Question

One third of your critically ill patients will have atrial fibrillation. 

More than one third of those patients will develop immediate hypotension because of it.

More than one in ten will develop ischemia or heart failure because of it.

This is what you should know for your next shift:

#1 Don't wait to use electricity. If your patient is hypotensive or ischemic because of atrial fibrillation, you do not need to wait for anticoagulation before you cardiovert.

#2 Electricity buys you time to load meds. Fewer than half of patients you cardiovert will be in sinus rhythm an hour later and fewer than a quarter at the end of a day.

#3 There is no perfect rate control agent. Beta blockers have a lower mortality in A-fib from sepsis. Esmolol has the benefit of being short-acting if you cause hypotension. Diltiazem has better sustained control than amiodarone or digoxin. 

#4 There is no perfect rhythm control agent. Magnesium is first-line in guidelines. Amiodarone can be used even when there is coronary artery or structural heart disease.

#5 Anticoagulation is controversial. In sepsis, anticoagulation does not reduce the rate of in-hospital stroke, but does increase the risk of bleeding. Use with caution if cardioversion isn't planned.

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Critical Care Management of AIS

• In addition to reperfusion therapy, the critical care management of patients with an acute ischemic stroke also includes airway and ventilation management, hemodynamic management, glucose control, anticoagulation management, and surgery in select cases.
• Consider the following management pearls:
  • Mechanical ventilation
    • Target SpO2 > 94% (avoid supplemental oxygen for non-hypoxemic patients)
    • Target normocarbia (PaCO2 35-45 mmHg)
  • Hemodynamics
    • Target euvolemia with isotonic saline
    • Target BP < 185/110 mmHg for 24 hrs after tPA
    • Target BP < 220/120 mmHg if tPA ineligible
    • Target SBP < 160 mmHg after endovascular therapy
  • Glucose
    • Target serum glucose 140-180 mg/dL

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A new study confirmed the previously-known antibiotics to be associated with Torsades de pointes and QT prolongation (Macrolides, Linezolid, Imipenem and Fluoroquinolones). However, this study found new association between amikacin and Torsades de pointes/QT prolongation.

Methods

The authors queried the United States FDA Adverse Event Reporting System (FAERS) from 01/01/2015 to 12/31/2017 for reports of Torsade de points/QT prolongation (TdP/QT).

Reporting Odd Ratio (ROR) was calculated as the ratio of the odds of reporting TdP/QTP versus all other ADRs for a given drug, compared with these reporting odds for all other drugs present in FAERS

Results

FAERS contained 2,042,801 reports from January 1, 2015 to December 31, 2017. There were 3,960 TdP/QTP reports from the study period (0.19%).

Macrolides               ROR 14 (95% CI 11.8-17.38)

Linezolid                  ROR 12 (95% CI 8.5-18)

Amikacin                 ROR 11.8 (5.57-24.97)

Imipenem-cilastatin ROR 6.6 (3.13-13.9)

Fluoroquinolones   ROR 5.68 (95% CI 4.78-6.76)

Limitations:

These adverse events are voluntary reports

There might be other confounded by concomitant drugs such as ondansetron, azole anti-fungals, antipsychotics.

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The Kidney Transplant Patient in Your ED

• Acute bacterial graft pyelonephritis is the most frequent type of sepis (bacterial pneumonia is the second most common source)
• Obtain renal transplant imaging to evaluate for sources of infection (i.e. urinary tract obstruction, renal abscess, or urine leakage)
• BK polyomavirus may reactivate and lead to nephritis, ureteral stenosis, or hemorrhagic cystitis
• Pneumocystis pneumonia is the most common fungal infection in patients without prophylaxis and after prophylaxis discontinuation (adjunctive steroids for treatment is controversial)
• Vascular access may be challenging. Avoid subclavian lines or femoral venous acess on the side of the graft
• Cardiovascular disease is the leading cause of mortality (accounts for 40-50% of deaths after the first year following renal transplant)

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Managing the intubated patient with exacerbation of severe obstructive lung disease, especially asthma, can be very challenging as it carries higher risks of barotrauma due to higher pulmonary pressures and circulatory collapse due to auto-PEEP and decreased venous return. When measures such as medical therapy and noninvasive positive-pressure ventilation fail to prevent intubation, here are some tips to help:

1. Utilize a volume control ventilation mode to ensure a set tidal volume delivery / minute ventilation, as pressure-targeted modes will be more difficult due to the high pulmonary pressures in acute obstructive lung disease.

