UMEM Educational Pearls - Critical Care

The Macklin Effect

Pneumomediastinum (click here for image) may be caused by many things:

  1. Esophageal perforation (e.g., complication from EGD)
  2. Tracheal / Bronchial injury (e.g., trauma, complication of bronchoscopy, etc.)
  3. Abdominal viscus perforation with translocation of air across the diaphragmatic hiatus
  4. Air may reach mediastinum along the fascial planes of the neck.
  5. Alveolar rupture, also known as the "Macklin Effect"

The "Macklin Effect" is typically a self-limiting condition leading to spontaneous pneumomediastinum and massive subcutaneous emphysema after the following:

  1. Alveolar rupture from increased alveolar pressure (e.g., asthma, blunt trauma, positive pressure ventilation, etc.)
  2. Air released from alveoli dissects along broncho-vascular sheaths and enters mediastinum
  3. Air may subsequently track elsewhere (e.g., cervical subcutaneous tissues, face, epidural space, peritoneum, etc.)

Pneumomediastinum secondary to the Macklin effect frequently leads to an extensive workup to search for other causes of mediastinal air. Although, no consensus exists regarding the appropriate workup, the patient's history should guide the workup to avoid unnecessary imaging, needless dietary restriction, unjustified antibiotic administration, and prolonged hospitalization.

Treatment of spontaneous pneumomediastinum includes:

  • Supplemental oxygen and observation for airway obstruction secondary to air expansion within the neck
  • Avoiding positive airway pressure, if possible
  • Avoiding routine chest tubes (unless significant pneumothorax is present)
  • Administering prophylactic antibiotics are typically unnecessary
  • Ordering imaging as needed

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Monitoring Hyperosmolar Therapy

  • Hyperosmolar therapy (mannitol or hypertonic saline) is commonly used in the treatment of neurocritical care paitents with elevated ICP.
  • When administering mannitol, guidelines recommend monitoring serum sodium and serum osmolarity.  Though targets remain controversial, most strive for a serum sodium of 150-160 mEq/L and a serum osmolarity between 300 - 320 mOsm/L.
  • Unfortunately, serum osmolarity is a poor method to monitor mannitol therapy.
  • Instead of serum osmolarity, follow the osmolar gap.  It is more representative of serum mannitol levels and clearance.  If the osmolar gap falls to normal, the patient has cleared mannitol and may be redosed if clinically indicated. 

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Fluid boluses are often administered to patients in shock as a first-line intervention to increase cardiac output. Previous literature states, however, that only 50% of patients in shock will respond to a fluid bolus. 

Several validated techniques exist to distinguish which patients will respond to a fluid bolus and which will not; one method is the passive leg raise (PLR) maneuver  (more on PLR here). A drawback to PLR is that it requires direct measurement of cardiac output, either by invasive hemodynamic monitoring or using advanced bedside ultrasound techniques.

Another technique to quantify changes in cardiac output is through measurement of end-tidal CO2 (ETCO2). The benefits of measuring ETCO2 is that it can be continuously measured and can be performed non-invasively on mechanically ventilated patients.

A 5% or greater increase in end-tidal CO2 (ETCO2) following a PLR maneuver has been found to be a good predictor of fluid responsiveness with reliability similar to invasive measures.


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Neuromuscular Blocking Agents in the Critically Ill

  • NMBAs are used in critically ill patients for RSI, patient-ventilator asynchrony, reducing intra-abdominal pressure, reducing intracranial pressure, and preventing shivering during therapeutic hypothermia.
  • There are a number of alterations in critical illness that affect the action of NMBAs
    • Electrolyte abnormalities
      • Hypercalcemia: decreases duration of blockade
      • Hypermagnesemia: prolongs duration of blockade
    • Acidosis: can enhance effect of nondepolarizing agents
    • Hepatic dysfunction: prolongs effects of vecuronium and rocuronium
  • In addition, there are a number of medications that may interact with NMBAs
    • Increased resistance: phenytoin and carbamazepine
    • Prolongs effect: clindamycin and vancomycin
  • Key complications of NMBAs in the critically ill include:
    • ICU-aquired weakness (controversial)
    • DVT: NMBAs are one of the strongest predictors for ICU-related DVT
    • Corneal abrasions: prevalence up to 60%

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Necrotizing fasciitis (NF) is a rapidly progressive bacterial infection of the fascia with secondary necrosis of the subcutaneous tissue. In severe cases, the underlying muscle (i.e., myositis) may be affected.

