May 2014 Critical Care Case of the Month: Second Wind

Kenneth K. Sakata, MD

Sudheer Penupolu, MD 

Robert W. Viggiano, MD

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

History of Present Illness

A 65 year old woman was admitted for gastrointestinal bleeding as evidence by hematochezia. At the time of admission she denied any respiratory symptoms other than mild dyspnea. However, she rapidly developed respiratory failure, was transferred to the ICU and required emergent intubation.

PMH, FH, SH

She has a history of rheumatoid arthritis with a cervical spine fusion. There is also a history of sarcoidosis and she was receiving prednisone 30 daily up until the time of admission. There is no significant family history. She does not smoke or drink.

Physical Examination

Afebrile. Pulse 78. BP 105/65 mm Hg. Respirations: 28. SpO2 96% while receiving an FiO2 of 60% at the time of transfer to the ICU.

Neck: No jugular venous distention.

Lungs: Scattered rales and rhonchi.

Cardiovascular: Regular rhythm. 

Abdomen: no hepatosplenomegaly.

Radiography

A portable chest x-ray taken after intubation is shown in figure 1.

Figure 1. Portable chest x-ray taken shortly after intubation.

Which of the following best describe the chest x-ray? (Click on the correct answer to move to the next panel)

1. Chronic interstitial disease
2. Diffuse consolidation
3. Endotracheal tube in the right mainstem bronchus
4. Small right pneumothorax
5. All of the above

Reference as: Sakata KK, Penupolu S, Viggiano RW. May 2014 critical care case of the month: second wind. Southwest J Pulm Crit Care. 2014;8(5):258-65. doi: http://dx.doi.org/10.13175/swjpcc033-14 PDF

Ultrasound for Critical Care Physicians: The Big Squeeze

A 57 year-old man without significant past medical history presented with difficulty swallowing and pleuritic chest pain.  He was undergoing evaluation for his dysphagia when he was noted to be tachycardic and hypotensive shortly after admission to the medical-surgical ward.  His initial chest x-ray revealed bilateral pleural effusions and what appeared to be cardiomegaly. A cardiac ultrasound was performed (Figure 1).

Figure 1. Subxiphoid view of patient's heart, inferior vena cava and hepatic vein.

What is the cause of the patient's tachycardia and hypotension?

1. Aortic dissection
2. Cardiac tamponade
3. Cardiomyopathy
4. Mitral insufficiency
5. Pulmonary embolus

Reference as: Siddiqi T, Assar S, Malo J. Ultrasound for critical care physicians: the big squeeze. Southwest J Pulm Crit Care. 2014;8(4):221-2. doi: http://dx.doi.org/10.13175/swjpcc036-14 PDF

April 2014 Critical Care Case of the Month: Too Much, Too Fast

Kenneth Sakata, MD

Richard A. Helmers, MD

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

History of Present Illness

A 69 year old man was admitted to the intensive care unit with shortness of breath and atrial fibrillation with a rapid ventricular response.

PMH, FH, SH

He has a history of peripheral vascular disease, end-stage renal disease and is receiving chronic hemodialysis.

Physical Examination

Afebrile. Pulse 135 and irregular. BP 105/65 mm Hg. SpO2 96% while receiving oxygen at 2L/min by nasal cannula.

HEENT: Unremarkable.

Neck: Jugular venous distention to the angle of the jaw while the head is elevated at 45 degrees.

Lungs: Decreased breath sounds at the right base.

Cardiovascular: Irregularly, irregular rhythm. 2-3+ pretibial edema.

Abdomen: no hepatosplenomegaly.

Radiography

The admission chest x-ray is shown in figure 1.

Figure 1. Admission portable chest x-ray.

Which of the following is the best interpretation of the chest x-ray given the clinical situation? (Click on the correct answer to move to the next panel)

1. Hepatomegaly elevating the right diaphragm
2. Large right pleural effusion
3. Paralyzed right diaphragm
4. Right lower lobe pneumonia
5. Right middle lobe pneumonia

Reference as: Sakata K, Helmers RA. April 2014 critical care case of the month: too much, too fast. Southwest J Pulm Crit Care. 2014;8(4):205-12. doi: http://dx.doi.org/10.13175/swjpcc031-14 PDF

Ultrasound for Critical Care Physicians: Hypotension After a MVA

A 25 year old woman was a restrained driver in a rollover motor vehicle accident (MVA) and suffered a C5-C6 fracture-dislocation with spinal cord injury. She was lucid and able to follow commands and could move her upper extremities but not her lower extremities. She was given approximately 6 liters of fluid but required vasopressors to maintain her blood pressure. Initial ECG revealed a normal sinus rhythm without significant ST changes (Figure 1).

Figure 1. Initial ECG.

Upon initial evaluation her blood pressure was low. Bedside ultrasound of the left anterior second intercostal space revealed a sliding lung sign and a 4 chamber view of her heart  was performed (Figure 2).

Figure 2. Four chamber view from the cardiac ultrasound.  

Which of the following is the most likely cause of her hypotension?

1. Blunt cardiac injury
2. Intravascular volume depletion
3. Neurogenic stunned myocardium
4. Pericardial tamponade
5. Pneumothorax

Reference as: Schmitz ED. Ultrasound for critical care physicians: hypotension after a MVA. Southwest J Pulm Crit Care. 2014;8(3):176-8. doi: http://dx.doi.org/10.13175/swjpcc023-14 PDF

March 2014 Critical Care Case of the Month: Interstitial Lung Disease

Seongseok Yun, MD PhD

Konstantin Mazursky, DO

Kahroba Jahan, MD

Enas Al Zaghal, MD

Department of Medicine

University of Arizona

Tucson, AZ 85724

History of Present Illness

An 80 year-old man with a history of chronic obstructive pulmonary disease, asbestosis and interstitial lung disease, presented to the outpatient clinic with cough, sinus congestion and mild sputum. He was sent home with amoxicillin for the treatment of a sinus infection. However, he came back to emergency department with worsening respiratory symptoms including shortness of breath and persistent cough. He required 8-10 L/min of oxygen to maintain an oxygen saturation above 90 %.

PMH

• COPD
• Asbestosis
• Interstitial lung disease
• Diabetes mellitus,  type II
• Hypertension
• Aortic valve replacement

Medications

• Fluticasone-salmeterol 250-50 mcg inhaler
• Mometasone 50 mcg/actuation nasal spray
• Furosemide 40 mg PO daily
• Felodipine 5 mg PO BID
• Warfarin 3 mg PO daily
• Insulin aspart 5 units SC injection before meals
• Insulin glargine 15 units SC injection night time

Social History

• 50 pack-year prior smoking history
• No ethanol or recreational drugs
• No recent travel history      

Physical Examination

Vital signs: temperature 37.2 °C, pulse 116 beats/min, respiratory rate 32-34 breaths/min, blood pressure 179/77 mmHg, SpO2 90 % on 10 L/ min non-rebreathing mask (NRB).

General: Alert and oriented but appearing distressed, tachypneic and dyspneic

Skin: Diaphoretic, no rash or lesions noted.

HEENT: Unremarkable.

Respiratory: Diffuse rales but no wheezing or stridor.

CVS: Tachycardic, regular rhythm, soft systolic murmur.

Abdomen: Soft, non-tender, no tenderness, no guarding, no hepato-splenomegaly

Lymph: No cervical lymphadenopathy

Extremities: No peripheral edema, normal tone, normal range of movement  

Laboratory

CBC: WBC 20.2 X 10³ /μL, hemoglobin 9.3 g/dL, hematocrit 29.8 %, platelets 272,000/μL.

Chemistries: Na⁺ 134 meq/L, K⁺ 4.8 meq/L, Cl^- 108 meq/L, CO₂ 19 mmol/L, blood urea nitrogen (BUN) 58 mg/dL, creatinine 1.7 mg/dL, glucose 272 mg/dL, calcium 9.7 mg/dL, albumin 2.2 g/dL, liver function test-within normal limits.

Prothrombin time (PT) 28.0 sec, international normalized ratio (INR) 2.5, partial thromboplastin time (PTT) 44.5 sec

An old chest x-ray and CT scan were reviewed (Figure 1).     

Figure 1. Old PA (panel A) and lateral (Panel B) and representative image from an old CT scan (panel C).

