization, over 100,000 infants were born worldwide with congenital rubella syndrome (CRS). By 2014, a 95% decrease in cases of CRS was observed in countries that followed the immunization schedule [4]. Thus, it is critically important that research efforts continue to prioritize the development of immunizations and treatments plans for all viruses that can result in congenital fetal infection in an attempt to minimize the substantial long-term morbidities that result.
Chorioamnionitis is the term that has been used for decades to describe infection and/or inflammation of the chorion, amnion, or both. This has been further delineated into a “clinical” diagnosis based on maternal symptoms, and a “histological” diagnosis based on the pathology of the placenta following delivery. Clinical signs and symptoms are used to diagnose clinical chorioamnionitis, and include maternal fever, uterine fundal tenderness, maternal and/or fetal tachycardia and purulent amniotic fluid [5]. The most common bacterial organisms to cause chorioamnionitis are Ureaplasma urealyticum and Mycoplasma hominis. Histological chorioamnionitis is diagnosed by observing neutrophil infiltration into the chorion and amnion [6]. The variation in the definition of chorioamnionitis has resulted in confusion in neonatal management as well as difficulty in assessing the long-term impact of chorioamnionitis on development. Therefore, intra-amniotic infection (IAI) has been developed to replace the prior diagnosis of chorioamnionitis [7].
IAI was updated in 2017 by the American College of Obstetricians and Gynecologists into three categories which are readily diagnosed. Isolated maternal fever (IMF) is the first category, in which the mother has a single intrapartum temperature of ≥39.0°C or a temperature of 38.0–38.9°C that persists for 30 min, with treatment recommendations including the consideration of broad-spectrum antibiotics [7, 8]. Given the numerous potential causes of maternal fever, the utilization of antibiotics is at the providers’ discretion. Suspected IAI is diagnosed when the mother has an elevated temperature (≥39.0°C) or a slightly elevated temperature (38.0–38.9°C) along with one of the following risk factors: maternal leukocytosis, purulent cervical drainage or fetal tachycardia [7, 8]. Confirmed IAI is diagnosed with a positive amniotic fluid test or placental pathology demonstrating histologic evidence of infection [7]. Similar to the previously used histological chorioamnionitis, a criticism of this diagnosis is that it is made after the clinical situation has resolved, and thus does not aid in the acute management of the mother or the infant. Both suspected and confirmed IAI diagnoses should result in treatment with intrapartum antibiotics and antipyretics [7].
IAI is present in nearly 50% of very early preterm birth [9], after which multiple complications can occur and a wide array of neonatal morbidities and mortalities are observed. This has led to speculation that IAI is directly impacting the fetal and neonatal development and outcomes, as well as potentially resulting in preterm birth, which then impacts development and outcomes. The majority of studies that have investigated this question utilized diagnoses of chorioamnionitis, which included both clinical and histological cases. Given the variation of diagnoses included in these studies, it is not surprising that the results have also been varied. A large study of 2390 extremely preterm infants (born <27 weeks’ gestational age) from sixteen centers across the United States found infants exposed to histological and clinical chorioamnionitis had an increased risk of cognitive impairment at 18–22 months’ corrected age [10]. A separate study of 350 infants found that while gestational age was significantly lower among those with exposure to histological chorioamnionitis, there was no association with intraventricular hemorrhage, white matter injury around birth, or differences in cognitive or motor outcomes at 18–24 months’ corrected age [11]. Additional studies have found weak causal or associative roles of chorioamnionitis with cerebral palsy risk [12] and no increased risk of white matter injury on magnetic resonance imaging (MRI) following histological chorioamnionitis in premature infants [13]. Additional investigation is required with the new IAI definitions to determine if there are consistent findings with developmental outcomes in those diagnosed with IAI.
TORCH infection is a mnemonic that has classically been used to describe congenital infections that can impact fetal development. In the past, TORCH represented Toxoplasmosis, Other (syphilis, varicella-zoster, parvovirus B19 and newer pathogens such as Zika), Rubella, Cytomegalovirus and Herpes Simplex Virus. However, as more pathogens are being discovered and the “other” category is expanding, some experts feel the mnemonic is not as relevant today.
Toxoplasma gondii is an obligate intracellular protozoan which typically causes mild illness in most immunocompetent individuals [14, 15]. While a large portion of infected children and adults are asymptomatic, Toxoplasmosis is considered one of the major causes of death linked to foodborne illness in the United States. If an immunocompromised individual, pregnant woman, or fetus/infant acquires the infection, there can be severe, even fatal, consequences [14, 15]. Illness can range from non-specific systemic symptoms such as fever, lymphadenopathy and hepatosplenomegaly to congenital toxoplasmosis (CT), which is classically described as a triad of chorioretinitis, intracranial calcifications and hydrocephalus. CT can lead to loss of vision and hearing, decreased cognitive function, and neurodevelopmental delay if untreated [14, 16–18].