Risk factors for NF include immunosuppression (e.g., transplant patients), HIV/AIDS, diabetes, etc.

There are three categories of NF:

  • Type I (poly-microbial infections)
  • Type II (Group A streptococcus; sometimes referred to as the “flesh-eating bacteria)
  • Type III (Clostridial myonecrosis; known as gas gangrene)

In the early stage of disease, diagnosis may be difficult; the physical exam sometimes does not reflect the severity of disease. Labs may be non-specific, but CT or MRI is important to diagnose and define the extent of the disease when planning surgical debridement.

Treatment should be aggressive and started as soon as the disease is suspected; this includes:

  • Aggressive fluid and/or vasopressor therapy
  • Broad spectrum antibiotics covering for gram-positive, gram-negative, and anaerobic bacteria; clindamycin should be added initially as it suppresses certain bacterial toxin formation
  • Emergent surgical consult for debridement
  • Once the patient is stable, other treatments may include intravenous immunoglobulin and hyperbaric oxygen therapy


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Category: Critical Care

Title: Massive Transfusion Pearls

Posted: 4/16/2013 by Mike Winters, MD (Emailed: 4/17/2013)
Click here to contact Mike Winters, MD

Massive Transfusion Pearls

  • As discussed in previous pearls, massive transfusion (MT) is defined as the transfusion of at least 10 U of packed red blood cells (PRBCs) within 24 hours.
  • While the optimal ratio of PRBCs, FFP, and platelets is not known, most use a 1:1:1 ratio.
  • Though scoring systems have been published to identify patients who may benefit from MT (ABC, TASH, McLaughlin), they have not been shown to be superior to clinical judgment.
  • A few pearls when implementing massive transfusion for the patient with traumatic shock:
    • Monitor temperature and aggressively treat hypothermia.
    • Monitor fibrinogen levels and replace with cryoprecipitate if needed.
    • Monitor calcium and potassium.  MT can induce hypocalcemia and hyperkalemia.

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Category: Critical Care

Title: Keeping the Beat: Strategies in Shock Refractory VF

Keywords: Resuscitation, ventricular fibrillation, cardiac arrest, emergency, cardiology (PubMed Search)

Posted: 4/6/2013 by Ben Lawner, DO (Updated: 4/24/2024)
Click here to contact Ben Lawner, DO

Recent advances in resuscitation science have enabled emergency physicians to identify factors associated with good neurologic and survival outcomes. Cases of persistent ventricular dysrhythmia (VF or VT) present a particular challenge to the critical care provider. The evidence base for interventions in shock refractory ventricular VF mainly consists of case reports and retrospective trials, but such interventions may be worth considering in these difficult resuscitation situations:

1. Double sequential defibrillation
-For shock-refractory VF, 2 sets of pads are placed (anterior/posterior and on the anterior chest wall). Shocks are delivered as "closely as possible."1,2

2. Sympathetic blockade in prolonged VF arrest
-"Eletrical storm," or incessant v-fib, can complicate some arrests in the setting of VF. An esmolol bolus and infusion may be associated with improved survival.3  Left stellate ganglion blockade has been identified as a potential treatment for medication resistant VF.4

3. Don't forget about magnesium! 
-May terminate VF due to a prolonged QT interval 

4. Invasive strategies
-Though resource intensive, there is limited experience with intra-arrest PCI and extracorporeal membrane oxygenation. Preestablished protocols are key to selecting patients who may benefit from intra-arrest PCI and/or ECMO. 5

5. Utilization of mechanical CPR devices 
-Though mechanical CPR devices were not officially endorsed by the AHA/ECC 2010 guidelines, there's little question that mechanical compression devices address the complication of provider fatigue during ongoing resuscitation. 


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Hormonal Dysfunction in Neurologic Injury

  • In the critically ill patient with neurologic injury (SAH, TBI), the initial treatment focus is to maintain adequate cerebral perfusion pressure, control intracranial pressure, and limit secondary injury.
  • Once stabilized, however, it is important to consider endocrine dysfunction in the brain injured patient.
  • Endocrine dysfunction is common in neurologic injury and may lead to increased morbidity and mortality.  In fact, over half of SAH patients develop acute dysfunction of the HPA, resulting in low growth hormone, ACTH, and TSH. 
  • In addition to hormonal dysfunction, sodium abnormalities (i.e. hyponatremia) are present in up to 80% of critically ill SAH patients.
  • Consider hormonal replacement therapy (or hypertonic saline in cases of severe hyponatremia) for patients with evidence of endocrine dysfunction.  For some, this therapy can be life-saving.

