Imaging Flashcards
Question 20
A 54-year-old woman with lupus is hypoxaemic in a Durban intensive care unit after abdominal surgery. She is supported on the following ventilatory parameters
Calculate the alveolar-arterial gradient, D(A-a)O2, and give 2 possible causes of hypoxaemia
in the above patient. What is the limitation of this equation? (5)
This patient has a high A-a gradient which could be secondary to ventilation defect vq mismatch or perfusion defect shunting of blood
PAO2= FiO2 (PB-SVH20)-PaCO2/R+F
Norma gradient <20mmhg(<2.7KPA)
Hg A-a gradient = VQ mismatch or diffusion abnormality
Normal gradient with hypoxia = hypercarbia
A 67 year old man is scheduled for repair of his inguinal hernia. On closer questioning he reviled history of haemoptysis,. Hi P CXR is shown.
1. Describe the xray
2. What is the underlying diagnosis
Diagnosis: COPD
Features:
° Hyperinflation a flat diaphragms , there should be 7 intercostals spaces seen
° Horizontal orientation of ribs
° osteopenic ribs 2° chronic steroid use
What does above image
show?
The image shows a large right-sided pneumothorax with visible margins of the collapsed lung. Pneumothorax is the presence of gas within the pleural space owing to disruption of the parietal or visceral pleura
How do you treat tension pneumothorax?
○ Tension pneumothorax is a surgical emergency, and if suspected on clinical grounds, time should not be spent seeking radiological evidence.
○ A large-bore needle should be placed in the second intercostal space in the midclavicular line, allowing air to drain freely (Fig. 44.3).
○ The needle should be left in place until a tube thoracotomy is performed.
What are the indications for surgical intervention for a pneumothorax?
An air leak from the lung that persists for more than 10days may be an indication for surgical intervention. Recurrent pneumothorax can be treated by chemical pleurodesis without a thoracotomy by instilling tetracycline into the pleural space [3].
Is there a way to classify this condition (pneumothorax)?
Classification Neonatal, spontaneous, traumatic
• Pediatric pneumothorax– neonates with respiratory distress syndrome, especially if they are mechanically ventilated with positive and expiratory pressure and are prone to pneumothorax.
• Congenital diaphragmatic hernia results in underdeveloped lung ipsilateral to the defect in diaphragm. The more compliant contralateral lung is prone to barotrauma and pneumothorax.
○ Spontaneous pneumothorax occurs without trauma and most often in males between 20 and 35years of age. These patients are often tall and slender, and most of the patients are smokers. Recurrent spontaneous pneumothorax is common during the first year after the initial event. Primary spontaneous pneumothorax occurs in tall, thin males aged 20–40 and who are smokers. Secondary spontaneous pneumothorax occurs in patients with underlying pulmonary disease, and the presentation may be more serious with symptoms and sequelae due to comorbid conditions. ○ Traumatic pneumothorax Blunt or penetrating trauma to the chest wall can cause a pneumothorax; the most common cause is iatrogenic and is caused by subclavian line placement. ○ Tension pneumothorax This occurs when air enters the pleural cavity on inspiration but, because of a ball-valve mechanism, is unable to exit. This progressively enlarges the pleural space, shifting the mediastinum and trachea to the contralateral side and also decreasing venous return.
○ Tension pneumothorax is a medical emergency and without prompt intervention leads to rapid deterioration in the patient’s condition leading to death [1].
Name some causes for the changes seen in the image?
What’s the most valuable x-ray finding used to help differentiate the etiology of this finding
The most common causes of unilateral lung whiteout on chest radiograph (Fig. 45.1) are pneumonia, pleural effusion (including hemothorax), and collapse/atelectasis. The ability to differentiate between collapse and pleural effusion is essential beca
2. The most important finding that may help differentiate the etiology of unilateral whiteout is tracheal deviation or mediastinal shiftuse they require distinct treatments, which, if applied erroneously, could harm the patient [1].
What is the differential diagnosis of this finding when there is no tracheal deviation or mediastinal shift on chest x-ray?
○ With a finding of central mediastinum, diagnostic considerations include consolidation/pneumonia, pulmonary edema/ARDS, small to moderate pleural effusions (most likely would cause a partial rather than a complete whiteout), and mesothelioma. ○ Small and moderate pleural effusions tend to gravitate posteriorly without producing mediastinal shift.
○ Encasement of the lung in a mesothelioma patient limits mediastinal shift.
What is the differential diagnosis when there is mediastinal shift away from the opacity?
○ With tracheal displacement away from the diffuse opacity, diagnostic considerations include a moderate to large pleural effusion, large pulmonary mass, and a diaphragmatic hernia.
○ Diaphragmatic hernias on the right side usually consist of liver herniation, while on the left, from herniated bowel.
What is the differential diagnosis when there is mediastinal shift toward the opacity?
Mediastinal shift toward the side of the opacity is seen in lung collapse (endobronchial intubation, mucus plugging), post-pneumonectomy, and pulmonary agenesis/hypoplasia. The figure above (Fig. 45.1) illustrates a case of mucus plugging in the ICU in a young patient with high-level spinal cord injury compromising the strength of his cough and therefore his ability to clear secretions. This scenario can be encountered by the anesthesiologist quite often. Endotracheal tube repositioning with or without bronchoscopy is a simple fix to main stem intubation, whereas endotracheal suctioning or bronchoscopy are easily performed to clear secretions and/or mucus plugs [1, 2, 3].
A 65-year-old female after a motor vehicle collision requires emergency surgery for an open lower extremity fracture; the patient tells you she has a “bad heart,” she has no history in your institution, and no signs of heart failure. An EKG shows wide QRS with dual-chamber pacing. A CXR on admission show (See Fig.46.1). 1. What type of device is shown in the image?
This patient has an implantable biventricular cardio-defibrillator (BiV ICD) [1].
(a) The radiographic image of a pacemaker would show (See Fig.46.2):
• Smaller generator
• Discreet right ventricular lead (stable diameter)
• With or without right atrial lead or coronary sinus lead
(b) The radiographic image of an ICD would show above image:
• Larger generator.
• Prominent right ventricular lead, otherwise known as shock coils.
They appear as two metallic segments along the length of the ICD lead.
(c) The radiographic image of a BiV ICD would show (See Fig.46.4):
• Larger generator
• Prominent right ventricular lead (shock coils)
• Right atrium lead
• Coronary sinus lead
Manufacturer ID can be seen in the CXR as well
What are the indications for cardiac implantable electronic device placement?
Indications for cardiac implantable electronic device placement [2]:
(a) Pacemaker:
• Patients with symptomatic sinus node dysfunction and bradycardia
• Patients with complete AV block (symptoms less relevant)
• Hypersensitive carotid sinus syndrome and neurocardiogenic syncope
(b)ICD:
• Patients at risk of sudden cardiac death: Prior ventricular tachycardia or fibrillation, low ejection fraction [3]
• Long QT syndrome
• Hypertrophic cardiomyopathy
• Arrhythmogenic right ventricular dysplasia • Cardiac transplantation
•Primary electrical disease: idiopathic ventricular fibrillation, short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia
(c) BiV ICD:
• Treatment of left ventricular dysfunction and heart failure, with prolonged ventricular conduction and heart failure symptoms.
• Required ventricular pacing and low EF:– RV pacing in patients with low EF increases CHF admissions and mortality. • Cardiac resynchronization therapy [4]:– Improved exercise tolerance and mortality.– Continuous pacing provides better hemodynamic stability.
What is the effect of placing a magnet over the device (pacemaker and/or ICD)?
Chapter 38 millers
○ Effect of a magnet on a device [5]: depends on manufacturer type and whether the magnet application is turned on. ST Jude vs Meditronic
(a) Pacemaker:
• Suspend sensing of intrinsic rhythm.
• Pacing in an asynchronous mode: the rate depends on the manufacturer and the battery life; if the battery life is low, the rate may not be adequate for surgery.
• Turns off “rate response.”
(b)ICD:
• Varies depending on device, manufacturer, and programming of the device.
• In general it turns off detection of tachycardia and tachycardia therapy (discharge and pacing).
• In general, it has no effect on the pacemaker (pacing will not become asynchronous). In patients that are pacemaker dependent due to the risk of electrical interference and pacemaker malfunction, it is best to reprogram the device to address both the tachycardia and bradycardia therapy.
In the OR, you place a magnet over the device. The patient goes pulseless after prolonged use of electrocautery. What is your diagnosis?
○ Most probably this patient has a BiV ICD and low ejection fraction and is pacemaker dependent.
° The device functioned appropriately with the magnet, which suspended the tachyarrhythmia detection.
° Pacing was inhibited by the prolonged use of electrocautery.
° Pacing returns to an unresponsive myocardium, after a prolonged period of asystole that might have led to PEA arrest.
What are the effects of electrocautery, radiation therapy, and radiofrequency on a pacemaker and an ICD?
Pacemaker [1, 6]:
(a) Electrocautery:
• Faulty sensing of intrinsic activity causing inappropriate inhibition of pacemaker activity– More prominent with monopolar cautery– More likely with above the waist surgery
• Possible device reset or damage to the generator, or the leads, but unlikely
(b)Radiation therapy:
• Possible device reset when performed near the device
(c) Radiofrequency:
• Electrocautery-like electromagnetic interference that could cause inappropriate inhibition of pacemaker activity which is more likely with procedures above the waist • Possible device reset or damage to the generator, or the leads, but unlikely
ICD:
(a) Electrocautery:
• Faulty sensing of intrinsic activity causing inappropriate sensing of arrhythmias– More prominent with monopolar cautery • Possible device reset or damage to the generator, or the leads, but unlikely (b)Radiation therapy:
• Possible device reset when performed near the device
(c) Radiofrequency:
• Electrocautery-like electromagnetic interference that could cause inappropriate arrhythmia sensing inhibition
• Possible device reset or damage to the generator, or the leads, but unlikely
What measures can you take to ensure proper intraoperative device functioning? Pacemaker
When facing a patient with a device one must ascertain [1, 5]: 243 46 CXR III
(a) Device type and obtain as much information as possible
• Is there a history of cardiac arrest, arrhythmias, or VT/VF?
• Evaluate medical record, registration card.
• Contact the manufacturer.
(b) Procedure type: Location and presence of electromagnetic interference
(c) Patients characteristics:
• Pacemaker dependence:– Usually can tell just from the monitor or EKG.If pacing spikes are not visible, then usually they are not dependent.– If there are spikes in front of all or most P waves and/or QRS complexes, then assume pacemaker dependency.
• Chambers being paced
• Presence of low EF? (d) Urgency of the case
• Elective cases:– Contact patient’s provider, pacemakers should be seen every year, and ICDs every 6 months.– Follow recommendations.
• Emergency cases:
(1) General recommendations:
a. Have magnet immediately available.
i. If magnet impossible to place, must call EP; the device might require reprograming before the procedure.
b. Monitor patient with plethysmography or arterial line.
i. All other forms of monitoring are unreliable due to noise with electromagnetic interference.
c. Transcutaneous pacing and defibrillation pads should be placed (anterior/posterior).
d. Evaluate the pacemaker or ICD before leaving a cardiac-monitored environment.
e. ICD patients should be on monitor at all times while ICD is deactivated.
f. If any device is programmed specifically for surgery, patient cannot be taken off the monitor until the device is reprogrammed. (2)
○ Recommendations for patients—not pacemaker dependent
a. No ICD present:
i. If the surgery is not within 6 inches (15cm) of the device, then no other actions are necessary.
ii. If the surgery is within 6 inches of the device, then a magnet can be placed or the device reprogramed by a device specialist to asynchronous mode (AOO, VOO, DOO).
b. ICD or BiV ICD present:
i. Place magnet to stop tachyarrhythmia detection.
ii. If magnet is impossible to place, or surgery is within 6inches of the device, or is a cardiac/thoracic procedure, then you must call the device specialist to turn off the tachyarrhythmia detection to avoid unwarranted discharges during the procedure if electrical interference is present.
