UMEM Educational Pearls - By Mike Winters

Title: Mechanical Ventilation in Pulmonary HTN

Category: Critical Care

Posted: 11/1/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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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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Title: Hyponatremia and SAH

Category: Critical Care

Posted: 10/18/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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SAH and Electrolyte Disorders

Hyponatremia can be seen in up to 40% of patients with a SAH.
Most often, hyponatremia in patients with an SAH is due to SIADH or the cerebral salt wasting syndrome.
To date, hyponatremia has not been associated with poor outcome.
Treatment should focus on the underlying cause and often includes volume replacement with isotonic crystalloids (0.9% NaCl).

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Title: Fever and ICH

Category: Critical Care

Posted: 10/4/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Fever and ICH

Fever is a common event in patients with intracerebral hemorrhage (ICH) and is associated with an increased length of ICU stay, cognitive impairment, and poor outcome.
While much of the management (and controversies) of the patient with ICH focuses on blood pressure control and reversal of oral anticoagulants or antiplatelet agents, don't forget about temperature control.
Aggressively treat temperatures ≥ 38.3^oC in patients with an ICH.
Importantly, there is currently insufficient evidence to support a superior method of fever control (antipyretics or surface/intravascular cooling devices).

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Title: Spontaneous Bacterial Peritonitis

Category: Critical Care

Posted: 9/20/2011 by Mike Winters, MBA, MD
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Spontaneous Bacterial Peritonitis

Critically ill patients with end-stage liver disease (ESLD) may be some of the sickest patients you'll ever manage.
Recall that patients with ESLD have higher rates of infection and worse outcomes.
Always consider spontaneous bacterial peritonitis (SBP) in the sick patient with ESLD. In fact, SBP is the most common infection in ESLD patients.
Physician impression alone has been repeatedly shown to be inaccurate in ruling out SBP.
In the critically ill patient with ESLD and ascites, tap the belly!

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Title: Fungal Sepsis

Category: Critical Care

Posted: 9/6/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Fungal Sepsis in the Critically Ill

In recent years, the incidence of invasive fungal infections has risen dramatically.
Candida species (C. albicans, C. glabrata, C. parapsilosis, C tropicalis, C. krusei) account for the majority of invasive infections in the critically ill patient.
Key risk factors for invasive candidal infections include:
- Exposure to broad spectrum antibiotics
- Cancer chemotherapy
- Indwelling catheters
- TPN administration
- Neutropenia
- Hemodialysis
Given the significant mortality of invasive fungal infections, early and appropriate antifungal therapy is paramount.
First-line empiric antifungal therapy recommendations from the Infectious Disease Society of America include caspofungin, micafungin, or fluconazole. Amphotericin B is now reserved for patients who are either intolerant or not responding to the echinocandins (caspofungin, micafungin).

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Title: Re-Expansion Pulmonary Edema

Category: Critical Care

Posted: 8/23/2011 by Mike Winters, MBA, MD
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Re-expansion Pulmonary Edema After Chest Tube Placement

Tube thoracostomy is a common procedure in the emergency department.
For patients who develop respiratory distress after chest tube placement, think about re-expansion pulmonary edema.
While a rare occurrence, re-expansion pulmonary edema is reported to have a mortality rate of up to 20%.
The mechanism by which edema forms remains controversial, but is thought to be due to increased alveolar-capillary membrane permeability in the expanding lung.
Treatment is supportive with supplemental oxygen and diuretics. Some patients may require mechanical ventilation depending on the degree of distress and hypoxia.

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Title: ED Thoracotomy

Category: Critical Care

Posted: 8/9/2011 by Mike Winters, MBA, MD
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When may an ED thoracotomy be futile?

Performing an ED thoracotomy is incredibly stressful and a resource-intense procedure.
While we've all learned that stab wounds to a ventricle have the highest survival rate, what about indicators that an ED thoracotomy may be futile?
A recent study of 18 trauma centers across the US found that ED thoracotomy was unlikely to yield productive survival in the following:
- Blunt trauma patients that require > 10 min of prehospital CPR without response
- Penetrating trauma patients that require > 15 min of prehospital CPR without response
- Patients presenting in asystole without evidence of pericardial tamponade on bedside ultrasound.

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Title: Blood Pressure Measurements in the Critically Ill Obese Patient

Category: Critical Care

Posted: 7/26/2011 by Mike Winters, MBA, MD
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Blood Pressure in the Critically Ill Obese Patient

Recall that incorrectly sized cuffs can significantly overestimate blood pressure, especially in obese patients.
In fact, some studies show that false BP readings can occur in up to 75% of obese patients.
By relying solely on noninvasive BP measurements, many of your critically ill obese patients may actually be hypotensive and under perfused.
When you've got a sick obese patient, strongly consider early placement of an arterial line to assess and monitor blood pressure.

