Airway Pressure Release Ventilation (APRV) is an "advanced" mode of mechanical ventilation that has long been considered a "rescue" mode of ventilation and has recently garnered much more attention during the COVID pandemic.  Given the long boarding times of critical care patients in the ED with widespread improvement in sight, I wanted to send out some great resources that have come out recently delineating the difference in thought process between APRV as a "rescue" mode and as a "primary" mode.

Rory Spiegel of EMNerd and former UMMC CCM fellow has recently given a great talk on APRV and its use as a rescue mode of ventilation. See also Phil Rola's recent paper listed on that webpage.

https://emcrit.org/emcrit/aprv-for-lung-rescue/

 

APRV as a primary mode of ventilation has been used in the STC for years and is often referred to in the literature according to the basic ventilatory philsophy called Time Controlled Adaptive Ventilation. I realize this may be heresy to some and perhaps a curiousity to others. I recommend you take some time to peruse the following resources:

1. Dr. Habashi has done a great deal of work in the basic and translation literature on APRV and TCAV. His recent review dispels many myths and concerns surrounding APRV

Myths and Misconceptions of Airway Pressure Release Ventilation: Getting Past the Noise and on to the Signal - https://www.frontiersin.org/articles/10.3389/fphys.2022.928562/full

2. The TCAV Network has great resources for those who want to do a deeper dive into this topic. 

https://www.tcavnetwork.org/

(Can also find their recommended protocols at the Multi Trauma Critical Care education website: https://stcmtcc.com/handouts/)

 

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• 2211021655_fphys-13-928562_(2).pdf (5,575 Kb)
• 2211021655_Standard_Settings_for_APRV_using_the_TCAV_Method.pdf (1,525 Kb)
• 2211021655_APRV_TCAV_Rescue_Strategy_Strategy_Guidelines_2020.pdf (1,614 Kb)

Traditional trauma teaching is to admit trauma patients with abdominal wall ecchymosis caused by seat belts (seat belt sign) for fear of missing a hollow viscus injury leading to peritonitis and sepsis.  

Over the past few years there have been studies pointing toward the safety of discharging blunt abdominal trauma patients with a negative CT even if they do have a seat belt sign.

In this most recent study, a negative CT was defined as 

1. No free fluid (free fluid was the leading indicator of occult hollow viscus injury)

2. No solid organ injury

3. No bowel wall irregular contours, thickening, hematoma or air

4. No abdominal wall soft tissue contusion

5. No mesenteric stranding or hematoma

6. No bowel dilatation

If the patient’s CT did not include any of these findings, there was a 0.01% chance of finding a delayed hollow viscus injury. The authors conclude it is safe to discharge patients meeting these criteria. 

If we include no rebound or guarding on physical exam along with a negative CT scan, it appears to be safe to discharge trauma patient’s with seat belt sign.

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Arterial line waveform interpretation and troubleshooting are essential skills for any physician caring for critically ill patients. Overdamping and underdamping of the arterial line waveform leads to inaccurate systolic and diastolic blood pressure readings which can lead to unidentified hypertension or hypotension. In addition to scrutiny of the arterial waveform pattern, the square-wave test is a tool to identify overdamped or underdamped arterial lines. 

Overdamped arterial waveforms will underestimate systolic blood pressure and overestimate diastolic blood pressure. Underdamping will have the opposite effect and overestimate systolic blood pressure and underestimate diastolic blood pressure. In both cases, the mean arterial pressure (MAP) often remains the same.  

The square-wave test is a rapid flush that is applied to the arterial line for approximately 1 second. This rapid high-pressure surge results in vibration and oscillation of the arterial catheter. These oscillations are then read by the pressure transducer and the number and amplitude of these oscillations can be measured. 0 or 1 oscillations is suggestive of overdamping. 3 or more oscillations is suggestive of an underdamped system. 

Major causes of an overdamped arterial line waveform include low infusion bag pressure, loose connectors, air bubbles in the tubing, blood clot in the circuit, or kinking of vascular catheter. An underdamped arterial line, however, is caused by overly stiff circuit tubing or a defective transducer.   

 

Scrutiny of the arterial waveform and utilization of the square-wave test can be helpful to both identify erroneous arterial line blood pressure readings as well as suggest likely corrective measures.  

 

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This meta-analyisis looked at whether obesity was a protective factor for penetrating trauma (the armour phenomenon). The authors concluded that insteaed of being protective, obesity added to morbidity and mortality.

