UMEM Educational Pearls - Critical Care

Mediastinitis is an infection of the mediastinum; a rapidly fatal surgical emergency if not recognized and treated early.

Causes include esophageal perforation, oropharyngeal infections (e.g., Ludwig’s angina), prevertebral or carotid space infections, and iatrogenically (endoscopy, hypopharyngeal perforations during intubation, etc.).

Plain films (neck / chest) may serve as a screening tool, but CT best defines the source and extent of disease; the CT below demonstrates gas within the soft-tissues and the mediastinum (red arrrows).

Infections may be polymicrobial and broad-spectrum antibiotics with anaerobic coverage (e.g., pipercillin-tazobacam) should be started initially.

Immediate treatment should also include:

• Intubation (with co-existing soft tissue swelling)
• Fluid resuscitation and hemodynamic support
• Surgical consult for necrotic tissue debridement

Bonus Pearl

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Cuff Pressures and the Prevention of VAP

• As highlighted in a recent pearl, ventilator-associated pneumonia (VAP) is the second most common nosocomial infection in the US and is associated with increases in ICU length of stay and mortality.
• With increasing ED lengths of stay for many critically ill patients receiving mechanical ventilation, measures to prevent VAP should be initiated in the ED.
• In addition to elevating the head of the bed to 30-45 degrees, another low cost intervention is the measurement of endotracheal tube cuff pressures.
• Cuff pressures below 20 cm H₂O increase the risk of VAP.
• Measure cuff pressure within 4 hours of inflation and maintain between 20-30 cm H₂O.

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Sepsis is one of the top 10 causes of death in the U.S. and its incidence is on the rise.

The financial burden of sepsis is also growing; it is estimated that between 2000 and 2005 the overall cost of ICU hospitalization rose from $56.6 billion to $81.7 billion per year with severe sepsis accounting for $16.7 billion.

Although we may not be able to immediately modify the incidence of community-acquired sepsis, hospital-acquired sepsis can be reduced; for example, many cases of nosocomial sepsis are associated with catheter blood stream infections secondary to central-lines.

There are several simple strategies to prevent catheter-related blood-stream infections:

• Ensure proper hand hygiene prior to central-line insertion
• Use maximum sterile procedures during insertion of central venous catheters
• Use skin antiseptics and proper dressings at catheter insertion sites
• Rapid discontinuation of central venous catheters once no longer needed

Remember: We play a large role in reducing nosocomial sepsis; be vigilant about your sterile techniques during central catheter insertions and question the need for every single line.

Bonus pearl (only for iPhone): MDRNTools is a FREE app (that’s right, FREE!) with lots of ED and ICU applications such as an IV med calculator, an RSI handbook, a Stroke Scale calculator, and more.

Download http://itunes.apple.com/us/app/mdrntools/id505794224?mt=8&ls=1

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Transferring Multidrug-Resistant Organisms

• Hospital-associated infections are a major cause of morbidity and mortality, especially among the critically ill.
• Worldwide, the emergence of multidrug-resistant (MDR) bacteria has caused significant problems.
• A recent study from the University of Maryland examined the impact of environmental contamination on the rate of transfer of MDR bacteria to healthcare workers clothing.
• Two important findings from this study of ICU patients were:
  • Up to 8% of healthcare workers entered a patient's room with MDR bacteria on their hands
  • Almost 5% of healthcare workers had MDR bacteria (most notably Acinetobacter) on their hands upon exiting the room despite using gloves and a gown
• Take Home Point: Be sure to use hand hygiene upon entering and exiting a patient's room who is colonized with MDR bacteria!

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The supine position during rapid sequence intubation may result in posterior lung atelectasis thereby reducing lung volumes, oxygenation reserve, and ultimately apnea time.

Several studies have shown that elevating the head of the bed by at least 20 degrees or placing a patient in reverse Trendelenberg position (for patients with contra-indications to elevating the head of the bed) during RSI may significantly increase apnea time.

Elevating the head of the bed may be especially helpful for patients with BMIs >35

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High-Frequency Oscillatory Ventilation for ARDS?