Which of the followings are the findings of asbestos related disease on chest x-ray? (click on correct answer to move to next panel)  

1. Reticular or patchy opacity
2. Calcified pleural plaque
3. Bilateral consolidation
4. Pulmonary edema
5. 1 + 2
6. 3 + 4

Reference as: Yun S, Mazursky K, Jahan K, Al Zaghal E. March 2014 ciritcal care case of the month: interstitial lung disease. Southwest J Pulm Crit Care. 2014;8(3):152-60. doi: http://dx.doi.org/10.13175/swjpcc013-14 PDF

Resuscitative EChocardiography for the Evaluation and management of Shock: The RECES protocol

Jarrod M. Mosier^1,2

Lori Stolz^1,

John Bloom²

Josh Malo²

Linda Snyder²

Albert Fiorello¹

Srikar Adhikari¹

¹ Department of Emergency Medicine, University of Arizona, Tucson, AZ

²Department of Medicine, Section of Pulmonary, Critical Care, Allergy and Sleep, University of Arizona, Tucson, AZ

Abstract  

Purpose: Ultrasound use by emergency medicine and critical care physicians in the evaluation of the critically ill patient has increased in recent years. Several protocols exist to aid in diagnosing the etiology of shock and identifying rapidly reversible conditions in the undifferentiated hypotension patient. Currently, no protocol provides hemodynamic data or is designed to guide ongoing resuscitation of the critically ill patient with hypotension.

Methods: An evidence-based protocol was developed based on the components of echocardiography that have been supported in the literature for bedside evaluation of the critically ill patient.

Results: The RECES protocol provides diagnostic and hemodynamic information regarding volume responsiveness , presence of pericardial effusion with tamponade physiology (right ventricular diastolic collapse), systolic failure (poor contractility, decreased stroke volume and cardiac output), diastolic dysfunction (mitral valve inflow velocities and tissue Doppler), Right ventricular systolic failure, acute valvular rupture, obvious wall motion abnormalities, and signs of pressure or volume overload (septal flattening on parasternal short axis).

Conclusion: The RECES protocol is a proposed instrument for rapidly and repeatedly assessing the etiology and initial hemodynamic parameters of the patient in shock. Additionally, repeated exams will allow monitoring interventions and guide ongoing resuscitation.

Introduction  

Ultrasound has become indispensible for emergency medicine physicians and intensivists in the evaluation and management of patients in shock. Bedside ultrasound is no longer used solely for central line placement and the diagnosis of intra-abdominal free fluid. The emergency bedside applications being used with frequency span nearly every body system. The body of literature substantiating the ability of clinicians to accurately perform and interpret point-of-care ultrasound studies is robust and growing.

For patients in shock, several goal-directed ultrasound protocols have been described in the literature. Each of these is aimed at finding rapidly reversible etiologies of shock in the undifferentiated hypotensive patient (i.e. tamponade, pneumothorax, intra-abdominal hemorrhage) (1-6). Though similar in their aim, they each differ in respect to the pathology sought, views obtained and the scope of the exam. Of these protocols, systematic study has been undertaken in only two. Jones et al. (2) have demonstrated that goal-directed ultrasound early in the presentation of patients with shock can improve the accuracy of the treating physician’s diagnosis within 15 minutes of patient arrival from 50% accuracy at baseline to 80% accuracy with the use of ultrasound. Manno et al. (6) found a bedside ultrasound protocol in all admitted ICU patients changed the admitting diagnosis in 25.6% of patients, prompted further testing in 18.4% of patients and altered medical therapy in 17.6% of patients.

Bedside cardiac ultrasound in particular has been adopted as a key component of the emergent evaluation of critically ill patients (7,8). Cardiac ultrasound in the hands of non-cardiologist and non-radiologist clinicians has been shown to be accurate and reliable in diagnosing a wide array of pathologies. One paper has described a limited echocardiography protocol for use in trauma intensive care patients with the aim of evaluating for pericardial effusion, ventricular function and volume status (9). All whole-body sonography protocols that have been described for the evaluation of shock incorporate a limited cardiac exam. Within both studies described above, the cardiac portion yielded positive findings most frequently (2,6). However, despite these advances in clinical practice, to our knowledge no standardized, goal-directed bedside echocardiography protocol currently exists to guide the ongoing resuscitation of patients in shock.

This novel goal-directed echocardiography protocol was developed to provide immediate diagnostic information as to the etiology of shock similar to other protocols as well as provide hemodynamic information useful to guiding and assessing therapy during ongoing resuscitation. The protocol is taught to critical care and emergency ultrasound fellows at our institution as well as emergency medicine residents rotating in the ICU. It is designed to go beyond diagnosing the etiology of shock and to guide on-going resuscitation of critically ill patients through their hemodynamic crisis. The initial exam serves as a benchmark to which future exams are compared, and subsequent exams monitor the hemodynamic response to interventions. The intention is that this protocol be used on a recurring and as-needed basis to supplement the standard hemodynamic monitoring in a patient with shock

This protocol [Table 1] is evidence-based.

Table 1. Evaluation parameters: Goal-directed Assessment.  (Editor's note: the size on your browser may need to be enlarged to adequately view the table).  

It incorporates the elements of the bedside cardiac exam that have been proven in the literature to be accurate and useful in the emergency setting. It is not designed to replace standard comprehensive echocardiography but rather to be used in locations or situations where obtaining a complete echocardiogram is not possible or feasible given time of day, availability of formal echo services and clinical condition of the patient. Additionally, the protocol can be repeated after an intervention to assess progress during resuscitation whereas repeated formal echocardiograms are not reasonable. The information obtained at the bedside from this protocol is potentially useful for diagnosing the etiology of shock, and guiding resuscitation of patients with hemodynamic instability. It is not intended to manage the subtleties of chronic cardiovascular disease or valvular disease.

A key element to the use of this protocol is the potential to determine response to therapy to help on-going resuscitation of patients with hemodynamic instability. In a volume-depleted patient, for example, a repeat exam could be performed following each fluid bolus. Traditionally, clinical exam findings of excessive fluid administration can be monitored but occur after the desired intravascular volume status has been surpassed and possible patient harm has been done. A patient in shock who, after several liters of fluid, no longer demonstrates intravascular volume depletion can be assuredly started on vasopressors. Additionally, a patient who continues to demonstrate volume responsiveness with a large stroke volume may be started on vasopressors in the setting of diastolic failure. This phenomenon is also seen as a result in increased arterial elastance which is unlikely to improve from further fluid administration.

This protocol [Table 1] proceeds with several qualitative questions along with obtaining several quantitative hemodynamic parameters in the process. Following is a description of each step in the protocol:

1. Pericardial effusion

Q: Is there a pericardial effusion present? Yes or No

Q: If there is a pericardial effusion present, is there evidence of tamponade physiology (i.e. right ventricular diastolic collapse and/or plethoric inferior vena cava)? Yes or No

This protocol begins with an evaluation for pericardial effusion. The use of bedside ultrasound to diagnose pericardial effusion was one of the first applications employed by emergency medicine and critical care specialists. Emergency physicians can detect pericardial effusion on bedside ultrasound with a sensitivity of 96% and a specificity of 98% (10). Hand-carried ultrasound units have been used in cardiac ICUs to identify pericardial effusion (11). Although the sensitivity and specificity of these handheld units was 75% and 88% respectively, for all effusions, all false negatives had less than 20 mls of pericardial fluid on contrast enhanced CT and all false positives were estimated to be trace as well (11). Bedside ultrasound in undifferentiated dyspneic patients found pericardial effusion in 13.6% of patients, 29% of which required pericardiocentesis (12). If identified, the clinician can then evaluate for echocardiographic signs of tamponade. The elements of comprehensive echocardiographic evaluation for tamponade that are likely to be obtainable with a bedside machine by a non-cardiologist clinician are right ventricular diastolic collapse and inferior vena cava plethora (Figure 1) (13,14). However, as described below, inferior vena cava plethora can be caused by any elevation of right-sided pressures and should be interpreted in the context of the other findings on the exam.

Figure 1. Panel A: Plethoric, non-collapsible IVC suggests elevated right sided pressures or tamponade physiology. Panel B: Presence of pericardial effusion on subxyphoid view is small, but shows diastolic right ventricular collapse. Panel C: M-mode on parasternal long axis suggests tamponade physiology.

2. Global systolic function

Q: Is the left ventricular global systolic function decreased, normal, or hyperdynamic?

Q: What is the stroke volume and cardiac output?