(3) Recommendations for patients—pacemaker dependent
a. No ICD present:
i. Use short electrosurgical bursts.
ii. Place magnet over device for procedures not within 6 inches (15cm) of the device.
iii. If magnet is impossible to place or surgery is within 6 inches of the device, then the device specialists must be called to reprogram to an asynchronous mode. b. ICD or BiV ICD present:
i. Use short electrosurgical bursts.
ii. If the surgery is not within 6 inches of the device, then place magnet over device to suspend tachyarrhythmia detection and contact the device specialist to reprogram the device to an asynchronous mode.
iii. If magnet is impossible to place or surgery within 6 inches of the device, then contact in-hospital device specialist to reprogram the device to an asynchronous mode to avoid electrical interference and to turn off tachyarrhythmia detection to avoid unwarranted discharges during the procedure.
What do the images above show and what is the differential diagnosis based on the appearance seen in the images above?
○ The chest X-ray (Fig. 47.1) shows diffuse bilateral coalescent opacities, whereas the CT chest (Fig. 47.2) shows ground-glass opacification, reflecting an overall reduction in the air content of the affected lung. It is also possible to visualize bronchial dilatation within areas of ground-glass opacification.
Differential diagnosis include
(a) ARDS,
(b) congestive heart failure,
(c) pulmonary hemorrhage,
(d) pneumonia,(
e) transfusion-related acute lung injury, and
(f) non-cardiogenic pulmonary edema.
What is the current definition of acute respiratory distress syndrome?
○ The Berlin definition, dated 2012, states that acute respiratory distress syndrome is an entity characterized by hypoxemia and stiff lungs that occurs within a week of a known clinical insult or new/worsening respiratory symptoms.
° It presents with bilateral opacities on the chest X-ray involving at least three quadrants that are not fully explained by effusions, atelectasis, or nodules.
° Chest computed tomography (CT) findings are opacification that is denser in the most dependent regions as compared to more normal and hyper-expanded lung in the nondependent ones. In addition, CT chest shows widespread ground-glass attenuation, which is a nonspecific sign that reflects an overall reduction in the air content of the affected lung.
○ Respiratory failure in ARDS must not be fully explained by cardiac failure, and an objective assessment for exclusion of such cause may be necessary by echocardiography.
○ Finally, ARDS is classified as mild, moderate, or severe based on PaO2/ FiO2 ratio and PEEP.
° If PaO2/FiO2 ratio is between 200 and 300mmHg with PEEP ≥5, it is classified as mild.
° If PaO2/FiO2 ratio between 100 and 200mmHg with PEEP ≥5, it is moderate.
° PaO2/FiO2 ratio less than 100mmHg with PEEP ≥5 is classified as severe.
Note that the term acute lung injury has been removed, as well as the requirement of pulmonary capillary wedge pressure ≤18mmHg.
Name some common triggers for the development of ARDS.
Common risk factors for ARDS are divided into two categories: direct and indirect.
(a) Direct causes are pneumonia, aspiration of gastric contents, inhalational injury, pulmonary contusion, pulmonary vasculitis, and drowning.
(b) Indirect causes are non-pulmonary sepsis, major trauma, pancreatitis, severe burns, non-cardiogenic shock, drug overdose, and multiple transfusions or transfusion-associated acute lung injury (TRALI).
What is the approach for mechanical ventilation on patients with the above diagnosis? ARDS
○ Protective lung strategy (also known as open lung approach or lung protective ventilation) is the standard of care for the management of patients with ARDS.
○ The ARDS Network was a randomized controlled trial designed based on the concept that the limitation of end inspiratory lung stretch may reduce mortality in this patient population.
°Patients that received lower tidal volume (Vt 4–6ml/kg ideal body weight) and maintenance of plateau pressure between 25 and 30mmHg had a survival benefit, with a decrease in mortality from 40% to 31%.
°Drawbacks from this mode of ventilation were hypoventilation leading to permissive hypercapnia and shear injury due to repetitive opening and closing of alveoli with each cycle. For that reason, PEEP should be set at above lower inflection point to prevent cyclic atelectasis.
○It is difficult to describe an efficient method of applying optimal PEEP in any given patient.
°Applying the highest PEEP that allows for maintenance of goal plateau pressure could be a reasonable approach.
°In that study, the survival benefit was also associated with a reduction of plasma IL-6, supporting the hypothesis that a lung protective strategy limits the spill of inflammatory mediators into the systemic circulation, which may induce multiple system organ failure.
○In refractory hypoxemia, prolonging the inspiratory time by increasing the I:E ratio may improve oxygenation; however, close attention must be directed to avoid air trapping, auto-PEEP, barotrauma, and hemodynamic compromise
Is there an indication for steroids, statins, or neuromuscular blockade (NMB) in ARDS
○ The use of glucocorticoid treatment for ARDS remains contradictory.
° The ARDS Network LaSRS study showed no benefit in mortality from the routine use of steroids in patients with ARDS.
° In addition, it was associated with increased risk of neuromuscular complications, as well as risk of death if started 2weeks after onset of ARDS.
° The potential adverse effects of steroids also include immunosuppression, superadded infection, and higher blood glucose levels. The mineralocorticoid component contributes to fluid/sodium retention; both of which could result in positive fluid balance, a known factor associated with poor outcomes in lung injury.
***At the moment, there is insufficient evidence to justify the routine use of steroids in patients with ARDS.
○ The SAILS trial published in 2014 compared statin with placebo in patients with ARDS in the setting of sepsis.
° Statin therapy did not reduce mortality or increase ventilator free days; therefore there is no evidence to support its use in ARDS.
○Neuromuscular blockade therapy for hypoxia has a few potential benefits.
° Avoidance of large tidal volumes that predispose to volutrauma decreased oxygen consumption from lack of muscle activity and improved patient–ventilator synchrony.
° Literature shows that the use of NMB in early (first 48h) ARDS is associated with improved mortality rate. Having said that, judicious use is warranted since paralysis interferes with neurological exam and has been linked to ICU-acquired weakness and posttraumatic stress disorder
Which nonconventional therapies can be used to enhance oxygenation in severe ARDS?
- Airway pressure release ventilation (APRV) is a combination of pressure- controlled ventilation and inverted ratio ventilation on a time-triggered, pressure- targeted, and time-cycled mode (Fig. 47.3).
○ A higher and a lower PEEP are set, and 80–95% of the respiratory cycle is spent during inspiration at the higher PEEP.
○The patient is allowed to breathe spontaneously during both high and low PEEP.
○ The mean airway pressure increases without much increase in the peak pressure, favoring lung protection.
○ This mode has been found to be associated with shorter ICU stay and duration of ventilation in patients with ARDS, but contradictory literature still exists, mostly in regard to the lack of evidence of mortality benefit. - High-frequency oscillatory ventilation (HFOV) has been evaluated recently by two randomized controlled trials (OSCAR, and OSCILLATE) as well as by a meta- analysis.
○ HFOV has failed to show any mortality benefit.
○ The HFOV group in the OSCILLATE trial had higher mortality, higher requirement for sedatives, paralytics, and vasopressors, and therefore no evidence to support its use. - Prone positioning takes advantage of gravity and repositioning of the heart in the thorax to recruit lung regions and improve ventilation–perfusion matching.
○ The mechanisms for the proposed benefit are change in diaphragm movements, increased functional and residual capacity, better secretion clearance, and reduced ventilator-induced lung injury.
○ The PROSEVA trial, published in 2013, brought attention back to this rescue mode after showing association with major decrease in 28-day and 90-day mortality, increase in ventilation-free days, and reduced time to extubation. ○ An increase in PaO2 by 10mmHg over the first 30min of prone ventilation usually predicts a sustained increase in PaO2 and deems the patient as a “responder.” - Finally, extracorporeal membrane oxygenation (ECMO) remains an important tool for managing refractory hypoxemia that is life-threatening but often considered as a last resort. Literature on its benefit is scarce and controversial.
○ Guidelines suggest it should be used in scenarios that have a potential reversible cause, less than 7days on mechanical ventilation, age <65years, no significant comorbidities, no contraindication to anticoagulation, and no significant neurological dysfunction. In case of isolated respiratory failure, a veno-venous approach is advised, whereas in case of hemodynamic instability, a venoarterial approach should be used. More evidence is needed to support its use as standard of care [5].
What is the role of nitric oxide and prostaglandins in ARDS?
○ Inhaled vasodilators reduce pulmonary arterial pressure and redistribute blood flow to well-ventilated lung regions with little to no systemic side effects, improving the ventilation–perfusion matching.
○ Inhaled nitric oxide has been shown to improve oxygenation as measured by PaO2/FiO2 ratio and oxygenation index.
○ It is expensive, gets rapidly inactivated by hemoglobin, can result in methemoglobinemia, and carries an increased risk of renal failure.
***No beneficial effect on mortality or ventilator-free days has been shown with the use of nitric oxide.
○ Inhaled prostaglandins demonstrate similar vasodilator effects when compared to nitric oxide, including improved oxygenation and reduction in pulmonary hypertension; however evidence with large randomized clinical trials is lacking.
○ Patients on these vasodilators are considered “responders” if an improvement on oxygenation is observed within the first 1h of administration.
○ Based on current evidence, inhaled vasodilators must be considered only as a rescue and temporary therapy for patients with refractory hypoxemia (with or without pulmonary hypertension) when other methods have failed.
A 58-year-old man with a diagnosis of Hodgkin’s disease presents to the anesthesia preoperative clinic prior to placement of a port. He complains of mild difficulty in sleeping totally supine and clinically shows fullness of the veins of the neck. CT scan (Fig.48.1) shows that he has a mediastinal mass with both tracheal deviation and crescentic compression. 1. What are the symptoms of a mediastinal mass?
- Symptoms of a mediastinal mass:
(a) A mediastinal mass may be asymptomatic even when it reaches a significant size. It may be discovered during routine radiological testing for the disease causing the mass or just incidentally [1].
(b) When the mass reaches a critical size within the restricted mediastinal space, it can cause signs and symptoms related primarily to the cardiac or pulmonary system.
° This can include diminished venous return via the superior vena cava (SVC) leading to fullness of the neck veins and in extreme cases cardiac dysfunction from direct compression.
° Respiratory symptoms could range from dyspnea, progressive orthopnea, voice changes (nerve palsy), and in late stages stridor
What are the physical ramifications of a significant mediastinal mass on the airway?
Physical ramifications of the mediastinal mass on the intrathoracic airway:
(a) Deviation of the trachea. This could include:
• “C”-shaped bowing of the trachea
• “S”-shaped trachea
(b) Narrowing and invasion of the lumen of the trachea and/or major bronchus:
• The trachea when externally compressed becomes crescentic as the membranous posterior wall is the first to collapse.
• Narrowing can be a short segment or a long segment of the trachea.
• Encroachment can be around the entire carinal trifurcation of the trachea.
What are the anesthesia considerations for a significant mediastinal mass?
Anesthesia considerations for a significant mediastinal mass:
(a) Lack of symptoms should not be considered as reassuring.
° This is especially true with superior or anterior mediastinal masses.
° With spontaneous ventilation, the mechanics of thoracic cage cause a distracting force on the larger airways by maintaining the intrapleural pressure gradient, helping to maintain the patency of the lumen.
° The loss of bronchial tone due to general anesthesia can also decrease lumen size.
°Thirdly, the distension of the major airways will be diminished with smaller ventilatory volumes [2]. The loss of normal spontaneous ventilation during general anesthesia can thus precipitate intrathoracic airway obstruction in such cases with catastrophic results [3].
(b) Once the airway has been secured, the anesthetic plan is determined by the surgery and patient’s other comorbidities.
(c) Placement of a regular endotracheal tube (ETT) in a trachea with “S”-shaped deviation can lead to the distal bevel end pushing up against the wall of the trachea leading to obstruction.
(d) A smaller ETT size must be chosen against the measured diameter of the lumen by CT scan.
(e) Securing the “lost” airway can possibly be done only by rigid bronchoscopy (RB).
(f) Long-segment tracheal narrowing is a cause for concern for ETT placement or for the performance of rescue rigid bronchoscopy.
(g) Extracorporeal oxygenation (ECO) which takes time with significant prior organization and access placement is the only rescue for loss of the intrathoracic airway with failed rigid bronchoscopy [4, 5].