"Obese patients that sustained stab injuries underwent more nontherapeutic operations. Obese patients that sustained gunshot injuries had longer intensive care and total hospital length of stay. Obese patients suffered more respiratory complications and were at an increased risk of death during their admission."

Further evidence that obesity is a major health concern in both medical and trauma pateints. 

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Developmental dysplasia of the hip (DDH) 

 

• A spectrum of conditions related to hip development in infants & young children
• Results from abnormal development of the acetabulum and proximal femur
• Results in mechanical instability of the hip joint 
• Left hip (3:1) vs Right
• Female sex (5:1)
• Breech presentation (20%)
• Family history of DDH
• Infants and young children with untreated hip dislocation rarely have pain or other limitations.
• Most affected children begin to walk and reach developmental milestones at the appropriate time.
• In cultures where tight swaddling with the lower limbs in extension is common, significantly higher rates of DDH have been reported.
• In South Australia 79% of those with DDH were tightly swaddled
• In Japan, when traditional swaddling was used, the incidence of DDH was 5%.
• A public campaign to switch to wrapping techniques encouraging hip flexion and abduction led to DDH rates falling to less than 0.4%.
• https://res.cloudinary.com/dbwozcf0d/images/f_auto,q_auto/v1589948650/10624649_794826423982877_5167788043433556178_n/10624649_794826423982877_5167788043433556178_n.jpg

 

Once the diagnosis of intussusception is made, there are often delays in 1) getting the patient to a center where reduction can be performed and 2) getting the staff available to perform an air enema, especially during evenings and nights. Previous studies have shown worse outcomes when there is longer than a 24 hour delay in reduction. This was a retrospective single center study looking at 175 cases of intussusception and evaluating the time between the radiology final read of intussusception and the timing of reduction and if enema based reduction was successful. In this group of patients, there was no statistically significant difference in reduction efficacy, requirement for surgical reduction or complication rate (bowel resection or perforation) in the patients studied which included delay intervals up to 8 hours. Successful first attempt reductions ranged from 72-81% in each study group (1hr, 1-3hr, 3-6hr and 6+ hr). The caveat to this study is that there were only 11 patients included in the 6-8 hour group. This study also did not take into account the timing from symptom onset to reduction time. Bottom line: More evidence is needed, but this small study provides evidence that up to 8 hours from radiology diagnosis of intussusception to the 1st reduction attempt was not less efficient compared to those with an attempt in under 1 hour.

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Emergency physicians are familiar with posterior reversible [leuko]encephalopathy syndrome as an entity associated with untreated hypertension. It also happens to be a well-documented entity amongst solid organ transplant patients.  

While the exact pathophysiology remains unclear, PRES is characterized by posterior subcortical vasogenic edema due to blood-brain barrier disruption, usually in the setting of elevated blood pressure with loss of cerebral autoregulation and/or endothelial dysfunction.

The immunosuppressants used in this population, namely calcineurin inhibitors (CNI) such as tacrolimus and cyclosporine, are thought to contribute most to this endothelial dysfunction and development of PRES in transplant patients, although high-dose corticosteroids, ischemia-reperfusion injury during surgery, and antibiotics have also been implicated. 

Presentation of PRES post-transplant:

Clinical symptoms:

• Seizures (75-85%)
• AMS - confusion/somnolence (30-40%)
• Headache (25-50%)
• Vision disturbance (20-40%)

Time course:

• Within weeks to a year posttransplant, rarely after a year
• Rapid onset once it starts, can develop over hours to days

Diagnostics:

• Labs nonspecific, although supratherapeutic CNI levels are often associated with:
  • Acute renal injury
  • Hyperchloremic metabolic acidosis
  • Hyperkalemia
  • Hypomagnesemia
  • Hypercalciuria
• Thoughts on checking FK506 (tacrolimus) levels
  • For transplant patients, usually advise only checking troughs (~12 hrs after last dose)
  • A low random level may rule out CNI toxicity but not PRES
  • A high random level isn't really helpful
• MRI is diagnostic modality of choice >> subcortical edema, usually bilateral, symmetric, in parieto-occipital regions

Management:

1. Stabilization via supportive care – seizure, cerebral edema, BP management as applicable, etc.
2. Withdrawal/holding of offending agent – will require consultation with transplant physician and pharmacist usually by inpatient team
   • Mixed data re: use of CYP-inducers to lower CNI levels in CNI toxicity

Bottom Line: 

Patients with a history of solid organ transplant are at risk for PRES. While ED stabilization of these patients remains the same, recognition of PRES as a potential etiology for a transplant patient's presentation is crucial to proceed with important testing and necessary changes to their immunosuppressive regimen. 

