UMEM Educational Pearls - By Mike Winters

Category: Critical Care

Title: Acalculous Cholecystitis

Posted: 11/12/2013 by Mike Winters, MD (Updated: 8/17/2022)
Click here to contact Mike Winters, MD

Acalculous Cholecystitis in the Critically Ill

  • Acute acalculous cholecystitis (AAC) accounts for almost 50% of cases of acute cholecystitis in the critically ill ICU patient.
  • Importantly, the mortality rate for AAC can be as high as 50%.
  • Risk factors for AAC include:
    • CHF
    • Cardiac arrest
    • DM
    • ESRD on hemodialysis
    • Postoperative
    • Burns
  • Unfortunately, the physical exam is unreliable, especially in intubated and sedated patients.
  • Furthermore, less than half of patients with AAC are febrile or have a leukocytosis.  LFTs can also be normal in up to 20% of patients.
  • Ultrasound remains the most common imaging modality for diagnosis.
  • Take Home Point: Consider AAC in the septic critically ill patient without a source.

Show References


Peri-Intubation Cardiac Arrest

  • Emergency intubation is a common critical care procedure that carries the risk of life-threatening complications.
  • Although cardiac arrest (CA) is an established complication, there is scant literature on the actual incidence ad factors associated with CA in the peri-intubation period.
  • In a recent retrospective analysis from Carolinas Medical Center, investigators found:
    • Peri-intubation CA occurred in 4.2% of patients and was associated with a 14-fold increase in hospital mortality.
    • A pre-RSI shock index > 0.9 was indepedently associated with CA.
    • Obese patients had a higher incidence of CA; odds of CA increased 1.37 times for every 10 kg increase in weight.
  • Take Home Point: Peri-intubation CA may be more common than previously thought and, not suprisingly, is associated with an increased risk of in-hospital death.

Show References


Clostridium Difficile Associated Diarrhea and The Elderly Patient

  • Infectious diseases remain the leading cause of mortality in the elderly.
  • An infection that is increasing in prevlance among elderly patients is Clostridium difficile-associated diarrhea (CDAD).
  • Mortality rates are up to 3.5 times higher in elderly patients with CDAD compared to younger patients.
  • Antimicrobial therapy within the previous 6 weeks is the strongest risk factor for CDAD.
  • Though any antibiotic may cause CDAD, clindamycin, fluoroquinolones, and cephalosporins have the highest risk.
  • Importantly, the diarrhea may not always bloody.
  • Metronidazole remains the treatment of choice for uncomplicated infections.

Show References


Category: Critical Care

Title: HIV, ART, and the ICU

Posted: 7/23/2013 by Mike Winters, MD (Updated: 8/17/2022)
Click here to contact Mike Winters, MD

HIV, ART, and the ICU

  • Though survival has dramatically improved for patients with HIV, there has been no decrease in the quantity of ICU admissions for this select patient population.
  • One of the most common reasons for ICU admission is now adverse effects of antiretroviral therapy (ART).
  • When managing a critically ill HIV patient in the ED or ICU, consider the following effects of ART as an etiology:
    • Lactic acidosis
      • Seen with nucleoside reverse transcriptase inhibitors (NRTIs): greatest risk with didanosine, stavudine, and zidovudine
      • Presentation: fatigue, malaise, vomiting, abdominal pain, hepatomegaly
      • Lactate often > 10 mmol/L
    • Abacavir hypersensitivity
      • Usually within first 6 weeks of drug initiation
      • Presentation: rash, fever, shortness of breath, vomiting, abdominal pain
      • Can rapidly progress to cardiovascular collapse

Show References


Category: Critical Care

Title: CVP and Fluid Responsiveness

Posted: 6/25/2013 by Mike Winters, MD (Updated: 8/17/2022)
Click here to contact Mike Winters, MD

CVP and Fluid Responsiveness

  • Central venous pressure (CVP) has been used over the last 50 years to assess volume status and fluid responsiveness in critically ill patients.
  • Despite widespread practice habit, CVP has not been shown to reliably predict fluid responsiveness in the critically ill.
  • In a recent updated meta-analysis, Marik et al reviewed 43 studies, totaling over 1800 patients.
    • 57% of patients were fluid responders
    • The mean CVP was 8.2 mm Hg for fluid responders and 9.5 mm Hg for non-responders
    • For studies performed in ICU patients, the correlation coefficient for CVP and change in cardiac index was just 0.28.
  • Bottom line: Current literature does not support the use of CVP as a reliable marker of fluid responsiveness.