(h) Significant and chronic tracheal compression can lead to tracheomalacia [6].
○ This weakness of tracheal wall and airway swelling due to the ETT in a narrowed lumen must be considered before extubation.
(i) Occlusion beyond the carina in one of the major bronchi is significant but less concerning than total tracheal obstruction.
(j) Intravenous lines should be placed in the lower extremities if the SVC is compromised
What are techniques for the safe administration of an anesthetic for a significant mediastinal mass?
Techniques for safe administration of anesthesia in a patient with a significant mediastinal mass:
(a) Ascertain the significance of the mass and its encroachment of the airway preoperatively—this consultation should include the surgeon (and CVT surgeon), radiologist, and anesthesiologist [7].
° The factors in risk assessment include symptoms, type of tumor, and airway compromise.
(b) Many tumor masses will show amazing resolution with chemotherapy or radiation prior to surgery. The CT scan in the above patient was repeated after short definitive therapy and showed near-total resolution of tracheal deviation and compression (Fig.48.2). This should be done if appropriate. (c) When feasible, consider avoidance of general anesthesia. In the case presented, if venous access for treatment was critically needed, this should be done under monitored anesthesia care (MAC). If SVC drainage is compromised, venous access should be secured in the lower extremity.
(d) Even if MAC or regional anesthesia is considered, every precaution to prevent loss of spontaneous ventilation must be employed. Rigid bronchoscopy must be available in the OR.
(e) If MAC or regional anesthesia is not feasible, the choices are maintenance of spontaneous ventilation with either an inhalational induction or perform awake fiber-optic intubation followed by general anesthesia with appropriate ETT placement. This should include proper selection of the appropriate ETT for size and made with reinforced material.
(f) In cases of significant compromise or long-segment stenosis, awake fiber- optic intubation after placement of access catheters for extracorporeal oxygenation in the groin is warranted [5, 8]. In extreme cases of carinal encroachment, the patient can be placed on ECO and rigid bronchoscopy performed under TIVA for airway securement (personal experience). After the anesthetic, due caution must be given to the airway, as described above (3H), before removing the ETT which must preferably be done in the fully awake and recovered patient.
Case presentation: A 44-year-old man was brought into the hospital after being hit by a truck while riding a bicycle. Glasgow Coma Scale (GCS) was 5 on presentation. CT images of his head on arrival are shown below (Fig.49.1A–C).
1. Define Glasgow Coma Scale.
○ Teasdale and Jennett first described the Glasgow Coma Scale (GCS) in 1974 as a neurological tool to assess the level of consciousness following head injury.
○ The scale is since widely used by medical professionals worldwide as a reliable and objective way of recording the conscious state of a person for initial as well as subsequent assessments.
○ The scale ranges from a minimum score of 3 (not zero) to a maximum score of 15.
○ As described in Fig.49.2, GCS has three elements: eye response, verbal response, and motor response.
How do you grade traumatic brain injury
Traumatic brain injury (TBI) can be classified as mild, moderate, or severe, based on patient’s Glasgow Coma Scale (GCS) on presentation.
○ A TBI with a GCS of 13 or above is classified as mild, 9–12 as moderate, and 8 or below as severe.
○ The patient described above, therefore, has suffered a severe traumatic brain injury.
○ Other classification systems exist secondary to the limited ability of GCS alone in predicting the outcome.
○ The model developed by the US Department of Defense and Department of Veterans Affairs uses three criteria: GCS after resuscitation, duration of post-traumatic amnesia (PTA), and loss of consciousness (LOC) .
○ It has also been proposed that changes visible on neuroimaging, such as swelling, focal lesions, or diffuse injury, should also be taken into consideration
What are the common types of traumatic brain injuries?
○ Some of the common types of traumatic brain injury include epidural hematoma, subdural hematoma, subarachnoid hemorrhage, intraparenchymal hemorrhage, contusion, intraventricular hemorrhage, and diffuse axonal injury.
○ An epidural hematoma is the bleeding from an artery leading to collection of blood between the skull and dura.
° It can present with the characteristic feature of a lucid interval following which the patient decompensates acutely.
° It is often a neurosurgical emergency requiring emergent craniotomy and hematoma evacuation.
○ Subdural hematoma is secondary to bleeding from ruptured bridging veins leading to collection of blood between the dura and arachnoid layers of meninges.
° In elderly, subdural hematomas can occur even from minor trauma and present with symptoms such as new onset headache, seizures, and focal neurological deficits.
○ Subarachnoid hemorrhage is the bleeding into the space between arachnoid membrane and pia mater.
° Trauma is the leading cause of subarachnoid hemorrhage.
○ Intraparenchymal or intracerebral hemorrhage is the bleeding into the brain tissue itself.
○ A contusion is a small intracerebral hemorrhage commonly noted in orbitofrontal and anterior temporal cortices.
○ Intraventricular hemorrhage is the bleeding into the ventricles of the brain. ° This is often accompanied by intraparenchymal hemorrhage.
° An external ventricular drain is usually placed to drain the intraventricular hemorrhage.
○ Diffuse axonal injury (DAI) happens when there is widespread damage to the white matter tracts of the brain secondary to shearing forces.
° It is one of the most devastating types of traumatic brain injury and can result in persistent vegetative state.
What are the abnormal findings in the images shown above?
○ The CT images (Fig.49.3A–C) show some of the common CT findings that can be present in cases of traumatic brain injury following high-velocity motor vehicle collisions.
○ Figure49.3A shows subdural hematomas (blue arrows) in the midline and bilaterally (right larger than left), skull fracture (red circle), and soft tissue swelling on the right (yellow arrow).
○ Figure49.3B shows significant subarachnoid hemorrhage in the basal cisterns (blue margins).
○ Figure49.3C shows a nondepressed skull fracture running obliquely through the bifrontal and left parietal calvarium (blue arrows) and comminuted depressed fractures of the bilateral nasal bones and the nasal septum (green circle).
What are the usual aspects of medical care of a patient with acute traumatic brain injury
○ Guidelines for the management of severe traumatic brain injury have been published [6, 7].
○ Broadly, the acute management of a patient with traumatic brain injury revolves around ensuring hemodynamic stability; airway protection; control of elevated intracranial pressure by emergent medical and surgical measures such as intravenous mannitol/hypertonic infusion, hyperventilation, and placement of external ventricular drain and/or emergent craniotomy and surgical intervention; rapid identification and management of other injuries; and multimodal monitoring.
○ The initial approach to a trauma patient involves the primary and secondary surveys with rapid assessment of the airway, breathing, circulation, neurologic status (GCS), and associated injuries.
○ Signs and symptoms of severe traumatic brain injury and elevated intracranial pressure (such as low GCS, pupillary dysfunction, Cushing’s triad) usually indicate the need for emergent surgical interventions.
○ Airway management in such circumstances may be complicated by the status of the cervical spine, laryngopharyngeal integrity, and full stomach.
Describe some of the important elements of perioperative anesthetic care in a patient with acute traumatic brain injury
Some of the key elements of perioperative anesthetic care in a patient with acute severe traumatic brain injury include:
(a) Treat hypotension first and then intracranial pressure (ICP).
° The cerebral blood flow is more affected by the decrease in blood pressure than by elevated ICP.
(b) Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) management:
° treat if ICP is above 20mmHg but avoid prophylactic hyperventilation. ° Define target MAP based on ICP to maintain a normal CPP and cerebral blood flow: CPP=MAP−ICP or CPP=MAP−CVP (take the higher of ICP or CVP).
° Avoid CPP<50mmHg or >70mmHg.
(c) Avoid hypotension: avoid SBP<90mmHg.
(d) Avoid hypoxia: avoid PaO2<60mmHg or O2 SaO2<90%.
(e) Maintain normovolemia.
° Avoid using hypotonic solutions such as lactated ringer, free water, or glucose containing intravenous fluids. These can increase ICP by increasing cerebral edema.
° The first choice for IV fluids in patients with brain injury is normal saline and plasmalyte.
(f) The objective is to avoid secondary injuries from hypoxemia, hypercapnia, hypotension, elevated ICP, and metabolic derangements.
Case presentation: A 51-year-old woman initially presented to the hospital with 1-month history of confusion. Figure50.1A, B illustrates the initial CT and MRI f indings. She underwent awake craniotomy with maximal resection of the mass followed by outpatient chemotherapy and radiation. She was reoperated 6months later for recurrence of the lesion noted on surveillance imaging (Fig.50.1C, D). Eight months after that, she presented with progressive weakness, confusion, aphasia, and gaze preference and was found to have further progression of the disease (Fig.50.1E, F).
1. Identify and describe the abnormal findings in the images shown above.
○ The CT and MRI images of the brain depicted in Figs.50.1A, B and 50.2A, B show an irregular heterogeneously enhancing mass lesion centered in the region of the splenium of the corpus callosum, slightly to the left of the midline.
° This mass extends to involve the left lateral ventricle and bilateral thalami. ○ These findings are concerning for a high-grade glioma, likely glioblastoma multiforme.
° This patient underwent awake craniotomy and resection of the mass followed by outpatient chemotherapy and radiation.
° The pathology confirmed the diagnosis of glioblastoma.
○ Figures50.1C, D and 50.2C, D depict the local recurrence of the tumor sixmonths later. Following this, the patient underwent repeat craniotomy and tumor resection.
○ Figures50.1E, F and 50.2E, F depict the pre- and post- contrast MRI images which reveal recurrence in the right frontal region eightmonths later (encircled region).
° Radiation-induced changes are also noted (blue arrows). The decision was made to pursue hospice care at this point.
How are brain tumors classified?
○ Brain tumors can be classified in a number of ways.
°A primary brain tumor is a tumor that starts in the brain, as opposed to metastatic brain disease.
° Primary brain tumors can be classified as benign tumors that tend to have slower growth and distinct borders vs. malignant tumors that grow rapidly, invade the surrounding tissues and structures, and have grave prognosis.
○ Brain tumors are also commonly graded using the WHO grading system.
° Grade I tumors such as craniopharyngiomas and pilocytic astrocytomas grow slowly and are associated with good long-term prognosis.
° Grade II brain tumors are also slow growing but can spread into adjacent tissue.
°Grade III and IV tumors are malignant. Glioblastoma is the most common example of a grade IV primary brain tumor.
○ A very extensive WHO classification of brain tumors was recently published and serves as the guideline for neurosurgeons and neuropathologists.
List some of the common brain tumors.
○ The most common brain tumors include meningiomas, gliomas, and metastatic brain disease.
○ Meningiomas are the most common primary brain tumors.
° A meningioma is a tumor that arises from the meninges, which are the linings of the brain.
°They occur most frequently in middle-aged women.
°They are benign, WHO grade I tumors, and surgery is the usual first-line treatment. Small asymptomatic meningiomas can also just be observed. °Approximately 5% of meningiomas are malignant in nature.
○ Gliomas are tumors arising from glial cells which form the supportive tissue of the brain.
°They are the second most common primary brain tumors but comprise the most common malignant brain tumor.
°An astrocytoma is a glioma arising from the glial cells called astrocytes.
°A grade IV astrocytoma is also called Glioblastoma multiforme or GBM. °GBM can present with a variety of neurological signs and symptoms such as headache, seizures, and focal neurologic deficits. Usual treatment is maximal surgical resection followed by radiation and chemotherapy, but recurrence is frequent and prognosis is usually grave.
○ Craniopharyngioma is a benign tumor that arises from a nest of cells located near the pituitary stalk.
°These tumors can present with signs of increased intracranial pressure by causing obstruction of CSF outflow across the foramen of Monro.
°Surgery is the first-line treatment.
○Medulloblastoma is a high-grade cerebellar tumor usually seen in children. °They can extend into the fourth ventricle and cause hydrocephalus by obstructing CSF outflow and metastasize to the spinal cord.
°Treatment included resection followed by radiation and chemotherapy.
°Metastatic brain disease is the spread of a primary tumor elsewhere in the body to the brain.
°The common cancers that spread to the brain are those arising in the thyroid, lung, breast, kidney, prostate, and colon, as well as melanomas.