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There are several reasons why a mechanically ventilated patient may decompensate post-intubation. Immediate action is often needed to reverse the problem, but it can be difficult to remember where to start as the vent alarm is sounding and the patient is decompensating.

Consider using the mnemonic “D.O.P.E.S. like D.O.T.T.S.” to assist you in first diagnosing the problem (D.O.P.E.S.) and then fixing the problem (D.O.T.T.S.). You can view an entire lecture on the Crashing Ventilated Patient here.

Step 1: Could this decompensation be secondary to D.O.P.E.S.?

  • Displaced ET tube / ET tube cuff not inflated or has a leak
  • Obstruction of ET tube
  • Pneumothorax
  • Equipment malfunction (disconnection of the ventilator, incorrect vent settings, etc.)
  • Stacking (breath stacking / Auto- PEEP; click here for a review)

Step 2: Fix the problem with D.O.T.T.S.

  • Disconnect – Disconnect patient from the ventilator
  • Oxygen – Oxygenate patient with a BVM and feel for resistance as you bag
  • Tube position / function – Did the ET tube migrate? Is it kinked or is there a mucus plug?
  • Tweak the vent – Are the settings correct for this patient?
  • Sonogram (ultrasound) – Sonogram to look for pneumothorax, mainstem intubation, etc. 

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Category: Critical Care

Title: Extubating in the ED

Posted: 3/19/2013 by Mike Winters, MD (Updated: 4/24/2024)
Click here to contact Mike Winters, MD

Extubating in the ED

  • With the increasing LOS for many of our intubated critically ill ED patients, it is possible that select patients may be ready for extubation while still in the ED.
  • Patients who remain intubated unnecessarily are at increased risk for pneumonia, increased hospital LOS, and increased mortality.
  • To be considered for extubation, patients should meet the following criteria:
    • The condition that resulted in intubation is improved or resolved
    • Hemodynamically stable (off pressors)
    • PaO2/FiO2 > 200 with PEEP < 5 cm H2O
  • If these criteria are met, perform a spontaenous breathing trial (SBT).
    • Discontinue sedation
    • Adjust the ventilator to minimal settings: pressure support or CPAP (5 cm H2O) or use a T-piece.
    • Perform the trial for at least 30 minutes.
    • If the patient develops a RR > 35 bpm, SpO2 < 90%, HR > 140 bpm, SBP > 180 mm Hg or < 90 mm Hg, or increased anxiety, the SBT ends and the patient should remain intubated.
  • Before removing the endotracheal tube, be sure to assess mentation, the quantity of secretions, and strength of cough.

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Mechanically ventilated patients can develop a condition in which air becomes trapped within the alveoli at end-expiration; this is called auto-PEEP.

Auto-peep has several adverse effects:

  • Barotrauma from positive pressure trapped within the alveoli 
  • Increased work of breathing
  • Worsening pulmonary gas exchange
  • Hemodynamic compromise secondary to increased intra-thoraic pressure

Auto-PEEP classically occurs in intubated patients with asthma or emphysema, but it may also occur in the absence of such disease. The risk of auto-PEEP is increased in patients with:

  • Short expiration times (i.e., inadequate time for the evacuation of alveolar air at end-expiration)
  • Bronchoconstriction
  • Plugging of the bronchi (e.g., mucus or foreign body) creating a one-way valve and air-trapping

Auto-PEEP may be treated by:

  • Reducing tidal volume
  • Reducing the respiratory rate
  • Decreasing inspiratory time
  • Increasing PEEP

Patients may need to be heavily sedated to accomplish the above ventilator maneuvers.

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Ventilator-associated Pneumonia

  • Ventilator-associated pneumonia (VAP) is a well known complication of mechanical ventilation (MV) and is associated with increased duration of MV, hospital length of stay, and cost.
  • VAP is commonly associated with multi-drug resistant organisms, including Pseudomonas, Acinetobacter, Klebsiella, and Enterobacteriaceae.
  • Given the significant impact upon morbidity, a number of organizations have recommended "bundles" of care for the prevention of VAP.
  • Important measures for the prevention of VAP include:
    • Strict hand hygiene
    • Head of bed elevation to 30-45 degrees
    • Closed endotracheal suctioning
    • Maintaining endotracheal tube cuff pressure > 20 cm H2O
    • Oral chlorhexidine rinses
    • Orogastric tube placement

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Excessive and improper administration of local anesthetic (a.k.a. local anesthetic systemic toxicity or L.A.S.T.) can lead to cardiac toxicity with symptoms ranging from benign arrhythmias to overt cardiac arrest. 