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In this prospective, observational study performed at 25 urban trauma centers, police transport (18%) was compared to Advanced Life Support (ALS) transport (81%) for mortality in penetrating trauma patients with an injury severity score over 16. There was no difference in outcome for those transported by ALS.

The authors conclude "Police transport of penetrating trauma patients in urban locations results in similar outcomes compared with ALS. Immediate transport to definitive trauma care should be emphasized in this patient population."

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Needless to say, therapeutics for COVID-19 pneumonia have been controversial.  From hydroxychloroquine to ivermectin to remedesivir to steroids to bleach (sorry, but it had to be said...),  it depends on who you ask whether medications make a difference in COVID, how much of a difference, when they should be given, and what the correct dose is. 

Dexamethasone, however, ala the RECOVERY trial, is one of the relatively few therapies supported by the majority of the literature and guidelines, and generally is recommended when respiratory support is required for COVID-19 pneumonia.  Further add to this that steroids for ARDS is a long-running point of critical care controversy (e.g. DEXA-ARDS, Meduri, etc), and all you need to say to an intensivist is "how much steroid should I give this patient?" and you can walk away and come back 10 minutes later to find them having not noticed you had ever left.

Wu et all did a fairly small (n=107) single-centered RCT looking at dexamethasone 6 mg daily vs dexamethasone 20 mg daily for COVID-19 requiring O2.  There are several notable limitations to this study, but in short it did NOT add support to the notion that higher dose dexamethasone is a good thing for COVID-19 pneumonia.  In fact, the 20 mg group trended towards worse outcomes.  Small sample size, single-center, limited follow up, variable use of biologics between the groups, and failure to investigate intermediate doses between 6 and 20 are all significant limitations of this trial. Of note, DEXA-ARDS, which was conducted before COVID (2013-2018), looked at 20 mg x 5 days followed 10 mg x 5 days and DID find a significant benefit, as well as pretty darn good NNT and p values (and was a higher quality trial), so in my opinion it is also not unreasonable to use DEXA-ARDS dosing if the patient meets moderate-severe ARDS (P:F < 200) criteria, even though of course DEXA-ARDS was before COVID and Wu et al slightly contradicts it. 

When faced with a very sick COVID-19 pneumonia patients many intensivists will do either RECOVERY or DEXA-ARDS dexamethasone (with relatively limited basis to choose one vs the other), and some will do Meduri protocol methylprednisolone (1-2 mg/kg/day).  Relatively few nowadays will omit steroids unless there's a contraindication.

 

Bottom Line: It probably remains a good idea to give dexamethasone to your COVID-19 pneumonia patients with hypoxia, but you can probably stick to RECOVERY (see reference below; 6 mg daily x 10 days) dosing as opposed to higher doses.  If they're REALLY sick (P:F < 200), consider DEXA-ARDS (20 mg x 5 days followed by 10 mg x 5 days) dosing.

 

The use of the shock index (systolic blood pressure/heart rate) value under 0.9 has been shown to be effective in predicting the need for mass blood transfusion as well as mortality for trauma patients age 16-64. Using age times shock index has been shown to be an effective marker of mortality and the need for transfer/transport to a trauma center in those over age 65. The change in shock index over time is also useful for pre-hospital providers deciding the appropriate destination for traumatically injured individuals. 

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Popliteal artery entrapment syndrome (PAES)

 

 

CC:  Exertional lower leg pain, however, compression of posterior neurovascular structures can lead to nonspecific vascular and neurogenic symptoms.

Challenging diagnosis to make because of close overlap with chronic exertional compartment syndrome (CECS).

Anatomic PAES has a prevalence of 0.62% to 3.5% in the general population. Patients are more likely to be older be older, male, and have lower levels of activity.

Functional popliteal artery entrapment (FPAE) however has no anatomic anomaly. Sx’s are thought to be because of bulky surrounding muscle crowding with repetitive dynamic injury. This is most commonly from the medial head of the gastrocnemius.  Patients are younger and more likely to be involved in athletics. Most athletes were involved in sports that put high value on repetitive plantarflexion, such as track and field (45%), soccer (25%), water sports (8%), lacrosse (6%), basketball (6%), 

Sx’s:  bilateral (25-75% of cases) cramping in the region of the soleus and plantar paresthesias.