°The prognosis is grave.
What is the role of steroids in the acute management of brain tumors?
○ Steroids are often used acutely to treat the cerebral edema that can sometimes be caused by a brain tumor.
○ There are two broad categories of cerebral edema: cytotoxic edema and vasogenic edema.
°Cytotoxic edema happens after neuronal death and involves both grey and white matter. This is usually seen after a stroke.
°Vasogenic edema involves the white matter only and is often associated with tumors, infections, and hypertensive encephalopathy. Steroids are very effective for vasogenic edema from brain tumors and can temporarily relieve some of the neurologic signs and symptoms.
○They can be utilized before, during, or after surgery or to treat edema caused by radiation therapy.
○ Steroids can also be prescribed to improve quality of life in patients with advanced primary or metastatic neoplastic brain disease.
○ The usual dose in acute setting is dexamethasone 10mg IV followed by 4mg every 6h.
Describe important elements of anesthesia in a patient undergoing awake craniotomy for an intracranial mass lesion.
○ Awake craniotomy is utilized when the brain lesion (such as a tumor) is located in close proximity to an eloquent cortical region such as Broca’s area or the motor strip.
○ It provides the neurosurgeon the opportunity to preserve neurological function and limit deficits by performing awake functional cortical mapping during the resection.
○ The procedure, however, poses some unique challenges to the anesthesiologist [2].
° Patient cooperation during the procedure is critical, and loss of intraoperative cooperation may result in a failed awake craniotomy.
° Well- motivated and mature patients are the best candidates.
° Preoperative evaluation should include a discussion of the expectations and level of cooperation required during the procedure as well as eliciting risk factors for failed awake craniotomies such as history of alcoholism, low tolerance to pain, and anxiety or psychiatric disorders [3].
° Intraoperatively, the most critical element of anesthesia management is provision of a rapid and smooth transition of the anesthetic depth tailored to the different surgical stages while maintaining a stable hemodynamic and cardiopulmonary function. Comfortable positioning is mandatory. Several different anesthetic techniques have been described such as conscious sedation, asleep-awake-asleep technique, and asleep-awake technique. The choice of anesthetic agent is highly dependent upon the requirement for functional cortical mapping and intraoperative electrocorticography. Propofol infusion with a supplementary opioid is a common anesthetic choice for awake craniotomies.
A 38-year-old female has undergone an ORIF of the femur with a general anesthetic and epidural anesthesia for postoperative pain. On the second postoperative day, she is complaining of increasing back pain, numbness, and some weakness on the left leg. Her VSS show a blood pressure of 110/60mmHg, HR 85, RR 14, T-38.8 C.The surgeon would like you to remove the epidural catheter. She is on aspirin and subcutaneous heparin 5000 units three times a day
. What does the MRI show you in this picture?
○ Figure 51.1A and B shows a fluid collection in the epidural space in the thoracic spine in a T1-weighted image in sagittal and axial views, respectively. ○ Figure51.1C and D shows a hyperintense mass at the same level in a T2-weighted image.
○ Figure51.1D shows an intense mass pushing on the anterior aspect of the spinal cord (white arrows).
○ Spinal epidural hematoma can occur spontaneously or may follow spinal or epidural anesthesia [1].
° The peridural anterolateral venous plexus usually is most often the primary source, though arterial sources of hemorrhage can occur rarely. ° This is supported by the fact that hematoma usually develops over hours to days suggesting a slow accumulation of blood from a venous bleed.
° The hematoma usually extends to the dorsal aspect of thoracic or lumbar region over several vertebral levels. If the patient has any contraindication to obtaining a MRI, then a CT myelography scan may be substituted to make an early diagnosis. MRI is however more specific in detecting the various stages of hematoma compared to CT myelography and is considered the first choice diagnostic step to confirm the presence of an epidural hematoma.
°An acute hematoma usually presents as low signal intensity signal on T1-weighted image and high signal intensity on T2-weighted image [2].
What is the incidence of this condition?
Epidural hematoma after neuraxial anesthesia is fortunately a rare event. The true incidence is unknown but is estimated to occur at an incidence of 1:220,000 after a spinal block and 1:150,000 after an epidural block [3]. The risk is much higher at 1in 3000in certain patients with risk factors. The risk is much lower in the obstetric population compared to vascular patients. About 1in 430 patients with epidural catheters will be suspected to have an epidural hematoma and undergo a workup for it [4].
How does this condition present clinically?
○ Patients with epidural hematoma present with severe unrelenting, nonpositional, acute onset back pain and varying degrees of lower-limb weakness and sensory deficits.
○ Some patients may have motor weakness as a primary symptom in the absence of back pain.
○ If the compression is extensive, then it could cause bowel and bladder incontinence.
○ Symptoms could be absent or attenuated in the presence of a well-functioning epidural catheter infusing high concentrations of local anesthetics.
○ Symptoms rarely develop in the immediate postoperative period and typically take 2–3days. Once symptoms begin, they can progress from back pain to a complete or partial paraplegia or even quadriplegia in a fewhours.
A 38-year-old female has undergone an ORIF of the femur with a general anesthetic and epidural anesthesia for postoperative pain. On the second postoperative day, she is complaining of increasing back pain, numbness, and some weaknesco privation s on the left leg. Her VSS show a blood pressure of 110/60mmHg, HR 85, RR 14, T-38.8 C.The surgeon would like you to remove the epidural catheter. She is on aspirin and subcutaneous heparin 5000 units three times a day
What is the differential diagnosis for this patient?
○The differential diagnosis for this presentation can include
• epidural abscess,
• intradural hemorrhage,
• prolonged and exaggerated neuraxial block,
• anterior spinal artery syndrome,
• spinal cord compression due to presence of tumors,
• disc herniation,
• worsening of previous spinal stenosis,
• lumbar radiculopathy,
• compression fracture of the spine, and
• spinal cord infarction.
○ There should be a high index of suspicion for an epidural hematoma in an anticoagulated patient who has an epidural catheter and in the presence of back pain with neurological deficits.
A 38-year-old female has undergone an ORIF of the femur with a general anesthetic and epidural anesthesia for postoperative pain. On the second postoperative day, she is complaining of increasing back pain, numbness, and some weakness on the left leg. Her VSS show a blood pressure of 110/60mmHg, HR 85, RR 14, T-38.8 C.The surgeon would like you to remove the epidural catheter. She is on aspirin and subcutaneous heparin 5000 units three times a day
What are its risk factors?
○ The risk factors for developing an epidural hematoma include “patient-specific” factors or “surgery-related” issues.
○ “Patient-specific factors” include advanced age, needle size, presence of epidural catheter, females, trauma patients, spinal cord and vertebral column abnormalities, preexisting spinal stenosis, organ function compromise, presence of underlying coagulopathy, traumatic or difficult needle placement, as well as indwelling catheter in anticoagulated patient.
○ Spontaneous spinal epidural hematoma can sometimes occur with anticoagulation, thrombolysis, blood dyscrasias, coagulopathies, thrombocytopenia, neoplasms, or vascular malformations. ○ “Surgery-related factors” include prolonged surgery and high intraoperative blood loss
How could one prevent epidural haematoma occurrence?
○ The practice guidelines put forth by the American Society of Regional Anesthesia and Pain Medicine provide several preventive measures to avoid the occurrence of epidural hematoma.
○ The rarity of occurrence mandates that most guidelines come from the collective experience of recognized experts in the field of regional anesthesia and anticoagulation. They are based on case reports, clinical series, pharmacology, hematology, and risk factors for surgical bleeding.
○ The timelines to stopping and restarting anticoagulants after neuraxial anesthesia are summarized in Table51.1.
○ Multiple anticoagulants always pose an additional risk even in the case of aspirin, selective serotonin reuptake inhibitors, and nonsteroidal anti- inflammatory medications [5, 6].
○ Several newer anticoagulants in the past few years necessitate a thorough knowledge of these drugs and their impact on neuraxial anesthesia.
○ Optimal coagulation is necessary during needle placement, maintenance, and removal of catheters.
○ Close monitoring of anticoagulation status, frequent and regularly timed neurological checks, and the use of low- concentration local anesthetics are necessary to avoid this dreaded complication.
What treatment options are available? Spinal haematoma
The treatment of epidural hematoma is timely diagnosis, consultation with a neurosurgeon, and an emergency laminectomy to avoid persistent neurological deficits. The prognosis is best when the laminectomy is done within 8h. Treatment delay greater than 24h is associated with the worst prognosis [7].
An 82-year-old man with a history of hypertension, hyperlipidaemia and COPD presented from a nursing home for an emergent laparotomy for a ruptured appendix. A transoesophageal echocardiography (TEE) probe was placed intraoperatively for diagnosis and monitoring after several attempts at managing hypotension proved futile. Questions 1. What are some of the benefits of using TEE in managing patients for non-cardiac surgery?
TEE can provide immediate and accurate haemodynamic measurement of cardiac function including cardiac output and left ventricular filling pressure, chamber preload, atrial interaction and pulmonary arterial pressures. Doppler ultrasound principles are used to derive intracardiac flow across orifices and valves in order to calculate orifice area, stroke volume and cardiac output. Intraoperative cardiac output measurement provides a tool for assessing global cardiac function. The information obtained from the cardiac output measurement can be used in guiding therapeutic decision during cardiac and non-cardiac surgery. The use of TEE for cardiac output measurement thus provides a simple and reliable minimally invasive method of assessing cardiac function. Intraoperatively, TEE can be used to diagnose or redefine the cause of haemodynamic instability and detect new or unsuspected pathology like valvular (stenosis or regurgitation) and other lesions.
What physics principles underlie the calculation of valve area, stroke volume and cardiac output using TEE? (See Figs. 52.1, 52.2, 52.3, 52.4 and formula illustration)
○ Blood flow across valves and orifices of the heart can be obtained using the Doppler capabilities of echocardiography and applying the basic principle of physics and fluid dynamics.
○ According to the principles of physics and fluid dynamics,
° Volume in a cylinder = cross-sectional area of the cylinder or vessel × vessel length of cylinder or vessel
pr2L 2 ´=´ , where r is the radius of the cylinder or vessel and L is the distance between the two point (or the length of the cylinder or vessels).
Also, flow rate (Q) is calculated as Flowrate Q volume Area ()==´= ´p2 L t t where t is time for fluid to traverse from point A to B.
Intraoperative echo showed a severely calcified aortic valve with a left ventricular outflow tract diameter (LVOT) of 2.59cm, an LVOT VTI of 17.5, maximum LVOT velocity (Vmax) of 69.2cm/s, aortic valve VTI of 152cm and an aortic valve Vmax of 533cm/s. The heart rate on the monitor was 97beats/min. How would you calculate the stroke volume and cardiac out?
A 60-year-old-patient with a history of right upper lobe lung cancer, peripheral vascular disease, and chronic bronchitis is scheduled for a transthoracic echocardiography as part of workup for lung resection. Echocardiography evaluation revealed a severely calcified aortic valve, severe left ventricular hypertrophy, and a low normal ejection fraction (EF 50%): 1. What is the etiology and pathophysiology of aortic stenosis?
Causes of aortic stenosis (AS) in adults:
(a) Degeneration of tricuspid valve—commonest, seen after 60years age, caused by generalized atherosclerosis
(b) Degeneration of bicuspid valve—seen before 60, fusion of right and left cusps resulting in large anterior and small posterior cusp, associated with aortic dissection, aneurysm and coarctation
(c) Rheumatic—commonest cause worldwide, usually associated with mitral disease as well
(d)Outflow obstruction:
• Subvalvular—either membrane or hypertrophic obstructive cardiomyopathy (HOCM)
• Supravalvular—Williams syndrome Aortic sclerosis, defined as valve thickening without obstruction to LV outf low, is present in 25% of adults over 65years of age. Predisposing factors common to both aortic stenosis and sclerosis are hypertension, smoking, serum low-density lipoprotein, and diabetes mellitus.
○ Aortic sclerosis usually progresses to aortic stenosis in the presence of progressive inflammatory atherosclerosis. ○ Ten percent of patients with aortic sclerosis progress to AS within 5years.
