A 50yo man found dow in the snow was brought into our ER last week in cardiac arrest with a bladder temperature of 21° C. Let’s warm him up!

• Passive external warming (good for mild hypothermia > 34° C):  remove all wet clothing, use warm blankets, hot chocolate.
• Active external rewarming (Used for temp between 30-34° C): Radiant heat, electric blankets, Bair-Hugger. Disadvantages: “core temperature after drop” theory: drop in core temp because of peripheral vasodilatation. Therefore, focus on warming the chest and torso area.  May not occur with certain warming techniques.
• Active core rewarming (<30 °C, above techniques and several other options):

1. Heated humidified oxygen via mechanical ventilation at 42-46°
2. IV normal saline warmed to 41-43° C
3. Cardio-pulmonary bypass: 1-2° C increase every 5 minutes
4. ECMO (best option in cardiac arrest): Up to 4-6° C/hr. VV or VA ECMO. Provides Cardio-pulmonary support. Can continue CPR while placing a cannula.
5. CVVH: less costly, more available, 1-4°C/hr. Case reports only. 
6. Artic Sun; external rewarming pads: used in hypothermia protocols. Easy to use. Case reports only.

• Other methods (use if other methods are unavailable):

1. Pleural irrigation: one chest tube in the mid-clavicular line w saline at 42° and another chest tube in the post-axillary line and connected to a pleurovac.
2. Peritoneal lavage: 8 Fr catheter into the peritoneum using a standard paracentesis method. Use 40-45° C dialysate.
3. Gastric, bladder, colonic irrigations

We were able to get ROSC with CPR and ACLS and then used Artic Sun to re-warm successfully.

Other tips/tricks:

• Continue CPR while rewarming (This is debatable: monitor ECG for new rhythms)
• How warm is “warm and dead”? Probably around 32°C
• How fast to rewarm?  Would warm quickly in cardiac arrest and then 1-2° C/hr thereafter; (No good evidence here)
• Arrhythmias corrected by rewarming (bradycardia etc); no need for pacing
• Up to three defibrillations for V. fib/V. tach; hold if no benefit
• Can give epinephrine per ACLS protocol but would be cautious with further dosing
• Pressors: can use epinephrine drip cautiously for hypotension
• Cisaturacurium for paralysis w/ sedation to prevent shivering
• Rule out hypoglycemia, adrenal insufficiency, hypothyroidism, sepsis if patient does not rewarm as expected!
• Avoid IJ lines or irritating the myocardium with a guidewire.
• K>12 mmol /L: consider termination of CPR

Attachments

• 1402111256_nejm_hypothermia2012.pdf (581 Kb)

Mechanical Ventilation During ECMO

• ECMO is a rapidly emerging therapy for critically ill patients with severe acute respiratory failure (VV-ECMO) and circulatory failure (VA-ECMO).
• Mechanical ventilation (MV) settings may have important effects on patients receiving either VV- or VA-ECMO.
• Though no large, randomized trials, consensus guidelines and expert opinion recommend the following initial settings for patients receiving VV-ECMO:
  • Tidal volume: < 4 ml/kg predicted body weight
  • Plateau pressure: < 25 cmH₂O
  • PEEP: 10-15 cmH₂O
  • F_iO₂: titrated to maintain sats > 85%
  • RR: 4 to 6 breaths per minute

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NSSTIs occur secondary to toxin-secreting bacteria; NSSTIs are surgical emergencies with a high-morbidity / mortality

Risk factors: immunocompromised host (DM, AIDS, etc.), intravenous drug use, malnourishment, peripheral vascular disease

Type I (polymicrobial; most common), Type II (monomicrobial; typically clostridia, streptococci, staph, or bacteroides), Type III (Vibrio vulnificus; seawater exposure)

Signs / Symptoms: pain out of proportion to exam (occasionally no pain at all), skin findings (blistering / bullae, gray-skin discoloration, or “Dishwater-like” discharge), or systemic toxicity (altered mental status, elevated lactate, etc.)