In this protocol, left ventricular systolic function is assessed globally and is graded as decreased, normal, or hyperdynamic, rather than quantitatively estimating left ventricular ejection fraction (LVEF). Although LVEF is a numerical representation of left ventricular function, it is difficult to obtain in the acute setting and influenced by critical illness, as well as anatomic and physiologic factors limiting adequate endocardial visualization (15). Additionally, as LVEF is not influenced by hemodynamic parameters (preload, afterload), it is less useful for the acute hemodynamic evaluation of the patient in shock (16). E-point septal separation (EPSS) has been compared to magnetic resonance imaging methods of calculating ejection fraction with good correlation; however that correlation declines in the presence of wall motion abnormalities and valvular disease (17,18). Ahmadpour et al. (19) demonstrated EPSS to be a reliable index of ventricular performance in coronary artery disease patients but only as a predictor of decreased ejection fraction rather than estimating the exact ejection fraction. Secko et al. (20) showed that novice emergency physician obtained EPSS measurements correlated well with visual estimates of EF; however EPSS as a continuous variable did not correlate well with fractional shortening measurements in a study by Weekes et al. (21). These data would suggest that estimating LVEF by either estimating quantitatively or by EPSS is inconsistent and not indicative of the underlying hemodynamic state. Instead of attempting to quantify ejection fraction, this protocol uses visual estimates of LV systolic function obtained in each view, which have been shown to be accurate and easily performed at the bedside (16,22-24).

3.   IVC

Q: Is the IVC small (<2cm) or large (>2cm)?

Q: Is the IVC dynamic (>20% change in diameter with respiration)?

Assessing volume responsiveness in hypotensive patients is of paramount importance for restoring intravascular volume without deleteriously volume overloading the patient, which has been shown to worsen outcomes (25-28).Traditionally, central venous pressure (CVP) has been used as an endpoint of volume resuscitation (29). CVP as a measure of ventricular preload has been shown to poorly correlate with intravascular volume status and volume responsiveness (30-32). Rather than static CVP measurements, dynamic volume assessments reflected by cardiopulmonary interactions are more accurate and reliable for predicting improved cardiac index with volume infusion (33-40). Bedside ultrasound assessment of dynamic changes in inferior vena cava diameter with either distensibility (IVCd) in the case of a mechanically ventilated patient or collapsibility in a spontaneous breathing is a pre-heart/lung observation of cardiopulmonary interactions and has been shown to be reliable for predicting volume responsiveness (34,35,39,41,42). This protocol uses IVCd as one of three assessments of volume responsiveness along with obliteration of the LV cavity on parasternal short axis (papillary level) and left ventricular outflow tract VTi. Since evidence of IVCd measurement in the presence of cirrhosis and alternative ventilator modes such as airway pressure release ventilation (APRV) is lacking, it is not ideal as the sole assessment for volume responsiveness. A plethoric IVC can be seen in both high right-sided pressure (pulmonary embolism, RV infarct) and in tamponade physiology. A plethoric IVC in the absence of pericardial effusion should alert the physician to the presence of high right-sided pressure or RV volume overload. Additionally, determination of adequate intravascular volume status can guide clinicians in initiation or titration of pressor support.

4. Volume Responsiveness

Q: Does this patient appear to be volume responsive (i.e. in addition to IVC collapsibility, is there a hyperdynamic LV with cavity obliteration on systole and is there variability in the LVOT VTi)? Yes or No

In addition to IVCd, this protocol uses a global assessment of the left ventricular dynamics and the left ventricular outflow tract velocity time integral (LVOT VTi) respiratory variation as assessments of volume responsiveness (Figure 2).

Figure 2. Collapsibility of the IVC (Panel A, top left), hyperdynamic left ventricle with obliteration of the LV cavity on parasternal short axis (Panel B, top right), and variability of the left ventricular outflow tract with inspiration (Panel C, bottom) are indicators of volume responsiveness.

Left ventricular end diastolic area (LVEDA), if seen as cavitary obliteration or “kissing papillary muscles” on parasternal short axis, has been shown to correlate with the presence of hypovolemia (43,44). LVOT VTi variability has recently been shown to correlate well with non-invasive cardiac output monitors to determine volume responsiveness in hypotensive patients (45,46). The LVOT VTi obtained on an apical 5 chamber can be used with the LVOT diameter obtained in the parasternal long axis view to calculate the stroke volume and cardiac output (Figure 3) (47,48).

Figure 3. Stroke volume (SV) and cardiac output. The stroke volume is calculated by measuring the diameter of the LVOT on parasternal long axis (Panel A, left) and the LVOT VTi (Panel B, right) [SV= Vti x π(LVOTd/2)²]. Cardiac output is calculated by multiplying SV by the heart rate.

The LVOT VTi represents a Doppler assessment of cardiopulmonary interactions that translates to stroke volume variation, pulse pressure variation, and systolic pressure variation as seen on an arterial line tracing which has been well correlated with volume responsiveness (33,36,37,41,42,49).

Case 1:  A 48-year-old male is admitted to the intensive care unit (ICU) with septic shock secondary to spontaneous bacterial peritonitis. He had received several liters of crystalloid in the ED and remains hypotensive with poor perfusion. RECES protocol was performed on admission to the ICU, which demonstrated the patient was volume responsive; however the stroke volume and cardiac output were elevated suggesting increased vascular elastance rather than intravascular volume depletion. The patient was placed on a vasopressor with improved tissue perfusion and indicators of shock.

5. Diastolic dysfunction

Q: Is there diastolic dysfunction? Yes or No

Q: Is there evidence of elevated left atrial pressure? Yes or No

Diastoloic dysfunction plays an increased role as patients age or have chronic hypertension (50). Hemodynamically, this leads to an increased likelihood of pulmonary edema with aggressive fluid resuscitation, which has been shown to increase mortality (25,27,28). In this protocol, mitral valve inflow velocities by pulsed wave Doppler (PWD) are used to assess diastolic dysfunction. Mitral E and A waves accurately reflect the pressure gradient between the left atrium and left ventricle and have been shown to be superior to LVEF for estimation of left ventricular function (50). Mitral annulus tissue Doppler (TDI) is used to differentiate between pseudonormal inflow velocity patterns and decreased LV compliance as well as estimate left atrial pressure (50). In grade I diastolic dysfunction, mitral inflow velocities demonstrate an E-A reversal. As left ventricular compliance worsens, the E-A pattern returns to normal; however, the velocities increase, representing the left atrium “pushing” the blood into the left ventricle rather than the ventricle “sucking” blood from the atrium as the cavitary pressure drops below atrial pressure in the normal heart (51). In mechanically ventilated patients diastolic velocities may be altered to some degree by changes in left ventricular compliance, mainly through changes in right ventricular compliance via ventricular interdependence. Additionally, estimated pulmonary artery systolic pressures >40mmHg in the absence of known pulmonary hypertension, lung disease, or systolic failure may indicate undiagnosed diastolic dysfunction and caution over-resuscitation with fluids. Emergency physicians can accurately perform this exam at the bedside as shown by Unluer and colleagues (52).

Case 2:  An 81-year-old male presents with 3 days of productive cough and fever. The patient is found to be hypotensive and tachycardic with high suspicion for severe sepsis. Electrocardiogram demonstrates LVH with strain, and labs are consistent with a severe sepsis syndrome. RECES protocol is performed on this patient which demonstrates grade III diastolic dysfunction and moderate mitral regurgitation which limited the amount of crystalloid given to avoid worsened pulmonary edema and ARDS.

6. Wall motion abnormalities

Q: Is there any obvious wall motion abnormality (global or regional)? Yes or No

In a critically ill patient, differentiating shock-induced cardiac dysfunction from cardiogenic shock is difficult. Serial troponins may be helpful but may also be misleading, as in the case of sepsis-induced cardiomyopathy. The consensus statement on the use of focused cardiac ultrasound in the emergent setting recommends comprehensive echocardiography for the diagnosis of wall motion abnormalities (8). To our knowledge, there exists only one paper evaluating the ability of non-cardiologist clinicians to diagnose wall-motion abnormalities. This study showed that a 30-minute training module significantly improved the ability of emergency physicians to identify wall motion abnormalities (53). Though this has not been studied directly, we postulate that a negative exam performed and interpreted by a non-cardiologist clinician, given the skill required in image acquisition and interpretation, does not rule out the presence of wall motion abnormalities. However, a clearly positive exam noted by a bedside clinician in a patient with undifferentiated or multi-factorial shock could dramatically improve the quality of their resuscitation. A positive exam will require interpretation in consideration with the clinical picture and ancillary data. For example, sepsis-induced cardiomyopathy may present as global hypokinesia or unmask underlying ischemic cardiac disease especially in the presence of vasopressors or inotropes. 