○ In the 2014 ACC/AHA guidelines on valvular disease, aortic sclerosis is considered part of the AS continuum with sclerosis assigned stage A (at risk group).
How do you assess and grade aortic stenosis?
○ Diagnosis and assessment of severity of AS made on the basis of history, physical exam, and echocardiographic findings.
○ Patients with severe aortic stenosis (AS) usually present with angina, syncope, sudden death, or heart failure.
○ Physical exam may reveal a crescendo-decrescendo ejection murmur.
○ ECG will show signs of left ventricular hypertrophy and left atrial enlargement.
○ Two-dimensional echocardiography with Doppler evaluation (TTE or TEE) is the test of choice to confirm the diagnosis of AS and assess severity and also note the presence of coexisting diseases such as aortic regurgitation, mitral stenosis, mitral regurgitation, aortic root dilation, and coronary artery disease (Fig. 53.1).
○ The peak velocity and mean pressure gradient across the aortic valve are measured by means of Doppler interrogation of the aortic valve (Fig. 53.2).
○ Accurate Doppler measurement of aortic valve velocity (and pressure) requires a near parallel alignment of the ultrasound beam to the aortic valve.
○ The normal aortic valve area is approximately 3.0–4.0cm2.
○ The velocity and pressure gradients across the aortic valve are flow dependent.
○ In patients with low ejection fraction, dobutamine or exercise stress echo may be needed to confirm the diagnosis.
○ In the 2014 guidelines, severity of AS was divided into 4 stages (A, B, C, and D) based on valve anatomy, valve hemodynamics, hemodynamic consequence, and symptoms [1] (Table53.1
What is the natural history of patients with aortic stenosis?
○ Patients with aortic stenosis usually present when symptoms become severe enough to disrupt normal daily activity.
○ Prior to that, morbidity and mortality are very low.
○ The rate of progression to severe aortic stenosis varies, but in general it has been shown that in patients with at least moderate aortic stenosis, jet velocity across the aortic valve increases by 0.3m/s per year, mean gradient increases by 7mmHg per year, and AVA decreases by 0.1cm2 per year.
○ Patients with symptomatic or severe aortic stenosis present with angina, dyspnea, lightheadedness, syncope, and heart failure. Sudden death is a feared complication of severe aortic stenosis, and, although rare, it has been reported to occur without symptoms.
○ Average survival in patients with symptomatic aortic stenosis is 30–50% at 2years.
○ Patients with asymptomatic severe AS require close monitoring in order to detect sudden changes in symptoms.
○ Patients with mild-to-moderate aortic stenosis will not have symptoms of the disease, but due to the unpredictable disease progression, it is mandatory for these asymptomatic patients to have regular clinical follow-up and evaluation for development of symptoms and disease progression. During these follow-ups, patients should be educated on the signs and symptoms of disease progression such as exercise intolerance, exertional chest discomfort, dyspnea, and syncope.
What interventions are available for patients with aortic stenosis
○ Appearance of symptoms is the most important indication for intervention in patients with aortic stenosis.
○ There are no specific medical therapies to treat or slow the progression of aortic stenosis.
○ It is recommended to treat hypertension in patients with increased risk of developing AS (stages B and C)
○ Hypertension is prevalent in patients with AS and has been shown to be a risk factor for AS and also increase the morbidity and mortality risk associated with AS.
○ The treatment is started at low dose, and patients should be monitored closely by experienced cardiologist to avoid complications associated with the disease state or treatment in these high-risk patients.
○ Angiotensin-converting enzyme (ACE) inhibitors, diuretics, and vasodilators can be used in the acute setting in patients with severe decompensated AS.The use of these medications may require invasive hemodynamic monitoring.
○ Aortic valve replacement (AVR) is the only definite treatment for patient with AS.
°Early surgical intervention has been shown to decrease mortality in patients with severe AS.
° Decision to operate should be based on symptoms, valve anatomy, and hemodynamics.
°The ACC/AHA guideline recommends surgical AVR for all patients who meet an indication for AVR with low or intermediate surgical risk.
°Major indications for surgical AVR (class I recommendation) are severe symptomatic AS, asymptomatic severe AS with LVEF <50%, asymptomatic severe AS in patients undergoing CABG, other heart surgeries or surgery on the aorta.
°In patients with moderate AS undergoing other cardiac surgery, it is reasonable to perform surgical AVR if the aortic velocity is between 3 and 3.9m/s or the mean pressure gradient is between 20–39mmHg (class IIa recommendation).
° These patients are likely to have symptoms of the disease within 5years due to the progressive nature of aortic stenosis.
°Transcatheter aortic valve replacement (TAVR) is a minimally invasive surgical procedure for replacing the aortic valve. At present, it is indicated in patients with severe AS who are high risk for open surgical replacement of the aortic valve.
°It involves placing a valve mounted on balloon at the tip of a catheter over a diseased native aortic valve. °The catheter is fed through either the femoral artery or through the apex of the heart which require a small incision to be made on the left chest wall.
°According to the ACC/AHA 2014 guidelines on valvular disease, TAVR is recommended in AS patients with indications for AVR who have a high risk for open AVR, or a prohibitive surgical risk and a predicted post TAVR risk greater than 12months.
A 45-year-old Caucasian female with a recent history of breast cancer status post- chemotherapy and radiation therapy was admitted with high-grade fever, slurred speech, back pain, and petechial rash. Surveillance cultures had been inconclusive with one of three samples being positive for coagulase-negative Staphylococcus aureus. Transthoracic echocardiography, performed as part of initial workup, showed no valvular vegetation, preserved ejection fraction (55%), and mild aortic regurgitation. A diagnosis of infective endocarditis was suspected, and despite treatment with antibiotics, the patient continued to have intermittent high-grade fever and signs and symptoms of congestive heart failure. Transesophageal echocardiography performed 7days’ post-presentation showed a large mobile mass on the aortic valve, severe aortic regurgitation with a depressed ejection fraction of 40% (see Figs.54.1, 54.2, and 54.3). Therefore, cardiothoracic surgery was consulted for evaluation for possible valve replacement surgery.
What are the risk factors for infective endocarditis?
The following patients present a high risk for infective endocarditis [1–9]:
(a) Male, elderly (age>60)
(b) Prior history of prior IE
(c) Poor dental hygiene
(d) Patient undergoing dental procedures involving gingival tissues
(e) Patients with valvular heart disease (e.g., rheumatic valvular disease)
(f) Patients with uncorrected or partially corrected congenital heart disease
(g) IV drug use
(h)Prosthetic valves
(i) Immunosuppressed patient
(j) Patients with history of diabetes
(k) Patients with intracardiac devices
(l) Patients undergoing hemodialysis
What do Figs.55.1, 55.2, and 55.3 represent?
○ The figures show still echocardiographic frames for a patient with mitral valve regurgitation.
○ Figure55.1 is color flow Doppler with transesophageal echocardiography, and Figs.55.2 and 55.3 demonstrate continuous wave Doppler sampled across the mitral valve and pulsed wave Doppler sampled at the mitral valve using transthoracic echocardiography (TTE).
Define color flow Doppler and its application in mitral valve regurgitation.
○ Color flow Doppler displays intracavity blood flow in colors (red, blue, green, or their combinations) depending on the velocity, direction, and extent of turbulence.
○ Color flow Doppler is a widely used method for the detection of regurgitant valvular heart disease.
○ This technique provides visualization of the origin and width (vena contracta) of the regurgitation jet, spatial orientation of the jet area in the receiving chamber, and flow convergence into the regurgitant orifice.
○ The area of the regurgitant jet can provide a rapid quantitative assessment of the severity of the regurgitation; generally speaking, a large area may indicate a more significant regurgitation.
○ Vena contracta or regurgitant jet width (black double arrow in Fig.55.1) is the narrowest portion of a jet that occurs at/ or just downstream from the orifice of the valve, and it is an indirect measure of the regurgitant orifice.
○ Proximal isovelocity surface area (PISA) or flow convergence is another method to quantify the severity of mitral valve regurgitation.
°It is based on the continuity equation and the principle of flow conversation .
°As blood in the left ventricle approaches the mitral regurgitant orifice, there is convergence and flow acceleration. This is seen in hemispheric waves of decreasing area but of equal velocity (hence, the term isovelocity) .
○ PISA is identified by color flow Doppler as the “red-blue” aliasing interface (PISA radius is the distance between the “+” signs in Fig.55.1). ○ PISA radius is used to calculate the effective regurgitant orifice area (ERO), which is the cross-sectional area of the vena contracta, and regurgitant volume (which is the volume of the blood that is leaking back to the left atrium during systole) [1].
○ ERO and the regurgitant volume can also be calculated using the volumetric method.
○ In the absence of significant aortic valve regurgitation, the regurgitant volume is equal to the flow across the mitral valve minus the flow across the left ventricular outf low tract (systemic stroke volume) [1].
○ These calculations are made by obtaining the LVOT and mitral valve diameters and LVOT and mitral valve time-velocity integral (TVI).
○ Figure55.3 shows pulsed wave Doppler at the mitral valve which depicts the TVI of the mitral valve.
Describe the different grades of mitral valve regurgitation.
○ Mitral valve regurgitation is graded into mild, moderate, and severe.
○ This is based on quantitative as well as qualitative assessment, and it involves the use of Doppler echocardiography.
○ The visualization of the jet area and jet area to left atrium area ratio by color flow Doppler provides a quick assessment tool of the severity of mitral valve regurgitation [3].
○ This method tends to underestimate eccentric jets and overestimate the severity of mitral regurgitation in ventral jets.
○ Mitral valve regurgitation can be quantitatively assessed by measuring the vena contracta width, effective regurgitant orifice area, the regurgitant volume, and the regurgitant fraction (the ratio between the regurgitant volume and the flow across the mitral valve).
○ Table55.1 illustrates the different grades of mitral valve regurgitation using the different variables [3]. °Based on the data provided in the figures, this case represents severe mitral valve regurgitation (vena contracta 0.7cm and regurgitant volume of 63mL).
I.A 48-year-old male with history of uncontrolled hypertension and end-stage renal disease on hemodialysis presents for TTE as part of preoperative risk stratification prior to possible renal transplant. He has NYHA Class III symptoms at baseline. 2D images show moderately to markedly increased left ventricular wall thickness. LVEF calculated by the biplane Simpson’s method is 56%. The remainder of his diastolic parameters are as shown in Figs.56.1, 56.2, 56.3, and 56.4.
Describe what happens in normal diastole
○ Diastole is defined as the portion of the cardiac cycle between aortic valve closure and mitral valve closure.
○ It is normally divided into four phases: isovolumic relaxation, rapid early diastolic filling, diastasis, and atrial contraction.
○ Isovolumic relaxation occurs between aortic valve closure and mitral valve opening.
°Through an active, calcium-dependent process, left ventricular pressure decreases, while volume remains the same.
° When left ventricular end- diastolic pressure falls below left atrial pressure, the mitral valve opens and rapid early diastolic filling begins.
° This usually accounts for 70% of left ventricular filling.
° As pressures equalize between the left atrium and left ventricle, a small amount of filling continues via passive flow from the pulmonary veins; this is diastasis.
° Diastasis generally accounts for 5% of left ventricular filling and is only present at slower heart rates. If the patient is in sinus rhythm, atrial systole follows diastasis.
° Left atrial pressure again transiently increases, and there is further filling of the left ventricle.
° Atrial contraction generally accounts from 25% of left ventricular filling in the normal heart.
° Diastolic function is influenced by volume status, properties of the left ventricle (stiffness, recoil), atrial properties, and catecholamines.
What are the causes of diastolic dysfunction? What is the difference between diastolic dysfunction and heart failure with preserved ejection fraction (HF-pEF)?
○ Aging, hypertension, diabetes, obesity, coronary artery disease, renal disease, valvular heart disease, and infiltrative processes all affect left ventricular mechanics/stiffening and thus diastolic function.
○ In the presence of systolic dysfunction, diastolic function is always abnormal.
○ HF-pEF is defined as the presence of diastolic dysfunction accompanied by signs/symptoms of clinical heart failure in patients with an ejection fraction of at least 50%.