T. gondii exists in three forms: tachyzoite, bradyzoite, and sporozoite. The definitive hosts are members of the Felidae family, but warm-blood mammals can also serve as intermediate hosts [17]. Felines can acquire T. gondii through the ingestion of tissue cysts containing bradyzoites in infected prey or through the ingestion of oocysts containing sporozoites in anything contaminated with feces from an infected cat. They can excrete un-sporulated oocysts in their stools 3–30 days after infection and can shed for 7–14 days. If in the right climate (such as warm and humid), the oocysts can sporulate for 1–5 days, after which they can remain infectious for years. If the tissue cysts found in intermediate hosts or the sporulated oocysts are ingested by humans, they transform into active tachyzoites. The tachyzoites then primarily infect the central nervous system, eyes, musculoskeletal system, and placenta by infecting nucleated host cells to bypass the blood brain barrier and placental barricade. Incubation is 7 days with a range of 4–21 days [14, 15, 18].
For pregnant women who have an acute infection with T. gondii, the timing can be crucial and dictates the treatment course. Typically, the earlier in pregnancy that acute infection occurs, the lower the rate of transmission to the fetus. Unfortunately, there is an increased severity of illness if transmission occurs earlier in the pregnancy [14, 15]. The reverse is true for infection later in pregnancy (such as during the third trimester), during which there is a high rate of transmission but with less severe illness in the fetus.
The diagnosis of primary or latent infection is made primarily using serologic tests. Toxoplasma-specific Immunoglobulin G (IgG) and Immunoglobulin M (IgM) can be performed routinely at non-reference laboratories. Any positive IgM results are then submitted to reference laboratories that can perform additional testing for confirmation [18]. If a pregnant woman is found to have acute infection, then an amniocentesis can be performed, and the fluid can be sent for polymerase chain reaction (PCR) testing. If the PCR is negative and the fetus is believed to have not acquired the infection, the next best step is treatment in the mother with spiramycin in an attempt to prevent transmission [14, 15, 17, 18]. If, however, the fetus is thought to be infected, then the mother is started on a combination of pyrimethamine, sulfadiazine, and folinic acid. Spiramycin, a primarily bacteriostatic macrolide that has activity against some gram-negative and gram-positive organisms as well as some spirochetes, is unable to cross the placenta whereas the combination of anti-parasitic medications can cross the placenta and thus can aide in treatment of the fetus [18, 19]. The combination is also used for fetal infection confirmed at or after 18 weeks of gestation or maternal infection acquired during the third trimester [14, 17, 18]. As untreated CT can lead to fetal demise or death within the first few days of life, and chorioretinitis can develop in a significant proportion of infants whose mothers were untreated, it is imperative to diagnose and start treatment in a timely manner [18].
Once an infant with suspected CT is born, he or she should be thoroughly examined and evaluated. Serologies, a complete blood count (CBC), hepatic function tests, blood PCR, urine PCR, cerebrospinal fluid (CSF) PCR, and CSF studies including glucose level, protein, and cell count, should be sent [18]. The newborn should also have ophthalmologic, auditory, and neurologic evaluation including imaging of the brain [18]. Infected infants should receive treatment regardless of any clinically apparent symptoms, as a large proportion of infants with asymptomatic CT at birth go on to develop visual/hearing impairment, learning disabilities, and psychomotor delay [15, 16, 18, 20]. Treatment consists of the same anti-parasitic combination of pyrimethamine, sulfadiazine, and folinic acid [18, 19]. If CSF studies show an elevated protein concentration (greater than 1 g/dL) or there is evidence of severe chorioretinitis, then a corticosteroid such as prednisone is added until there is a decrease in protein concentration in the CSF or resolution of severe chorioretinitis [15, 18, 19]. Treatment is continued at least though 12 months of age, with consideration of shorter treatment duration for infants who remain asymptomatic for the first three months of life [18, 19]. For those infants who are asymptomatic with positive Toxo-specific IgG but negative IgM and Immunoglobulin A (IgA), there should be repeat IgG testing every four to six weeks until disappearance of IgG. There is no clear consensus on the treatment of these infants [18, 19].
Studies looking at the outcomes of infants with CT have shown significantly better neurologic and developmental outcomes in those that were treated than those who were not [21]. It is important to note that compared to their uninfected siblings, the children that received treatment had a lower level of cognitive function though there was no deterioration over time. In terms of ophthalmologic outcomes, it was found that when followed up to 22 years of age, new ocular lesions could be detected in adolescence which points to the importance of continued ophthalmologic evaluation.
Treponema pallidum, a thin, motile spirochete, is the organism that causes syphilis [18], a sexually transmitted infection that can also result in congenital infection to a fetus. While there was initially a decline in the cases of syphilis observed in the United States in 2000–2001, an alarming resurgence has recently been noted. There has been an increase of 72% in the number of reported primary and secondary cases in the United States from 2013 to 2017, with the number of congenital syphilis cases increasing more than 150% from 2013 to 2018 [22–24]. It is thought that the increase in methamphetamine use, having sex with a person who injects drugs, injection drug use and heroin use are the primary factors that are leading to this dramatic increase in syphilis cases [22, 25].