• High-frequency oscillatory ventilation (HFOV) is increasingly utilized for adult patients with ARDS who remain hypoxemic despite optimal settings of conventional mechanical ventilation (CMV).
• HFOV maintains a constant mean airway pressure and delivers very small tidal volumes (1-3 ml/kg) at very high respiratory rates (frequency range up to 10 Hz).
• Potential advantages to HFOV over CMV include greater alveolar recruitment, prevention of atelectrauma, and limiting excess alveolar distension (i.e. volutrauma).
• Studies on HFOV in adults are not as numerous as those in neonates.  As a result, optimal timing for initiation of HFOV is unclear.
• Nevertheless, some recommend considering HFOV for patients who persistently need an F_iO₂ > 60% with at least 10 cm H₂O of PEEP on CMV.
• Due to the ventilator settings, patients receiving HFOV often require significant sedation and often neuromuscular blockade.  

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Pre-oxygenation prior to rapid sequence intubation (RSI) is performed to prevent hypoxemia during endotracheal intubation.

An appropriate period of pre-oxygenation will potentially increase the amount of apnea time during intubation, however patients with certain critical illnesses (e.g., severe pneumonia) may desaturate faster than expected.

Apnea time can be increased by maintaining high-flow oxygen by nasal cannula (e.g., 15L), during application of the bag-valve mask and during the time of attempted endotracheal tube placement; this concept is known as apneic oxygenation.

Apneic oxygenation is based on the principle that when patients are apneic, alveoli absorb oxygen into the blood stream at a rate of approximately 250 mL/minute, creating a diffusion gradient from the pharynx (containing a high-density of oxygen from the nasal cannula) to a lower concentration of oxygen in the alveoli.

Although a patient’s oxygenation can be maintained longer using apneic oxygenation, its application does not remove the continuous buildup of CO2 in the alveoli during apena. Therefore, respiratory acidosis can result after a prolonged period of apneic oxygenation. 

The complete article describing the physiology and practical applications can be found here....it's free! http://www.annemergmed.com/article/S0196-0644(11)01667-2/fulltext

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Preventing VAP in the Intubated ED Patient

• Ventilator-associated pneumonia (VAP) occurs in 9-27% of patients receiving mechanical ventilation (MV).
• VAP increases the duration of MV and increases the ICU length of stay.
• VAP is primarily caused by aspiration of oropharyngeal secretions either during intubation or while receiving MV.
• While there are many interventions that may potentially reduce the incidence of VAP (aspiration of subglottic secretions, selective digestive decontamination, monitoring endotracheal cuff pressure), a simple, no cost intervention is patient positioning.
• Placing intubated patients in the semirecumbent position is associated with a lower risk of VAP.

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Ventricular assist devices (VAD) pump blood from the left, right or both ventricles for patients in severe ventricular failure.

VADs may be placed temporarily (as a bridge to transplant) or permanently in patients who are not transplant candidates (also known as Destination Therapy)

Certain types of VADs continuously pump blood in a non-pulsatile fashion. In these cases, a patient may be perfusing normally without a palpable pulse.

Familiarity with potential VAD complications is important as a patient with a VAD may be presenting to an ED near you. Complications include:

• Bleeding complications from anticoagulation; all VADs require some form of anticoagulation
• Infection; a portion of the VAD exits externally and this site can be a portal of entry for skin flora
• Embolic phenomenon from clots generated within the VAD
• Infection of the VAD itself, called VAD-itis; this can also lead to sepsis

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Ice-Cold Crystalloid for Therapeutic Hypothermia

• Therapeutic hypothermia (TH) is a critical component in the care of patients with ROSC from out-of-hospital cardiac arrest.
• Despite recent guidelines, initiation of TH in the ED for appropriate patients remains less than optimal.
• Reported barriers to the induction of TH in the ED include lack of familiarity, lack of collaboration with the ICU, access to special equipment, and the logistics of cooling.
• A recent analysis of studies on the use of ice-cold crystalloids (ICC) found that an infusion of 4⁰ C fluid is a safe, effective, inexpensive, and readily available method for inducing TH.
• Importantly, no study reported any significant hemodynamic complication (i.e. CHF) from the use of ICC.
• Lastly, once the target temperature has been reached, ICC alone cannot maintain TH.  Additional methods, such as surface cooling blankets or ice packs, should be used.