Common exacerbating mechanism: ascending stairs or climbing inclines because of leg/knee position of extension with plantarflexion 

 

In one review, 31% of patients who underwent debulking surgery for FPAES had been previously treated and extensively worked up at outside institutions for CECS, and already undergone various compartment releases.

 

Patients in one study underwent a dynamic CTA protocol. A positive test demonstrated normal flow in neutral position and compression or complete occlusion of the popliteal artery by the medial head of the gastrocnemius muscle against the lateral femoral condyle with provocative foot plantarflexion. Images below.

https://images.journals.lww.com/acsm-csmr/Original.00149619-202210000-00008.F1.jpeg

 

Nearly three-fourths of athletes limited by FPAES demonstrated full return to prior competitive levels with four compartment fasciotomy AND surgical debulking of the anterolateral quadrant of the medial head of the gastrocnemius muscle. 

 

 

 

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• Anomalous left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital defect in which there is an altered origin of the left coronary artery (also known as Bland-White-Garland syndrome)
• Generally asymptomatic at birth, but can present in late infancy, toddlerhood, or later with signs of congestive heart failure, a myocarditis picture, or sudden cardiac death
• Flow through the left coronary artery is normal at birth due to high pulmonary pressures, but as those pressures drop the blood flow drops as well and may become reversed due to the pressure gradient
• This can cause chronic myocardial ischemia, the severity of which, is dependent on collateral flow
• Most patients will also develop mitral regurgitation
• Cardiomegaly may be seen on CXR (and some patients will present with respiratory symptoms/wheezing)
• EKG findings include: findings consistent with ischemia (ST changes, q waves – specifically in the anterolateral leads), leftward axis (for age), abnormal R wave progression (loss of R wave amplitude in affected leads)
• Diagnosis can generally be made with echocardiogram (although not 100% sensitive) and the disease is generally treated with surgical repair

 

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Optimal Timing of Source Control in Sepsis

• Sepsis is the most common critical illness encountered in the emergency department.
• Much of the resuscitation of patients with sepsis is focused on early and appropriate antibiotic administration, appropriate fluid resuscitation, vasopressor support, and continued hemodynamic monitoring.
• Another critical pillar in sepsis resuscitation is source control.  To date, there is varying literature on the optimal timing of source control in sepsis.
• In a recent cohort study of approximately 5,000 patients with community-acquired sepsis, Reitz and colleagues report a 29% reduction in risk-adjusted odds of 90-day mortality for patients who had early source control (< 6 hours) compared to those with late source control (6-36 hours).
• The greatest reduction in risk-adjusted 90-day mortality with early source control occurred in patients with gastrointestinal/abdominal and soft-tissue sources of infection.
• Take Home Pearl: Early source control matters in sepsis resuscitation, especially in sicker patients with a GI or soft-tissue source of infection.

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Piperacillin-tazobactam is one of the most commonly used antipseudomonal antibiotics in the empiric management of patients with septic shock. The package insert recommends dose reductions for renal impairment in other infectious etiologies, but the impact of dose reduction has not been previously studied in patients with septic shock.

A recent retrospective, observational cohort study compared outcomes of patients with septic shock who received ≥ 27 grams (at least 3.375 gm q6 hours x 48 h-“NORM”) versus those who received < 27 grams (“LOW”) over the initial 48 h of septic shock (defined as concomitant norepinephrine infusion).  

Patients were excluded if they had death or hospice disposition within the 48h study period. The primary outcome was the number of norepinephrine free days (NFD) at day 28. Propensity matching was utilized to account for confounders.

Results: 351 in the LOW group, 928 in the NORM group with 608 pairs in the propensity matched assessment.

• Patients in the LOW group were
  • Older (65 v 61, p < 0.001)
  • More likely to have lower renal function (20% with CrCl < 20, 35% with CrCl 20-40) which corresponds to package insert dose reduction recommendations
  • Received lower doses of piperacillin/tazobactam (20.3 g v 30.4 g, < 0.001)
• Norepinephrine free days were statistically significantly higher in the NORM dosing group when looking at all patients and the propensity score matched patients.
• In-hospital mortality/hospice disposition was also lower in the NORM group (25.9% v 35.5%, p=0.014

Bottom Line: Dose reductions of piperacillin-tazobactam appears to be harmful early in the management of patients with septic shock.

