Aneasthesia Pearls Jan 2014

ANAESTHESIA PEARLS

Rapid Sequence Induction (RSI)

Rapid Sequence Induction (RSI)
What is new in Rapid Sequence Induction (RSI)
Introduction

RSI results in rapid unconsciousness (induction) and neuromuscular blockade (paralysis) and is the preferred method of endotracheal intubation for patients who have not fasted and are at greater risk for vomiting and aspiration. The goal of RSI is to intubate the trachea without the use of Bag-Valve-Mask ventilation, which is often necessary when using sedatives alone (titrated to effect).

Standard set-up for RSI.
Adjust head/neck position prior to starting.
Optimal preoxygenation.
Induction agent and suxamethonium.
Cricoid cartilage identified before induction by assistant.
Light pressure (no more than 10 N force) on the cricoid cartilage prior to loss of consciousness.
30 N cricoid force (equivalent to registering 3 kg on a weighing machine) after loss of consciousness.
Direct laryngsocopy undertaken.
If difficult try alternative blade (long, straight, McCoy etc), bougie, and the limited amount of external laryngeal manipulation possible with cricoid force.
If intubation unsuccessful – stop further attempts. Do not give second dose of relaxant.
Announce ‘Failed intubation’ to stop yourself carrying on with further attempts and to alert assistant that Plan a has failed.
What is new in Rapid Sequence Induction (RSI)
1. What is the rationale for providing Preoxygenation before tracheal intubation?
Preoxygenation allows a safety buffer during periods of hypoventilation and apnea. It extends the duration of safe apnea, defined as the time until a patient reaches a saturation level of 88% to 90%, to allow for placement of a definitive airway.
In a patient breathing room air before rapid sequence tracheal intubation (PaO2 90 to 100 mm Hg), desaturation will occur in the 45 to 60 seconds between sedative/paralytic administration and airway placement.
Studies by Heller and Watson and Heller et al show markedly increased time to desaturation if the patients received preoxygenation with 100% oxygen rather than room air before tracheal intubation.
2. For what period of time should the patient receive Preoxygenation?
Ideally, patients should continue to receive preoxygenation until they denitrogenate the functional residual capacity of their lungs sufficiently to achieve greater than 90% end-tidal oxygen level.
Three minutes’ worth of tidal-volume breathing (the patient’s normal respiratory pattern) with a high FiO2 source is an acceptable duration of preoxygenation for most patients. This tidal-volume breathing approach can be augmented by asking the patient to exhale fully before the 3-minute period.
Cooperative patients can be asked to take 8 vital-capacity breaths (maximal exhalation followed by maximal inhalation). This method generally can reduce the preoxygenation time to approximately 60 seconds.
The above times are predicated on a source of FiO2 greater than or equal to 90% and a tightly fitting mask that prevents entrainment of room air.
3. Can increasing mean airway pressure augment Preoxygenation?
Mean airway pressure may be increased during preoxygenation through the use of techniques such as noninvasive positive-pressure ventilation. If patients have not achieved a saturation greater than 93% to 95% before tracheal intubation, they have a higher likelihood of desaturation during their apneic and tracheal intubation periods.
If patients do not achieve this saturation level after 3 minutes of tidal-volume breathing with a high FiO2 source, it is likely that they are exhibiting shunt physiology; any further augmentation of FiO2 will be unhelpful.
CPAP masks, noninvasive positive pressure ventilation, or PEEP valves on a bag-valve-mask device should be considered for preoxygenation and ventilation during the onset phase of muscle relaxation in patients who cannot achieve saturations greater than 93% to 95% with high FiO2.
4. In what position should the patient receive Preoxygenation?
Supine positioning is not ideal to achieve optimal preoxygenation. When one is placed flat, it is more difficult to take full breaths and more of the posterior lung becomes prone to atelectatic collapse, which reduces the reservoir of oxygen contained within the lungs and therefore reduces safe apnea time.
Patients preoxygenated in a 20-degree head-up position improves preoxygenation. Similarly Reverse Trendelenburg position (head of stretcher 30 degrees higher than the foot) also improves preoxygenation.
Patients should receive preoxygenation in a head-elevated position whenever possible. For patients immobilized for possible spinal injury, reverse Trendelenburg position can be used.
5. How long will it take for the patient to desaturate after Preoxygenation?
Although breathing at a high FiO2 level will slightly increase the bloodstream stores of oxygen, the primary benefit of preoxygenation is the creation of a reservoir of oxygen in the alveoli.
When a patient is breathing room air, 450 mL of oxygen is present in the lungs; this amount increases to 3,000 mL when a patient breathes 100% oxygen for a sufficient time to replace the alveolar nitrogen. A patient breathing room air will have a total oxygen reservoir in the lungs and bloodstream of approximately 1.0 to 1.5 L, whereas an optimally preoxygenated patient will have 3.5 to 4.0 L.
Oxygen consumption during apnea is approximately 250 mL/minute (3 mL/kg per minute); in healthy patients, the duration of safe apnea on room air is approximately 1minute compared with approximately 8 minutes when breathing at a high FiO2 level.
Oxyhemoglobin dissociation curve demonstrates the SpO2 from various levels of PaO2. Risk categories are overlaid on the curve. Patients near an SpO2 of 90% are at risk for precipitous desaturation, as demonstrated by the shape of the curve.
Given the unique variables involved in each ED tracheal intubation, it is impossible to predict the exact duration of safe apnea in a patient. Patients with high saturation levels on room air or after oxygen administration are at lower risk and may maintain adequate oxygen saturation as long as 8 minutes. Critically ill patients and those with values just above the steep edge of the desaturation curve are at high risk of hypoxemia with prolonged tracheal intubation efforts and may desaturate immediately.
6. Can apneic oxygenation extend the duration of safe apnea?
Apneic oxygenation is not a new concept; it has been described in the medical literature for more than a century, with names such as apneic diffusion oxygenation, diffusion respiration, and mass flow ventilation.
Alveoli will continue to take up oxygen even without diaphragmatic movements or lung expansion. In an apneic patient, approximately 250 mL/minute of oxygen will move from the alveoli into the bloodstream. Conversely, only 8 to 20mL/minute of carbon dioxide moves into the alveoli during apnea, with the remainder being buffered in the bloodstream. The difference in oxygen and carbon dioxide movement across the alveolar membrane is due to the significant differences in gas solubility in the blood, as well as the affinity of hemoglobin for oxygen. This causes the net pressure in the alveoli to become slightly subatmospheric, generating a mass flow of gas from pharynx to alveoli. This phenomenon, called apneic oxygenation, permits maintenance of oxygenation without spontaneous or administered ventilations.
Under optimal circumstances, a PaO2 can be maintained at greater than 100mm Hg for up to 100 minutes without a single breath, although the lack of ventilation will eventually cause marked hypercapnia and significant acidosis.
To provide apneic oxygenation during ED tracheal intubations, the nasal cannula is the device of choice.
An additional benefit to the use of nasal cannula devices is that they can be left on during the tracheal intubation attempts. This has been described with an acronym, NO DESAT (nasal oxygen during efforts securing a tube); it allows the continued benefits of apneic oxygenation while tracheal intubation techniques are performed.
The nasal cannula can be placed under a facemask (or bag-valve-mask device) during preoxygenation, and then it remains on, administering oxygen through the nose throughout oral tracheal intubation with direct or video laryngoscopy.
A Nasal cannula set at 15 L/minute is the most readily available and effective means of providing apneic oxygenation.
9. Does the choice of paralytic agent affect Preoxygenation?
In patients at high risk of desaturation, rocuronium may provide a longer duration of safe apnea than succinylcholine.
It is hypothesized that the fasciculations induced by succinylcholine may cause increased oxygen use. Pretreatment medications to prevent fasciculations minimize the difference in desaturation times.
RISK STRATIFICATION AND CONCLUSIONS:
Patients requiring emergency airway management can be risk stratified into 3 groups, according to pulse oximetry after initial application of high-flow oxygen. The recommended techniques to use for patients in each group are shown in Table 1, and a logistic flow of preoxygenation steps is shown in Table 2.
Table I: Risk categorization of patients during Preoxygenation:

RSI results in rapid unconsciousness (induction) and neuromuscular blockade (paralysis) and is the preferred method of endotracheal intubation for patients who have not fasted and are at greater risk for vomiting and aspiration. The goal of RSI is to intubate the trachea without the use of Bag-Valve-Mask ventilation, which is often necessary when using sedatives alone (titrated to effect).gkggkghghgkfghhjjjjhghfd

Rapid Sequence Induction (RSI)
What is new in Rapid Sequence Induction (RSI)
Introduction
RSI results in rapid unconsciousness (induction) and neuromuscular blockade (paralysis) and is the preferred method of endotracheal intubation for patients who have not fasted and are at greater risk for vomiting and aspiration. The goal of RSI is to intubate the trachea without the use of Bag-Valve-Mask ventilation, which is often necessary when using sedatives alone (titrated to effect).
Standard set-up for RSI.
Adjust head/neck position prior to starting.
Optimal preoxygenation.
Induction agent and suxamethonium.
Cricoid cartilage identified before induction by assistant.
Light pressure (no more than 10 N force) on the cricoid cartilage prior to loss of consciousness.
30 N cricoid force (equivalent to registering 3 kg on a weighing machine) after loss of consciousness.
Direct laryngsocopy undertaken.
If difficult try alternative blade (long, straight, McCoy etc), bougie, and the limited amount of external laryngeal manipulation possible with cricoid force.
If intubation unsuccessful – stop further attempts. Do not give second dose of relaxant.
Announce ‘Failed intubation’ to stop yourself carrying on with further attempts and to alert assistant that Plan A has failed.
What is new in Rapid Sequence Induction (RSI)
1. What is the rationale for providing Preoxygenation before tracheal intubation?
Preoxygenation allows a safety buffer during periods of hypoventilation and apnea. It extends the duration of safe apnea, defined as the time until a patient reaches a saturation level of 88% to 90%, to allow for placement of a definitive airway.
In a patient breathing room air before rapid sequence tracheal intubation (PaO2 90 to 100 mm Hg), desaturation will occur in the 45 to 60 seconds between sedative/paralytic administration and airway placement.
Studies by Heller and Watson and Heller et al show markedly increased time to desaturation if the patients received preoxygenation with 100% oxygen rather than room air before tracheal intubation.
2. For what period of time should the patient receive Preoxygenation?
Ideally, patients should continue to receive preoxygenation until they denitrogenate the functional residual capacity of their lungs sufficiently to achieve greater than 90% end-tidal oxygen level.
Three minutes’ worth of tidal-volume breathing (the patient’s normal respiratory pattern) with a high FiO2 source is an acceptable duration of preoxygenation for most patients. This tidal-volume breathing approach can be augmented by asking the patient to exhale fully before the 3-minute period.
Cooperative patients can be asked to take 8 vital-capacity breaths (maximal exhalation followed by maximal inhalation). This method generally can reduce the preoxygenation time to approximately 60 seconds.
The above times are predicated on a source of FiO2 greater than or equal to 90% and a tightly fitting mask that prevents entrainment of room air.
3. Can increasing mean airway pressure augment Preoxygenation?
Mean airway pressure may be increased during preoxygenation through the use of techniques such as noninvasive positive-pressure ventilation. If patients have not achieved a saturation greater than 93% to 95% before tracheal intubation, they have a higher likelihood of desaturation during their apneic and tracheal intubation periods.
If patients do not achieve this saturation level after 3 minutes of tidal-volume breathing with a high FiO2 source, it is likely that they are exhibiting shunt physiology; any further augmentation of FiO2 will be unhelpful.
CPAP masks, noninvasive positive pressure ventilation, or PEEP valves on a bag-valve-mask device should be considered for preoxygenation and ventilation during the onset phase of muscle relaxation in patients who cannot achieve saturations greater than 93% to 95% with high FiO2.
4. In what position should the patient receive Preoxygenation?
Supine positioning is not ideal to achieve optimal preoxygenation. When one is placed flat, it is more difficult to take full breaths and more of the posterior lung becomes prone to atelectatic collapse, which reduces the reservoir of oxygen contained within the lungs and therefore reduces safe apnea time.
Patients preoxygenated in a 20-degree head-up position improves preoxygenation. Similarly Reverse Trendelenburg position (head of stretcher 30 degrees higher than the foot) also improves preoxygenation.