7. Right ventricle

Q: Is the right ventricle dilated? Yes or No

Q: Is there tricuspid regurgitation? Yes or No

Q: What is the systolic function of the right ventricle (TAPSE)?

Q: Is there evidence of right ventricular pressure or volume overload (i.e. septal flattening in systole or diastole)?

Q: What is the estimated pulmonary artery systolic pressure?

The right ventricular systolic movement differs greatly from the left ventricle. As opposed to the rotational component to left ventricular contraction, the right ventricular free wall moves towards the septum, followed by longitudinal contraction bringing the base towards the apex (54). As such, the tricuspid annular plane systolic excursion (TAPSE) using M-mode through lateral tricuspid annulus on an apical 4-chamber view is a reliable measurement of right ventricular systolic function (Figure 4) (54-57).

Figure 4. Tricuspid annular plane systolic excursion (TAPSE). M-mode through the lateral tricuspid annulus will demonstrate the amount of longitudinal excursion of the tricuspid annulus during systole. This has been shown to be a reliable indicator of right ventricular systolic function.

Elevations in RV afterload or decreases in contractility are reflected by a lower TAPSE (<16mm) (54,55). Septal movement is also used to demonstrate pressure or volume overload of the right ventricle. Obtained from a parasternal short axis view, septal flattening in systole represents pressure overload of the right ventricle whereas septal flattening in diastole represents volume overload (54). The presence of septal flattening along with a decreased TAPSE should alert the practioner to elevated pulmonary pressures and RV failure in the acutely hypotensive patient. Pulmonary artery systolic pressure can be calculated by continuous wave (CW) Doppler of the tricuspid regurgitation jet obtained on an apical 4 chamber view (p=4V²) (58). PA systolic pressure may be helpful to determine acute vs. chronic RV failure as the right ventricle is unable to overcome acute elevations in PA pressure >40mmHg (54,59,60).

Case 3:  A 56-year-old female presents by EMS with a seizure. She is found to be hypoxemic, unresponsive to supplemental oxygen, and hypotensive. She is given a fluid bolus immediately in the emergency department (ED), which worsens her hypotension and hypoxemia. The RECES protocol performed showed a dilated, hypodynamic right ventricle with a measured TAPSE of 12mm (severely decreased). tPA was administered and repeat RECES exam demonstrated an improved TAPSE of 16mm after 2 hours.  

8. Valves

Q: Is there obvious mitral, tricuspid, or aortic valve regurgitation? Yes or No

No systematic study has been performed evaluating the ability of emergency or critical care physicians to diagnose valvular pathology with bedside ultrasound. A study done comparing handheld bedside sonography performed by cardiologists to standard echocardiography found good agreement between studies in diagnosing morphologic aortic and mitral valvular pathology (61). Literature describing clinician-performed bedside echocardiography to diagnose valvular disease is limited to case reports (62-64). Despite this, a grossly abnormal valve could be recognizable by bedside clinician sonographers. In scenarios of papillary muscle rupture or valvular vegetations, recognition of these conditions would dramatically influence care. A strong regurgitant jet across the aortic or mitral valve in the setting of shock should alert the physician to acute valvular incompetence or, in the right clinical setting, endocarditis with valvular deterioration.

Limitations

The RECES protocol is not without its limitations. First, there requires a training period to not only learn the mechanics of acquiring the ultrasound images, but also gaining the knowledge base to interpret the findings and manipulate hemodynamics based on those findings. The protocol attempts to simplify complex echocardiographic principles into simple questions, however still requires somewhat intricate knowledge of hemodynamic principles to interpret. Although ultrasound training has become a required component of emergency medicine training and enthusiasm is increasing in critical care training, there still remains a large proportion of physicians in both specialties with limited to no ultrasound skills and would be required to attend a national course to gain the prerequisite skill. Secondly, although echocardiography is immensely helpful in the critically ill, it can also be very difficult in some patients. Many patients are intubated and cannot cooperate with positioning, obese, or have chronic lung disease limiting the ability to acquire appropriate views.

Conclusion

This protocol does not intend to replace comprehensive echocardiography. The machine quality and level of training of bedside clinicians cannot match the level of expertise available with comprehensive echocardiography. However, there are many scenarios in which comprehensive echocardiography cannot be feasibly obtained for a critically ill patient. This protocol is intended to be rapidly performed and allow a treating physician to make immediate clinical decisions when circumstances do not allow for comprehensive echocardiography. Additionally, a limitation of comprehensive echocardiography in the early period of resuscitation is that the information obtained can quickly become obsolete in the setting of a dynamic situation of disease progression and aggressive resuscitation. However, a key component of this protocol is re-evaluation throughout the resuscitation to account for these rapid changes.

Our experience with this protocol shows that others with similar or adequate training in echocardiography can use this protocol to determine the volume responsiveness (IVCd, LVOT VTi) of their patient as well as presence of pericardial effusion with tamponade physiology (RV diastolic collapse, MV inflow variability), systolic failure (poor contractility, decreased SV and CO), diastolic dysfunction (MV inflow velocities and TDI), RV systolic failure (TAPSE), acute valvular rupture, obvious wall motion abnormalities, and signs of pressure or volume overload (septal flattening on parasternal short axis). Future studies should evaluate the learning curve for mastering the ultrasound skills necessary for reliably performing the RECES protocol.