 

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A fourteen center study enrolling 1623 trauma patients (53% penetrating) comparing cold-stored whole blood vs. blood component products found no difference in AKI, thromboembolism, or pulmonary complications. And more interestingly, patients receiving whole blood were 48% less likely to die than those receiving standard blood component products. Add this data point to a growing trend toward cold-stored whole blood for trauma patients.

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Enter the WATERFALL trial into the present flood of fluid strategy trials, a multi-country (primarily Spain) open-label RCT of “Aggressive” versus “Moderate” fluid resuscitation with lactated ringers for early mild acute pancreatitis.

Population: 249 adults (1/3 of the planned enrollment) presenting to the ED within 24hrs hours of abdominal pain onset diagnosed with mild acute pancreatitis. Numerous exclusions for local pancreatic complications, acute or chronic organ dysfunction (including CHF and CKD), among many others. Average age of 57, 51% female, 61% due to gallstones, median Charleson index of 2, median BISAP of 1, and 52% clinically judged hypovolemic on enrollment.

Interventions: 1:1 randomization to two complex protocols, both with time points every 48 hours and same criteria for initiating oral diet.

• “Aggressive”: Immediate 20ml/kg bolus of LR hours with repeat 20ml/kg boluses for hypoperfusion followed by 3ml/kg/hr infusion for 12hrs, then 1.5-3ml/kg/hr for at least 36hrs
• “Moderate”: 10ml/kg bolus only if hypovolemic with repeat 10ml/kg boluses for hypoperfusion followed 1.5 ml/kg/hr infusion for 20hrs

Outcomes/Results: Primary outcome was development of moderate of severe pancreatitis with no difference found between the two strategies. Median fluid at 72 hours was 8.3L (IQR 7.1- 10.8) in the aggressive arm and 6.6L (IQR 4.1 - 8.0) in the moderate arm.  Several point estimates favor the moderate group, but none statistically significant and there was not a difference in symptom or SIRS improvement at 72 hours.  The trial was stopped after 1/3 enrollment when the monitoring board noted a significantly increased rate of fluid overload in the aggressive arm (20.5%) versus the moderate arm (6.6%). 

Discussion:

-Aggressive fluids for mild acute pancreatitis didn’t show benefit over a moderate strategy and showed some harms in contrast to previous smaller studies and some guideline recommendations in mild disease

-Only reached 1/3 of target enrollment significantly limiting analysis

-This was by design not a trial of severe or critical disease

-The open label nature may have affected some endpoints, including safetly endpoints

-Another trial to shift our thinking a bit about how to use and safely limit fluid resuscitation

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Finger thoracostomy is superior to needle decompression in the fifth mid-axiallary intercostal space which is superior to the traditionally taught needle decompression in the second mid-clavicular intercostal space for traumatic tension pneumothorax/trauamtic arrest.

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Pes Anserinus pain syndrome (formerly pes anserine Bursitis)

Occurs at the bursa of the pes anserinus which overlies the attachment of the 1) Sartorius 2) gracilis and 3) semi-tendinosis tendons. Insertions resemble a Goose’s foot.

An inflammatory condition of the medial knee

Location is 2-3 inches below the knee joint on the medial side

1^st layer of medial compartment

https://sportsclinicnq.com.au/wp-content/uploads/2019/01/Screen-Shot-2019-01-30-at-8.55.48-am-300x291.png

 

https://www.dramynrajani.com/wp-content/uploads/2018/05/pes-anserine-bursitis-clinical-test.jpg

 

Patients complain of knee pain just below medial joint line (esp with stairs)

History may include sudden increase in running distance especially with hills (common)

Associated with obesity, tight hamstring muscles and with knee OA

PE:  Tenderness to palpation of the bursa possibly with mild swelling

DDx: MCL tear, medial meniscus injury, medial (knee) compartment arthritis, tibial stress fracture

 

Treatment: Cessation/modification of offending activities, Icing and ice massage, NSAIDs, hamstring stretching and physical therapy. Failure of the above should prompt referral for bursal steroid injection.

 

 

Have you ever encountered an ESRD patient who missed dialysis because the patient "felt too sick to go to dialysis"? The patient then had hypotension from an infected catheter line? Do we give 30 ml/kg of balanced fluid now?

__________________________

 

Title: Outcomes of CMS-mandated ?uid administration among ?uid-overloaded patients with sepsis: A systematic review and meta-analysis.