Acquired syphilis is typically divided into three stages: primary, secondary and latent. During the primary stage, painless indurated ulcers form on the skin or mucous membranes of the areas exposed and heal spontaneously in a few weeks. The secondary stage, typically 1–2 months after the primary stage, is characterized by a maculopapular rash that typically includes the palms and soles, lymphadenopathy and mucocutaneous lesions including condylomata lata [18]. Finally, the latent stage occurs when there are no clinical signs or symptoms of infection, but an individual remains seroreactive [18]. T. pallidum can infect the central nervous system (CNS) during any stage, resulting in neurosyphilis. Transmission to the fetus during pregnancy can occur at any point, with primary and secondary syphilis having the highest rates of transmission at 60–100% [18].
It is recommended that all women be screened for syphilis early in pregnancy with a nontreponemal test, with repeat testing later in pregnancy for high risk individuals. These tests include the Venereal Disease Research Laboratory (VDRL) slide test and the rapid plasma reagin (RPR) test [18]. These nontreponemal tests utilize an antigen that reacts in the presence of antibodies (to syphilis). However, given that the antigen is not specific for syphilis and is a component of cell membranes, false positives may result from other infections including varicella and measles, or by tissue damage observed in connective tissue disease and even pregnancy itself [26]. Therefore, a positive nontreponemal test should be followed by a confirmatory test such as fluorescent treponemal antibody absorption (FTA-ABS) or T. pallidum particle agglutination (TP-PA) tests. Additionally, any person found positive for syphilis based on screening and confirmatory testing should also be screened for human immunodeficiency virus (HIV) given the high rate of co-infection.
Treatment for syphilis is parenteral penicillin G; if an individual is allergic to penicillin G, they should undergo desensitization due to the lack of proven efficacy of alternative agents in this setting. Lack of treatment during pregnancy can result in stillbirth and neonatal death in nearly 40% of women with primary and secondary stage disease, 40% of infants being infected and only 20% of infants being healthy and uninfected [27]. Additionally, fetal infection can result in anemia, hepatomegaly and hydrops [24]. Treatment of the infant should not be delayed, as early treatment may prevent neurologic sequelae [24].
A serological diagnosis is made on the infant if the nontreponemal titer (VDRL or RPR) is fourfold higher than that of the mother (both samples should be obtained around the same time), if the nontreponemal titer persists or increases after birth, or if the treponemal antibody titer (FTA-ABS or TP-PA) remains positive at 12–18 months of age. The choice of test on the infant is dependent on the test that the mother had received, as the titers will need to be compared [18]. A complete evaluation, including complete blood cell count (CBC), liver function tests, obtaining cerebrospinal fluid (CSF) to test for VDRL reactivity, ophthalmologic examination and long-bone radiographs to assess abnormal ossification, radiolucencies or dislocation of epiphyses is then needed [28]. Neuroimaging should be considered if there are any concerns for central nervous system involvement [18]. Ten days of treatment with parenteral penicillin G is typically used in infected infants, with close follow up required. Titers should be repeated by 3 months of age and noted to be declining, with nonreactivity noted by 6 months of age [28]. If the mother received appropriate treatment that was administered >4 weeks before delivery, and the infant has a normal physical examination with the titer equal to or less than fourfold the maternal titer, then no evaluation is recommended. However, inadequate treatment in the mother should result in evaluation of the infant and treatment with penicillin G for 10 days [28].
Clinically, nearly half of infants do not have any apparent signs of infection, although bone lesions and hematologic and hepatobiliary abnormalities may be present, with hepatomegaly one of the most common findings [24, 29]. Infants that develop symptoms may have rhinitis in the first week of life, in which persistent white discharge (“snuffles”) occurs which contains spirochetes [29]. Additional symptoms can include generalized lymphadenopathy and a maculopapular rash [29]. Long term outcomes of infants not appropriately treated can include sensorineural hearing loss, interstitial keratitis, secondary glaucoma, corneal scarring, vision impairment, Hutchinson teeth (smaller teeth that are widely spaced with notches), saber shins (sharp anterior bowing of the tibia), frontal bossing, saddle nose, gummas (soft, non-cancerous growth) and scarring [29]. Life-long disabilities can occur in congenital syphilis infections if infants are not appropriately screened and treated [28].
Varicella-zoster virus (VZV) is a herpesvirus that is transmitted by respiratory droplets, direct contact with skin lesions, and transplacentally during pregnancy [30]. Infants that are exposed to VZV during the last few weeks of pregnancy may develop neonatal varicella which can be quite severe; congenital varicella syndrome (CVS) develops in infants exposed during the pregnancy, with the risk being highest if the exposure occurs in the first trimester [30]. Infants exposed after 20 weeks’ gestation only have about 2% chance of developing CVS [31]. Infants with CVS most commonly have skin lesions in a dermatomal distribution followed by neurologic defects, eye disease and skeletal anomalies [31]. Neurologic defects can include cerebral cortical atrophy and ventriculomegaly. Unfortunately, CVS is fatal in about 30% of cases within the first month of life [32].