Diagnostic radiology

• Xray (shows gas); low sensitivity; CT scan (gas / tissue stranding); sensitivity is also low
• MRI can over-diagnose NSSTI and should not be used routinely
• Bedside ultrasound may demonstrate fluid or gas collections in deeper tissues (see clip below)

Treatment is emergent surgical debridement with simultaneous hemodynamic resuscitation PLUS broad-spectrum antibiotics; consider clindamycin becuase it has anti-toxin activity

Adjunctive therapies include Intravenous intraglobulin (neutralizes toxins secreted by bacteria) and hyperbaric oxygen

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Arterial Catheter-Related Blood Stream Infections

Whether arterial lines are a potential source of catheter-related blood stream infections (CRBSIs) is highly-debated; however, based on a recent systematic review they are an under recognized and significant source of CRBSIs.

• Incidence: In systematically cultured arterial catheters, the infection rate was 1.6 infections/1,000 catheter days which is similar to what has been reported for infections associated with short-term CVC's.
   
• Location: Femoral a-lines are more likely than radial a-lines to be a source of a CRBSI. Femoral a-line CRBSIs occurred in 1.5% of all catheters (95% CI, 0.8–2.2%), which is higher than radial CRBSI, with a relative risk of infection 1.94 times greater than those placed at the radial site.
   
• Technique: Only one study specifically evaluated the impact of full barrier precautions versus using sterile gloves only for peripheral a-lines, and it did not find any significant difference in BSI. No study has evaluated the impact of maximal barrier precautions for femoral, axillary, and brachial arterial catheters.
   
• Dressing: The risk of infection was significantly decreased with the use of chlorhexidine-impregnated dressings (ex: BioPatch).

Bottom Line(s) 

1. Arterial lines appear to be a significantly under recognized source of CRBSI's in critically-ill patients.  If you are deciding to place an a-line for invasive blood pressure monitoring, strongly consider the radial site and use a chlorhexidine sponge or dressing to try and minimize the risk of future BSI.
    
2. There is a paucity of data regarding the utility of maximal barrier techniques when inserting peripheral arterial lines.  With arterial catheter infection rates approaching that of central venous catheters, we should probably be inserting a-lines with the same sterile technique.

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Determination of Brain Death

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Attachments

• 1401141409_pitfalls_in_brain_death,_wijdicks.pdf (93 Kb)

Pearls for the Crashing LVAD Patient

• Left ventricular assist devices (LVAD) are placed as a bridge to transplant, bridge to recovery, or as destination therapy.
• As thousands of LVADs have been implanted, it is likely that a sick LVAD patient will show up in your ED or ICU.
• In addition to pump thrombosis (UMEM pearl 12/31/13), two complications to also consider in the crashing LVAD patient include infection and arrhythmias.
• Infection:
  • The driveline and pump pocket are the most common locations for device infection.
  • Most are caused by Staphylococcus and Enterococcus organisms.
  • For pump pocket and deeper wound infections be sure to also add coverage against Pseudomonas species. 
• Arryhthmias:
  • The highest incidence is within the first month after implantation.
  • Consider a "suction event," where the inflow cannula contacts the ventricular septum.
  • Suction events can be caused by hypovolemia, small ventricular size, or RV failure and are treated with fluid resuscitation and decreasing the LVAD speed.

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VAD thrombosis: A Must Know VAD Complication

The HeartMate left ventricular assist device (LVAD) is one of the most frequently placed LVADs today. Originally, it was thought to have a lower incidence of thrombosis due to its mechanical design. However, a recent multi-center study published in the NEJM reported a dramatic increase in the rate of thrombosis since 2011 in the HeartMate II device.  The report found:

• An increase in pump thrombosis at 3 months after implantation from 2.2% to 8.4%

• The median time from implantation to thrombosis was 18.6 months prior to March 2011, to 2.7 months after.

