UMEM Educational Pearls - By Mike Winters

Category: Critical Care

Title: Patient Positioning in the Critically Ill Obese Patient

Posted: 11/30/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Beware Trendelenburg Positioning in the Critically Ill Obese Patient

When inserting a central venous catheter (CVC) into the internal jugular or subclavian vein, clinicians often place patients in the Trendelenburg position to increase the size of the vein.
When possible, avoid Trendelenburg position for CVC placement in the morbidly obese patient.
These patients can quickly deteriorate in this position due to reduced lung volumes, increased right heart pressures, decreased cardiopulmonary reserve, and the effects in intra-abdominal pressure.

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Category: Critical Care

Title: Obesity and Mechanical Ventilation

Posted: 11/16/2010 by Mike Winters, MD
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Positioning for Ventilated, Critically Ill Obese Patients

Up to one-quarter of patients in the ICU are obese, as defined by a BMI > 35 kg/m²
Obesity can significantly alter pulmonary physiology causing
- reduced lung volumes
- decreased compliance
- abnormal ventilation to perfusion relationships
- respiratory muscle inefficiency
For intubated obese patients, body position can affect ventilatory management
In the supine position, obese patients can have collapse of lung segments along with increased impedance of the diaphragm
Elevating the head of the bed to 30-45 degrees in intubated obese patients has been shown to improve tidal volumes and lower respiratory rates.

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Category: Critical Care

Title: Ventilation in the Post-Cardiac Arrest Patient

Posted: 11/2/2010 by Mike Winters, MD
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Ventilation Pearls in the Post-Cardiac Arrest Patient

Some ventilation pearls from the recently released 2010 AHA guidelines include:
- Set the tidal volume to 6-8 ml/kg ideal body weight
- Titrate minute ventilation to achieve a P_aCO₂ between 40-45 mm Hg or P_ETCO₂ between 35-40 mm Hg
- Reduce the F_iO₂ to maintain S_pO₂ > 94%

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Category: Critical Care

Title: Ketamine for RSI in Unstable ED Patients

Posted: 10/19/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Ketamine for RSI in Hemodynamically Unstable ED Patients

Recall that ketamine acts as a sympathomimetic resulting in increases in heart rate, blood pressure, and ultimately cardiac output.
Because of its rapid transport across the blood-brain barrier, its sympathomimetic effects, and lack of significant adverse effects, ketamine is recommended by many organizations as a first line agent for RSI in unstable patients.
Important contraindications to ketamine include an acute coronary syndrome, aortic dissection, and acute heart failure.
Take Home Point: Consider using ketamine the next time you need to intubate a hypotensive, critically ill ED patient.

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Category: Critical Care

Title: Peak and Plateau Pressures in Intubated ED Patients with Respiratory Distress

Posted: 10/5/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Respiratory Distress in the Ventilated ED Patient

In the ventilated patient with respiratory distress, evaluation of peak and plateau pressures can help to identify the cause.
Isolated increases in peak pressure suggest increased resistance to airflow and should prompt consideration of the following:
- kinked or twisted ET tube
- patient biting ET tube
- obstructed ET tube
- bronchospasm
- lower airway obstruction
Increases in plateau pressure suggest decreased pulmonary compliance and should prompt consideration of the following:
- unilateral intubation
- pneumothorax
- pulmonary edema
- worsening pneumonia
- abdominal HTN/compartment syndrome

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Category: Critical Care

Title: Hemophilia A and Life-threatening bleeding

Posted: 9/21/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Life-threatening Bleeding in Hemophilia A Patients

Although an infrequent occurrence, patients with Hemophilia A can present with life-threatening hemorrhage (e.g. ICH).
Recall that normal clotting factor levels range from 50-150 IU/dL - reported by the lab as 50-150%.
Life-threatening bleeding requires Factor VIII levels between 80-100%. In general, each unit of FVIII/kg raises plasma levels by 2%.
Recombinant Factor VIII products are preferred over plasma derived concentrates or blood products and are dosed as:
- FVIII - 50 IU/kg loading dose followed by infusion of 3 IU/kg/hr
In the event you don't have access to recombinant or plasma derived FVIII concentrates, cryoprecipitate (contains FVIII) can be used.