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Title: MAP in the Post-Cardiac Arrest Patient

Category: Critical Care

Posted: 7/12/2011 by Mike Winters, MBA, MD
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Hemodynamic Optimization in the Post-Arrest Patient

Hemodynamic instability is common in the post-cardiac arrest patient.
While the optimal targets remain unclear, hemodynamic stabilization often consists of intravenous fluids, vasopressors, and in rare cases mechanical support, such as an intra-aortic balloon pump or left-ventricular assist device.
Based on recent literature, current recommendations for mean arterial pressure (MAP) in the post-arrest patient range from 65-100 mm Hg.
Depending upon the baseline blood pressure and degree of myocardial stunning, many post-arrest patients will need a higher MAP (80-100 mm Hg) in order to maintain critical perfusion pressure to vital organs such as the brain.

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Title: Hepato-Renal Syndrome

Category: Critical Care

Posted: 6/28/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Hepato-Renal Syndrome

Hepato-renal syndrome (HRS) is the development of acute kidney injury (AKI) in patients with advanced cirrhosis.
HRS is traditionally divided into two types based upon how quickly AKI develops:
- Type I: a rapid decline in function in less than 2 weeks
- Type II: a slow decline in function over weeks to months
Type I is more likely to be seen in the ED and is often due to a precipitating event such as:
- GI bleed
- Spontaneous bacterial peritonitis (SBP)
- Hypovolemia from aggressive diuresis
In ED patients with advanced cirrhosis and new, or worsening, AKI think about HRS.
If suspected, look for precipitants (i.e. SBP), restore volume with IVFs, avoid nephrotoxins (IV contrast), and administer vasopressor therapy when indicated.

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Title: AKI in Critically Ill Cancer Patients

Category: Critical Care

Posted: 6/14/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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AKI in the Critically Ill Cancer Patient

Acute kidney injury (AKI) is common in the critically ill cancer patient and associated with worse outcomes.
The incidence seems to be higher in patients with hematologic malignancies.
Despite many different etiologies for AKI in cancer patients (tumor lysis syndrome, hypercalcemia, chemotherapeutic drugs, etc) the most common cause is sepsis, accounting for 58-65% of causes.
Given the emphasis on early antibiotic administration in sepsis, be sure to double check the potential for nephrotoxicity of antibiotics for this patient population. When possible, avoid nephrotoxic meds, such as aminoglycosides, that can worsen AKI.

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Title: The Critically Ill Patient with ESLD

Category: Critical Care

Posted: 5/31/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Cardiovascular Complication of ESLD

Patients with end-stage liver disease (ESLD) can develop a number of complications that lead to, or complicate, critical illness.
Regarding the cardiovascular system, ESLD patients can develop:
- Hyperdynamic vasodilated cardiovasculature: low baseline blood pressure and high cardiac output
- "Cirrhotic cardiomyopathy": impaired systolic response to stress or altered diastolic relaxation
- Autonomic dysfunction: reduced responsiveness to vasoconstrictors
ESLD patients also tend to have a normal or near-normal lactate at baseline, despite lactate being cleared more slowly.
When managing the critically ill patient with ESLD, look for signs of heart failure, expect an abnormal response to vasopressors, think about steroids for persistent shock, and don't ascribe an elevated lactate simply to impaired hepatic clearance.

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Title: Acute Liver Failure

Category: Critical Care

Posted: 5/17/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Acute Liver Failure (ALF)

ALF is defined as sudden and severe liver failure in a patient without preexisting liver disease.
The clinical presentation can include altered mental status, coagulopathy, MODS, & cerebral edema.
In the US, the most common cause of ALF is drug-induced (e.g. acetaminophen).
Important components of the ED management of patients with ALF include:
- Monitoring and correcting hypoglycemia (may need infusion of D20)
- Monitoring and maintaining a normal sodium concentration
- Volume resuscitation with isotonic crystalloids or colloids
- Prophylactic administration of broad spectrum antibiotics (given high incidence of sepsis)
- Consideration for continuous veno-venous hemodiafiltration (CVVHD) for severe elevations in ammonia and acidosis (even if renal function is normal)
- Transfer to center capable of liver transplantation

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Title: GI Complications of Obesity in Critical Illness

Category: Critical Care

Posted: 5/3/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Gastrointestinal Changes of Obesity that Complicate Critical Illness

Obesity predisposes patients to several gastrointestinal abnormalities that can cause, or complicate, critical illness.
Important abnormalities to keep in mind when managing a critically ill obese patient include:
- Increased intra-abdominal pressure which predisposes to abdominal compartment syndrome
- Increased incidence of nonalcoholic fatty liver disease which may lead to prolonged drug metabolism
- Increased incidence of cholelithiasis which may result in pancreatitis or cholangitis

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Title: Combination Therapy for Bacteremia

Category: Critical Care

Keywords: staphylococcal aureus, aminoglycoside, monotherapy, combination therapy (PubMed Search)

Posted: 4/19/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Combination Antimicrobial Therapy for Gram (+) Bacteremia

Bacteremia is a major cause of morbidity and mortality in the critically ill patient.
S.aureus remains a common isolate in patients with either hospital-acquired or community-acquired bacteremia.
In cases of suspected endocarditis due to S.aureus, traditional teaching has been to give an aminoglycoside (i.e. gentamicin) in combination with vancomycin or an antistaphylococcal penicillin.
Importantly, there is no strong evidence to support this combination in patients with suspected S.aureus bacteremia.
Furthermore, patients receiving the aminoglycoside combination have higher rates of renal impairment without any added clinical benefit.