Pump thrombosis is a major cause of morbidity and mortality (up to almost 50%!!) and is a can't miss diagnosis.  It's important to keep thrombosis on the differential for any VAD patient presenting with:

• Power spikes or low pump flow alarms on the patient's control box

• Pump (VAD) failure

• Recurrent/new heart failure

• Altered mental status

• Hypotension (MAP < 65)

• Signs of peripheral emboli (including acute CVA)

Useful lab findings suggestive of thrombosis include:

• Evidence of hemolysis

• LDH > 1,500 mg/dL or 2.5-3 times the upper limit of normal

• Hemoglobinuria

• Elevated plasma free hemoglobin

Bottom Line: In the patient with suspected VAD thrombosis, it is important to contact the patient's VAD team immediately (CT surgeon, VAD coordinator/nurse, VAD engineer).  Treatment should begin with a continuous infusion of unfractionated heparin, while other treatment options can be discussed with the VAD team.

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The morbidity and mortality from pseudomonas aeruginosa infections is high and empiric double-antibiotic coverage (DAC) is sometimes given; quality evidence for this practice is lacking.

Although there is little supporting data, the following reasons have been given for DAC:

• DAC provides better empiric coverage through differing mechanisms of antibiotic action
• DAC prevents the emergence of antibiotic resistance during therapy

The potential harm of antibiotic overuse cannot be ignored, however, and include adverse reaction, microbial resistance, risk of super-infection with other organisms (e.g., Clostridium difficile), and cost.

There may be a signal in the literature demonstrating a survival benefit when using DAC for patients with shock, hospital-associated pneumonia, or neutropenia. The IDSA guidelines, however, do not support DAC for neutropenia alone; only with neutropenia plus pneumonia or gram-negative bacteremia.

Bottom line: Little data supports the routine use of DAC in presumed pseudomonal infection. It may be considered in patients with shock, hospital-associated pneumonia, or neutropenia (+/- pneumonia), but consult your hospital’s antibiogram or ID consultant for local practices.

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Hepatic Encephalopathy (HE)

Pathogenesis: Several theories exist that include accumulation of ammonia from the gut because of impaired hepatic clearance that can lead to accumulation of glutamine in brain astrocytes leading to swelling in patients with hepatic insufficiency from acute liver failure or cirrhosis.

Clinical Features:

• Impaired mental status
• impaired neuromotor function (hyperreflexia, hypertonicity, asterixis)
• Subtle signs include personality changes, decreased energy level, and impaired sleep-wake cycle

Diagnostic tests: Ammonia levels are routinely drawn but must be drawn correctly without the use of a tourniquet, transported on ice, and analyzed within 20 minutes to get an accurate result. Severity of HE does not correlate with increasing levels.

Management:

1.     Airway protection as needed

2.     Correct precipitating factors (GI bleed, infection-SBP, hypovolemia, renal failure)

3.     Consider neuro-imaging if new focal neurologic findings are found on exam

4.     Correct electrolyte imbalances

5.     Lactulose by mouth (PO/Naso-gastric tube or Rectally)

a.     10-30 g every 1-2 hours until bowel movement or lactulose enema (300 mL in 1 L water)

b.     Facilitates conversion of NH3 to NH4+, decreases survival of urease-producing bacteria in the gut

6.     Rifaximin 550 mg by mouth BID (minimally absorbed antibiotic with broad-spectrum activity)

7.     Do not limit protein intake acutely

8.     TIPS reduction in certain patients with recurrent HE

9.     Transplant referral as needed

10.  Consider other causes if patient does not improve within 24-48hrs. 

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The Concentrated Overview of Resuscitative Efforts (CORE) Scan

• Ultrasound has become an essential tool in the evaluation and management of the crashing patient.
• The CORE scan utilizes emergency bedside ultrasonography to systematically evaluate and resuscitate the rapidly deteriorating patient.
• Essentially steps in the CORE scan include:
  • Endotracheal tube assessment
  • Lung assessment
    • Pneumothorax?
    • Pleural effusion?
    • Hemothorax?
  • Cardiac assessment
    • Pericardial effusion?
    • Massive PE?
    • Estimated ejection fraction?
  • Aorta assessment
    • Abdominal aortic aneurysm?
    • Aortic dissection?
  • IVC assessment
  • Abdominal assessment
    • Intraperitoneal fluid?