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A fluid bolus is often the first-line therapy for patients with pericardial tamponade. A fluid bolus, however,  may not always improve hemodynamics.

The cardiac index of forty-nine patients with cardiac tamponade was assessed before and after a 500 cc normal saline bolus:

• 47% increased their cardiac index
• 22% did not demonstrate a change
• 31% decreased their cardiac index

Bottom-line: A fluid bolus may a reasonable first choice in a hypotensive patient with tamponade, but remember that fluid boluses may not always work. Attempts at fluid resuscitation should never delay definitive treatment with pericardiocentesis.

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ECMO for ARDS and Refractory Hypoxemia

• Extracorporeal membrane oxygenation (ECMO), or extracorporeal life support (ECLS), is increasingly being used for a variety of cardiac and pulmonary conditions.
• Venovenous ECMO (VVE) should be considered in the treatment of patients with profound gas-exchange abnormalities that are refractory to accepted standards in ventilator management.
• Although indications vary slightly by institution, general indications for VVE include:
  • Severe hypoxemia: P_aO₂/F_iO₂ < 80 despite high levels of PEEP for at least 6 hours
  • Uncompensated hypercapnia with pH < 7.15
  • Excessively high plateau pressures (> 45 cm H₂0)

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AGE occurs when gas bubbles enter arteries or veins; AGE may cause clinical symptoms even with very small volumes of air. 

Air enters the circulatory system via:

· Barotrauma – Alveolar injury allows air to enter systemic bloodstream; occurs in divers following rapid ascent after breath holding, during mechanical ventilation, chest tube placement, or bronchoscopy

· Decompression sickness – Dissolved gas precipitates out of bloodstream as bubbles; typically following scuba diving without appropriate time to ascend or prolonged flying in unpressurized aircrafts

· Direct injection of air into arterial or venous circulation – Examples include accidental IV injection of air, needle biopsy of lung, or aspiration of air during central line placement

Serious clinical manifestations include:

· Neurologic changes - loss of consciousness, confusion, or focal neurological deficits

· Hemodynamic changes – hypotension, arrhythmias, cardiac ischemia, or cardiac arrest.

· Respiratory changes – obstruction of pulmonary circulation, pulmonary edema, or hypoxemia

Treatment:

· Strict attention to ABC’s using high-flow O2.

· Keep head of bed elevated to minimize/reduce cerebral edema.

· Hyperbaric Oxygen (HBO) therapy is recommended for neurological manifestations or cardiovascular instability. Good outcomes associated with shorter intervals from air embolism to HBO. Typically only 1 to 2 treatments are needed; occasionally additional treatments are necessary.

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SAH and Pulmonary Edema - Think Twice About Diuresis!

• Delayed cerebral ischemia (DCI) is the most common cause of secondary neurologic injury in patients with aneurysmal subarachnoid hemorrhage (SAH).
• Intravascular volume depletion is one of several factors thought to cause, or worsen, DCI.
• Pulmonary edema frequently occurs in patients with SAH.
• A recent study in patients with SAH and pulmonary edema demonstrated that many were not volume overloaded.  In fact, many were intravascularly volume depleted.
• Think twice about aggressive diuresis in patients with SAH and pulmonary edema, as this may exacerbate volume depletion and may worsen DCI.

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Fungal endopthalmitis is an intraocular infection of the aqueous and/or vitreous humor secondary to fungal pathogens; Candida and Aspergillus species are the most common pathogens.

Risk factors: intravenous drug abuse (#1 risk factor), critical illness, systemic fungal infection, immunosuppression (from cancer or medications), diabetes, and alcoholism.

Have a high-index of suspicion for endopthalmitis when patients with systemic fungal disease have visual symptoms; endopthalmitis is present in up to 33% of patients with systemic fungal disease.

Symptoms include:

• Visual disturbances / visual loss
• Eye pain
• Photophobia
• Red eye
• “Floaters”
• Asymptomatic

Inspection of both the anterior and posterior chamber is essential to during evaluation; several small yellow-white circular or “fluffy” lesions with surrounding hemorrhage are demonstrated.