References

1. Atkinson PR, McAuley DJ, Kendall RJ, et al. Abdominal and Cardiac Evaluation with Sonography in Shock (ACES): an approach by emergency physicians for the use of ultrasound in patients with undifferentiated hypotension. Emerg Med J. 2009;26(2):87-91. [CrossRef] [PubMed]
2. Jones AE, Tayal VS, Sullivan DM, Kline JA. Randomized, controlled trial of immediate versus delayed goal-directed ultrasound to identify the cause of nontraumatic hypotension in emergency department patients. Crit Care Med. 2004;32(8):1703-8.[CrossRef] [PubMed]
3. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically lll. Emerg Med Clin North Am. 2010;28(1):29-56, vii. [CrossRef] [PubMed] 
4. Rose JS, Bair AE, Mandavia D, Kinser DJ. The UHP ultrasound protocol: a novel ultrasound approach to the empiric evaluation of the undifferentiated hypotensive patient. Am J Emerg Med. 2001;19(4):299-302. [CrossRef] [PubMed] 
5. Schmidt GA, Koenig S, Mayo PH. Shock: ultrasound to guide diagnosis and therapy. Chest. 2012;142(4):1042-8. [CrossRef] [PubMed] 
6. Manno E, Navarra M, Faccio L, et al. Deep impact of ultrasound in the intensive care unit: the "ICU-sound" protocol. Anesthesiology. 2012;117(4):801-9. [CrossRef] [PubMed]
7. Emergency ultrasound guidelines. Ann Emerg Med. 2009;53(4):550-70. [CrossRef] [PubMed] 
8. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23(12):1225-30. [CrossRef] [PubMed]
9. Gunst M, Sperry J, Ghaemmaghami V, O'Keeffe T, Friese R, Frankel H. Bedside echocardiographic assessment for trauma/critical care: the BEAT exam. J Am Coll Surg. 2008;207(3):e1-3. [CrossRef] [PubMed] 
10. Mandavia DP, Hoffner RJ, Mahaney K, Henderson SO. Bedside echocardiography by emergency physicians. Ann Emerg Med. 2001;38(4):377-82. [CrossRef] [PubMed] 
11. Schleder S, Dittmar M, Poschenrieder F, et al. Diagnosis of pericardial effusion with a new generation hand-carried ultrasound device in cardiothoracic intensive care unit patients. Acta Radiol. 2012;53(10):1133-6. [CrossRef] [PubMed]
12. Blaivas M. Incidence of pericardial effusion in patients presenting to the emergency department with unexplained dyspnea. Acad Emerg Med. 2001;8(12):1143-6. [CrossRef] [PubMed] 
13. Nagdev A, Stone MB. Point-of-care ultrasound evaluation of pericardial effusions: does this patient have cardiac tamponade? Resuscitation. 2011;82(6):671-3. [CrossRef] [PubMed] 
14. Goodman A, Perera P, Mailhot T, Mandavia D. The role of bedside ultrasound in the diagnosis of pericardial effusion and cardiac tamponade. J Emerg Trauma Shock. 2012;5(1):72-5. [CrossRef] [PubMed]
15. Hu K, Liu D, Niemann M, et al. Methods for assessment of left ventricular systolic function in technically difficult patients with poor imaging quality. J Am Soc Echocardiogr. 2013;26(2):105-13. [CrossRef] [PubMed] 
16. Marwick TH. Techniques for comprehensive two dimensional echocardiographic assessment of left ventricular systolic function. Heart. 2003;89 Suppl 3:iii2-8. [CrossRef] [PubMed] 
17. Silverstein JR, Laffely NH, Rifkin RD. Quantitative estimation of left ventricular ejection fraction from mitral valve E-point to septal separation and comparison to magnetic resonance imaging. Am J Cardiol. 2006;97(1):137-40. [CrossRef] [PubMed] 
18. Lehmann KG, Johnson AD, Goldberger AL. Mitral valve E point-septal separation as an index of left ventricular function with valvular heart disease. Chest. 1983;83(1):102-8. [CrossRef] [PubMed] 
19. Ahmadpour H, Shah AA, Allen JW, Edmiston WA, Kim SJ, Haywood LJ. Mitral E point septal separation: a reliable index of left ventricular performance in coronary artery disease. Am Heart J. 1983;106(1 Pt 1):21-8. [CrossRef]
20. Secko MA, Lazar JM, Salciccioli LA, Stone MB. Can junior emergency physicians use E-point septal separation to accurately estimate left ventricular function in acutely dyspneic patients? Acad Emerg Med. 2011;18(11):1223-6. [CrossRef] [PubMed] 
21. Weekes AJ, Reddy A, Lewis MR, Norton HJ. E-point septal separation compared to fractional shortening measurements of systolic function in emergency department patients: prospective randomized study. J Ultrasound Med. 2012;31(12):1891-7. [PubMed] 
22. Weekes AJ, Tassone HM, Babcock A, et al. Comparison of serial qualitative and quantitative assessments of caval index and left ventricular systolic function during early fluid resuscitation of hypotensive emergency department patients. Acad Emerg Med. 2011;18(9):912-21. [CrossRef] [PubMed] 
23. Randazzo MR, Snoey ER, Levitt MA, Binder K. Accuracy of emergency physician assessment of left ventricular ejection fraction and central venous pressure using echocardiography. Acad Emerg Med. 2003;10(9):973-7. [CrossRef] [PubMed] 
24. Moore CL, Rose GA, Tayal VS, Sullivan DM, Arrowood JA, Kline JA. Determination of left ventricular function by emergency physician echocardiography of hypotensive patients. Acad Emerg Med. 2002;9(3):186-93. [CrossRef] [PubMed] 
25. Vincent JL, Sakr Y, Sprung CL, et al. Sepsis in European intensive care units: results of the SOAP study. Crit Care Med. 2006;34(2):344-53. [CrossRef] [PubMed] 
26. Rosenberg AL, Dechert RE, Park PK, Bartlett RH. Review of a large clinical series: association of cumulative fluid balance on outcome in acute lung injury: a retrospective review of the ARDSnet tidal volume study cohort. J Intensive Care Med. 2009;24(1):35-46. [CrossRef] [PubMed] 
27. Stewart RM, Park PK, Hunt JP, et al. Less is more: improved outcomes in surgical patients with conservative fluid administration and central venous catheter monitoring. J Am Coll Surg. 2009;208(5):725-35; discussion 735-37. [CrossRef] [PubMed]
28. Boyd JH, Forbes J, Nakada TA, Walley KR, Russell JA. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med. 2011;39(2):259-65. [CrossRef] [PubMed] 
29. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368-77. [CrossRef] [PubMed] 
30. Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med. 2004;32(3):691-9. [CrossRef] [PubMed] 
31. Osman D, Ridel C, Ray P, et al. Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge. Crit Care Med. 2007;35(1):64-8. [CrossRef] [PubMed] 
32. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134(1):172-8. [CrossRef] [PubMed] 
33. Berkenstadt H, Margalit N, Hadani M, et al. Stroke volume variation as a predictor of fluid responsiveness in patients undergoing brain surgery. Anesth Analg. 2001;92(4):984-9. [CrossRef] [PubMed] 
34. Barbier C, Loubieres Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med. 2004;30(9):1740-6. [CrossRef] [PubMed] 
35. Feissel M, Michard F, Faller JP, Teboul JL. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intensive Care Med. 2004;30(9):1834-7. [CrossRef] [PubMed] 
36. Kramer A, Zygun D, Hawes H, Easton P, Ferland A. Pulse pressure variation predicts fluid responsiveness following coronary artery bypass surgery. Chest. 2004;126(5):1563-8. [CrossRef] [PubMed] 
37. Michard F, Lopes MR, Auler JO, Jr. Pulse pressure variation: beyond the fluid management of patients with shock. Crit Care. 2007;11(3):131. [CrossRef] [PubMed]
38. Cannesson M. Arterial pressure variation and goal-directed fluid therapy. J Cardiothorac Vasc Anesth. 2010;24(3):487-497. [CrossRef] [PubMed]
39. Moretti R, Pizzi B. Inferior vena cava distensibility as a predictor of fluid responsiveness in patients with subarachnoid hemorrhage. Neurocritical Care. 2010;13(1):3-9. [CrossRef] [PubMed] 
40. Maguire S, Rinehart J, Vakharia S, Cannesson M. Technical communication: respiratory variation in pulse pressure and plethysmographic waveforms: intraoperative applicability in a North American academic center. Anesth Analg. 2011;112(1):94-6. [CrossRef] [PubMed] 
41. Michard F, Teboul JL. Using heart-lung interactions to assess fluid responsiveness during mechanical ventilation. Crit Care. 2000;4(5):282-289. [CrossRef] [PubMed]
42. Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med. 2000;162(1):134-8. [CrossRef] [PubMed]
43. Scheuren K, Wente MN, Hainer C, et al. Left ventricular end-diastolic area is a measure of cardiac preload in patients with early septic shock. Eur J Anaesthesiol. 2009;26(9):759-65. [CrossRef] [PubMed]
44. Vincent JL. Intensive Care Medicine: Annual Update 2008. 1 ed: Springer; 2008.
45. Levitov A, Marik PE. Echocardiographic assessment of preload responsiveness in critically ill patients. Cardiol Res Prac. 2012;2012:819696. [CrossRef] [PubMed]
46. Slama M, Masson H, Teboul JL, et al. Respiratory variations of aortic VTI: a new index of hypovolemia and fluid responsiveness. Am J Physiol Heart Circ Physiol. 2002;283(4):H1729-1733. [PubMed]
47. Lewis JF, Kuo LC, Nelson JG, Limacher MC, Quinones MA. Pulsed Doppler echocardiographic determination of stroke volume and cardiac output: clinical validation of two new methods using the apical window. Circulation. 1984;70(3):425-31. [CrossRef] [PubMed]
48. Dinh VA, Ko HS, Rao R, et al. Measuring cardiac index with a focused cardiac ultrasound examination in the ED. Am J Emerg Med. 2012;30(9):1845-51. [CrossRef] [PubMed] 
49. Cannesson M, Tran NP, Cho M, Hatib F, Michard F. Predicting fluid responsiveness with stroke volume variation despite multiple extrasystoles. Crit Care Med. 2012;40(1):193-8. [CrossRef] [PubMed] 
50. Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echocardiogr. 2009;22(2):107-33. [CrossRef] [PubMed] 
51. Ommen SR, Nishimura RA. A clinical approach to the assessment of left ventricular diastolic function by Doppler echocardiography: update 2003. Heart. 2003;89 Suppl 3:iii18-23. [CrossRef] [PubMed]
52. Unluer EE, Bayata S, Postaci N, et al. Limited bedside echocardiography by emergency physicians for diagnosis of diastolic heart failure. Emerg Med J. 2012;29(4):280-3. [CrossRef] [PubMed] 
53. Kerwin C, Tommaso L, Kulstad E. A brief training module improves recognition of echocardiographic wall-motion abnormalities by emergency medicine physicians. Emerg Med Int. 2011;2011:483242. [CrossRef] [PubMed]
54. Haddad F, Hunt SA, Rosenthal DN, Murphy DJ. Right ventricular function in cardiovascular disease, part I: Anatomy, physiology, aging, and functional assessment of the right ventricle. Circulation. 2008;117(11):1436-48. [CrossRef] [PubMed] 
55. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography. J Am Soc Echocardiogr. 2010;23(7):685-713; quiz 786-8. [CrossRef] [PubMed]
56. Doutreleau S, Talha S, Di Marco P, Lebourg F, Rouyer O, Geny B. Does tricuspid annular plane systolic excursion (TAPSE) or systolic velocity (Sm) allow an easier determination of right ventricular function after heart transplantation? J Heart Lung Transplant. 2007;26(3):302-303. [CrossRef] [PubMed]
57. Tousignant C, Kim H, Papa F, Mazer CD. Evaluation of TAPSE as a measure of right ventricular ouptut. Can J Anaesth. 2012;59(4):376-383. [CrossRef] [PubMed]  
58. Piazza G, Goldhaber SZ. The acutely decompensated right ventricle: pathways for diagnosis and management. Chest. 2005;128(3):1836-52. [CrossRef] [PubMed] 
59. Haddad F, Doyle R, Murphy DJ, Hunt SA. Right ventricular function in cardiovascular disease, part II: pathophysiology, clinical importance, and management of right ventricular failure. Circulation. 2008;117(13):1717-31. [CrossRef] [PubMed] 
60. Chin KM, Kim NH, Rubin LJ. The right ventricle in pulmonary hypertension. Coronary artery disease. 2005;16(1):13-8. [CrossRef] [PubMed] 
61. Giusca S, Jurcut R, Ticulescu R, et al. Accuracy of handheld echocardiography for bedside diagnostic evaluation in a tertiary cardiology center: comparison with standard echocardiography. Echocardiography. 2011;28(2):136-41. [CrossRef] [PubMed]
62. Riley DC, Cordi HP. Emergency department diagnosis of mitral stenosis and left atrial thrombus using bedside ultrasonography. Acad Emerg Med. 2010;17(5):e30-1. [CrossRef] [PubMed] 
63. Sautner J, Budhram G. Diagnosis of acute mitral valve insufficiency using emergency bedside echocardiography. Acad Emerg Med. 2009;16(7):685-6. [CrossRef] [PubMed] 
64. Seif D, Meeks A, Mailhot T, Perera P. Emergency department diagnosis of infective endocarditis using bedside emergency ultrasound. Crit Ultrasound J. 2013;5(1):1. [CrossRef] [PubMed] 