The monovalent vaccine approved in 1995 and the quadrivalent vaccine introduced in 2005 have impacted the prevalence of congenital infection as seroprotection is nearly 100% after 2 doses of the vaccine [18]. Thus, at this time, CVS is considered an extremely rare disorder.
Human parvovirus B19 is a nonenveloped, single-stranded deoxyribonucleic acid (DNA) virus with humans as the only host [18]. The virus replicates in erythrocyte precursors and is transmitted via respiratory tract secretions, exposure to blood or blood products, and vertically [18]. While it often causes a mild respiratory tract infection with a “slapped cheek” rash, it can be lethal to a fetus, with the risk of death being as high as 10% [33]. The incidence of parvovirus B19 infection during pregnancy is 3–4%, with the transplacental transmission rate approaching 30% [34]. Fortunately, approximately 50–75% of women of reproductive age are immune to parvovirus B19 [35]. The timing of infection during pregnancy does alter the risk of fetal death, with first trimester infections resulting in up to 71% risk of fetal loss [34]. The difficulty in diagnosing the virus during pregnancy arises in the lack of symptoms that most adults experience, and as many as 70% of women would have no symptoms if infected during pregnancy [34]. Arthropathies are one of the most common symptoms and should raise suspicion for possible infection [34]. Additionally, the presence of fetal ascites or pericardial effusions on ultrasound should trigger high suspicion as well [33].
Fetal hydrops, or abnormal accumulation of fluid/edema in two or more compartments, is common in the setting of Parvovirus B19 infection, with a meta-analysis finding a 9.3% pooled incidence, as well as an increased risk of fetal loss, spontaneous abortion and stillbirth [36]. Parvovirus B19 is among the most common causes of non-immune fetal hydrops, and while spontaneous resolution of infection can occur, only about 5% of cases with hydrops will show spontaneous resolution of the infection with disappearance of hydrops on follow up ultrasounds [37].
Severe anemia and thrombocytopenia occur in utero following parvovirus B19 infection, along with myocardial dysfunction [38]. These factors together are likely the etiology of the fetal hydrops. In utero transfusions (IUT) are often necessary and reduce mortality rates when compared to expectant management. A meta-analysis found IUT was performed in 78% of hydropic fetuses compared to 29% of non-hydropic fetuses, with the difference likely due to the hydropic fetuses at higher risk of demise [37]. Complications may occur in up to 5% of cases, especially if the fetus is likely more sensitive to vascular overload [38]. Thus, intrauterine exchange transfusions (IUET) have also been attempted in cases of fetal hydrops in the setting of parvovirus B19 infection. Unfortunately, thus far it results in similar survival rates as IUT and does not seem to be clinically superior as a treatment modality [38].
Longer-term testing reveal abnormal neurodevelopment following intrauterine parvovirus B19 infections in those also diagnosed with hydrops. Brain abnormalities including parenchymal calcifications, venous infarction, arterial infarction, cerebellar hemorrhage, and cortical malformations including diffuse cortical dysplasia and polymicrogyria have been described in congenital parvovirus infections [39]. If there are no abnormalities on imaging and hydrops resolves prior to delivery, one study found normal neurodevelopment in survivors at 1- and 5-year follow-up [40]. While the overall risk of mortality and morbidity are high, there is the potential for a normal outcome in select cases of congenital parvovirus infections.
Zika virus, ZIKV, is an emerging flavivirus that first became apparent internationally after Brazil declared a national public health emergency in 2016 followed by the World Health Organization declaring the outbreak a public health event of international concern [41]. The virus was first identified in 1947 in Uganda, after which cases of human infection have been infrequent and fairly localized [41]. ZIKV is transmitted by infected Aedes spp. mosquitoes, sexual contact and blood transfusions [42]. Around 80% of ZIKV that occur in adults are asymptomatic, with other cases having a mild febrile illness, headache, rash, fever and conjunctivitis [42]. However, severe neurologic sequalae can also occur in adults.
Congenital Zika syndrome (CZS) is variable in the presentation and severity with only a subset of infants that were exposed having apparent signs and symptoms at birth [41]. Infants exposed to ZIKV in utero are expected to survive, however a severe phenotype can result, particularly when exposure occurs in the first trimester [43]. ZIKV replication in brain tissue can continue after birth, and thus infants that are initially asymptomatic may develop symptoms within the first year of life [41]. The phenotype of CZS appears to consist of severe microcephaly and possibly a partially collapsed skull, thin cerebral cortices with subcortical calcifications, macular scarring, congenital contractures and marked early hypertonia [41]. Microcephaly is the most common symptom, occurring in up to 91% of CZS, and is often severe with the mean occipitofrontal head circumference falling 3–4 standard deviations below normal [43]. Both the central and peripheral nervous systems are impacted, with resultant effects on musculoskeletal, auditory and ophthalmologic systems and symptoms including conductive hip dysplasia, abnormal posturing of extremities, conductive hearing loss and abnormalities of the retina and optic nerve [43]. Up to 55% of infants with CZS have structural ocular abnormalities, making visual screening and interventions critically important to occur early in life to allow for neuroplasticity optimizing the outcomes [44]. This has led to the recommendation of any infant with suspected CZS or exposure to ZIKV to have an ocular examination before hospital discharge and again at 3 months of age [44].