Definitive diagnosis made by vitreous biopsy, culture, or PCR; presumptive treatment is acceptable if systemic fungal disease has been demonstrated.

Treatment with Amphotericin B or Voriconazole may be used for broad-spectrum fungal coverage until specific culture and sensitivities return.

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Hypertonic Saline for Intracranial Hypertension

• Mannitol is commonly used to treat acute increases in intracranial pressure in patients with TBI, ICH, tumor, and CVA.
• While there is currently no conclusive evidence of superiority, a growing body of literature suggests hypertonic saline (HTS) may be more favorable than mannitol for acute increases in ICP.
• HTS is believed to work by:
  • osmotic effect
  • increasing cardiac output and MAP, thereby increasing cerebral oxygen delivery
  • improving microcirculatory flow
  • anti-inflammatory effects
• When administering HTS, concentrations ranging from 1.5% - 23.4% can be used, titrating to a serum Na concentration of 145-155 and a serum osm > 350 mOsm/L.

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Carotid or vertebral artery injury following blunt trauma is a rare (%1 of blunt trauma), but a potentially serious injury potentially causing stroke and long-term disability.

Injury leads to an intimal tear becoming a nidus for platelet aggregation; thrombosis and/or distal emboli may subsequently develop.

Mechanisms of injury include:

• Blunt trauma to the neck
• Hyper-extension of neck with contralateral rotation of the head
• Intra-oral trauma
• Arterial laceration secondary to adjacent sphenoid or petrous bone fracture.

Symptoms of carotid injury may include contralateral sensorimotor deficits; Symptoms of vertebral injury may include ipsilateral facial pain and numbness, headache, ataxia, or dizziness.

Angiography is the diagnostic “gold standard” but these days a 16-slice CT angiography (or greater) is a reliable screening tool.

Anticoagulation with heparin is the treatment of choice for severe injury, if there are no contraindications (e.g., intracranial bleeding). Anti-platelet drugs may be acceptable in certain cases.

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VBG to Assess Respiratory Function?

• Arterial blood gas (ABG) analysis is often used in to evaluate pulmonary function in critically ill ED patients.
• In recent years, venous blood gas (VBG) analysis has replaced ABG analysis for assessing acid-base status (pH, HCO₃^-) in conditions such as DKA.
• Some key points about the VBG for assessing pulmonary function:
  • VBG does not replace an ABG in determining the exact P_aO₂
  • The agreement between the VBG and ABG PCO₂ is often poor and unpredictable
  • There is emerging literature on the use of VBG PCO₂ as a screen for hypercarbia but more data is needed
• Bottom line: With the possible exception of screening for hypercarbia, VBG has limited utility in the assessment of pulmonary function.

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Amiodarone-induced lung toxicity (ALT) is a serious and sometimes fatal complication of amiodarone use.

Symptoms range from mild (e.g., dyspnea with exertion) to acute respiratory distress syndrome and risk of death.

ALT is secondary to either release of toxic oxygen radials that are directly toxic to the lung or the reaction is secondary to an indirect immunologic reaction.

Risk factors for ALT: use > 2 months, dose > 400mg/day, advanced age, or pre-existing lung injury

ALT is typically a diagnosis of exclusion so suspect ALT through a detailed history; physical exam and radiology are non-specific. Lung biopsy is the only confirmatory test.

Treat ALT by discontinuing the drug, steroids, and supportive care. In rare cases where amiodarone cannot be safely discontinued (i.e., life-threatening arrhythmia), dosage should be reduced and steroids added immediately.

Generally, ALT is reversible with a good prognosis.

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The Crashing Patient with PAH

• In recent weeks, we've highlighted some pearls regarding the management of patients with pulmonary arterial hypertension (PAH).
• In the crashing patient with PAH, think about the following:
  • Catheter occlusion or malfunction (for those receiving IV prostacyclin analogues)
  • PE (for those inadequately anticoagulated)
  • Pneumonia
  • RV ischemia
  • GI bleeding
  • Ischemic bowel
• In the patient receiving IV epoprostenol (Flolan) who presents with a catheter occlusion or malfunction, time is of the essence. Restart the medication through a peripheral IV as soon as possible.

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