Patients should receive preoxygenation in a head-elevated position whenever possible. For patients immobilized for possible spinal injury, reverse Trendelenburg position can be used.
5. How long will it take for the patient to desaturate after Preoxygenation?
Although breathing at a high FiO2 level will slightly increase the bloodstream stores of oxygen, the primary benefit of preoxygenation is the creation of a reservoir of oxygen in the alveoli.
When a patient is breathing room air, 450 mL of oxygen is present in the lungs; this amount increases to 3,000 mL when a patient breathes 100% oxygen for a sufficient time to replace the alveolar nitrogen. A patient breathing room air will have a total oxygen reservoir in the lungs and bloodstream of approximately 1.0 to 1.5 L, whereas an optimally preoxygenated patient will have 3.5 to 4.0 L.
Oxygen consumption during apnea is approximately 250 mL/minute (3 mL/kg per minute); in healthy patients, the duration of safe apnea on room air is approximately 1minute compared with approximately 8 minutes when breathing at a high FiO2 level.
Oxyhemoglobin dissociation curve demonstrates the SpO2 from various levels of PaO2. Risk categories are overlaid on the curve. Patients near an SpO2 of 90% are at risk for precipitous desaturation, as demonstrated by the shape of the curve.
Given the unique variables involved in each ED tracheal intubation, it is impossible to predict the exact duration of safe apnea in a patient. Patients with high saturation levels on room air or after oxygen administration are at lower risk and may maintain adequate oxygen saturation as long as 8 minutes. Critically ill patients and those with values just above the steep edge of the desaturation curve are at high risk of hypoxemia with prolonged tracheal intubation efforts and may desaturate immediately.
6. Can apneic oxygenation extend the duration of safe apnea?
Apneic oxygenation is not a new concept; it has been described in the medical literature for more than a century, with names such as apneic diffusion oxygenation, diffusion respiration, and mass flow ventilation.
Alveoli will continue to take up oxygen even without diaphragmatic movements or lung expansion. In an apneic patient, approximately 250 mL/minute of oxygen will move from the alveoli into the bloodstream. Conversely, only 8 to 20mL/minute of carbon dioxide moves into the alveoli during apnea, with the remainder being buffered in the bloodstream. The difference in oxygen and carbon dioxide movement across the alveolar membrane is due to the significant differences in gas solubility in the blood, as well as the affinity of hemoglobin for oxygen. This causes the net pressure in the alveoli to become slightly subatmospheric, generating a mass flow of gas from pharynx to alveoli. This phenomenon, called apneic oxygenation, permits maintenance of oxygenation without spontaneous or administered ventilations.
Under optimal circumstances, a PaO2 can be maintained at greater than 100mm Hg for up to 100 minutes without a single breath, although the lack of ventilation will eventually cause marked hypercapnia and significant acidosis.
To provide apneic oxygenation during ED tracheal intubations, the nasal cannula is the device of choice.
An additional benefit to the use of nasal cannula devices is that they can be left on during the tracheal intubation attempts. This has been described with an acronym, NO DESAT (nasal oxygen during efforts securing a tube); it allows the continued benefits of apneic oxygenation while tracheal intubation techniques are performed.
The nasal cannula can be placed under a facemask (or bag-valve-mask device) during preoxygenation, and then it remains on, administering oxygen through the nose throughout oral tracheal intubation with direct or video laryngoscopy.
A Nasal cannula set at 15 L/minute is the most readily available and effective means of providing apneic oxygenation.
7. When and how should we provide manual ventilations during the apneic period?
Practitioners should not initiate laryngoscopy before full muscle relaxation to maximize laryngeal exposure and to avoid triggering the patient’s gag reflex and active vomiting just before apnea.
Ventilation during the onset phase of muscle relaxation can create alveolar distention and lengthen the duration of safe apnea during tracheal intubation efforts.
If a bag-valve-mask device is used during the onset of muscular relaxation, a PEEP valve will provide sustained alveolar distention. Ventilations should be delivered slowly (during 1 to 2 seconds), involve a low volume (6 to 7 mL/kg), and be administered at as low a rate as tolerable for the clinical circumstances (6 to 8 breaths/min).