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Category: Critical Care

Title: Pulmonary Contusion Ventilator Management

Posted: 9/7/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Pulmonary Contusion and Ventilator Management

Pulmonary contusion is the most common injury in blunt thoracic trauma.
Patients with pulmonary contusion often present with hypoxia, hypercarbia and increased work of breathing.
Importantly, patients with pulmonary contusion have a low cardiopulmonary reserve. Maintain a low threshold for initiating mechanical ventilation is these patients.
When starting mechanical ventilation, think about the following:
- Patients are at high risk for developing ARDS
- Most centers use a low tidal volume ventilatory strategy
- Higher levels of PEEP may be necessary to recruit collapsed alveoli
- High frequency oscillatory ventilation (HFOV) and airway pressure release ventilation (APRV) are modes of ventilation that are gaining in popularity for ventilating patients with pulmonary contusions.

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Category: Critical Care

Title: Hemostatic Therapy for ICH

Posted: 8/24/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Hemostatic Therapy for ICH - Updated Guidelines

The AHA/ASA just published updated guidelines for the diagnosis and treatment of acute spontaneous intracerebral hemorrhage (ICH).
Regarding hemostatic therapy, new/revised recommendations from the 2007 AHA/ASA guidelines include:
- Patients with severe thrombocytopenia or factor deficiency should receive platelets or factor replacement
- Patients with ICH due to oral anticoagulants (warfarin) should receive intravenous vitamin-K and vitamin-K dependent factor replacement
  - Prothrombin complex concentrates (PCCs) are being increasingly used and are considered a reasonable alternative to FFP. To date, studies have not shown improved outcome with PCCs.
  - Recombinant factor VIIa (rFVIIa) is not recommended as a sole agent for warfarin-related ICH
- rFVIIa is not recommended in unselected patients
- Usefulness of platelet transfusions for patients using antiplatelet medications is unclear and currently investigational.

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Category: Critical Care

Title: Drug-Induced Hypophosphatemia

Posted: 8/10/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Drug-Induced Hypophosphatemia

Hypophosphatemia is seen in almost 30% of critically ill patients.
As discussed in a prior pearl, hypophosphatemia can result in respiratory failure along with cardiac and neurologic abnormalities.
Although common ED causes of hypophosphatemia include sepsis, hypothermia, and dialysis, don't forget about medications.
Medications that can cause significant hypophosphatemia in the critically ill (along with their mechanism) include:
- Decreased GI intake: antacids, sucralfate
- Transcellular shift: aspirin overdose, albuterol, catecholamines, insulin, and bicarbonate
- Increased urinary excretion: diuretics, acetaminophen overdose, and theophylline overdose

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Category: Critical Care

Title: Hypocapnia and the Injured Brain

Posted: 8/3/2010 by Mike Winters, MD
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Hypocapnia and Brain Injury

Hypocapnia indirectly reduces cerebral blood volume through reductions in arterial cerebral blood flow.
Despite its continued and frequent use, hypocapnia can actually aggravate cerebral hypoxia through reductions in oxygen supply and increases in cerebral oxygen demand.
In addition to inducing further cerebral injury, hypocapnia can cause deleterious effects on the heart, lung, and GI tract.
To date, there is no evidence that hypocapnia improves outcome in patients with traumatic brain injury or acute stroke.
Induced hypocapnia in critically ill ED patients with acute brain injury should primarily be reserved for those with imminent brain herniation.