Administration of a 20% intra-lipid emulsion has been experimentally known to reverse L.A.S.T in animal models, but in 2006 the first documented human case of ILE was successfully used during cardiac arrest secondary to L.A.S.T. with hemodynamic recovery and good neurologic outcome. Many case reports have emerged since then, including the use of ILE in toxicity with other lipophilic drugs (e.g., calcium channel blockers, tricyclic antidepressants, etc.)

Several mechanisms have been proposed explaining how ILE works. They include:

  • binding circulating toxins in the blood stream, minimizing its exposure to tissues
  • improving mitochondrial metabolism (which is inhibited in L.A.S.T.) 
  • reducing re-perfusion injury and cellular apoptosis post cardiac-arrest

Dosing of ILE:

  • 1.5 mL/kg intravenous bolus of 20% ILE over 2-3 minutes (may be repeated, if necessary) then,
  • starting a continuous infusion of 0.25-0.5 mL/kg/min and continuing infusion for 10 minutes after vital signs return.

Check out this video by our own Dr. Bryan Hayes(@PharmERToxGuy) and for more information.

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Managing Traumatic Hemorrhagic Shock

  • When managing the critically ill patient with traumatic hemorrhagic shock, the primary objectives are to stop bleeding, maintain tissue perfusion and oxygen delivery, and limit organ dysfunction.
  • Pearls to consider when resuscitating these patients include:
    • In the patient without brain injury, target an SBP of 80 - 100 mm Hg until major bleeding has been controlled.
    • Limit aggressive fluid resuscitation
    • Avoid delays in blood and blood component transfusion.  Transfuse early. Though the optimal ratio remains controversial, most transfuse PRBCs and FFP in a 1:1 ratio.
    • Consider point-of-care testing, such as thromboelastography (TEG), to assess the degree of coagulopathy and guide transfusion strategies.
    • Consider the use of tranexamic acid

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Propofol is generally a well-tolerated sedative / amnestic but occasionally it can lead to the propofol infusion syndrome (PRIS); a metabolic disorder causing end-organ dysfunction.

Suspect PRIS in patients with increasing lactate levels, worsening metabolic acidosis, worsening renal function, increased triglyceride levels, or creatinine kinase levels. End-organ effects include:

  • Myocardial dysfunction / Arrhythmias
  • Rhabdomyolysis
  • Acute renal failure

The true incidence of PRIS is unknown, however, certain risk factors have been identified:

  • Doses >4-5mg/kg/hour
  • <18 years of age
  • Critically-ill patients; especially receiving vasopressors or steroids
  • History of mitochondrial disorders
  • Infusions >48 hours

Prevent PRIS by using adequate analgesia (with morphine or fentanyl) post-intubation, which may reduce the overall dosage of propofol ultimately reducing the risk.

If PRIS develops, stop propofol and provide supportive care; IV fluids, ensuring good urine output, adequate oxygenation, dialysis (if indicated), vasopressor and inotropic support.

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Needle Decompression - Are we Teaching the Right Location?

  • Tension pneumothorax frequently results in circulatory collapse and may lead to cardiopulmonary arrest.
  • In the event that tube thoracostomy cannot be immediately performed, traditional teaching is to perform needle decompression in the second intercostal space, mid-clavicular line using a 5-cm angiocath needle.
  • Recent literature, however, has challenged the traditional location for needle decompression.  In fact, researchers found:
    • Needles placed in the second intercostal space often failed to enter the chest cavity and relieve tension physiology.
    • Needles placed in the fifth intercostal space in the anterior axillary line were more likely to enter the chest cavity with a lower failure rate.
  • Take Home Point: It may be time to reconsider the optimal position for needle decompression of tension pneumothorax.

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Category: Critical Care

Title: Hemodynamic Pearls from the Surviving Sepsis Guidelines

Posted: 1/29/2013 by Haney Mallemat, MD (Emailed: 1/30/2013) (Updated: 1/30/2013)
Click here to contact Haney Mallemat, MD

The updated Surviving Sepsis Guidelines have been released (click here) and here are some recommendations as they pertain to hemodynamic management (grades of recommendations in parenthesis).