How do you use echocardiography to grade diastolic dysfunction?
○ In the 2016 American Society of Echocardiography/European Association of Cardiovascular Imaging guidelines, there are four main echocardiographic parameters used to assess diastolic dysfunction: mitral inflow pulse wave (PW) Doppler, annular tissue Doppler imaging (TDI), peak tricuspid regurgitant (TR) velocity, and left atrial end-systolic volume index (LAESVi).
○ Mitral inflow PW Doppler is measured in the apical four chamber (A4C) view with the Doppler cursor placed at the mitral leaflet tips.
° The initial wave of early diastolic filling is labeled the E wave.
°The second wave represents filling due to atrial contraction and is labeled the A wave.
°In normal hearts the E/A ratio is typically between 0.9 and 1.5.
°As relaxation becomes impaired, but before left atrial pressures (LAP) rise, there is an increased reliance on atrial contraction to maintain diastolic filling, and the E/A ratio is <0.9.
°As LAP continues to rise, there is again more filling happening in early diastole due to the increased pressure gradient between the left atrium (LA) and left ventricle (LV), and the E/A ratio becomes “pseudo normal.”
°As left ventricular compliance decreases and LAP rises further, there is initial brief filling in early diastole with relatively little filling happening during atrial contraction, and the E/A ratio increases to ≥2.
○ Mitral inflow PW Doppler varies with volume status, mitral valve disease, and atrial arrhythmias.
○ Annular TDI velocities are measured with PW Doppler in the A4C view with the cursor placed at both the septal and at the lateral mitral annulus.
°Myocardial relaxation in early diastole is labeled e′.
°Septal and lateral e′ velocities are normally >7cm/s and >10cm/s, respectively [3].
° As myocardial relaxation becomes impaired, annular tissue Doppler velocities decrease. °The ratio of mitral inflow during early diastolic filling (E) and tissue Doppler early myocardial relaxation (e′) has been shown to correlate with LAP.
°Specifically, an average E/e′ ratio>14, a septal E/e′ ratio>15, and a lateral E/e′ ratio>13 are consistent with elevated LAP [2].
° Annular TDI velocities are not dependent on volume status but are unreliable in the presence of significant mitral annular calcification, a mitral prosthesis, or a mitral annuloplasty ring.
○ The peak TR velocity (Fig. 56.3) also positively correlates with LAP and pulmonary capillary wedge pressure (PCWP) in the absence of pulmonary vascular or pulmonary parenchymal disease.
°It should be measured using continuous wave (CW) Doppler in multiple views with an attempt to get the cursor as parallel as possible to the direction of regurgitant flow.
°A peak TR velocity>2.8m/s is consistent with elevated LAP [3]. Finally, left atrial size is related to chronic elevations in LAP (in the absence of mitral valve disease, atrial arrhythmias, or post-cardiac transplant).
°Left atrial size is best assessed by the left atrial end-systolic volume index (LAESVi), with left atrial area traced in atrially focused A4C, and apical 2-chamber (A2C) views one to two frames before mitral valve opening.
°Left atrial volume is calculated using either Simpson’s method of disks or the area-length method (0.85×A1×A2)/ (L1–L2/2) and is indexed to body surface area (BSA). A LAESVi >34mL/m2 is consistent with chronic elevations in left atrial pressure [2].
⊙ Currently, the main purpose in grading diastolic dysfunction is to evaluate whether LAP is elevated as elevated LAP is modifiable and correlates with symptoms and outcomes.
☆ Grade I diastolic dysfunction is characterized by impaired left ventricular relaxation with normal filling pressures. There is a decrease in early diastolic f illing and an increase in filling with atrial contraction.
☆ Filling pressures are elevated in grades II–IV diastolic dysfunction. In grade II diastolic dysfunction, the left atrium remodels and left atrial pressures increase to compensate for elevated left ventricular end-diastolic pressures.
☆ Grades III–IV diastolic dysfunction represent restrictive filling where left ventricular filling only occurs in the setting of markedly elevated left atrial pressures due to reduced left ventricular compliance (exaggerated change in pressure for a small change in volume). Grade III is reversible; grade IV is irreversible [1–3]. Table56.1 summarizes the findings for each of the four key variables in grades I–IV diastolic dysfunction.
What do Figs.56.1, 56.2, 56.3, and 56.4 show?
- With our patient, the mitral inflow PW Doppler E/A ratio is 1.2 (Fig.56.1). This is either normal or pseudo normal. Therefore, we need to assess his average E/e′ ratio, his peak TR velocity, and his LAESVi. His average E/e′ ratio is >14 at 19.3 (Fig.56.2). His peak TR velocity is >2.8m/s at 4.19m/s (Fig.56.3). His LAESVi is >34mL/m2 at 66.5mL/m2 (Fig.56.4). As all three parameters are abnormal, LAP is elevated, and he has grade II diastolic dysfunction
I. A 48-year-old male with history of uncontrolled hypertension and end-stage renal disease on hemodialysis presents for TTE as part of preoperative risk stratification prior to possible renal transplant. He has NYHA Class III symptoms at baseline. 2D images show moderately to markedly increased left ventricular wall thickness. LVEF calculated by the biplane Simpson’s method is 56%. The remainder of his diastolic parameters are as shown in Figs. 56.1, 56.2, 56.3, and 56.4.
Does this patient have normal or abnormal diastolic function? How would you grade it
Page 303
○ With our patient, the mitral inflow PW Doppler E/A ratio is 1.2 (Fig.56.1).
°This is either normal or pseudo normal.
°Therefore, we need to assess his average E/e′ ratio, his peak TR velocity, and his LAESVi.
°His average E/e′ ratio is >14 at 19.3 (Fig.56.2).
°His peak TR velocity is >2.8m/s at 4.19m/s (Fig.56.3).
° His LAESVi is >34mL/m2 at 66.5mL/m2 (Fig.56.4).
○ As all three parameters are abnormal, LAP is elevated, and he has grade II diastolic dysfunction.
A 70-year-old male presents to the ED after an industrialfate accident causing a traumatic below-knee amputation on the right side. The patient has been obtunded and dyspneic since arrival. A total of six pRBC units and 5L of crystalloids have been given in the last hour. You have been asked to evaluate this patient prior to operative BKA.HR, 120; BP, 90/60; RR, 35; SpO2, 84%.
Questions 1. What is the view shown in the picture and how do you obtain it (See Fig. 57.1)?
○ This is a longitudinal view of the subcostal inferior vena cava.
○ In the supine position, if possible with the knees bent, (relaxes abdominal wall) the probe is placed in the midline 2 or 3cm below the xyphoid perpendicular to the abdominal wall with the orientation marker pointing toward the 3 o’clock position (See Fig. 57.1A).
○ Focusing on the right atrium the probe is turned counterclockwise until the orientation marker is pointing toward the patient’s head or until the IVC is seen merging into the RA.
○ The IVC diameter is best-measured 2–3cm before the IVC-RA junction, where the IVC walls are parallel [1].
How do you interpret the following images?
○ The following ultrasound images are obtained from the patient:
° Figure 57.2 shows a longitudinal view of the subcostal inferior vena cava.
° Figure 57.3 shows a longitudinal view of the subcostal inferior vena cava in M-mode measuring the IVC diameter during inspiration and expiration
○ Ultrasound images of the IVC could be interpreted using the following criteria [1]:
(a) Hypovolemia: a reduced IVC diameter (<2.5cm) and collapse with inspiration greater than half or complete collapse
(b) Hypervolemia: an increase in IVC diameter (>2.5cm) and minimal collapse with inspiration.
• Other situations that can cause this appearance are cardiac tamponade, mitral regurgitation, or aortic stenosis.
Interpretation of IVC Diameter [5]:
(a) By measuring IVC diameter (normal 1.5–2.5cm):
• Less than 1cm: Very possible large blood loss necessitating blood transfusion
• Less than 1.5cm: Possible hypovolemia
• More than 2.5cm: Possible hypervolemia
By measuring IVC diameter collapse with inspiration (Caval Index) preferably in M-mode as shown in Fig.57.3: =
• Cavalindex IVCdiameterinexpirationIVCdiameter ininspiratio n ()´ 100 IVCdiamterinexpiration
• Caval index >50% suggests fluid responsiveness.
(c) Central venous pressure estimated by IVC imaging.
• CVP of 0–5cm H2O: Findings include an IVC diameter of less than 1.5cm and a total collapse with inspiration.
• CVP of 5–10cm H2O: Findings include an IVC diameter between 1.5 and 2.5cm, and a caval index of >50%.
• CVP of 11–15cm H2O: Findings include an IVC diameter between 1.5 and 2.5cm, and a caval index of <50%.
• CVP of 16–20cm H2O: Findings include an IVC diameter larger than 2.5cm, and a caval index of <50%.
• CVP larger than 20cm H2O: Findings include an IVC diameter larger than 2.5cm, and no changes in the diameter with inspiration. The dynamic image of the IVC ultrasound obtained in this case shows volume overload in the patient based on criteria discussed.
A 70-year-old male presents to the ED after an industrial accident causing a traumatic below-knee amputation on the right side. The patient has been obtunded and dyspneic since arrival. A total of six pRBC units and 5L of crystalloids have been given in the last hour. You have been asked to evaluate this patient prior to operative BKA.HR, 120; BP, 90/60; RR, 35; SpO2, 84%.
Would you change this patient’s management, based on the ultrasound findings, and how?
○ The ultrasound images (see answer to question 3) appear to show a patient that could be in acute congestive heart failure, secondary to massive transfusion of blood products/crystalloids (flash pulmonary edema).
○ This finding needs to be confirmed (see answer to question 5). If congestive heart failure is strongly suspected continuing fluid resuscitation will worsen the situation.
○ A more precise measurement of his fluid status and cardiac function is necessary to guide further therapy. Other supportive measures like ventilatory support, forced diuresis, and inotropic support might be necessary [6].
A 70-year-old male presents to the ED after an industrial accident causing a traumatic below-knee amputation on the right side. The patient has been obtunded and dyspneic since arrival. A total of six pRBC units and 5L of crystalloids have been given in the last hour. You have been asked to evaluate this patient prior to operative BKA.HR, 120; BP, 90/60; RR, 35; SpO2, 84%.
How would you confirm your suspicion?
○ Clinical examination of the patient followed by further testing which should include EKG, chest X-Ray, and formal transthoracic echocardiography.
○ Invasive tests include CVP and PA pressure measurement and cardiac catheterization.
○ Laboratory tests include N-terminal pro-B-type natriuretic peptide and markers of cardiac ischemia.
A 50kg patient receives a supraclavicular peripheral nerve block in the preoperative area for anesthesia and postoperative pain for open reduction and internal fixation of an ulnar fracture on the left arm. The patient received a total of 20cc of 0.5% ropivacaine during the block (See Fig. 58.1). 55min later, the surgery starts and the patient complains of pain in the area of the surgery.
1. Based on the ultrasound image above what is the most likely cause of the patient’s pain?
○ Most probably this patient experienced ulnar sparing due to poor distribution of the injection to the lower trunk.
○ This occurs commonly when the injection is made superficial to the plexus and does not cover the lower trunk (in the “eight ball corner pocket,” which is the area formed by the angle between the brachial plexus and first rib).
○ These patients will report adequate motor and sensory block over the median, radial, and musculocutaneous distribution; however, the area of the ulnar nerve, and medial cutaneous nerve of the forearm retain sensation and function.
How would you supplement the block?
○ Time permitting, the block could be supplemented by placing more local anesthetic in the “eight ball corner pocket,” since the patient could safely still receive more local anesthetic.
○ The maximum dose of ropivacaine in this patient is 150mg (3mg/kg).
° So we could safely repeat the block targeting the area of interest and inject up to another 10cc of ropivacaine 0.5%.
° Awake patients might complaint of tourniquet pain.
° All patients experience neuropathic pain after a few minutes of a tourniquet being inflated to 100mmHg above the systolic blood pressure.
° With enough time this manifests as pain, sometimes severe in awake patients, or a sympathetic response in patients under general anesthesia.