The risk/benefit of active ventilation during the onset phase of muscle relaxants must be carefully assessed in each patient. In patients at low risk for desaturation (_95% saturation), manual ventilation is not necessary. In patients at higher risk (91% to 95% saturation), a risk-benefit assessment should include an estimation of desaturation risk and the presence of pulmonary pathology. In hypoxemic patients, low-pressure, low-volume, low-rate ventilations will be required.
8. What positioning and maneuvers should the patient receive during the apneic period?
Patients should be positioned to maximize upper airway patency before and during the apneic period, using ear-to–sternal notch positioning. Nasal airways may be needed to create a patent upper airway. Once the apneic period begins, the posterior pharyngeal structures should be kept from collapsing backwards by using a jaw thrust. Cricoid pressure may negatively affect apneic oxygenation.
9. Does the choice of paralytic agent affect Preoxygenation?
In patients at high risk of desaturation, rocuronium may provide a longer duration of safe apnea than succinylcholine.
It is hypothesized that the fasciculations induced by succinylcholine may cause increased oxygen use. Pretreatment medications to prevent fasciculations minimize the difference in desaturation times.
RISK STRATIFICATION AND CONCLUSIONS:
Patients requiring emergency airway management can be risk stratified into 3 groups, according to pulse oximetry after initial application of high-flow oxygen. The recommended techniques to use for patients in each group are shown in Table 1, and a logistic flow of preoxygenation steps is shown in Table 2.
Table I: Risk categorization of patients during Preoxygenation:
Risk Category, Based on Pulse Oximetry While Receiving High- Flow Oxygen Preoxygenation Period (3 Minutes) Onset of Muscle Relaxation (_60 Seconds) Apneic Period During Tracheal Intubation (Variable Duration, Depending on Airway Difficulty; Ideally <30 Seconds)
Low risk, SpO2 96%–100% Non rebreather mask with maximal oxygen flow rate Non rebreather mask and nasal oxygen at 15 L/min Nasal oxygen at 15 L/min
High risk, SpO2 91%–95% Non rebreather mask or CPAP or bag – valve – mask device with PEEP Non rebreather mask, CPAP, or bag valve – mask device with PEEP and nasal oxygen at 15 L/min Nasal oxygen at 15 L/min
Hypoxemic, SpO2 90% or less CPAP or bag-valve-mask device with PEEP CPAP or bag-valve-mask device with PEEP and nasal oxygen at 15 L/min Nasal oxygen at 15 L/min
Table 2: Logistic flow of Preoxygenation and prevention of desaturation:
Sequence of Preoxygenation and prevention of desaturation
(Assuming 2 oxygen regulators)
Pre-oxygenation Period
Position the patient in semi recumbent position (≈20˚) or in reverse Trendelenberg. Position the patient’s head in the ear-to-sternal- notch position using padding if necessary.
Place a nasal cannula in the patient’s nares. Do not hook the nasal cannula to oxygen regulator.
Place patient on a non-breather mask at the maximal flow allowed by the oxygen regulator ( at least 15 lpm, but many allow a much greater uncalibrated flow)
If patient is not saturating >90% remove face mask and switch to non invasive CPAP by using ventilator, non invasive ventilation machine, commercial CPAP device or BVM with PEEP valve attached. Titrate between 5-15 cm H2O of PEEP to achieve oxygen saturation > 98%. Consider this step in patient saturating 91-95%.
Allow patient to breathe at tidal volume for 3 minutes or ask the patient to perform 8 maximal exhalations and inhalations.
Attach a BVM to oxygen regulator and set it to maximal flow (at least 15lpm). If the patient required CPAP for preoxygenation, attach a PEEP valve to the BVM set at the patient’s current CPAP level.
Apneic Period
Push sedative and paralytic ( preferably rocuronium if the patient is at risk for rapid desaturation)
Detach face mask from the oxygen regulator and attach the nasal cannula. Drop the flow rate to 15 lpm.
Remove the face mask from the patient.
Performance jaw thrust to maintain pharyngeal patency.
If the patient is high risk (required CPAP for preoxygenation), consider leaving on the CPAP during the apneic period or providing 4-6 ventilation with the BVM with a PEEP valve attached. Maintain a two hand mask seal during the entire apneic period to maintain the CPAP.
Intubation Period
Leave the nasal cannula on throughout the airway management period to maintain apneic oxygenation.
If 3 regulators are available, attach reservoir face mask, BVM and nasal cannula to them. If only one regulator is available, consider using a standalone oxygen tank to offer a second source of oxygen.
Source:
Preoxygenation and Prevention of Desaturation During Emergency Airway Management. Annals of Emergency Medicine, March 2012 (Vol. 59 | No. 3 | Pages 165-175.e1)
Ref:
Rapid sequence induction – Guidelines. Difficult Airway Society.