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Title: Aspiration Pneumonitis/Pneumonia

Category: Critical Care

Posted: 3/22/2011 by Mike Winters, MBA, MD
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Aspiration Pneumonitis and Pneumonia

Aspiration of low pH gastric fluid or food matter is common in critically ill patients and often underdiagnosed.
Patients with aspiration initially develop a pneumonitis that, in some, can be complicated by bacterial pneumonia. Up to 33% develop severe ALI/ARDS, with an associated 30% mortality rate.
Aspiration pneumonitis presents with hypoxia and a CXR demonstrating infiltrates in the dependent portion of the lungs. Often, the degree of respiratory distress is worse than the CXR appearance.
Since it is challenging to differentiate aspiration pneumonia from aspiration pneumonitis, current recommendations suggest initiating empiric antibiotics with agents that have adequate Gram-negative coverage. Routine coverage against anaerobic bacteria is not currently recommended, except in patients with severe periodontal disease and those with a lung abscess on CXR or CT.
Despite the initial inflammatory response, steroids are not indicated for patients with aspiration.

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Title: The Severely Hypoxemic ED Patient

Category: Critical Care

Posted: 3/8/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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The Severely Hypoxemic ED Patient

Most define hypoxemia as a P_aO₂ < 60 mm Hg.
Perhaps a better definition of hypoxemia is a P_aO₂ that is associated with continued tissue hypoxia (rising lactate, low S_cvO₂), the need for vasopressor medications, or severe metabolic acidosis.
For ED patients that remain hypoxemic despite increased F_iO₂ and high levels of PEEP, consider the following rescue therapies:
- Recruitment maneuvers - brief periods of high PEEP (35-50 cm H₂O) or pressure-controlled breaths to reopen collapsed alveoli
- High-frequency oscillatory ventilation - employs a high airway pressure to recruit closed alveolar segments
- Prone positioning - believed to improve oxygenation through a redistribution of ventilation and perfusion
- Extracorporeal membrane oxygenation

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Title: Hemodynamic Monitoring in the Ventilated Patient

Category: Critical Care

Posted: 2/22/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Hemodynamic Monitoring in the Ventilated Patient

Consider pulse pressure variation (PPV) as a method to monitor volume responsiveness in your mechanically ventilated ED patients.
The theory behind PPV:
- When a positive pressure breath is delivered via the ventilator, pleural pressure rises and causes a decrease in venous return, right heart filling, and right heart output.
- Simultaneously, the positive pressure breath causes an increase in left heart filling and a decrease in left heart afterload. This is reflected clinically as an increase in blood pressure.
- Within a few beats, the decreased right heart output is transmitted to the left heart resulting in a decrease in blood pressure during expiration.
Patients who are volume depleted can have significant differences in blood pressure between inspiration and expiration - i.e. a large variation in pulse pressure.
PPV values > 12% have been shown to identify patients who are volume responsive.
Importantly, PPV works best in vented patients who have no spontaneous respiratory effort, are in sinus rhythm, and receiving 8 ml/kg tidal volumes.

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Title: LV Dysfunction in the Critically Ill

Category: Critical Care

Posted: 2/8/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Acute LV Dysfunction in the Critically Ill

Approximately one-third of critically ill hospitalized patients develop acute LV dysfunction, most often due to a stress-induced cardiomyopathy.
In these patients, up to 25% develop an acute dynamic LV outflow tract obstruction.
Consider acute LV outflow tract obstruction in hypotensive patients with a new systolic ejection murmur in the left parasternal area.
Aggressive IVFs is central to the management of these patients with LV outflow tract obstruction.

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Title: Valproic Acid and Status Epilepticus

Category: Critical Care

Posted: 1/26/2011 by Mike Winters, MBA, MD (Updated: 11/22/2024)
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Valproic Acid in Status Epilepticus

In previous pearls, we have discussed the treatment of status epilepticus (SE) with first-line (benzodiazepines) and second-line agents (phenytoin/fosphenytoin).
Refractory SE is defined as the failure to respond to both first- or second-line antiepileptic medications.
Valproic acid is listed in many algorithms as a third-line agent for treating SE.
Avoid valproic acid in refractory SE patients who have hepatic disease or dysfunction.
Although rare, valproic acid can cause a fatal hepatotoxicity in these patients.