Corresponding Author: 

Jarrod M. Mosier, MD

Assistant Professor

Department of Emergency Medicine

Department of Medicine, Section of Pulmonary, Critical Care, Allergy and Sleep

University of Arizona

1609 N Warren

FOB 122C

Tucson, Az 85719

Phone: 775-527-1292

Fax: 520-626-2480

jmosier@aemrc.arizona.edu

Disclosures: None for any authors

Reference as: Mosier JM, Stolz L, Bloom J, Malo J, Snyder L, Fiorello A, Adhikari S. Resuscitative EChocardiography for the Evaluation and management of Shock: The RECES protocol. Southwest J Pulm Crit Care. 2014;8(2):110-25. doi: http://dx.doi.org/10.13175/swjpcc177-13 PDF

Ultrasound for Critical Care Physicians: Dyspnea

A 62 year old man with metastatic melanoma presented to the Emergency Department with dyspnea, hypoxemia, and tachycardia. A bedside ultrasonography was performed (Figure 1).

Figure 1. Four chamber view of the beside ultrasonography

Which of the following diagnosis is most compatible with the ultrasound findings? (Click on the correct answer to proceed to the next panel)

1. Cardiac thrombus
2. Cardiogenic shock
3. Mitral stenosis
4. Pericardial effusion
5. Pulmonary embolism

Reference as: Thompson MJ. Ultrasound for critical care physicians: dyspnea. Southwest J Pulm Crit Care. 2014;8(2):96-8. doi: http://www.dx.doi.org/10.13175/swjpcc009-14 PDF

February 2014 Critical Care Case of the Month: A Rush of Blood

Maja Udovcic MD

Sudheer Penupolu MD

Robert W. Viggiano MD

Lewis J. Wesselius MD

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

History of Present Illness

A 51 year old African-American woman was admitted from the emergency department with hemoptysis. She had blood tinged sputum earlier in the day followed by about ½ cup of hemoptysis which led her to seek care.

PMH, SH, FH

She is known to have stage IV sarcoidosis with bronchiectasis and cavitation. A right upper lobectomy was performed in 1996 and embolization of  

3 left bronchial arteries in 2011 for hemoptysis. She has a history of anaphylaxis with iodinated radiocontrast dye. However, no reaction occurred with premedication in 2011. She also has a history of asthma, but has been out of her medications for several days. Since this time she has noted increased cough. She is a nonsmoker and a Jehovah’s Witness. Her family history is noncontributory.

Medications

• Albuterol HFA
• Montelukast
• Fluticasone propionate nasal spray
• Loratidine

Physical Examination

VS:  36.9°C, 106 beats/min, 135/83 mm Hg, 26 breaths/min, SpO2 100% on room air

General: She is in no acute distress.  

Respiratory: coarse breath sounds with scattered wheezing, inspiratory crackles, and diminished air movement throughout

Which of the following laboratory tests should be ordered? (click on correct answer to move to next panel)

1. Blood urea nitrogen
2. Coagulation profile (PT, INR, APTT)
3. Complete blood count
4. 2 + 3
5. All of the above

Reference as: Udovcic M, Penupolu S, Viggiano RW, Wesselius LJ. February 2014 critical care case of teh month: a rush of blood. Southwest J Pulm Crit Care. 2014:8(2):79-87. doi: http://dx.doi.org/10.13175/swjpcc165-13 PDF

Ultrasound for Critical Care Physicians: Hypotension

A 68 year old man is transferred to the intensive care unit because of hypotension. An ultrasound of the heart and inferior vena cava (IVC) were performed (Figure 1).

Figure 1. Upper panel: subxiphoid view of heart. Lower panel: inferior vena cava.

What is the cause of the hypotension? (Click on the correct answer)

1. Cardiogenic shock secondary to cardiomyopathy
2. Intracardiac thrombus
3. Intravascular volume depletion
4. Massive pulmonary embolism
5. Pericardial effusion

Reference as: Mosier JM. Ultrasound for critical care physicians: hypotension. Southwest J Pulm Crit Care. 2013;8(1):41-3. doi: http://dx.doi.org/10.13175/swjpcc176-13 PDF

January Critical Care Case of the Month: Bad Cough

Bhupinder Natt MD

Linda Snyder MD

Janet Campion MD

University of Arizona Medical Center

Tucson, AZ

History of Present Illness

A 41 year-old man was admitted with a five-day history of cough, shortness of breath, and fever to 102° F. He was recently diagnosed with a high-grade astrocytoma of the brain and had undergone resection followed by chemotherapy with temozomide (an alkylating agent) and radiation therapy. 

PMH

• Renal transplantation (1993)
• Glioblastoma (astrocytoma grade 4)
• Crohn’s disease treated with budesonide and meselamine

Medications

• Dexamethasone 2 mg PO BID
• Keppra 500 mg PO BID
• Tacrolimus 1.5 mg PO AM and 1mg PO PM
• Mycophenolate 750 mg PO BID
• Budesonide 3 mg PO daily
• Meselamine 1600 mg PO TID
• Sulfamethoxazole/trimethoprim DS PO on Mon/Wed/Fri
• Temozolomide 75 mg IM with radiotherapy

Social History

Nonsmoker, no ethanol or recreational drugs, no recent travel, and no occupational exposures.

Physical Examination

T 38.6°C, P 112 beats/min, RR 32-40 breaths/min, BP 119/76 mm Hg, SpO2 100% on NRB

General: Fatigued, ill appearing and dyspneic.

Skin: No rash or lesions, well-healed craniotomy scar

HEENT: Dry oral mucosa, pupils and extra-ocular muscles normal

Respiratory: Reduced breath sounds, fine crackles throughout all lung fields, no wheezing

CVS: Hyperdynamic precordium, tachycardia without murmur, no elevation of jugular venous pressure (JVP), peripheral vascular exam normal.

Abdomen: Soft, non-distended, no hepato-splenomegaly, normal bowel sounds.

Lymph: No cervical lymphadenopathy

Extremities: No edema, normal muscle bulk and tone.