2. Set a low RR in order to allow for full exhalation, avoiding air-trapping / breath-stacking and circulatory collapse due to decreased venous return. This may require deep sedation and potentially paralysis.

• Permissive hypercapnea to >7.2 is generally well-tolerated except for pregnant patients, patients with high ICP, or patients with severe pulmonary hypertension

3. Increase your inspiratory flow by shortening your inspiratory time (thereby increasing your time for exhalation.

4. Monitor for auto-PEEP:

• Check your flow curve -- the waveform should return to zero before the start of the next inhalation, otherwise the next breath has been given before the patient has fully exhaled.
• Perform an expiratory hold at the end of exhalation. PEEP greater than set PEEP = auto-PEEP.

5. Peak inspiratory pressures will be high -- what is more important is the plateau pressure, measured by performing an inspiratory hold at the end of inspiration. Provided your plateau pressure remains <30, you don't need to worry as much about the peak pressure alarms.

6. If your patient acutely decompensates in terms of hemodynamics and oxygenation -- first attempt to decompress their likely auto-PEEPed lungs by popping them off the ventilator and manually press on their chest to assist with exhalation of stacked breaths allowing venous return to the heart.

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With increasing critical care boarding and the opioid crisis leading to more intubations for overdose, extubation - which was once a very rare event in the ED - is taking place downstairs more often.  Prolonged mechanical ventilation is associated with a ton of complications, so it's important for the ED physician to be comfortable assessing extubation readiness.  There is no single accepted set of criteria, but most commonly used are some variant of the following:

• Reason for intubation (e.g. overdose, pneumonia, pulmonary edema, AMS, etc) has resolved
• Minimal vent settings - Typically FiO2 < 40%, PEEP <= 5
• Spontaneous breathing present (i.e. pt breathes with reasonable rate on PS, SIMV, VS, PPS, etc) and able to maintain reasonable pH and pCO2 on these settings
• Neuromuscular function adequate - Ask patient to lift head off bed
• Mental status adequate - Ask patient to give thumbs up or squeeze hands
• Secretions tolerable - Ask RN or RT for frequency of suctioning and sputum character.  Think twice about extubation if getting purulent, thick secretions every 15 minutes.
• Clinical course does not require further intubation (i.e. no immediate trips planned to OR, MRI; pt not hemodynamically unstable, etc.)

If the above criteria are met, two additional tests are frequently considered:

• Spontaneous Breathing Trial (SBT) - Typically done by placing pt on PS with low settings (0/0 to 5/5).  Let pt equilibrate (time of SBT is variable) on these settings, then calculate RSBI (RR/Vt). RSBI < 105 is traditionally considered acceptable for extubation.  Remember - lower is better.  Ask RT for this. 
• Cuff Leak Test - becoming less popular, but may consider in patients at risk for laryngeal edema (e.g. prolonged intubation, angioedema, etc). Historically thought to predict airway swelling, but data is mixed.  Ask RT for this.

And don't forget to consider extubating high risk patients directly to BiPAP or HFNC!

Bottom Line: For conditions requiring intubation where significant clinical improvement may be expected while in the ED (e.g. overdose, flash pulmonary edema, etc), be vigilant about, and have a system for, assessing readiness for extubation.

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Question

The incidence of empyema as a complication of pneumonia has been increasing since the 1990's and source control requires removing the pus from the chest as soon as possible, but how large should the drain be? The American Association for Thoracic Surgery (AATS) released the most recent guidelines for identifying and managing empyema in June 2017 and at the time had no certain evidence to guide the choice of large-bore vs small-bore catheters. Most studies to guide us are flawed (not randomized), but no recently published randomized studies exist to provide a definitive answer. 

Bottom line: a small-bore pigtail catheter is a reasonable choice to drain empyema and flushing it every 6 hours has been shown to prevent clogging.