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Vent Management: Finding the AutoPEEP!

OK, so we all know not to, "...Fall asleep on Auto-PEEP" thanks to Dr. Mallemat's pearl that can be seen here.  But now the question is, how do you know if your patient is air-trapping?

There are 3 ways you can look for evidence of Auto-PEEP on the ventilator:

1. Do an end-expiratory hold:  If the measured PEEP is more than the PEEP set on the vent after a 2-3 second hold, the difference is your Auto-PEEP.


2. Look at the expiratory flow waveform:  If the waveform does not return to baseline (still expiring when inspiratory ventilation occurs), there's Auto-PEEP!


3. Compare the inspiratory vs. expiratory volumes.  If the inspiratory volumes are much higher then the expiratory volumes, consider Auto-PEEP.

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The management of alcohol withdrawal syndrome (AWS) includes supportive care focusing on the ABC’s and administration of benzodiazepines (BDZ). 

While BDZ are effective in the treatment of AWS, some patients may require very high doses of BDZ to control symptoms (tachycardia, hypertension, diaphoresis, etc.); unfortunately, high-doses of BDZ may lead to suppression of the respiratory drive and endotracheal intubation.

Dexmedetomidine (DEX) is a sedative agent that is an intravenous alpha2-agonist (it's like clonidine); it reduces sympathetic outflow from the central nervous system and it may help treat withdrawal syndromes. The major benefit of DEX is that it does not suppress the respiratory drive, thus intubation is not required.

Smaller trials and case series have shown that patients with AWS who were treated with BDZ in addition to DEX had better symptom control, lower overall BDZ doses, and less respiratory depression/intubation.

Bottom-line: While more trials are needed, consider adding DEX for patients with AWS who require high-doses of BDZ.

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Ottawa Rules for Subarachnoid Hemmorhage (SAH)

Background

• Headache is a common reason for ER visits
• 1-3% of headaches are SAH
• Misdiagnosis of SAH can be fatal
• Lumbar puncture can be a painful/time-consuming procedure
• Goal is to design a decision rule to help guide the clinician

Design

• Multi-center study at ten Canadian emergency departments.
• 2131 adults with a headache peaking within 1 hour and no neurologic deficits
• Non-traumatic headaches only; GCS of 15 required
• SAH defined as: 1. CT evidence of SAH; 2. Xanthochromia in CSF; or 3. RBCs in the final tube of CSF, WITH positive angiography findings.

Results

132 (6.2%) had SAH

Decision rule including any:

1. age 40 years or older
2. neck pain or stiffness
3. witnessed LOC
4. onset during exertion

Had 98.5% sensitivity (95% CI, 94.6%-99.6%) and 27.5% specificity (95% CI, 25.6%-29.5%)

Adding “thunder-clap” headache and “limited neck flexion on examination” (inability to touch chin to chest or raise the head 8cm off the bed if supine) resulted in 100% (95% CI, 97.2%-100%) sensitivity.

The rule was then evaluated using a bootstrap analysis on old cohort data to validate the rule.