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Category: Critical Care

Title: Drug Induced Thrombocytopenia in the Critically Ill

Posted: 7/27/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Drug-Induced Thrombocytopenia

Thrombocytopenia is common in critically ill patients and is associated with increased mortality.
Up to 25% of critically ill patients will develop thrombocytopenia as a result of a medication, termed drug-induced thrombocytopenia (DIT)
Antibiotcs are a common, yet infrequently recognized, cause of DIT.
Antibiotics reported to cause DIT include linezolid, vancomycin, trimethoprim/sulfamethoxazole, and the beta-lactams.
In fact, piperacillin/tazobactam has been associated with DIT more frequently than any other penicillin.

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Category: Critical Care

Title: ICU Acquired Weakness

Posted: 7/19/2010 by Mike Winters, MD (Emailed: 7/20/2010) (Updated: 4/25/2024)
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ICU Acquired Weakness

ICU acquired weakness (ICU-aw) is a general term that refers to the weakness that develops in critically ill patients during the course of their illness - especially in patients with sepsis and those receiving mechanical ventilation.
ICU-aw is an very common complication of critical illness that can develop within hours and has been shown to increase the duration of mechanical ventilation and ICU/hospital LOS. Observational studies have also reported an association with mortality.
Risk factors associated with ICU-aw include medications (neuromuscular blocking agents, corticosteroids), hyperglycemia and immobility.
For the critically ill ED patient, current recommendations suggest limiting the administration of neuromuscular blocking agents and corticosteroids, when possible.

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Category: Critical Care

Title: Drug-Drug Interactions in the Critically Ill

Posted: 7/13/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Drug-Drug Interactions in the Critically Ill

Critically Ill ED patients are at risk for drug-drug interactions (DDIs) due to altered organ function, polypharmacy, and altered drug kinetics.
DDIs involving the cytochrome isoenzyme CYP3A4 are of particular importance.
CYP3A4 inhibitors, such as macrolides and azoles (fluconazole, voriconazole), can cause serious DDIs when given concomitantly with meds that are a subtrate for CYP3A4 - midazolam, cyclosporine, tacrolimus, diltiazem, amiodarone.
Pay particular attention to your transplant patients, as administration of an azole can result in significant cyclosporine or tacrolimus toxicity.

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Category: Critical Care

Title: Asthma, Peak Pressures, and the Ventilator

Posted: 7/6/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Asthma, Peak Pressures, and the Ventilator

In previous pearls, we have highlighted ventilator settings for the asthmatic, along with the differences between peak and plateau pressure measurements.
When ventilating the asthmatic, pay attention to the ventilator settings placed by your respiratory therapist.
In general, the respiratory therapist will set the ventilator to stop delivering tidal volumes when the peak pressure exceeds 40-60 cm H₂O.
For asthmatics, this practice can result in very low tidal volumes.
Thus, peak pressure limits must be set higher.
As you know, high peak pressures have not been shown to be injurious, provided that the plateau pressure remains < 30 cm H₂O

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Category: Critical Care

Title: Acidosis and Intubation

Posted: 6/29/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Pre-existing acidosis and mechanical ventilation

Not surprisingly, many critically ill ED patients often develop a metabolic acidosis.
To compensate, patients hyperventilate, thereby producing a respiratory alkalosis.
When these patients require intubation and mechanical ventilation, be sure to provide the same level of respiratory compensation when setting the ventilator.
Failing to provide a rate sufficient to compensate for the pre-intubation acidosis leads to a rapid drop in pH, bradycardia and eventually asystole.
In general, rates can be increased to about 30-35 breaths per minute, after which auto-PEEP becomes problematic.

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Category: Critical Care

Title: Hypotension and MV

Posted: 6/15/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Hypotension after intubation and initiation of mechanical ventilation

Approximately 25-30% of patients develop hypotension after intubation and initiation of mechanical ventilation (MV).
Although the literature is not robust, risk factors for hypotension after initiation of MV include:
- hypotension prior to intubation
- tachycardia prior to intubation
- obesity
- high intrathoracic pressure (COPD)
- excess catecholamine states (ETOH withdrawal, cocaine intoxication) with rapid relaxation during RSI
In addition to administering isotonic intravenous fluids (IVFs) while preparing for intubation, consider having a vasopressor medication, such as phenylephrine, available if IVFs alone prove insufficient at maintaining blood pressure.