Show References


Rhabdomyolysis in the Critically Ill

  • Rhabdomyolysis can be disastrous in the critically ill patient, resulting in metabolic acidosis, life-threatening hyperkalemia, acute kidney injury, and acute renal failure (ARF).  In fact, mortality can be as high as 60% for those that develop ARF secondary to rhabdomyolysis.
  • Although creatine kinase (CK) is a sensitive marker of muscle injury and used for diagnosis, it is actually the presence of myoglobinuria that results in ARF.
  • Current guidelines recommend treatment when the CK level is > 5000 U/L.
  • The mainstay of treatment remains aggressive fluid resuscitation with crystalloids.
  • The administration of bicarbonate to alkalinize the urine, diuretics to increase urine output, and osmotic agents (mannitol) to augment urine output remain controversial and are not supported by current literature.

Show References


Category: Critical Care

Title: End-Expiratory Occlusion Test

Posted: 5/28/2013 by Mike Winters, MD (Updated: 8/17/2022)
Click here to contact Mike Winters, MD

End-expiratory Occlusion Test

  • Volume expansion is a cornerstone of resuscitation for circulatory failure.
  • As discussed in previous pearls, only 50% of unstable critically ill patients respond to fluid therapy.  For the 50% that don't respond, additional fluids may increase morbidity and mortality.
  • In recent years, there has been tremendous focus on dynamic markers of fluid responsiveness, including respirophasic changes in IVC diameter, passive leg raising, and pulse pressure variation (PPV).
  • An additional dynamic marker of fluid responsiveness is the end-expiratory occlusion test.
  • Unlike PPV, this test can be performed on patients with spontaneous breathing activity and those with cardiac arrhythmias.
  • Recent literature indicates that a 5% increase in cardiac output during a 15-second end-expiratory occlusion test predicts a positive response to a 500 ml saline infusion.

Show References


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. 

Show References


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%

Show References


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.

Show References


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.

Show References


Category: Critical Care

Title: Extubating in the ED

Posted: 3/19/2013 by Mike Winters, MD (Updated: 8/17/2022)
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.

Show References


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

Show References


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

Show References


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.

Show References


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.

Show References


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.  

Show References


VV-ECMO for Refractory Hypoxemia

  • In the absence of significant cardiac disease, patients with refractory hypoxic respiratory failure should be considered for venovenous extracorporeal membrane oxygenation (VV-ECMO).
  • Though indications vary slightly among organizations, the Extracorporeal Life Support Organization states that ECMO is indicated when the PaO2/FiO2 is < 80 mm Hg on FiO2 > 90% or safe plateau pressures (< 30 cm H2O) cannot be maintained.
  • A few pearls when initiating VV-ECMO:
    • Fluids are often needed in the first few hours after initiation of ECMO
    • Reduce tidal volumes to maintain plateau pressures < 25 cm H2O
    • Decrease FiO2 to maintain oxygen saturations > 88%
    • Use a hemoglobin threshold of 7-8 g/dL for blood transfusion

Show References


Ultrasound-Guided Pericardiocentesis

  • Though emergent pericardiocentesis is a relatively rare procedure in the ED, it is a critical intervention in patients with effusion and life-threatening instability/PEA arrest.
  • Ultrasound-guided pericardiocentesis is preferred over the traditional "blind" approach, as it allows the provider to choose an optimal position and is associated with fewer complications.
  • A few pearls when using ultrasound for emergent pericardiocentesis:
    • Consider placing an NGT for abdominal decompression.
    • Don't mistake the epicardial fat pad for an effusion; fat pads don't change size and usually move in concert with the ventricle.
    • The apical 4-chamber view tends to be the most common probe position, as the largest collection of fluid is usually around the apex.
    • If you are unsure about your needle location, inject 5-ml of agitated saline to confirm you are in the pericardial space.

Show References


Category: Critical Care

Title: Management of AKI

Posted: 11/27/2012 by Mike Winters, MD (Updated: 8/17/2022)
Click here to contact Mike Winters, MD

Managing Critically Ill Patients with AKI

  • Acute kidney injury (AKI) occurs in almost 50% of hospitalized patients and is an independent risk factor for mortality. 
  • Updated guidelines have recently been published on the management of patients with AKI.
  • Pearls for the management of patients with, or at risk of, AKI include:
    • Optimize volume status and perfusion pressure
      • Crystalloids preferred over colloids
      • Consider vasopressors to maintain MAP > 65 mm Hg
    • Avoid nephrotoxic drugs
    • Control co-factors
      • Monitor intra-abdominal pressure
      • Avoid hyperglycemia - target glucose < 150 mg/dL

Show References