A meta-analysis of 42 articles revealed the most common brain abnormalities following ZIKV exposure in utero, including decreased brain volume, increased extra-axial cerebrospinal fluid space, subcortical calcifications, microcephaly, ventriculomegaly, malformation of cortical development, basal ganglia calcifications, and mega cisterna magna [45]. These findings support the concept that ZIKV interferes with normal neuronal migration during development which then impacts the brain development. The major neuronal migration is occurring before the 25th week of gestation, making exposure to the virus in the first and second trimesters the most devastating. Infants with ZIKV exposure and no apparent congenital syndrome are also at risk for abnormal neurodevelopmental outcomes, as evidenced in a recent study of 70 infants followed to age 18 months [46]. These infants had confirmed exposure to ZIKV but no findings to support CZS, and despite the normal head circumference, had subsequent neurodevelopmental deficits develop over the first year of life [46]. As studies continue and longer-term outcomes become known, it is critically important to follow any infant with ZIKV exposure closely.
Rubella is caused by a single stranded ribonucleic acid (RNA) virus which is highly contagious and only transmitted between humans [18, 47]. It is usually spread through respiratory droplets and in most cases will result in a mild viral disease. Symptoms may include fever, rash, malaise and adenopathy. The virus is able to infect cells of the respiratory tract and then spread via the systemic circulation to multiple organ systems, including the placenta [48]. When the infection occurs during pregnancy the virus can be transmitted to the fetus and result in death of the fetus or a range of congenital anomalies known collectively as Congenital Rubella Syndrome (CRS) [18]. The timing of when a pregnant woman contracts the virus appears to be related to the risk of congenital infection and fetal defects. Studies estimate that maternal infection occurring during the first 12 weeks of gestation has roughly a 90% chance of congenital infection with the risk of defects nearly 85% [49]. When congenital infection occurs during the first trimester, hearing defects, heart defects, neurologic damage, and ocular defects appear more commonly. CRS is a combination of these defects but most classically is described as a triad of cataracts, congenital heart disease, and sensorineural deafness [49, 50]. Other manifestations include intrauterine growth restriction (IUGR), hepatomegaly, splenomegaly, thrombocytopenia and dermal erythropoiesis (commonly known as a “blueberry muffin rash”) [18].
Pregnant women in the United States are tested for rubella immunity by serologic screening. Those who have had a natural infection or have received at least one dose of the rubella vaccine tend to have lifelong immunity [18]. Those women who are found to be non-immune should receive one dose of the vaccine after childbirth, as vaccination during pregnancy has theoretical teratogenic risks due to the vaccine being live [18]. If a pregnant woman is exposed to the rubella virus, they should have serologic testing for rubella-specific IgM and IgG. If she is found to have rubella-specific IgG, then she is considered immune. However, if there is no IgG detectable at the time of exposure then convalescent serologies are obtained 3 and 6 weeks after exposure, with IgG reactivity at these time points indicating a recent infection [18]. Unfortunately, there is no treatment for rubella outside of supportive measures.
When congenital infection is suspected, diagnosis can be done by testing for rubella-specific IgM in fetal blood or detection of the virus in amniotic fluid [49]. Postnatally, an enzyme-linked immunosorbent assay (ELISA) can also be done for rubella-specific IgM. If positive, then confirmatory testing is done by reverse transcription polymerase chain reaction (RT-PCR) of nasopharyngeal swabs, urine, or oral fluid [47, 49]. In some infants the virus can be detected in nasopharyngeal secretions and urine for over a year [18, 49]. While there is no treatment for CRS, diagnosis is important in terms of follow up. Due to the risk of cataracts among other ocular abnormalities (including microphthalmia, glaucoma, chorioretinitis), hearing loss, neurologic manifestations (such as developmental delay, autism), and endocrine disorders (including diabetes, thyroid disease) children with CRS must be evaluated periodically for management of these potential complications [48–50]. The introduction of the vaccine has resulted in a significant decline in cases of rubella infection and CRS in the United States, with an average of 14 reported rubella cases a year and 4 CRS cases a year from 2001 to 2004 [51].
Cytomegalovirus (CMV) is a double stranded deoxyribonucleic acid (DNA) virus that is universally found and generally causes mild or subclinical symptoms in most children and adults [18, 52]. It can be transmitted via contact with infected secretions, transfusion of blood products from infected donors, organ transplants from infected individuals, or vertically [18]. When it is vertically transmitted, CMV has the potential to cause severe and permanent sequelae [18, 52, 53]. CMV is known as one of the most common congenital viral infections and is the leading, non-genetic cause of sensorineural hearing loss in children in the United States [18]. It can be transmitted to the fetus by crossing the placenta, through contact of infected cervical secretions during birth, or perinatally by ingestion of breast milk containing the virus [18]. When CMV is transmitted in utero, it can be due to primary maternal infection during pregnancy, reactivation of a prior infection, or reinfection with a different strain despite presence of maternal antibodies [54, 55]. Reactivation and reinfection are more common than a primary infection; however, the latter tends to cause more severe sequelae especially if infection occurs earlier in pregnancy.