Conclusion/Limitations

• Exciting new rule for SAH that needs to be validated in a new, independent cohort
• The rule may not decrease the rate of investigation (CT, LP, or both)
• It may decrease the amount of SAH that are missed on first visit to the ER
• Limited by narrow criteria for inclusion in the rule/not meant for other causes of headache
• See the JAMA editorial with the article for a nice discussion of the difficulties with decision making rules.
• The rule:
  The Ottawa SAH Rule

  • For alert patients older than 15 y with new severe nontraumatic headache reaching maximum intensity within 1 h

  • Not for patients with new neurologic deficits, previous aneurysms, SAH, brain tumors, or history of recurrent headaches (≥3 episodes over the course of ≥6 mo)

  • Investigate if ≥1 high-risk variables present:

  1. Age ≥40 y

  2. Neck pain or stiffness

  3. Witnessed loss of consciousness

  4. Onset during exertion

  5. Thunderclap headache (instantly peaking pain)

  6. Limited neck flexion on examination

   

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Attachments

• 1311191832_ottawa_editorial.pdf (109 Kb)

Acalculous Cholecystitis in the Critically Ill

• Acute acalculous cholecystitis (AAC) accounts for almost 50% of cases of acute cholecystitis in the critically ill ICU patient.
• Importantly, the mortality rate for AAC can be as high as 50%.
• Risk factors for AAC include:
  • CHF
  • Cardiac arrest
  • DM
  • ESRD on hemodialysis
  • Postoperative
  • Burns
• Unfortunately, the physical exam is unreliable, especially in intubated and sedated patients.
• Furthermore, less than half of patients with AAC are febrile or have a leukocytosis.  LFTs can also be normal in up to 20% of patients.
• Ultrasound remains the most common imaging modality for diagnosis.
• Take Home Point: Consider AAC in the septic critically ill patient without a source.

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Ineffective triggering is the most common type of ventilator dyssynchrony.  The differential diagnosis includes:

• Auto peep (the most common cause) 
• Neuromuscular weakness 
• Improper ventilator settings

Auto peep is the most common cause of ineffective triggering and will often occur as a patient cannot create enough inspiratory force to overcome their own intrinsic peep (PEEPi).  Patients who are severely tachypnic or those with obstructive lung disease are at high risk for auto peep (not enough time to exhale).

Ineffective triggering can also occur if the patient cannot create enough of a negative inspiratory force to trigger the vent to deliver a positive pressure breath. Prolonged period of mechanical ventilation, over sedation, high cervical spine injuries, or diaphragmatic weakness are common causes.

Lastly, improper trigger sensitivities may make it difficulty for the ventilator to sense when the patient is attempting to take a spontaneous breath.  

For an example of a patient with ineffective triggering, check out: http://marylandccproject.org/2013/10/28/vent-problems1/

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The pregnant patient normally has increased cardiac output and minute ventilation by the third trimester. Despite this increase, however, these patients have little cardiopulmonary reserve should they become critically-ill.

Remember the mnemonic T.O.L.D.D. for simple tips that should be done for the pregnant patient who presents critically-ill or with the potential for critical illness: 

• Tilt: The supine-hypotension syndrome occurs after the 20th week of pregnancy as the gravid uterus compresses the IVC and aorta, reducing cardiac output by up to 30%. Placing a 30-degree right hip-wedge under the patient will relieve this obstruction.
• Oxygen: the growing uterus pushes up on the base of the lungs reducing the functional residual capacity meaning there is less oxygen reserve and rapid oxygen desaturations. Supplemental oxygen may increase the patient's reserve.
• Lines: The circulatory system reserve is reduced, so early and large bore venous access is important. Remember that lines should be placed above the diaphragm because the enlarging uterus compresses pelvic veins, reducing venous return to the heart.
• Dates: Rapidly determine the gestational age of the fetus as 24 weeks is a critical date to remember (e.g., increased risk of supine-hypotension syndrome, fetal viability, etc.)
• Delivery: Call labor and delivery early on, not only for the consultation, but also for the fetal monitoring that this service provides. 

