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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Up until recently, a tight-fitting mask was one of the only ways to deliver non-invasive positive-pressure ventilation.

High-flow nasal cannulas (HFNC) have been adapted from use in neonates to adults to deliver continuous positive airway pressure (CPAP).

HFNC provides continuous, high-flow (up to 60 liters), and humidified-oxygen via nasal cannula providing positive pressure to the pharynx and hypopharynx. Patients tolerate it well and it is less claustrophobic than tight-fitting masks.

HFNC does not generate the same amount of pressure as CPAP so it may be best utilized as an intermediate step between low-flow oxygen (i.e., traditional nasal cannula) and non-invasive positive pressure ventilation with tight-fitting masks.

Check with your respiratory department if these devices are locally available.

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Hypotension in the PAH Patient

• Hypotension in the critically ill patient with pulmonary arterial hypertension (PAH) must be rapidly treated to avoid cardiovascular collapse.
• Hypotension in the PAH patient is not always due to hypovolemia.  In fact, excessive volume loading may further decrease LV stroke volume.  Consider starting with a fluid bolus of 250 ml of an isotonic crystalloid solution and monitoring response.
• Patients with severe PAH may present to the ED with a continuous flow pump of a pulmonary vasodilator (epoprostenol, treprostinil).  These medications can also cause hypotension at excessive doses.  Consider decreasing the rate of the infusion by 25% to see if overdosing is the cause.

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Determining the exact etiology of hypotension / shock can sometimes be difficult in the Emergency Department.

The Rapid Ultrasound for Shock / Hypotension (RUSH) exam is a sequential, 5 step-protocol (typically requiring less than 2 minutes) that can be used to determine the cause(s) of hypotension.

The mnemonic for the exam is “HI MAP”, and is easy to remember because a "HI MAP" is our goal with hypotensive patients.

H - Heart (parasternal and four-chamber views)
I  - Inferior Vena Cava (for volume responsiveness)
M - Morrison’s pouch (i.e., FAST exam) and views of thorax (looking for free fluid)
A - Aortic Aneurysm (ruptured abdominal aneurysm)
P - Pneumothorax (i.e., Tension PTX)

Refer to the link for a more detailed discussion and podcast from the creators of this exam: emcrit.org/rush-exam

Hypertensive Emergency Pearls

• Recent literature indicates that many patients with a true hypertensive emergency are mismanaged.
• Patients with a hypertensive emergency should have an arterial line placed and receive a continuous infusion of a short-acting, titratable medication to reduce blood pressure.  Avoid oral, sublingual, and intermittent IV bolus administration of antihypertensives. 
• Recall that most patients with a hypertensive emergency are volume depleted.  Providing IV fluids can help to prevent marked drops blood pressure when you start an IV antihypertensive medication.
• Avoid diuretics (due to volume depletion) and hydralazine.  Hydralazine can cause precipitous drops in blood pressure and is felt by many to have no role in the treatment of hypertensive emergencies.

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Positive-pressure ventilation (e.g., mechanical ventilation) increases intrathoracic pressure potentially reducing venous return, right-ventricular filling, and cardiac output.

Pericardial tamponade similarly causes hemodynamic compromise through increased pericardial pressure which reduces right-ventricular filling and cardiac output.

When mechanically ventilating a patient with known or suspected pericardial tamponade the mechanisms above may be additive, causing cardiovascular collapse and possibly PEA arrest.

For the patient with known or suspected pericardial tamponade consider draining the pericardial effusion prior to intubation or delaying intubation until absolutely necessary.

If intubation is unavoidable, consider maintaining the intrathoracic pressure as low as possible (by keeping the PEEP and tidal volumes to a minimum) to ensure adequate cardiac filling and cardiac output.

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Mechanical Ventilation in Patients with Pulmonary HTN 

• In the critically ill patient with pulmonary HTN and respiratory failure, improper mechanical ventilator settings can be disastrous.
• Large lung volumes and high levels of PEEP can result in acute cardiovascular collapse.
• When setting the ventilator is these patients, select low tidal volumes and relatively low levels of PEEP (3-5 cm H₂O).
• In addition, small studies suggest avoiding permissive hypercapnia, as this may increase pulmonary vascular resistance and mean pulmonary arterial pressure.

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• On October 25, 2011, Eli Lilly announced a voluntary-recall of activated drotrecogin alfa (Xigris) following a recent trial (PROWESS-SHOCK), which demonstrated no survival benefit when using the drug when compared to placebo.

• Activated drotrecogin alfa is a recombinant form of human activated protein C previously recommended for adults with severe sepsis and a high-risk of death (APACHE II > 25 or multi-organ failure); it is included in the 2008 International Sepsis Guidelines (Grade 2b recommendation).

• The PROWESS-SHOCK trial reported an all-cause mortality rate of 26.4% in the drotrecogin alfa group compared with 24.2% in the placebo group; this difference was not statistically significant.

• Interestingly, the study also found that severe bleeding (the drug's main side-effect) was found to be 1.2% in the activated drotrecogin alfa group compared to 1.0% for the placebo group (also non-significant) suggesting it does not increase the risk of bleeding as it had previously been reported.

• Hospitals should revise their sepsis guidelines based on this recent news.

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