Laboratory

WBC 11 X 10³/µL, Hemoglobin 9.8 g/dL, Hematocrit 30%, Platelets 264,000/ µL

Na⁺ 135 meq/L, K⁺ 4.2 meq/L, Cl⁻ 111 meq/L, CO2 14 mmol/L, blood urea nitrogen (BUN) 46 mg/dL, creatinine 1.7 mg/dL, glucose 132 mg/dL, calcium 10.5 mg/dL, albumin 1.5 g/dL, liver function tests-within normal limits

Prothrombin time (PT) 15 sec, international normalized ratio (INR) 1.2, partial thromboplastin time (PTT) 29.9 sec

Chest X-ray

Figure 1. Admission PA (Panel A) and lateral (Panel B) chest x-ray.

What is the best description of the chest x-ray? (click on correct answer to move to next panel)

1. Bibasilar consolidation
2. Bilateral diffuse nodules
3. Pneumomediastinum with subcutaneous emphysema
4. Pulmonary edema with evidence of pulmonary hypertension
5. Subdiaphragmatic free air

Reference as: Natt B, Snyder L, Campion J. January critical care case of the month: bad cough. Southwest J Pulm Crit Care. 2014;8(1):20-6. doi: http://dx.doi.org/10.13175/swjpcc161-13 PDF

Ultrasound for Critical Care Physicians: Unique

A 22-year-old man is seen for shortness of breath. Cardiac ultrasound / echocardiography is performed (Figure 1).

Figure 1. Cardiac ultrasound.

Which of the following best describes the ultrasound? (click on correct answer to move to next panel)

1. Enlarged left atrium
2. Enlarged left ventricle
3. Enlarged right atrium
4. Enlarged right ventricle
5. Normal

Reference as: Gotway MB. Ultrasound for critical care physicians: unique. Southwest J Pulm Crit Care. 2013;7(6):336-7. doi: http://dx.doi.org/10.13175/swjpcc148-13 PDF

December 2013 Critical Care Case of the Month: I Don’t Have a Drinking Problem

Robert Raschke MD

Elijah Poulos MD

Adam Bosak MD

Critical Care Medicine

Banner Good Samaritan Medical Center

Phoenix, AZ

History of Present Illness

A 69-year-old male retired diabetic police officer was admitted to the ICU with intractable vomiting, severe abdominal pain and acute blindness. About a week prior, he suffered urinary frequency and was prescribed ciprofloxacin at urgent care with a presumptive diagnosis of urinary tract infection.  Over the course of the week his urinary frequency resolved and he became anuric, he developed progressively worsening nausea and eventually vomiting to the point that he was unable to keep anything down, and severe bilateral lower abdominal and pelvic pain.    His wife and son actually forced him into the ER when he became blind the day of admission. He denied fever, dysuria, cough and headache.   In our emergency room he was noted to be in moderate distress with tachycardia, tachypnea, hyperpnoea and completely blind in both eyes unable to discern even simple shadows.

PMH, SH, FH

The patient is a retired police officer with a past medical history of diabetes mellitus and benign prostatic hypertrophy.  The patient denied alcohol, tobacco, or illicit drug use. He works out at a local gym almost daily since being diagnosed with diabetes a couple of years ago.

Medications

• Glipizide
• Metformin
• Tamsulosin

Physical Exam

Blood pressure160/95 mmHg with a heart rate of 110, respiratory rate 35, SpO2 99% on 2 lpm nasal cannula, and temp 36.0° C.  He appeared uncomfortable and moderately distressed, lethargic but arousable with GCS 13. He was able to briefly answer simple questions. His eyes were conjugate, but did not track nor fix on objects placed in front of his eyes, and he could vaguely discern the light of a bright flashlight shined into both eyes. His pupils were 3-4 mm and fixed, with no light reflex elicitable, even with magnified examination of the pupil using an ophthalmoscope.  On fundoscopic exam his discs were flat, and there were no hemorrhages or other lesions seen.  He was tachycardic but regular with normal heart tones, and a bedside echocardiogram showed good left ventricular function.  He had Kussmaul breathing with an odor of ketones and clear lungs. The lower abdomen was distended and tender, and a Foley catheter insertion returned 2 liters of yellow urine which resolved his abdominal pains.  He had no peripheral edema and his hands were cool.  The rest of his physical examination was unremarkable.

Laboratory Evaluation

Initial laboratory evaluation included a white blood count 24.3 K/mm3 with 79% segmented neutrophils and no bands, hemoglobin 14.7 g/dL; sodium 138 mmol/L;  potassium 5.1 mmol/L; chloride 92 mmol/L; and CO₂ 4 mmol/L, yielding an anion gap of 44 when corrected.  His BUN was 116 mg/dL; creatinine of 7.7 mg/dL.  A venous blood gas showed a pH 6.77 pCO₂ 17 mmHg; pO₂ 73 mmHg; bicarbonate of 3 mmol/L. Urinalysis showed negative leukocyte esterase, 1-5 leukocytes per HPF, glycosuria and ketonuria.

Radiology Evaluation

Admission chest x-ray is in Figure 1. 

Figure 1. Admitting chest radiograph.

Computerized tomography of the abdomen showed no urinary tract obstruction (was performed after the Foley catheter was placed) and no other significant findings. Piperacillin/tazobactam and gentamicin were started for possible urinary tract infection with sepsis.

Which of the following is the best fits the clinical presentation explaining both his metabolic abnormalities and blindness? (click on correct answer to move to next panel)

1. Acute renal failure
2. Alcoholic ketoacidosis
3. Diabetic ketoacidosis
4. Ethylene glycol ingestion
5. Methanol ingestion

Reference as: Raschke RA, Poulos E, Bosak A. December 2013 critical care case of the month: I don't have a drinking problem. Southwest J Pulm Crit Care. 2013;7(6):328-35. doi: http://dx.doi.org/10.13175/swjpcc141-13 PDF

Ultrasound for Critical Care Physicians: Atypical Headache

A 76 year old woman presented with complaints of a new onset of headache especially on the right. Brain CT scan and MRI were unremarkable. Her erythrocyte sedimentation rate was markedly elevated. An ultrasound of the chest was performed (Figures 1 and 2).

Figure 1. Long axis view through the aortic valve area (movie has been slowed).

Figure 2. Transverse view through the aorta (movie has been slowed).

What does the ultrasound show?

1. Aortic aneurysm
2. Aortic insufficiency
3. Aortic stenosis
4. Aortic wall thickening
5. 1 and 2
6. 1 and 4
7. 2 and 4

Reference as: Gotway MB. Ultrasound for critical care physicians: atypical headache. Southwest J Pulm Crit Care. 2013;7(5):289-90. doi: http://dx.doi.org/10.13175/swjpcc125-13 PDF

November 2013 Critical Care Case of the Month: A Series of Unfortunate Infections

Kenneth K. Sakata, MD

Karen L. Sapienza, MD

Lewis J. Wesselius, MD 

Department of Pulmonary Medicine

Mayo Clinic Arizona

Scottsdale, AZ

History of Present Illness

A 22 year old man was admitted with fever for 2 weeks. He had a history of acute lymphocytic leukemia (ALL) and had received a stem cell transplant in (SCT) in May 2013.

PMH, SH, FH

Other than the ALL and STC transplant there was no significant PMH, SH, or FH. The STC was uneventful.

Physical Examination

T 38.6°C with a pulse of 110 beats/min. Otherwise the physical examination was unremarkable.

CT scan

A CT scan of the thorax was performed in a search for the source of the fever (Figure 1).

Figure 1. Admission thoracic CT scan showing an abnormality. The remainder of the CT scan was unremarkable.

Which of the following best describes the CT abnormality?

1. Chest wall abnormality in the left chest
2. Focal area of consolidation in the left lung
3. Focal area of consolidation in the right lung
4. Mass in the left lung
5. Mass in the right lung

Reference as: Sakata KK, Sapienza KL, Wesselius LJ. November 2013 pulmonary case of the month: a series of unfortunate infections. Southwest J Pulm Crit Care. 2013;7(5):280-8. doi: http://dx.doi.org/10.13175/swjpcc139-13 PDF

Fat Embolism Syndrome: Improved Diagnosis Through the Use of Bedside Echocardiography

Douglas T. Summerfield, MD

Kelly Cawcutt, MD

Robert Van Demark, MD

Matthew J. Ritter, MD

Departments of Anesthesia and Pulmonary/Critical Care Medicine

Mayo Clinic

Rochester, MN

Case Report

A 77 year old female with a past medical history of dementia, chronic atrial fibrillation requiring anticoagulation, hypertension, biventricular congestive heart failure with a preserved left ventricular ejection fraction, pulmonary hypertension, and chronic obstructive pulmonary disease (COPD) presented to the emergency room after she sustained a ground level fall while sitting in a chair. The patient reportedly fell asleep while sitting at the kitchen table, and subsequently fell to her right side. According to witnesses, she did not strike her head, and there was no observed loss of consciousness. As part of her initial evaluation, at an outside hospital, radiographs of the pelvis, hip, and knee were obtained. These identified a definitive right superior pubic ramus fracture with inferior displacement and a questionable fracture of the right femoral neck. Shortly thereafter, the patient was transferred to our hospital for further management. On exam, the patient had a painful right hip limiting active motion and her right lower extremity was neurovascularly intact without paresthesias or dysesthesias. The remainder of the exam was unremarkable. In the emergency room, a repeat radiograph showed no evidence of a right femur fracture. Later in the evening a CT scan of the pelvis with intravenous contrast showed acute fractures through the right superior and inferior pubic rami with associated hematoma. Multiple tiny bony fragments were noted adjacent to the superior pubic ramus fracture (Figure 1).