Of those infants whose mother had an acute infection during pregnancy, 30–40% will have congenital CMV (cCMV) [18, 55]. Infants with cCMV are symptomatic in 10–15% of the cases, with half to two-thirds of these infants developing sensorineural hearing loss (SNHL) later in life [55]. Symptoms at birth can include thrombocytopenia, hepatomegaly, splenomegaly, microcephaly, periventricular calcifications in the brain, chorioretinitis, hepatitis, and SNHL. Long term outcomes include progressive SNHL and neurodevelopmental delay [18, 53, 55]. Of the infants who are asymptomatic at birth, around 15% will later develop SNHL [18]. Imaging of the fetal brain can be completed in utero via transvaginal ultrasound or with magnetic resonance imaging (MRI). cCMV can result in germinolytic cysts, lenticulostriate vasculopathy, temporal lobe and occipital cysts as well as cerebellar hypoplasia and migrational disorders including polymicrogyria [52]. Periventricular calcifications is the most frequently reported finding on brain imaging of cCMV cases, impacting 34–70% of diagnosed patients [56].
Testing during pregnancy is not routinely done, but serologic testing can be performed if a pregnant woman has been exposed or is suspected of having CMV infection. CMV-specific IgM has low specificity as it can persist for 6–9 month following primary infection and can also be detected during reactivation [54]. CMV IgG avidity index however can be used to confirm primary infection; avidity testing is a method to measure the strength of the bonding between antibodies and the virus. Low avidity would indicate recent infection while high avidity takes time to occur and would indicate a past infection. There is no current recommended treatment for acute CMV infection during pregnancy [18, 54].
There is also no current routine testing for CMV in infants. Some states have mandated targeted CMV screening for those who fail their routine newborn hearing screen, however it is important to note that targeted screening will miss those newborns who are asymptomatic at birth but still at risk for developing SNHL later in life [18]. For symptomatic infants, the diagnosis of cCMV can be made postnatally if testing is done within 3 weeks of birth as to avoid the difficulty of differentiating between intrauterine and perinatal infection [18, 54, 57]. CMV can be isolated from the urine, saliva, respiratory secretions, blood, or cerebrospinal fluid [18]. Viral cultures, rapid shell vial cultures, and PCR can be completed [54]. Treatment for those infants who are symptomatic regardless of CNS involvement includes intravenous ganciclovir or oral valganciclovir [18, 54, 58]. The latter is preferred due to ease of administration as duration of treatment is six months. If there are concerns for abnormal gastrointestinal absorption due to other factors, treatment can be started with IV ganciclovir [54]. Studies have found that those who have anti-viral treatment started within the first month of life have significantly improved audiologic and neurodevelopmental outcomes at 12 and 24 months of age compared to those who do not [53]. Treatment with either valganciclovir or ganciclovir can cause significant neutropenia; absolute neutrophil counts should be monitored weekly for the first six weeks of treatment, followed by screening at eight weeks of treatment, and thereafter monthly for the duration of treatment [54]. Infants with mild symptoms or isolated SNHL are not recommended to receive antiviral treatment at this time due to lack of data in this population [54].
Long term outcomes to consider in children with cCMV include SNHL and neurodevelopmental delay. These children should have frequent audiologic assessments as SNHL can develop and/or progress after the newborn period [54]. While there are no established universal guidelines for hearing evaluation, studies indicate that screening should continue for at least the first four years of life after which late-onset SNHL is seldom seen.
Herpes simplex viruses are large, double-stranded DNA viruses with two types, HSV-1 and HSV-2 [18]. Traditionally, HSV-1 can cause vesicular lesions in areas above the waist while HSV-2 involves areas below the waist. It is, however, becoming increasingly more common to see genital HSV-1 lesions. Both types are able to cause herpetic disease in neonates when acquired from the mother. Transmission can occur during the birthing process via contact with genital lesions, an ascending infection, intrauterine, or postnatally from contact with lesions [18, 52]. A primary genital HSV infection in the mother near delivery has 10–30 times the risk of transmission compared to a recurrent infection. This is thought to be due to lower concentrations of transplacental HSV antibodies in the neonate [18, 59]. Unfortunately, defining an infection as primary versus recurrent may not be straightforward, as women can be asymptomatic and may be unaware that they have had a prior infection with HSV. Furthermore, viral shedding can occur in the absence of clinical symptoms [59].
If a pregnant woman does have genital lesions characteristic of HSV near delivery, then swabs of the lesions can be sent for viral culture and PCR with serologic testing to determine the type. From these results, women can be classified into four different categories: documented first primary infection, documented first episode non-primary infection, assumed first episode (primary or non-primary), or recurrent infection (see Table 1 adapted from Kimberlin et al.).