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POCUS in the Critically Ill Pregnant Patient

• POCUS can be a valuable tool in the assessment and management of critically ill pregnant patients.
• Conditions to consider in the critically ill pregnant patient who presents with acute RUQ pain include acute fatty liver of pregnancy (AFLP), liver infarction, liver hematoma, and Budd-Chiari Syndrome.
• POCUS findings for these conditions include:
  • AFLP: a "bright" liver
  • Infarction: a wedge-shaped hypoechoic area (late finding)
  • Hematoma: a heterogeneous fluid collection below the capsule or intraparenchymal
  • Budd-Chiari Syndrome: lack of blood flow or thrombus in a hepatic vein or within the IVC.

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With a shortage of push dose epi, this may be an opportune time to review alternative options (see also Ashley's email on the subject).

The dose of vasopressor required to reverse hypotension has been most studied in pregnant women undergoing c-section who get epidurals and experience spinal-induced vasoplegia and hypotension (not necessarily our patient population, but we can extrapolate...)  

Phenylephrine was found to reverse hypotension 95% of the time at a dose of 159 micrograms (a neo stick has 100 ug/mL, so around 1-2 mL out of the stick)

Norepinephrine reversed hypotension in 95% of patients at a dose of 5.8 ug.  The starting dose for our norepi order in Epic is 0.01 ug/kg/min, so if you have a levophed drip hanging and have an acutely hypotensive patient, you may want to briefly infuse at a higher rate such as 0.1 ug/kg/min (for a typical weight patient), or bolus approximately 3-7 ug for a typical patient.  Of course the degree of hypotension, particular characteristics of your patient and clinical context should be taken into consideration.  When your a lucky enough to have this resource, always consult your pharmacist.

Bottom Line: To reverse acute transient hypotension you may consider:

-A bolus of phenylephrine 50-200 ug (0.5-2 mL from neo-stick)

-A bolus of norepinephrine 3-7 ug

-Briefly increasing your norepinephrine drip (if you have one) to something around 0.1 ug/kg/min in a typical weight patient

-Always search for other causes of hypotension and consider clinical context.

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Question

Wound botulism presents as descending paralysis when Clostridium botulinum spores germinate in anaerobic necrotic tissue. There have been hundreds of cases in the last decade, but it is poorly reported outside of California.

Black tar heroin and subcutaneous injection (“skin popping”) carry the highest risk, but other injected drugs and other types of drug use suffice. C botulinum spores are viable unless cooked at or above 85°C for 5 minutes or longer and this is not achieved when cooking drugs. 

Early administration of botulism anti-toxin (BAT) not only saves lives but can prevent paralysis and mechanical ventilation. An outbreak of 9 cases between September 2017 and April 2018 cost roughly $2.3 million, in part because patients didn’t present on average until 48 hours after symptom onset and it took an additional 2-4 days before the true cause of their respiratory depression and lethargy were understood. One patient died.

PEARL: talk to your injecting drug users about the symptoms of botulism: muscle weakness, difficulty swallowing, blurred vision, drooping eyelids, slurred speech, loss of facial expression, descending paralysis, and difficulty breathing. Consider botulism early in your patients who inject drugs but who do not respond to naloxone or who exhibit prolonged symptoms. Testing at the health department is performed with mouse antibodies to Botulism Neurotoxin (BoNT) combined with the patient’s serum.

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Post-Arrest Prophylactic Antibiotics?

• Pneumonia is the most common infective complication in post-cardiac arrest patients. It may develop in up to 60% of patients and is associated with an increased ICU length of stay.
• Given the challenges in diagnosing pneumonia in the post-cardiac arrest patient, many clinicians consider prophylactic antibiotic administration.
• A recent systematic review and meta-analysis sought to evaluate the effect of early antibiotic use on survival and survival with good neurologic outcome in adult patients resuscitated from cardiac arrest. Key study results include:
  • 11 studies (3 RCTs, 8 observational trials)
  • 6149 patients
  • No change in overall survival or survival with good neurologic outcome
• Take Home Point: Current data does not support the prophylactic administration of antibiotics to adults resuscitated from cardiac arrest.