 

Settings: This is a meta-analysis

Patients: Septic patients who have underlying fluid overload conditions (CHF or ESRD).

Intervention: intravenous fluid administration according to the mandate by the Center for Medicare/Medicaid as 30 ml per kilograms of bodyweight.

Comparison: fluid administration at less than 30 ml/kg of body weight.

Outcome: 30-day mortality, rates of vasopressor requirement, rates of invasive mechanical ventilation

Study Results:

• Random-effects meta-analysis of 5 studies, including 5804 patients.  There were 5260 (91%) patients receiving non-aggressive IVF at < 30 ml/kg versus 544 (9%) patients received aggressive IVF at rates > 30 ml/kg.
• Patients who received aggressive IVF > 30 ml/kg were associated with 30-day all-cause mortality OR 1.42 (95% CI 0.88-2.3, P = 0.15, I² =35%).
• The need for vasopressor during stay was similar: OR 0.69 (95%CI 0.42-1.15, P=0.21, I² = 33%)
• The need for invasive mechanical ventilation during hospitalization was similar: OR 0.85 (95% CI 0.57-1.26, P = 0.42, I² = 0)
• Both groups had similar ICU length of stay: Standard Difference in Means -0.002 (Very small magnitude), 95% CI -0.35 to 0.34, P= 0.99, I² = 53)
• Similar hospital length of stay: Standard Difference in means -0.11 (small magnitude), 95% CI -0.62 to 0.38), P= 0.67, I²=77%

 

Discussion:

• All studies were retrospective studies, as it’s hard to do RCT when the treatment is required by guidelines.  Although the studies were graded as high quality but there was still risk of bias.
• Until there is significant evidence to change the guidelines, please document thoroughly in your charts if you do not give sepsis patients who have fluid overload the required volume of IVF at 30 ml/kg.
• Consider early vasopressor.

Conclusion:

• Patients who have fluid overload and sepsis had similar outcomes when they were given IVF at rates < 30 ml/kg, compared to those given IVF > 30 ml/kg as required by CMS.

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Manageing the airway of a trauma patient presents difficulties because of both anatomic and physiologic derangement. 

The Bottom Line: Trauma patients requiring intubation are a challenge and should be managed by the most expereinced person in the room. No study shows superiority of direct vs.video laryngoscopy. Use the technique you are most facile with and develop more techniques through courses, mentoring, and expanding your repertoire in less ill patients first. Use induction agents with lower liklelihood of causing hypotension like Etomidate and ketamine (avoid propofol and benzodiazepenes). Avoid hypoxia, hypotension and hypocarbia by resucitating as much as possible prior to intubation (use blood products and pressors where appropriate). Have a plan, a back up plan, and know when to switch to a surgical airway approach. This ia a low frequency, high risk proceedure. Mentally visualize yourself doing this proceedure regualrly to create a comfort level when it is actually needed. 

PEARLS:

1. Blood/Emesis  A. Use a double suction set up with one suction placed into the airway near the esophagus and then moved to the left of the mouth with the second used by the intubator to clear their view. 

B. If you can't visualize becaue of vomit/emesis it is very likely BVM and super glotic airways are not going to be possible and you will need to move to a surgical (front of neck) airway.

2. Limited Jaw Opening  Cervical collars can impede jaw opening. Loosen/open the collar to allow more jaw opening. Studies show that there is limited movement of C-Spine when the intubator uses caution not to flex the neck during intubation meaning the collar does not have to be in place. No study shows diret or video laryngoscopy to be superior. 

3. Blunt or penetrating neck injury Highest level of difficulty. Should be most expereienced intubator. Can use an awake intubation technique if you are adept at this method. Go with the airway approach that gives YOU the best first pass success chance. Another situation where BVM or suprglotic airway device may not work and requires surgical airway. May require low tracheostomy approach. 

4. Hypoxia  Avoiding hypoxia is a must especially in traumatic brain injured patients. Pre-oxygenate and use the airway technique that is going to give you the best first past chance of success.

5. Hypotension:  A. Resuscitate with blood products as much as possible before intubation. B. Use induction agents that are the most hemodynamically neutral such as Etomidate or Ketamine (safe in head injury patients!)

6.. Hypocarbia: Congrats on getting the tube! Now slow down your bagging. Hypocarbia leads to increased injury in traumatic brain injured patients. 

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