Diagnostic tests for Herpes simplex virus (HSV) Antibodies and Culture/PCR. This table describes the classification of HSV infection based on culture or PCR test results as well as HSV-1 and HSV-2 antibody test results.
Women classified as having a primary infection or first episode can be treated with oral acyclovir for 7–10 days [18]. Those with a recurrent episode can be treated with the same or higher dose for 5 days [18]. If a woman has a known history of HSV then suppressive therapy should be started at 36 weeks’ gestation to decrease the risk of recurrence at delivery, although this will not entirely suppress shedding [60]. Other preventative methods include avoiding invasive fetal monitoring, such as fetal scalp electrodes, and opting for elective cesarean sections when lesions are present at the time of delivery [52, 60].
Neonatal HSV can have different manifestations. SEM disease includes disease of the skin, eyes and/or mouth; 45% of infants with HSV will have SEM. Another 30% of infants with HSV will have localized central nervous system (CNS) disease with or without skin involvement. The remaining 25% of infants with HSV will have disseminated disease which can involve multiple organs, most commonly the liver and lungs [18]. The onset of disease varies between the different manifestations, with SEM disease presenting at 5–11 days of life, CNS disease presenting between 8 and 17 days of life, and disseminated disease presenting between 10 and 12 days of life [61]. Initial symptoms may be non-specific and include feeding difficulties, lethargy, seizures, suspected sepsis, vesicular rash or severe liver dysfunction, with as many as 30% of infected neonates not having skin lesions [52, 60]. As there can be high morbidity and mortality rates in newborns with HSV, it is imperative to diagnose and initiate treatment as soon as it is suspected [18].
Guidelines have been published on the management of asymptomatic neonates born to women with active genital lesions [59]. In newborns whose mothers have a history of genital HSV prior to pregnancy and present with active lesions at delivery, there is a low risk of transmission. However, the infant should still have surface swabs of the mouth, nasopharynx, conjunctivae, and anus obtained for culture and PCR as well as serum HSV PCR sent at 24 h of life. Waiting to send samples until 24 h of life ensures that any positive results would represent active viral replication in the infant and not maternal contamination [59]. Intravenous acyclovir is not started in this situation unless the infant becomes symptomatic, or the surface swabs and/or serum are positive. This would confirm infection and require a lumbar puncture to obtain cerebrospinal fluid (CSF) for PCR testing. The result of the CSF PCR is key in determining treatment duration. If the CSF and serum HSV PCR are negative, then empiric IV acyclovir is administered for a total of 10 days to prevent progression from infection to disease. If the CSF PCR is positive, then treatment should be administered for 21 days [59]. After the treatment course has completed, a repeat lumbar puncture is necessary in cases of CNS disease to document clearance. If the repeat CSF HSV PCR is still positive, then acyclovir is continued for another 7 days. A repeat lumbar puncture is obtained to show clearance. This process is repeated until the CSF is negative. Any infant who undergoes a treatment course for HSV disease should have suppressive therapy with oral acyclovir for 6 months after the completion of parenteral treatment (see Figures 1 and 2) [59, 62].
Infant evaluation in suspected exposure to Herpes simplex virus (HSV). This flow diagram, adapted from Ref. [59], describes the infant evaluation(s) to complete if there was concern for maternal HSV infection around the time of delivery due to the presence of lesions.
Infant treatment recommendations for suspected congenital Herpes simplex virus (HSV) infection. Tis flow diagram, adapted from Ref. [59], describes treatment regimens based on infant symptoms.
In the case that an asymptomatic neonate is born to a mother with active genital lesions but does not have a history of genital HSV prior to pregnancy, then the importance lies in distinguishing whether it is a primary, non-primary or recurrent infection [59]. The mother should not only have the swabs sent for PCR testing and culture but should also have serum serological tests performed for HSV-1 and HSV-2 antibodies. The infant requires evaluation at 24 h of life with HSV surface cultures and PCR testing of the serum and CSF. The CSF samples should also be sent for cell count and chemistries, with screening serum alanine aminotransferase obtained. IV acyclovir would be started empirically after obtaining the samples at 24 h of age while awaiting results. Once the maternal testing is resulted, maternal classification can then be determined as shown in Table 1. If the mother is deemed to have a first episode primary or non-primary infection, then treatment of the infant would include 10 days of IV acyclovir for a normal evaluation (infant remains asymptomatic, negative CSF and serum HSV PCR, normal CSF indices, and normal serum ALT), 14 days for an abnormal evaluation (positive serum HSV PCR, symptomatic infant, or abnormal ALT) and 21 days for CNS infection (positive CSF PCR or abnormal indices) [59]. A neonate with a positive CSF HSV PCR, regardless of the maternal classification, would be managed as described above for HSV disease. It is important to note that if the infant becomes symptomatic at any point, even prior to the testing obtained at 24 h of life, then immediate evaluation and treatment should be initiated [59]. Other risk factors that may prompt testing and treatment prior the 24 h include: prolonged rupture of membranes (>4–6 h) and prematurity (<37 weeks’ gestation) in the setting of maternal genital lesions characteristic of HSV [59].