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Question

Little people (patients with achondroplasia or "dwarfism") have little lungs. Even though the trunk may appear to be a normal size with small limbs, the vital capacity is actually about 75% the predicted value based on the patient's sitting height. Macrocephaly and a decreased anterior-posterior depth are the cause for this. When you want to mechanically ventilate a little person, you can estimate their height based on a typical person with the same sitting height, but their actual volume will be about 3/4 the tidal volume predicted.

When intubating, remember these patients also have a high risk of basicranial hypoplasia (the foramen magnum may be small and key-hole shaped). These patients will be predisposed to compress the vertebral arteries when you tilt the head back and this itself can cause ischemia of the medulla and pons leading to central apnea.

Stokes DC, Wohl ME, Wise RA, et al. The lungs and airways in Achondroplasia. Do little people have little lungs? CHEST. 1990; 98(1):145-52

Pauli RM. Achondroplasia: A comprehensive review. Orphanet Journal of Rare Diseases. 2019; 14(1): 

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Some patients with severe pulmonary hypertension receive continuous infusions at home of prostacyclins, such as epoprostanol (flolan).  These are generally delivered via a pump that the patient wears, which is attached to an indwelling catheter.  As with any indwelling device, they are at risk for infection and other complications, including malfunction.

Interruption of delivery of the medication can result in rapid cardiovascular collapse, sometimes within minutes.  In this instance, the medication should be resumed as quickly as possible (by a traditional IV if the catheter is not functional), and the patients should be treated as one would approach a patient with decompensated right heart failure.

I once saw a patient in the ED whose listed chief complaint was "medication refill", but was actually there for dislodgement of her prostacyclin catheter (thankfully she was ok).  With more patients receiving devices they are dependent upon (insulin pumps, AICDs, prostacyclin catheters), be wary of chief complaints such as "medication refill" or "device malfunction."

Bottom Line: Interruption of continuous prostacyclin therapy for pulmonary hypertension can be rapidly fatal and should be addressed immediately.

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Question

In a study of alarms from 77 monitored ICU beds over the course of a month at the University of California, San Francisco, false alarms were common. Accellerated Ventircular Rhythms (AVRs) made up roughly one third of the alarms, and of the more than 4,361 AVRs, 94.9% were false while the remaining 5.1% did not result in a clinical action.

While this study had a majority of patients in the Med/Surg ICUs, a minority were from the cardiac and neurologic ICUs giving it some broad applicability. This study adds to the literature indicating there are subsets of alarms which may not be necessary or which may require adjustment to increase specificity.

Suba S, Sandoval CS, Zegre-Hemsey J, et al. Contribution of Electrocardiographic Accelerated Ventricular Rhythm Alarms to Alarm Fatigue. American Journal of Critical Care. 2019; 28(3):222-229

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• ANDROMEDA-SHOCK compared using capillary refill time versus lactate clearance as a guide for resuscitation in septic shock patients
• The cap refill group showed better SOFA scores at 72 hours, and a trend to lower mortality
• In the study, cap refill was performed by pressing a glass microscope slide to the ventral surface of the second finger distal phalanx, holding until blanched for 10 seconds, and releasing.  Cap refill > 3 seconds was considered abnormal.

Bottom Line: Consider using capillary refill as an alternate (or complimentary) endpoint to lactate clearance when resuscitating your septic shock patients.

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Management of Coagulopathy in Acute Liver Failure

• Patients with acute liver failure (ALF) frequently require rapid resuscitation to prevent decompensation and multiorgan failure.
• The most common cause of ALF remains drug-induced injury (i.e., acetaminophen).
• Though coagulopathy is common in patients with ALF, the prophylactic administration of blood products has not been shown to have clinical benefit.
• The routine correction of coagulation abnormalities is not currently recommended, unless the patient undergoes a major procedure (e.g., liver transplant).

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Many, if not nearly all, of our intubated patients in the ED have altered mental status, a potential to clinically worsen, or a requirement for medications that would alter their respiratory status (e.g. propofol, opioids, paralytics).  It is imperative to place these patients on appropriate ventilator modes to avoid apnea when their respiratory status changes.