PRONE

PRONE
PRONE – Basic Position
DESCRIPTION:
In the full horizontal prone position (also known as “ventral decubitus”), the patient rests horizontally facing the table, allowing maximum exposure of the posterior aspect of the body.
Used for:
Back or neck procedures (cervical to sacral)
Procedures of the occipital or postero-lateral cranium
Sacral, perianal & perineal procedures
POSITIONING STEPS:
Note preoperatively, any patient limitations in positioning (neck or arms). The patient is anesthetized and intubated, and the endotracheal tube is secured, while patient is lying in the supine position, on either a stretcher or bed. This is accomplished by moving the OR table to one side, so the patient (on stretcher or bed) can be pulled into position for induction, near the anesthesia machine and needed equipment. The OGT, EGS and humidifier should be placed at this time.
After intubation and induction are accomplished, the anesthesia provider gives permission for other OR team members to assist in moving the OR table back, next to the stretcher or bed, aligning both in front of the anesthesia machine. The anesthetist frees and secures all lines ( IV, Art-line, Central-lines, etc.) in preparation for turning of the patient. (Please note: There should be a draw sheet on the OR table before moving patient onto it, for later positioning of the patient arms.)
With multiple assistants, the anesthesia circuit is briefly disconnected by the CRNA as he or she simultaneously commands the head, with one hand securing the airway (or ETT), and attends to the position of all lines. At the command or 1-2-3count of the CRNA, the patient is carefully flipped prone onto the OR table.
While other OR team members assist in the prone positioning of the patient, the CRNA continues to maintain the airway, reconnects the circuit, ensures proper functioning of the ventilator (or ability to hand ventilate patient in the case of a LMA), and checks and secures lines.
Parallel thoracic or chest rolls (made from tightly rolled sheets and blankets or manufactured gel rolls) are placed under the thorax, lateral to the breasts, following the long line of the body to free the abdomen from compression. Care is given not to compress the breasts with the rolls or cause undue pressure under the axilla.
The head is positioned prone, with face placed in a foam prone-cutout pillow (with ETT, OGT and EGS exiting out the side), in a skull-pin head clamp, or in a rocker-based face/forehead rest. It can alternatively be placed laterally, using a gel donut, pillow or blankets, while avoiding forced rotation of the pronated head . Eyes, ears, and nose should be checked to assure that these areas are free from pressure. Most important: The C-spine should be in neutral alignment (check for neutral position of the neck in all 3 planes). The tube should be free without kinking or undue traction, and the anesthesia provider should be able to visually see or reach in and check all connections.
The arms are padded and positioned to prevent nerve stretch or compression. This can be accomplished in a variety of ways depending on the exact nature of the surgery and access required (check with the surgeon). The arms are secured to prevent accidental dislocation or trauma from movement or falling off of table during the procedure.
Legs are maintained in the long axis of the body. Knees should be padded with egg crate or gel. Pillows should be placed under the calves and feet to take pressure off the lumbar spine and prevent pressure sores on toes.
The patient is secured to the table with tape or a belt across the thighs immediately under the buttocks.
EQUIPMENT:
Thoracic/Chest Rolls
Blankets
Gel Pads
Egg crate
Pillows
Belt
Arm Boards
Foam Face Pillow
Tape
Straps
PRONE – Arms caudad
DESCRIPTION:
Positioning of the arms along the long axis of the body (at sides) while in the ventral decubitus position to prevent against injury, nerve damage, vessel compression, pressure ulcers or other trauma during the procedure.
Used for:
Surgical procedure requiring the surgeon to be right alongside of the patient for close access to the surgical site where arms would otherwise be in the way of procedure, as in head, neck and upper spine (cervical and thoracic) procedures.
PRONE – Arms Cephalad
DESCRIPTION:
Positioning of the arms while in the ventral decubitus position along side of the head to prevent against injury, nerve damage, vessel compression, pressure ulcers or other trauma during the procedure.
Used for:
surgeon desires access to the middle to lower spine
procedures involving the sacral, perianal or perineal area
procedures involving posterior iliac crests for bone harvesting
procedures of posterior thighs or hips
PRONE – Horizontal with mayfield’s
DESCRIPTION:
While prone, the head is placed in Mayfield tongs by the surgeon to facilitate surgical access to the neck or cranium.
Used for:
Back or neck procedures (cervical to sacral)
Procedures of the occipital or postero-lateral cranium
PRONE – Horizontal with horseshoe headrest
DESCRIPTION:
While prone, the head is rested on a horseshoe headrest to facilitate surgical access to the neck or cranium.
Used for:
Back or neck procedures (cervical)
Procedures of the occipital or postero-lateral cranium
PRONE – Wilson Table
DESCRIPTION:
A specialized table for the prone position that allows the thorax and abdomen to hang freely.
Used for:
Back or neck procedures (cervical to sacral)
Procedures of the occipital or postero-lateral cranium
PRONE – Jackson Table
DESCRIPTION:
A specialized table for the prone position that allows the thorax and abdomen to hang freely.
Used for:
Back or neck procedures (cervical to sacral)
Procedures of the occipital or postero-lateral cranium
PRONE – Jack Knife
DESCRIPTION:
While prone, the patient is bent from the hips so that both the thorax and thighs are lower than the hips to facilitate access to the perianal, sacral, perineal, and lower alimentary canal areas.
Used for:
Procedures of the occipital or postero-lateral cranium
Sacral, perianal & perineal procedures
Andrews Frame (Seated Prone)