○ Other reasons for pain are due to surgical stimulation in the area covered by the intercostobrachial nerve, the upper, inner aspect of the upper arm, which is not routinely covered by brachial plexus blocks.
° This area can be anesthetized with a field block of the medial side of the arm or a PECS II (pectoralis nerves) block.
A 50 kg patient receives a supraclavicular peripheral nerve block in the preoperative
area for anesthesia and postoperative pain for open reduction and internal fixation
of an ulnar fracture on the left arm. The patient received a total of 20 cc of 0.5%
ropivacaine during the block (See Fig. 58.1). 55 min later, the surgery starts and the
patient complains of pain in the area of the surgery.
Are there other reasons for pain during surgery? Apart from ulner sparing
Other reasons for pain are due to surgical stimulation in the area covered by the intercostobrachial nerve, the upper, inner aspect of the upper arm, which is not routinely covered by brachial plexus blocks. This area can be anesthetized with a field block of the medial side of the arm or a PECS II (pectoralis nerves) block.
A 50 kg patient receives a supraclavicular peripheral nerve block in the preoperative
area for anesthesia and postoperative pain for open reduction and internal fixation
of an ulnar fracture on the left arm. The patient received a total of 20 cc of 0.5%
ropivacaine during the block (See Fig. 58.1). 55 min later, the surgery starts and the
patient complains of pain in the area of the surgery.
Should a continuous nerve catheter been placed?
○ A catheter is indicated if it’s expected that the patient will require continuous analgesic coverage beyond the first 24h after surgery, would need strenuous physical therapy, and has unresolved trauma or a chronic pain syndrome among others.
○ A peripheral nerve catheter placed under ultrasound guidance has a better chance of success, with fewer complications, than the one placed with stimulation alone.
○ It also prolongs the pain relief in the postoperative setting, which might contribute to better patient satisfaction and active participation in rehabilitation with selective sensory blockade.
○ In this particular case, a catheter is not indicated since the pain of the trauma and surgery is expected to decrease after surgery; there is no need for strenuous physical therapy, and the patient has no chronic pain.
Figure 59.1 image is obtained from a patient (80yo M, 60kg) in the PACU after a repeat femoral peripheral nerve block for postoperative pain of a knee arthroplasty. The patient received a total of 30cc of 0.5% bupivacaine and 20cc of 0.5% ropivacaine. Patient is complaining of persistent pain in the area of the surgery
What are the structures labeled a, b, and c?
a, femoral vein; b, femoral artery; c, femoral nerve.
Figure 59.1 image is obtained from a patient (80yo M, 60 kg) in the PACU after a
repeat femoral peripheral nerve block for postoperative pain of a knee arthroplasty.
The patient received a total of 30 cc of 0.5% bupivacaine and 20 cc of 0.5% ropiva-
caine. Patient is complaining of persistent pain in the area of the surgery.
What are the possible causes of persistent postoperative pain?
Persistent pain might be due to:
(a) Inadequate distribution of the local anesthetic in the correct plane, possibly due to difficult and distorted anatomy after multiple attempts
(b) Lack of coverage of the sciatic nerve area on the back of the knee or the obturator nerve on the medial aspect of the thigh
If the patient develops seizures after peripheral nerve block how would you treat him?
○ Seizures in this setting would be very suspicious for local anesthetic systemic toxicity (LAST).
○ According to the American Society of Regional Anesthesia and Pain Medicine (ASRA), management in this setting should include [1]:
(a) Airway management: ventilate with 100% oxygen.
(b) Seizure suppression: benzodiazepines are preferred; avoid propofol in patients having signs of cardiovascular instability.
(c) Alert the nearest facility having cardiopulmonary bypass capability.
d) Lipid emulsion therapy (not propofol):
• Bolus 1.5mL/kg.
• Continuous infusion at 0.25mL/kg/min.
• Bolus may be repeated and the infusion raised to 0.5mL/kg/min for persistent hypotension.
• Continue treatment for 10min after attaining stability.
• Maximum dose of lipid—10mL/kg in first 30min.
(e) Other possibilities of seizure activity in this setting are pseudo-seizures, cryptogenic, metabolic insult, toxic insult, CNS infection, stroke, brain trauma, cerebral hemorrhage, and alcohol or drug withdrawal. 5. Management of cardiovascular collapse in this setting differs from the one caused by other etiologies and current recommendations by ASRA are [1]:
(a) Advanced Cardiac Life Support (ACLS):
• Avoid vasopressin, calcium channel blockers, beta-blockers, or local anesthetics.
• Reduce individual epinephrine doses to <1mcg/kg, to avoid onset of malignant arrhythmias.
(b) Lipid emulsion (20%) therapy:
• Bolus 1.5mL/kg (lean body mass) intravenously over 1min.
• Continuous infusion 0.25mL/kg/min.
• Repeat bolus once or twice for persistent cardiovascular collapse.
• Double the infusion rate to 0.5mL/kg/min if blood pressure remains low.
• Continue infusion for at least 10min after attaining circulatory stability.
• Recommended upper limit: Approximately 10mL/kg lipid emulsion over the first 30min.
(c) Consider placing the patient on cardiopulmonary bypass if prolonged resuscitation with no return of cardiac function is present
If the patient with LAST develops hypotension and asystole how would you treat him?
Management of cardiovascular collapse in this setting differs from the one caused by other etiologies and current recommendations by ASRA are [1]:
(a) Advanced Cardiac Life Support (ACLS):
• Avoid vasopressin, calcium channel blockers, beta-blockers, or local anesthetics.
• Reduce individual epinephrine doses to <1mcg/kg, to avoid onset of malignant arrhythmias.
(b) Lipid emulsion (20%) therapy:
• Bolus 1.5mL/kg (lean body mass) intravenously over 1min.
• Continuous infusion 0.25mL/kg/min.
• Repeat bolus once or twice for persistent cardiovascular collapse.
• Double the infusion rate to 0.5mL/kg/min if blood pressure remains low.
• Continue infusion for at least 10min after attaining circulatory stability.
• Recommended upper limit: Approximately 10mL/kg lipid emulsion over the first 30min.
(c) Consider placing the patient on cardiopulmonary bypass if pprolonged resuscitation with no return of cardiac function is present.
An ultrasound of the chest/lung is obtained on a multi-trauma patient with chest drains and on a ventilator in the ICU.
What is lung sliding?
Lung sliding is the movement of the pleural interface in a synchronous fashion with spontaneous or mechanical ventilation. The parietal and visceral pleura constitute the pleural interface, which is a hyperechoic structure between two ribs on bidimensional ultrasound. It is maximized in the lower lung fields, as the lung descends toward the abdomen. Lung sliding identification is the most commonly used artifact in the exclusion of pneumothorax as well as in the confirmation of endotracheal intubation
What is lung point?
○ On two-dimensional ultrasound, lung point is the transition point between the presence and absence of a lung sliding.
○ It represents the border of the pneumothorax and the intact pleural interface.
○ In M-mode, the absence of lung sliding will create a series of black and white horizontal lines called the “stratosphericor barcode” sign.
○ In this mode, the lung point can be identified by the transition of a seashore sign to a stratospheric sign (Fig. 60.1). This is a pathognomonic sign for the presence of pneumothorax, with 100% specificity [3].
Besides lung sliding, what other two common artifacts can help with differential diagnosis?
○ A-lines are multiple horizontal regularly spaced hyperechogenic lines which represent reflections of the pleural interface.
○ Each A line is separated by a distance equivalent to the thickness of the subcutaneous tissue between the ultrasound probe and the pleural interface (Fig. 60.2).
○ They are present in a normal lung as well as in the presence of pneumothorax.
○ B-lines, also known as comet tails or lung rockets, are artifacts created by repetitive reflections of the ultrasound wave within the lung parenchyma because of a higher concentration of physiologic or pathologic fluid.
○ They are vertical white lines, originating from the visceral pleura and reaching the bottom of the screen (Fig. 60.3). B-lines will erase the A-lines on their passage.
○ A few B-lines (less than 3) may be seen in a healthy lung and more so in the dependent regions. Their presence is utilized in the diagnosis of alveolar interstitial syndrome (pulmonary edema, ARDS) and exclusion of pneumothorax [4].
What are the indications for a feeding tube placement?
○ Early records note that Capivacceus placed a tube to deliver nutrients into the foregut [1].
○ The practice became more common during the seventeenth century.
○ The tubes are inserted to decompress the stomach or for intestinal ileus or obstruction.
○ Patients that most frequently need a naso-enteric tube (NET) are in surgical intensive care settings.
○ Other indications include prematurity, failure to thrive (or malnutrition), neurologic and neuromuscular disorders, inability to swallow, anatomical and postsurgical malformations of the mouth and esophagus, cancer and digestive disorders.
○ The feeding tubes could be for short-term or even long-term use.
○ Feeding tubes are placed in patients either through the nose or percutaneously.
What do these images show?
○ Figure 62.1 is computed tomography showing a large pulmonary embolism (PE) involving the right pulmonary artery (red arrow).
○ Figure62.2 is pulmonary angiography of the same patient showing the same finding.
How does one assess the pretest probability for this finding? PE
○ Wells score (Table62.1) is used to calculate the pretest probability of PE.
○ In patients with high pretest probability for PE, imaging is the test of choice.
○ Pulmonary arteriography is the gold standard for diagnosis of PE.
○ Current generation multi-detector helical computed tomography (CT) has high sensitivity and specificity, comparable to pulmonary arteriography, in detection of PE [2].
○ Helical CT is the most widely used modality in current clinical settings and would be the diagnostic test of choice in this case.
○ However, in patients with high pretest probability for PE (as in our case) and a negative CT, further investigation in the form of duplex ultrasound of lower extremities or pulmonary arteriography should be considered [3].
How does imaging play a role in diagnosis of PE?
○ In patients with high pretest probability for PE, therapeutic anticoagulation should be initiated immediately while awaiting further diagnostic testing (CT, duplex ultrasound, etc.) [4].
○ Treatment for PE has evolved with the introduction of novel oral anticoagulants or non-warfarin oral anticoagulants (NOAC).
○ Treatment for acute PE can be one of the following:
(a) Weight-based low-molecular-weight heparin (LMWH) for 5days followed by dabigatran, edoxaban, or warfarin (NOACs)
(b) Rivaroxaban or apixaban without initial LMWH
○ The treatment for acute PE is divided into the following treatment phases:
•acute phase of 5–10days, short-term phase 3–6months, and long-term phase beyond 6months.
○ The duration of therapy depends on the underlying cause for the PE and the risk to benefit ratio of anticoagulation.
○ Outcomes in PE patients depend on the clinical presentation.
○ Based on clinical presentation, they can be further classified into [5]:
(a) Massive PE: Acute PE with sustained hypotension (systolic BP<90mmHg sustained for over 15min or requiring ionotropic support) in the absence of any other cause, pulselessness, or profound bradycardia (highest risk of adverse outcomes).
(b) Sub-massive PE: Acute PE without sustained hypotension, with signs of hypoperfusion, right ventricular dysfunction on echocardiography, elevated cardiac troponins, and elevated brain natriuretic peptide (intermediate risk of adverse outcomes).
(c) Low-risk PE: Acute PE with normal blood pressures, normal cardiac biomarkers, and normal RV function (low risk of adverse outcomes).
○ Further risk stratification using Pulmonary Embolism Severity Index (PESI) scores (Table62.2), signs of cardiovascular decompensation, and signs of shocklike state allows for consideration of inpatient versus outpatient treatment setting for further management and for the consideration for advanced therapies including thrombolytic therapy [6].
What are the acute therapeutic options in this situation? PE
○ The role of systemically administered thrombolysis in acute PE is reserved for patients with clinically massive PE who are not at risk for major bleeding.
○ As mentioned above, massive PE is defined as PE with resulting hypotension (SBP<90mmHg) [7]. In low-risk PE, antithrombotic therapy is sufficient.
○ Thrombolytic therapy may be considered down the road in these patients if they acutely develop hypotension while on antithrombotic therapy.