• Spontaneous modes (see partial list below) REQUIRE patients to initiate breaths on their own.  No ventilation occurs in a true spontaneous mode without patient effort.  
• Patients who have alterations in respiratory drive, neuromuscular function, or are receiving paralytics should NOT be placed on:
  • Pressure Support (PSV),
  • Volume Support (VSV),
  • CPAP/BiPAP/APAP,
  • Pressure-Assisted Ventilation (PAV) / Proportional Pressure Support (PPS),
  • or other spontaneous modes
• Our hypothermia order set includes a prn paralytic (cisatracurium infusion, vecuronium bolus) to combat shivering.  Discontinue these medications for patients on spontaneous modes.
• Our Servo-I ventilators automatically backup to a control mode (VS-->VC, PS-->PC) after a period of apnea (default is anywhere from 15-45 seconds, but it depends on how the RT has set the ventilator) as a safety mechanism, but this could still cause dangerous hypoxia or hypercapnea in severely ill patients.
• If the mechanics of pressure support are desired in patients at risk of apnea, there are other methods to achieve this (PC, descending flow VC, SIMV VC+PS with a low rate, and others).
• Always consult your RT when changing ventilator settings, and be sure to take vent alarms seriously.

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Question

Gallstones account for 35-40% of cases of pancreatitis and the risk increases with diminishing stone size. Bile reflux into the pancreatic duct can form stones there, beyond where they can be visualized by ultrasound. Biliary colic may precede the pancreatitis, but not necessarily. The pain typically reaches maximum intensity quickly but can remain for days.

Alanine aminotransferase (ALT) > 3x normal is highly suggestive of biliary pancreatitis.

Abdominal ultrasound is not sensitive to common bile duct stones but may find dilation.

In the absence of cholangitis, endoscopic ultrasound or MRCP are sensitive tests and permit intervention. Patients who recover are much more likely to develop cholangitis, therefore cholecystectomy is indicated in patients after they recover from gallstone pancreatitis.

Bottom Line: a patient presenting with days of abdominal pain but an absence of gallstones or cholangitis may still suffer from gallstone pancreatitis which requires further intervention, including cholecystectomy.

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Mechanical Ventilation in the Obese Critically Ill

• Rates of obesity have steadily risen over the past three decades.  In fact, the prevalance of obesity in the ICU is now estimated at 20%.
• Obesity affects numerous organ systems and impacts the resuscitation and management of these patients.
• The pulmonary systems undergoes several changes that include decreased lung compliance, decreased chest wall compliance, increased O2 consumption, increased CO2 production, and increased work of breathing.
• When initiating mechanical ventilation in the obese patient without ARDS, consider the following initial settings:
  • Tidal volume 6 ml/kg ideal body weight
  • PEEP of 10-12 cm H2O
  • RR to achieve a PaCO2 35-45 mmHg
  • FiO2 to maintain SpO2 92-95%
  • Driving pressure < 15 cm H2O

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Background:  Previous systematic reviews^1,2,3 have indicated that the absence of cardiac activity on point-of-care ultrasound (POCUS) during cardiac arrest confers a low likelihood of return of spontaneous circulation (ROSC), but included heterogenous populations (both traumatic and atraumatic cardiac arrest, shockable and nonshockable rhythms).

The SHoC investigators⁴ are the first to publish their review of nontraumatic cardiac arrests with nonshockable rhythms, evaluating POCUS as predictor of ROSC, survival to admission (SHA), and survival to discharge (SHD) in cardiac arrests occurring out-of-hospital or in the ED.

• 10 studies, 1485 patients
• Compared to absence of cardiac activity, presence of cardiac activity = higher odds, increased incidence of ROSC, SHA, and SHD
• Pooled sensitivity for ROSC, SHA, SHD relatively low (60%, 75%, 69%, respectively)
  • On subgroup analysis, sensitivity higher in PEA group (77%) than asystole group (25%)

Bottom Line:  In nontraumatic cardiac arrest with non-shockable rhythms, the absence of cardiac activity on POCUS may not, on its own, be as strong an indicator of poor outcome as previously thought.

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