Physiological changes - prone

Physiological changes in the prone position
Cardio Vascular System:
Decrease in cardiac index (CI of 24%).
Mean arterial pressure (MAP) was maintained by increased systemic vascular resistance (SVR), and pulmonary vascular resistance (PVR).
No changes were noted in mean right atrial or pulmonary artery pressures (PAP)
The position of the heart at a hydrostatic level above the head and limbs may have caused reduced venous return to the heart and consequently a decreased CI
It has been suggested that the decrease in CI could be attributed to increased intra-thoracic pressures causing a decrease in arterial filling, (also decrease in left ventricular compliance) leading to an increase in sympathetic activity via the baroceptor reflex.
Obstruction of the IVC is likely to play a role in reducing cardiac output.
Increased surgical bleeding: Obstruction to venous drainage forces blood to return to the heart by an alternative route (usually the vertebral column venous plexus of Batson). As these veins are thin walled, containing little or no muscle tissue and few valves, any increase in pressure is transmitted and causes distension. This causes increased blood loss during lumbar spinal surgery.
Respiratory
There is a relative increase in functional residual capacity when a patient is moved from supine to prone position. FVC and FEV1 change very little. The increase in FRC seems to be related to a reduction of cephalad pressure on the diaphragm and the reopening of atelactatic segments.
In the prone position, blood flow may be relatively uniform as gravitational forces are opposing rather than augmenting the regional differences in pulmonary vascular resistance
Redistribution of lung ventilation is a proposed mechanism by which gas exchange is thought to improve in the prone position.
A recent review suggested that pulmonary vascular and bronchiolar architecture may be more important than gravity in supine and prone positions in determining ventilation and perfusion distribution.
Complications associated with the prone position
Injury to the central nervous system
Injuries from arterial occlusion
Turning a patient from the supine to the prone position should be performed carefully, avoiding excessive neck movement and allowing normal blood flow in the carotid and vertebral arteries.
Occlusion of the vertebral arteries has been reported.
It would seem prudent to maintain neutral neck alignment to minimize the risk of occluding the carotid or vertebral arteries.
Injuries from venous occlusion
Cervical laminectomy in the prone position supported by chest rolls developed new neurological deficits immediately after the operation (hemiparesis, quadriparesis, and paraparesis). It was thought that the use of chest rolls caused a degree of increased venous pressure which, when combined with mild arterial hypotension led to decreased perfusion pressure in the spinal cord and ischemia.
Air Entrapment
Entrainment of air into the cranial cavity is common after neurosurgical procedures and occurs in all operative positions.
There is a case report of quadriplegia as a result of air entrapment into the spinal cord after posterior fossa exploration. It was thought to have occurred as a result of the head down prone position allowing entrapped air in the posterior fossa to pass through the foramen magnum.
Cervical Spine Injury
Excessive neck flexion in a patient undergoing an 8.5h operation in the ‘Concorde’ position with the neck flexed and the chin approximately one finger breadth from the sternum resulted in complete and permanent C5/6 sensory and motor deficit level after operation. This was presumed to result from overstretching of the cervical cord in a narrow spinal canal and bulging C/6 disc with consequent ischemia.
Another patient undergoing lumbar spine surgery awoke with a T6 sensory level as a result of a prolapsed intervertebral disc at C6/7. Excessive neck extension together with the muscle relaxation of general anesthesia was blamed.
Injury to the peripheral nervous system
Peripheral nerve injury may occur in patients under anesthesia in any position and is thought to be the end result of nerve ischemia from undue stretching or direct pressure. Prone positioning may lead to a different pattern or frequency of injury than supine positioning.
Distribution of peripheral nerve injuries
Brachial plexus damage.
Ulnar neuropathy
Axillary nerve injury attributed to arms being abducted above the head.
Musculocutaneous and radial nerve injuries have also been reported.
In the lower limb sciatic nerve injury and Damage to the lateral cutaneous nerve of the thigh is a much more commonly recognized complication of prone positioning.
Pressure Injuries
A. Direct pressure injuries
Pressure necrosis of the skin
Direct pressure is a common cause of anesthesia related injury which can occur in the prone position. Close attention to positioning of the face, ears, breasts, genitalia, and other dependent areas to prevent pressure sores or skin necrosis has been advocated
Tracheal compression
There are reported cases of tracheal compression occurring in the prone position.
Salivary gland swelling
Bilateral painful swelling of the submandibular glands after surgery in the prone position with the head rotated has been reported. It probably resulted from stretching of the salivary ducts leading to stasis and acute swelling.
Shoulder dislocation
The distribution of pressure in the prone position can lead to anterior dislocation of the shoulder.
B. Indirect pressure injuries
Macroglossia and oropharyngeal swelling