○ Thrombolysis may also be considered in those patients who were initially stable, if blood pressure decreases but is still >90mmHg, and they develop a shock-like state along with supplemental signs of cardiac decompensation including acute right ventricular failure, elevated cardiac troponins, and brain natriuretic peptide levels (sub-massive PE) [4].
When is thrombolytic therapy used in PE?
○ The role of systemically administered thrombolysis in acute PE is reserved for patients with clinically massive PE who are not at risk for major bleeding.
○ As mentioned above, massive PE is defined as PE with resulting hypotension (SBP<90mmHg) [7].
○ In low-risk PE, antithrombotic therapy is sufficient.
○ Thrombolytic therapy may be considered down the road in these patients if they acutely develop hypotension while on antithrombotic therapy.
○ Thrombolysis may also be considered in those patients who were initially stable, if blood pressure decreases but is still >90mmHg, and they develop a shock-like state along with supplemental signs of cardiac decompensation including acute right ventricular failure, elevated cardiac troponins, and brain natriuretic peptide levels (sub-massive PE) .
○ Contraindications to systemic thrombolysis are mentioned in Table62.3.
○ Thrombolytic agents approved by the FDA are alteplase (100mg infusion over 2h), urokinase (4400U/kg as a loading dose given at a rate of 90mL/h over a period of 10min, followed by continuous infusion of 4400U/kg/h at a rate of 15mL/h for 12h), and streptokinase (250,000U as a loading dose over 30min, followed by 100,000U/h over 12–24h).
A sixty-one-year-old male with known descending thoracic aortic aneurysm with Stanford-type B aortic dissection underwent thoracic endovascular aortic repair (TEVAR) due to ongoing pain and rapidly expanding aneurysm. The procedure was complicated due to significant curvature of the thoracic aorta; patient was subsequently discharged home.
Patient was readmitted 2weeks later with worsening chest pain, back pain, and dizziness. At the time of presentation, patient was in distress. Examination revealed sinus tachycardia HR 120bpm, no obvious cardiovascular exam findings were noted, pulses were equal in all four extremities, and serum chemistry was unremarkable except for mild renal insufficiency. Due to recent TEVAR procedure, CT angiography was obtained; images are displayed below.
What is seen in the images?
○ Figure 63.1 is a triple phase computed tomographic image (CT) showing a type III endoleak in the descending thoracic aorta originating from the stent graft.
○ Figure63.2 is also a triple phase CT image of the same patient showing the extension of the type III endoleak proximally.
○ This patient underwent a thoracic endovascular aortic repair (TEVAR) procedure for urgent repair of acute type B thoracic aortic dissection with ongoing chest pain and rapid aneurysmal expansion.
○ TEVAR is the procedure of choice in patients with complicated type B dissections. ○ The CT images are consistent with an endoleak.
○ Endoleak is defined as blood collection outside the stent graft but within the aneurysm sac.
° This is a known complication following TEVAR.
° According to reported data, it occurs in about 5–20% of cases [1].
How is the above complication classified?
○ The most widely used method classifies endoleaks depending on the mechanism of formation of the endoleak:
(a) Type I endoleak: Proximal or distal reperfusion of the aneurysmal sac.
° This occurs due to malapposition of the stent graft to the aortic wall.
° This is an early complication following TEVAR and needs urgent intervention.
° This is considered to be a form of treatment failure.
(b) Type II endoleak: Retrograde reperfusion of the aneurysmal sac from branch vessels. ° These have a benign course and usually need surveillance only.
(c) Type III endoleak: Leak into the aneurysmal sac due to structural damage to the stent graft in the form of tears, fractures, or junctional separation.
° This requires urgent intervention and is considered to be a form of treatment failure.
(d) Type IV endoleak: Leakage into the aneurysmal sac due to endograft porosity.
(e) Type V endoleak: Increase in the aneurysm sac in the absence of leak (endotension). This is poorly understood.
What is the recommended surveillance to detect this complication?
○ Lifelong surveillance is recommended following TEVAR since complications like type III endoleaks can occur many years down the line .
○ Triple phase CT (images obtained before, during, and after contrast administration) angiography is the modality of choice in many centers.
○ As in our case, endoleak on a triple phase CT angiography will show up as contrast outside the stent graft structure in delayed imaging after the contrast has cleared the aortic lumen.
○ Patients receive CT angiography immediately post procedure, then at 1month, 6month, and then yearly with clinical follow-up.
○ Magnetic resonance imaging (MRI) can be used as an alternative modality to reduce cumulative radiation in cases where MRI compatible grafts have been used.
○ Ultrasound is not as reliable in the setting of TEVAR due to chest wall interference.
○ Transesophageal echocardiography as a follow-up tool has some disadvantages due to its invasive nature.
A 46-year-old male presents to the ER after a syncopal event. The patient developed severe precordial chest pain while lifting weights, immediately followed by syncopal event lasting 30seconds. Currently in the ER, he continues to have chest pain that radiates to the back. He describes it as a tearing sensation. Pain does not respond to nitroglycerine. On exam patient appears in distress, diaphoretic, HR 120bpm, BP 150/70mmHg on right, and 120/60mmHg on left; chest exam is within normal limits. EKG is consistent with sinus tachycardia and ST depressions anterolaterally. CXR reveals widened mediastinum. Creatinine 2.0ng/ml (0.0–0.399ng/ml) Troponin 0.2ng/ml (0.0–0.399ng/ml) D-dimer 800 BNP 240pg/ml (0–100pg/ml) Echocardiography is performed next and a couple of images are displayed below.
What do the images show?
Figure 64.1 shows a transthoracic echocardiographic image of a Stanford type A acute aortic dissection. Figure64.2 shows a transesophageal echocardiographic image of the same patient confirming the same finding.
What are the presenting features of this condition?
○ Presenting symptoms are sudden onset and severe chest, back, or abdominal pain that is described as tearing or ripping in quality .
○ Some patients with acute aortic dissections may not have any chest pain at all and may present with syncope and shock like state.
○ Patients also present with perfusion defects and end organ damage depending on the extension of the dissection flap, with resulting neurological deficits, myocardial ischemia, renal insufficiency, mesenteric ischemia, or limb ischemia.
○ On physical exam, patients may demonstrate perfusion deficits in the form of a pulse deficit and systolic blood pressure deferential.
○ Vascular examination of all four extremities should be conducted in all patients with suspected aortic dissection.
How is this condition classified?
○ Thoracic aortic dissections are classified according to the involvement of the various segments of the thoracic aorta.
○ Accurate classification is necessary to decide on surgical versus medical management.
○ Two classification schema have been proposed: DeBakey and Stanford.
○ The Stanford classification is more widely used, it classifies thoracic aortic dissections based on the involvement of the ascending aorta into:
(a) Stanford A: involving ascending aorta (before the brachiocephalic artery). Urgent surgery is recommended.
(b) Stanford B: involving the descending aorta only (after the left subclavian artery). Surgery usually not recommended.
○ The DeBakey classification: Acute limb ischemia
(a) Type I: Originates in ascending aorta and propagates distally. Urgent surgery is recommended.
(b) Type II: Dissection is limited to the ascending aorta only. Urgent surgery is recommended.
(c) Type III: Originates in the descending thoracic aorta and propagates distally. Surgery is usually not recommended.
What end organ complications can we expect from aortic dissection?
○ As mentioned previously, acute thoracic aortic dissections carry high morbidity and mortality.
○ This is largely due to the end organ complications that arise due to obstruction to blood flow via the dissection flap.
○ The various end organ complications are listed in (Table64.1).
- How do pediatric chest X-rays differ from those of an adult?
○ Pediatric chest X-Ray differ from those of adults because:
(a) They are difficult to obtain as cooperation is limited.
(b) Chest X-rays change with age.
(c) Children present with different conditions.
(d) There are specific areas to review when interpreting a pediatric chest X-ray.
(f) The thymus can cause confusion.
Consider this normal chest X-ray of an infant (Fig. 65.1). Is there a system for interpreting the image?
○ There are many ways of reading a CXR [2].
○ Adopt a method that suits you and stick to it.
○ Here is an example:
(a) Check ID and quality
(b)Bone structure
(c) Tracheobronchial tree and mediastinum
(d)Heart silhouette
(e) Contours of thorax
(f) Lung fields
(g)Abdomen
(h)Soft tissues
(i) Lines, tubes, and artefacts
What is the initial prehospital management of a choking child? [1]
○ Assess severity of choking episode [1].
(a) Effective cough (crying or verbal response to questions, loud cough, able to breath before coughing, normal GCS)
• Encourage cough—unless patient deteriorates or until obstruction is relieved. Transport to ED if indicated!
(b) Ineffective cough (unable to breath, cyanosis, decreasing GCS, unable to vocalize)
• Conscious—blind oropharyngeal finger sweep is not recommended. Alternating five back blows with five chest thrusts (infants) or five abdominal thrusts (child >1year). Repeat until object comes out or child becomes unconscious.
• Unconscious—start CPR.
What does the CXR in our patient show?
Hyperinflated right lung with increased translucency, flattened right hemidiaphragm, wider spaced right ribs, and mediastinal shift to the left are the radiological features of obstruction.
What do Figs.67.1 and 67.2 demonstrate?
Figures 70.1 and 70.2 show the classical 3D TEE surgeon’s view of the mitral valve in systole (Fig.67.1) and diastole (Fig.67.2). In the surgeon’s view, the left atrium has been opened and you are looking down at an en face view of the mitral valve. The aortic valve by convention is at the top of the image. In this view, the lateral commissure and left atrial appendage are to the left of the image, and the medial commissure and tricuspid valve apparatus are to the right of the image. PML scallops are labeled by the Carpentier convention, lateral to medial, P1, P2 and P3. The adjacent segments of the AML are labeled A1, A2, A3 from lateral to medial. These images show a flail P2 segment due to a ruptured cord (arrow). A flail segment is defined as the tip of the leaflet pointing towards the left atrium in systole and the left ventricle in diastole.
How is mitral regurgitation classified?
Mitral regurgitation (MR) is typically described by the Carpentier Classification (adapted from Tsang etal.) [2]. This patient’s mitral regurgitation would be described as type II (likely due to fibroelastic disease) with isolated flail P2 segment due to a ruptured cord (Table67.1).
II.A 40year old female with hypertension, diabetes, and end-stage renal disease on hemodialysis presents to the emergency room complaining of a 2week history of fevers, chills, night sweats and a 1day history of rapidly progressive shortness of breath. She is sitting upright, in moderate distress and appears dyspneic. Temperature is 38.4°C. 2/2 blood cultures grow S. aureus. Physical exam reveals an S3 and an early diastolic flow rumble.
What do Figs.67.3, 67.4, and 67.5 demonstrate?
○ These images show a 3D TEE surgeon’s view of the mitral valve in systole (Fig.67.3) and diastole (Fig.67.4).
○ The aortic valve is labeled at the top of the screen (Ao).
○ The lateral commissure is on the left by the left atrial appendage; the medial commissure is on the right by the tricuspid valve (TV) apparatus.
○ On the atrial aspect of the P2 scallop of the PML, there is an irregular, shaggy, echogenic mass (arrow in Fig.67.4) which involves the mitral valve annulus and is associated with local destruction of the P2 scallop.
○ The regurgitant orifice is marked with an arrow in Fig.67.3.
○ Figure67.5 shows the color doppler mitral regurgitation through the perforated leaflet.
○ The patient has positive blood cultures for a typical organism (S. aureus), suggestive echocardiographic findings, and is febrile.
○ She has two major and one minor Duke criteria which is diagnostic for infective endocarditis [7].
○ TEE confirmed severe MR which was likely acute given her clinical presentation.
○ Her lack of murmur is explained by rapid equilibration of left atrial and left ventricular diastolic pressures. If present, the murmur of acute severe MR occurs in early systole and terminates in early to mid-systole.
○ An S3 is often present due to acute left ventricular volume overload and a diastolic rumble flow murmur may be heard [8].
Using the Carpentier classification, what is the mechanism of mitral regurgitation?
In this patient, mitral valve leaflet motion is normal. The mechanism of MR is due to leaflet perforation from infective endocarditis (IE) (Carpentier class I) (Table67.1).