Only 10% of infants survive in untreated HSV disseminated disease with 50% of infants surviving in untreated HSV CNS disease [61]. Inadequately treated or untreated HSV SEM disease can progress to either disseminated or CNS disease; those that survive have a significant proportion that show some neurologic sequelae, namely in the form of motor, speech, and developmental delay [61]. Outcomes, especially mortality, improve the earlier that treatment is initiated, making it imperative to evaluate and begin empiric treatment whenever HSV infection is suspected [61]. Oral suppressive therapy has also been shown to improve neurodevelopmental outcomes at 12 months of age compared to those that did not receive long-term antivirals, suggesting that ongoing neurologic injury may occur in infants affected by HSV disease [62].
A review of additional viruses that can impact infants exposed during pregnancy is provided below. These viruses have been associated with a range of adverse outcomes in infants with prenatal/perinatal exposure, however they remain uncommonly diagnosed or the impact on the fetus remains extremely varied. However, given the increased risk of potential adverse outcomes, they are briefly discussed.
The hepatitis E virus (HEV) is a single-stranded RNA virus which is known as a major cause of acute viral hepatitis especially in developing countries through ingestion of contaminated water sources [18, 63]. While it generally causes a mild illness in most adults, pregnant women tend to have more severe disease. Mortality has been observed in pregnant women, especially if infected with genotype 1 [18, 63]. HEV is estimated to be responsible for up to 3000 stillbirths a year in developing countries and can commonly cause preterm delivery in infected mothers with resultant poor neonatal outcomes [63, 64]. When HEV is transmitted vertically, hepatitis can be present from birth and persist throughout the infant’s life but is not known to be associated with congenital anomalies.
Enteroviruses are a group of RNA viruses that can spread between humans via respiratory routes, vertically, and fecal-oral transmission [18]. Symptoms in adults and children can be varied and may include respiratory, dermatologic, neurologic, ocular, cardiac, muscular, and gastrointestinal manifestations [18]. When enterovirus is transmitted vertically or more commonly peripartum, the neonate may remain asymptomatic without sequelae or have severe symptoms including septic shock with multiorgan dysfunction [65]. There is limited evidence to suggest that infection with enterovirus during pregnancy is associated with congenital anomalies or fetal death [65].
Lymphocytic choriomeningitis virus (LCMV) is a single-stranded RNA virus spread by rodents which can cross the placenta; rarely it can be transmitted during delivery by exposure to maternal secretions or blood and cause congenital viral infection [66–68]. Infected pregnant women can have non-specific viral symptoms and may report direct exposure to or the presence of rodents in their homes [66, 68]. Common findings in an infant affected by LCMV are macrocephaly or microcephaly and ocular abnormalities; additionally, neurological abnormalities may be present and include hydrocephalus, periventricular calcifications, seizures, neurodevelopmental sequelae including intellectual disability, or even death [67, 68]. These symptoms suggest a similarity with other congenital infections previously discussed, such as CMV or toxoplasmosis, which may contribute to an underestimation of the prevalence of LCMV when congenital infection is suspected [66, 68].
The West Nile Virus (WNV) is a flavivirus that was initially isolated in 1937 and did not reach the United States until an outbreak in 1999 [69–71]. The primary mode of transmission is through the bite of an infected Culex species mosquito, with individuals ranging from no symptoms to 0.7% of infected individuals developing neuro-invasive disease with encephalitis, meningitis or acute flaccid paralysis possible [69]. There is no specific treatment or vaccine at this time [70]. Case reports of infants born to mothers with WNV have shown an array of outcomes, with follow up at 2–3 years of age not consistently showing any developmental delays [69]. Findings have included chorioretinitis, white-matter loss and cystic changes, and congenital defects such as lissencephaly, polydactyly, aortic coarctation and cleft palate [69]. Additional studies on the impact of infants with exposure during gestation, and longer-term outcomes are needed to truly delineate if WNV results in congenital anomalies.
Human adenoviruses (HAdV) are DNA viruses in the Adenoviridae family, with 7 subgroups and 52 serotypes [72]. While typically the cause of a “cold”, the severity of illness can range from mild to severe with gastroenteritis, pneumonia and neurologic disease possible [73]. Reports have not noted any specific fetal malformations, although infants with positive polymerase chain reaction (PCR) testing had a higher incidence of neural tube defects and echogenic liver lesions with and without hydrops [74].
Many of the maternal infections that previously resulted in significant impact and poor outcomes on the developing fetus have improved as treatments and vaccines have been introduced and refined. However, other pathogens are now becoming more apparent in their impact on fetal development, such as Zika virus. Some infections are declining in incidence, with a resultant decrease in congenital infections (such as the nearly 80% decline in Rubella infections) [51]. Other infections are continuing to increase, with the true impact on society yet to be determined. Thus, it is imperative that we monitor any infections in a pregnant woman, and complete a thorough examination and evaluation of each infant born with the hopes of identifying any abnormalities quickly and improving the outcomes of each infant to the best of our ability.
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