Three cases of macroglossia and oropharyngeal swelling have been described in the prone position.
The proposed mechanism for macroglossia and oropharyngeal swelling suggests that excessive flexion of the head and the presence of a tracheal tube cause kinking and obstruction of the internal jugular vein in the neck which in turn obstructs venous drainage from the lingual and pharyngeal veins.
Mediastinal compression
The chest wall is usually able to support the patient’s weight without compression of the structures within it. However this may not be the case with congenital anatomical abnormalities.
In pectus excavatum this is more pronounced.
Visceral ischemia
Hepatic ischemia with progressive metabolic acidosis and elevated LFTs has been described after prolonged surgery in the prone position. This was thought to be due to abdominal compression.
Avascular necrosis of the femoral head
There are reports of patients undergoing decompressive surgery for spinal stenosis with a hypotensive anesthetic technique developing collapse of the femoral head. The cause was thought to be a combination of deliberate hypotension and increased venous pressure from the prone position.
Peripheral vessel occlusion
There are reports of compression of the axillary artery being detected by pulse oximetry or radial artery monitoring.
• In a patient positioned on a four post Relton Hall spinal frame, shifting of the pelvis laterally on the frame caused occlusion of the femoral artery leading to mottling of one leg and absence of the dorsalis pedis pulse. Repositioning restored normal blood flow.
Limb compartment syndrome
It would seem that is this is associated with flexion of the hips and knees and resultant impaired blood flow.
Ophthalmic Injury
The two injuries most commonly described are ischemic optic neuropathy and central retinal artery occlusion.
Aetiology
Prone positioning can lead to ophthalmic injury by direct external pressure by a headrest or other support apparatus on the orbital contents causing an increase in intraocular pressure which may lead to retinal ischemia and visual loss. This is usually linked with examination findings consistent with central retinal artery occlusion.
Ischemic optic neuropathy is not associated with direct pressure and may be due to inadequate oxygenation of the optic nerve causing ischemic damage and failure of impulse transmission.
Perfusion pressure to the optic nerve can be defined as the difference between MAP and intraocular pressure or venous pressure, whichever is the greater.
Prone positioning tends to increase venous pressure and peak inspiratory pressure which in turn increase intraocular pressure. This increased orbital venous pressure, decreased choroidal blood flow and reduced outflow of aqueous humor could decrease perfusion pressure to the optic nerve head and contribute to ischemic optic neuropathy.
Visual loss after prone anesthesia and surgery is often characterized by long surgical duration, large blood loss and administration of large volumes of clear fluids.
Minimizing risk
It is important to position the head to maximize venous outflow from the eye and hence minimize any impairment of ocular perfusion.
It may also be the case that in high risk patients keeping the head above the heart by means of a slight head up tilt can reduce risk.
Embolic complications
Venous gas embolism
Venous gas embolism may result from atmospheric air entrainment or accidental direct delivery of exogenous gas.
Efforts to minimize abdominal compression and thus IVC pressure in the prone position can result in an increased negative pressure gradient between the right atrium and the veins at the operative site. This increases the risk of air entrainment.
Risks are minimized by maintaining intravascular volume and pressure and positioning the surgical site dependent relative to the heart.
Practical Procedures
Airway management
A variety of problems with the tracheal tube may occur while a patient is prone. Repeated obstruction of a tracheal tube after prone positioning as a result of bloody secretions draining under gravity from the right lower lobe.
Use of the LMA as a primary adjunct is controversial but it has been used effectively. The LMA has been placed after prone positioning with the patient positioning themselves awake. This may avoid other adverse events related to the prone position such as soft tissue and nerve injury or spinal destabilization, but runs the risk of inability to maintain an adequate airway once anesthesia is initiated.
Cardiovascular procedures
There are also several reports on the management of cardiac arrest in the prone patient. Conventional teaching has been that the patient should be returned to the supine position via the use of an additional table in the OR. However this may not always be possible, especially when there may be bulky surgical instrument protruding from the back. Chest compressions have been delivered successfully with the hands on the central upper back between the scapulae. A post cordial thump delivered between the shoulder blades to treat pulseless ventricular tachycardia has also been described.
Defibrillation has been successfully undertaken using the anterior-posterior paddle position or paddle orientation on the left and right sides of the back. However, the use of posterior paddle positions may not deliver enough energy to the myocardium owing to the anterior displacement of the heart in the prone position and also increased transthoracic impedance with PPV. Biphasic shocks and anterior paddle or pad positioning has been recommended.
To Minimise the Risks:

  • Avoid prone position in the first place
  • Position the patient carefully – head in neutral position, with no flexion, extension or rotation of the neck.
  • Make sure the eyes are free. I just tape with a transparent dressing to keep them closed
  • Head higher than the heart and no neck ties
  • Keep surgery short (95% cases of prone/blindness cases are >6 hours). Stage surgery if possible.
  • Avoid blood loss and anaemia, and think twice about induced hypotension
Source:
1. University of Pittsburgh
2. Anaesthesia in the prone position. Br. J. Anaesth. (2008) 100 (2): 165-183.

Vasopressin

What is New in CPR?
Vasopressin, Steroids, and Epinephrine and Neurologically Favorable Survival after Cardiac Arrest
Neurological outcome after cardiac arrest has been the main end point of several randomized clinical trials (RCTs).Neurologically favorable survival differs from overall survival. Among cardiac arrest survivors, the prevalence of severe cerebral disability or vegetative state ranges from 25% to 50%.
Combined vasopressin-epinephrine during cardiopulmonary resuscitation (CPR) and corticosteroid supplementation during and after CPR improve neurological outcome after cardiac arrest.
Patients in the vasopressin-steroids-epinephrine (VSE) group had more frequent return of spontaneous circulation (ROSC) and attenuated post resuscitation systemic inflammatory response and organ dysfunction.
A double-blind, placebo-controlled, parallel-group trial performed in 3 Greek tertiary care centers.
Patients received either vasopressin (20 IU/CPR cycle) plus epinephrine (1mg/CPR cycle; cycle duration approximately 3 minutes) (VSE group) or saline placebo plus epinephrine (1 mg/CPR cycle; cycle duration approximately 3 minutes) (control group) for the first 5 CPR cycles after randomization, followed by additional epinephrine if needed. During the first CPR cycle after randomization, patients in the VSE group received methylprednisolone (40mg) and patients in the control group received saline placebo. Shock after resuscitation was treated with stress-dose hydrocortisone (300 mg daily for 7 days maximum and gradual taper) (VSE group) or saline placebo (control group).
Patients with evidence of acute myocardial infarction received stress-dose hydrocortisone for 3 days or less to prevent retardation of infarct healing.
At the time of vasopressor cessation or on day 8 after arrest, daily hydrocortisone was consecutively reduced to 200mg and 100mg and then discontinued.
In this study of patients with cardiac arrest requiring vasopressors, the combination of vasopressin and epinephrine, along with methylprednisolone during CPR and hydrocortisone in postresuscitation shock, resulted in improved survival to hospital discharge with favorable neurological status, compared with epinephrine and saline placebo.
Cerebral microcirculatory flow is reduced by approximately 60% during chest compression–only CPR and is restored to prearrest levels in 3minutes or longer after ROSC. Periarrest cerebral ischemia depends on CPR duration. The present study’s experimental VSE-CPR regimen included methylprednisolone, which may enhance the vasopressor effects of vasopressin and epinephrine. As periarrest changes in cerebral blood flow may parallel changes in mean arterial pressure, the improved periarrest hemodynamics and shorter ALS duration of VSE patients vs control patients may reflect attenuated periarrest cerebral ischemia (hypothesis supported by post hoc cerebral perfusion pressure results), possibly contributing to improved neurological recovery.
The improved early post arrest mean arterial pressure and ScvO2, lower CPR dose of epinephrine, shorter ALS duration, and use of methylprednisolone during CPR are consistent with improved post arrest cardiac performance, possibly leading to better outcomes for patients in the VSE group.
Among patients with cardiac arrest requiring vasopressors, combined vasopressin-epinephrine and methylprednisolone during CPR and stress-dose hydrocortisone in post resuscitation shock, compared with epinephrine/saline placebo, resulted in improved survival to hospital discharge with favorable neurological status.
Ref:
Vasopressin, Steroids, and Epinephrine and Neurologically Favorable Survival After In-Hospital Cardiac Arrest A Randomized Clinical Trial.
JAMA. 2013;310(3):270-279.
Posted in ANAESTHESIA PEARLS 2014

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