Fluid therapy

  • An initial fluid bolus of at least 30 mL/kg is recommended; crystalloids should be the initial fluids (1B).
  • Consider albumin when “substantial” amounts of crystalloid have been given (2C).
  • Use of hydroxyethyl starch is not recommended (1B)

Vasopressors (targeting MAP of at least 65 mmHg)

  • Norepinephrine (NE) is the vasopressor of choice (1B)
  • Epinephrine (EPI) if an additional agent is required; can be added to or substituted for NE (2B)
  • Vasopressin (0.03 units/minute) can be added to NE; it should not be titrated or used as a single agent (ungraded).
  • In selected patients (e.g., bradycardia or low-risk of tachyarrhythmia), dopamine may be considered (2C). Low-dose dopamine (for renal protection) should not be used (1A).
  • Phenylephrine (PE) is not recommended, except if (1C):
    • Serious NE associated arrhythmias
    • Cardiac output can be measured and is increased with low MAP (PE can reduce cardiac output)
    • Other therapies cannot achieve the target MAP


  • Use if fluids and vasopressors cannot restore adequate perfusion
  • Total daily dose of 200 mg (2C) administered by continuous infusion (2D)
  • ACTH stimulation test is not recommended (2B)
  • Tapering hydrocortisone when vasopressors have been discontinued (2D)

Inotropic Therapy

  • Administer dobutamine if it is believed that cardiac filling pressures are elevated, cardiac output is low, or persistent signs of hypoperfusion despite other therapies (1C)

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Postintubation Hypotension

  • It is clear that preintubation hypotension is associated with increased mortality in critically ill patients who require mechanical ventilation.
  • Unfortunatley, the literature is less clear on the frequency and impact of hypotension that develops after intubation.
  • Two recent publications in the Journal of Intensive Care provide valuable information on postintubation hypotension.  Some highlights of the studies include:
    • Retrospective cohorts of over 300 patients who developed postintubation hypotension, defined as a SBP < 90 mm Hg within 60 min of intubation.
    • Postintubation hypotension occurred in almost 25% of patients.
    • Median time to hypotension was 11 minutes.
    • Patients with postintubation hypotension had a higher inhospital mortality (33% vs. 23%).
    • A preintubation Shock Index > 0.8 was the strongest predictor of cardiovascular collapse after intubation.
  • Take Home Point: Postintubation hypotension occurs frequently and may be associated with worse outcomes.

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Intra-aortic balloon pumps (IABP) are devices that provide hemodynamic support during cardiogenic shock; the balloon inflates during diastole (improving coronary artery perfusion) and deflates during systole (reducing afterload and improving systemic perfusion). Click here to see a 41 second video illustrating how it works. 

Several guidelines recommend placement of an IABP for patients in cardiogenic shock secondary to acute myocardial infarction (AMI), if early revascularization (e.g., CABG) is planned (Class I recommendation). Data behind this recommendation, however, is limited.

The IABP-SHOCK II trial was a randomized, multi-center, open-label study that enrolled 600 patients (598 in the analysis) with cardiogenic shock secondary to AMI (STEMI or NSTEMI). Patients were randomized to the control group (receiving standard therapy; N=298) or the experimental group (receiving IABP; N=300).

No significant difference was found between groups with respect to 30-day mortality (primary end-point), secondary end-points (e.g., time to hemodynamic stabilization, renal function, lactate levels, etc.), or complications (e.g., major bleeding, peripheral ischemic complications, etc.).

Bottom line: Perhaps it is time to reassess the approach to cardiogenic shock secondary to AMI when early revascularization is planned. At this time consultation with local expertise is recommended.

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The Crashing Cardiac Transplant Patient

  • Approximately 2000 patients receive a cardiac transplant each year in the United States.
  • With improvements in surgical techniques, immunosuppression, and management of complications, graft half-life is now approximately 13 years; thereby increasing the likelihood that a cardiac transplant patient will show up in your ED. 
  • In the crashing cardiac transplant patient, think of the following causes for acute decompensation:
    • Acute rejection
    • Primary graft failure
    • RV failure
    • Sepsis
  • For patients with primary graft failure initiate inotropic support with dobutamine, epinephrine, milrinone, or isoproteronol.  Those failing standard inotropes will likely require mechanical circulatory support (VAD) or ECMO.
  • Patients with acute RV failure will often require the combination of a pulmonary vasodilator (inhaled NO, prostaglandins) and inotropic agent. In addition, it is critical to avoid hypercapnia and hypoxia.  

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