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Background

• Acute lung injury that develops within 6 hours after transfusion of 1 or more units of blood or blood components.
• Increased risk with greater number of transfusions
• Incidence is 1 in 4000

Definition

• Acute onset
• Hypoxemia (PaO2/FiO2 < 300 mm Hg)
• Bilateral pulmonary opacities on chest x-ray
• Absence of left atrial hypertension

Pathogenesis

Two-hit hypothesis: first hit is underlying patient factors causing adherence of neutrophils to the pulmonary endothelium; second hit is caused by mediators in the blood transfusion that activate the neutrophils and endothelial cells.

Differential

Can be confused or overlap with TACO or transfusion-associated volume/circulatory overload, which presents similarly but has evidence of increased BNP, CVP, pulmonary wedge pressure, and left sided heart pressures. Patients with TACO tend to improve with diuretic treatment

Supportive tests

• Echocardiogram 
• BNP (tends to be low)
• Transient leukopenia

Treatment

• Supportive care
• Lung protective ventilation strategies
• Fluid restrictive strategy
• Aspirin (shown to be helpful in animal studies)
• Pre-washing of stored RBCs prior to transfusion
• Decrease the amount of transfusions!

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There have been so many great talks at ACEP 2013, but Dr. Michael Winters' talk "The ICU is NOT Ready for Your Patient" was chock full of great critical care pearls. Here are just a few:

• Increased mortality for ICU patients boarding in the Emergency Department; the increase is 1.5% per each hour of delayed transfer.
• Intubated patients should receive analgesia BEFORE sedation; fentanyl is recommended because hemodynamically stable, but you can use anything. Good analgesia will also reduce total sedative dosing
• Use continuous capnography for the intubated patient; can detect equipment malfunction and allow titration of ventilation
• Keep an eye out for abdominal compartment syndrome. Physical exam is not always conclusive, should obtain bladder pressures
• Reduce the risk of ventilator-associated pneumonia by keeping endotracheal cuff pressures adequate and keeping the head of bed elevated 30-45 degrees

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Want to improve your chances of success in the resus room?  Download a metronome app on your smartphone and set it to a rate of 100-120 beats per minute.  There are a number of cheap (usually free) metronome applications for both iOS and Android devices.

A recent review looked at the evidence behind CPR feedback devices and found:

• Compared to baseline, chest compression rates and end-tidal CO₂ improved after activation of the metronomes.

So instead of going to iTunes and downloading the Bee Gees, go over to the App store and download a free metronome.  Your resus team will be able to stay on track with their compressions and even better - they won't have to hear you sing!

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• The efficacy of epinephrine during out-of hospital cardiac arrest has been questioned in recent years, especially with respect to neurologic outcomes (ref#1).

• A recent study demonstrated both a survival and neurologic benefit to using epinephrine during in-hospital cardiac arrest when used in combination with vasopressin and methylprednisolone.

• Researchers in Greece randomized 268 consecutive patients with in-hospital cardiac arrest to receive either epinephrine + placebo (control group; n=138) or vasopressin, epinephrine, and methylprednisolone (intervention arm; n=130)

  • Vasopressin (20 IU) was given with epinephrine each CPR cycle for the first 5 cycles; Epinephrine was given alone thereafter (if necessary)

  • Methylprednisolone (40 mg) was only given during the first CPR cycle.

  • If there was return of spontaneous circulation (ROSC) but the patient was in shock, 300 mg of methylprednisolone was given daily for up to 7 days.

• Primary study end-points were ROSC for 20 minutes or more and survival to hospital discharge while monitoring for neurological outcome

• The results were that patients in the intervention group had a statistically significant:

  • probability of ROSC for > 20 minutes (84% vs. 66%)

  • survival with good neurological outcomes (14% vs. 5%)

  • survival if shock was present post-ROSC (21% vs. 8%)

  • better hemodynamic parameters, less organ dysfunction, and better central venous saturation levels

• Bottom-line: This study may present a promising new therapy for in-hospital cardiac arrest and should be strongly considered.

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