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Category: Critical Care

Title: Platelet Transfusions in the Critically Ill

Posted: 6/8/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Platelet Transfusions in the Critically Ill

Recommendations for the transfusion of platelets in the critically ill patient is primarily extrapolated from the oncology literature; literature that is predominantly observational and expert opinion.
Nevertheless, indications for the transfusion of platelets in a critically ill ED patient include:
- active bleeding with a plt count < 50 x 10⁹/L
- plt count < 10 x 10⁹/L (high risk of spontaneous bleeding)
- prior to an invasive procedure when the plt count is < 50 x 10⁹/L
Importantly, the decision to transfuse platelets should also take into account the clinical setting (ie. a uremic patient with active bleeding)

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Category: Critical Care

Title: PCAS: Controlled Reoxygenation

Posted: 5/25/2010 by Mike Winters, MD (Updated: 4/25/2024)
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Postcardiac Arrest Syndrome: Controlled Reoxygenation

In previous pearls, Dr. Marcolini has highlighted the poscardiac arrest syndrome (PCAS), comprised of brain injury, myocardial dysfunction, systemic ischemia/reperfusion response, and persistent precipitating disease.
Not surprisingly, postcardiac arrest brain injury is a major cause of morbidity and mortality, accounting for > 60% of deaths in some studies.
In addition to therapeutic hypothermia, consider "controlled reoxygenation" in order to optimize neurologic outcome.
Animal data has demonstrated that too much oxygen may worsen neuronal damage during the initial resuscitation phase.
Take Home Points:
- Use a minimum amount of F_iO₂ to maintain S_pO₂ of 94-96%
- Avoid unnecessary arterial hyperoxia

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Category: Critical Care

Title: PRBCs in Neurocritical Care

Posted: 5/11/2010 by Mike Winters, MD (Updated: 4/25/2024)
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PRBC Transfusions in Neurocritical Care

Historically, neurocritical care textbooks have favored a more liberal PRBC transfusion strategy, as the brain is very sensitive to decreases in oxygen delivery.
Despite these recommendations, limited studies have failed to show a mortality benefit to PRBC transfusion in critically ill patients with neurologic illness.
Postulated reasons for the lack of morbidity or mortality benefit center around the injured brain's response to attempts to increase oxygen delivery through transfusion.
- TBI: PET studies have shown an overall lower level of metabolic activity along with a lower oxygen extraction and loss of autoregulation
- SAH: transfusion may increase the risk of vasospasm in SAH and worsen flow
Although the evidence is not overwhelming, current recommendations from SCCM-Eastern Society for the Surgery of Trauma recommend a restrictive PRBC transfusion threshold (Hgb < 7 gm/dL) even in neurocritical care patients.

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Category: Critical Care

Title: PRBCs in the Critially Ill Patient with Cardiac Disease

Posted: 4/27/2010 by Mike Winters, MD (Updated: 4/25/2024)
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PRBC Transfusion Threshold for Patients with Cardiac Disease

As previously discussed, the PRBC transfusion threshold for the general population of critically ill patients is a Hgb < 7 gm/dL.
Traditional teaching has been to maintain a Hgb > 10 gm/dL in patients with a history of CAD.
This threshold stems from a 1950s cohort of Jehovah's Witness patients, and several observational studies, that demonstrated increased perioperative mortality in patients whose Hgb was < 10 gm/dL.
Recent studies, however, have found that patients with a history of CAD tolerate lower Hgb levels without increases in morbidity or mortality. In fact, current cardiovascular surgery guidelines favor a conservative Hgb threshold (7 gm/dL) for patients with CAD.
Importantly, the Hgb threshold of < 7 gm/dL for PRBC transfusion applies to patients with simply a history of CAD and not to patients with evidence of an acute coronary syndrome (STEMI, NSTEMI, unstable angina). Guidelines continue to recommend a Hgb > 10 gm/dL for patients with ACS.