Figure 1. CT scan demonstrating acute fractures through the superior and inferior pubic rami with associated hematoma. Multiple tiny bone fragments are adjacent to the superior pubic ramus fracture.

The CT did not show an apparent femur fracture. MRI of the pelvis and hip were ordered to assess for a femoral fracture; however this was not obtained secondary to patient confusion thus no quality diagnostic images were produced. The orthopedic service concluded that surgery was not required for the stable, type 1 lateral compression injury that resulted from the fall.

The patient was admitted to a general medicine floor for non-surgical management which included weight bearing as tolerated as well as therapy with physical medicine and rehabilitation. On admission, her vital signs were stable, including a heart rate of 89, blood pressure of 159/89, respirations of 20, with the exception of her peripheral oxygen saturation which was 89% on room air. Over the next several hospital days, she continued to have low oxygen saturations, began requiring fluid boluses to maintain an adequate mean arterial blood pressure (secondary to systolic blood pressure falling to the 70-80mmHg range intermittently) and she developed acute kidney injury with her creatinine increasing to 4.2 from her baseline of 1.1.  Nephrology was consulted to evaluate the acute kidney injury and their impression was acute renal failure secondary to contrast administration for the initial CT scan, in the setting of chronic spironolactone and furosemide use. The patient’s mental status remained altered, her speech although typically understandable was non-coherent, and she remained bed-bound. Due to her underlying dementia, her baseline mental status was difficult to determine and this combined with her opioids for pain control were felt to contribute to her mental status.

During her first dialysis session, the patient developed hypotension and hypoxemia which necessitated a rapid response call and transfer to the intensive care unit (ICU). The impression at the time of transfer to the ICU was septic shock with multi-organ dysfunction syndrome, presumably from a urinary source. The initial exam by the ICU team demonstrated what was thought to be considerable acute mental status change with agitation and moaning, hypotension, hypoxemia, and continued renal failure. Further review of her hospital course revealed that these changes had slowly been progressing since admission. Stabilization in the ICU included placement of a right internal jugular central venous catheter, blood pressure support with vasopressors, as well as intubation and high level of ventilatory support, including inhaled alprostadil, for severe hypoxemic respiratory failure. In addition, she was also placed on continuous renal replacement therapy.

In order to better assess the patient’s fluid status, the service fellow assessed the vena cava with the bedside ultrasound. While observing the collapsibility of the IVC, small hyperechoic spheres were observed traveling through the IVC proximally towards the right heart. A subcostal window focusing on the right ventricle demonstrated the same hyperechoic spheres whirling within the right ventricle. These same spheres were seen in both the four chamber view (Figure 2), as well as the short axis view and were present for several hours.

Figure 2. Four chambered view revealing right ventricular bowing as well as small hyperechoic spheres present in the right ventricle and atria.

Two hours later, a formal bedside echocardiogram was performed to evaluate the right heart structure and function. The estimated right ventricular systolic pressure was at 70 mm Hg, indicating severe pulmonary hypertension. The right ventricle was enlarged, and there was severe tricuspid regurgitation. Again there continued to be small hyperechoic spheres within her right ventricle as well as her right atria. Per the formal cardiologist reading, these were consistent with fat emboli. Further laboratory evaluation, including the presence of urinary fat, helped confirm the diagnosis of fat emboli syndrome.

Supportive care was continued, but without obvious improvement. After a family care conference, she was transitioned to palliative care and died.

Background

Fat emboli (FE) and fat emboli syndrome (FES) have been described clinically and pathologically since the 1860’s. Early work by Zenker in 1862 first described the pathologic significance of fat embolism with the link of fat to bone marrow release during fractures was discovered by Wagner in 1865. Despite the 150 years since its discovery, the diagnosis of Fat Embolism remains elusive. FE is quite common with the presence of intravascular pulmonary fat seen in greater than 90% of patients with skeletal trauma at autopsy (1). However, the presence of pulmonary fat alone does not necessarily mean the patient will develop FES. In a case series of 51 medical and surgical ICU patients, FE was identified in 28 (51%) of patients, none of whom had classic manifestations of FES (2).

The three major components of FES have classically consisted of the triad of petechial rash, progressive respiratory failure, and neurologic deterioration. The incidence following orthopedic procedures ranges from 0.25% to 35% (3). The wide variation of the reported incidence may in part be due to the fact that FES can affect almost every organ system and the classic symptoms are only present either transiently or in varying degrees, and may not manifest for 12-72 hours after the initial insult (4). The patient we present represents both the lack of the classic triad and the delayed onset of signs and symptoms, illustrating the elusiveness of the diagnosis.

Of the major clinical criteria, the cardio-pulmonary symptoms are the most clinically significant. Symptoms occur in up to 75% of patients with FES and range from mild hypoxemia to ARDS and/or acute cor pulmonale. The timing of symptoms may coincide with manipulation of a fracture, and there have been numerous reports of this occurring intraoperatively with direct visualization of fat emboli seen on trans-esophageal echo (TEE) (5-8).

The classic petechial rash, which was not noted in our patient, is typically seen on the upper anterior torso, oral mucosa, and conjunctiva. It is usually resolved within 24 hours and has been attributed to dermal vessel engorgement, endothelial fragility, and platelet damage all from the release of free fatty acids (9). The clinical manifestation of this “classic” finding varies widely and has been reported in 25-95% of the cases (4, 10).

Neurologic dysfunction can range from headache to seizure and coma and is thought to be secondary to cerebral edema due to multifactorial insults. These neurologic changes are seen in up to 86% of patients, and on MRI produce multiple small, non-confluent hyper intensities that appear within 30 minutes of injury. The number and size correlate to GCS, and subsequently reversal of the lesions is seen during neurologic recovery. (11,12).

Temporary CNS dysfunction usually occurs 24-72 hours after initial injury and acute loss of consciousness immediately post-operatively has been documented. Of note, this loss of consciousness may not be a catastrophic event. In a case report by Nandi et al., a patient with acute loss of consciousness made full neurologic recovery within four hours (13). In the retina, direct evidence of FE and FES manifests as cotton-wool spots and flame-like hemorrhages (1). However these findings are only detected in 50% of patient with FES (14)

FES also affects the hematological system, producing anemia and thrombocytopenia 37% and 67% of the time, respectively (15, 16). Thrombocytopenia is correlated to an increased A-a gradient, which Akhtar et al. noted that some clinicians include this finding in the criteria to diagnose FES (1).

Diagnosis

Given the broad and varying manifestations of FES, others have broadened the criteria. The Lindeque criteria require a femur fracture. The FES Index is a scoring system which includes vitals, radiographic findings, and blood gas results. Weisz and colleagues include laboratory values such as fat macroglobulenemia and serum lipid changes. Miller and colleagues (17) even proposed an autopsy diagnosis using histopathic samples. The most widely used criteria are set forth by Gurd and Wilson and require two out of three major criteria be met, or one major plus four out of five minor criteria. Major criteria include pulmonary symptoms, petechial rash, and neurological symptoms. Minor criteria include pyrexia, tachycardia, jaundice, platelet drop by >50%, elevated ESR, retinal changes, renal dysfunction, presence of urinary or sputum fat, and fat macroglobulinemia (1). Of note, none of the proposed diagnostic criteria include direct visualization of fat emboli via ultrasound or echocardiography (18-22) (Table 1).

Table 1: Gurd's Criteria for Diagnosis of FES

Gurd AR. Fat embolism: an aid to diagnosis. J Bone Joint Surg Br. 1970;52(4):732-7. [PubMed]

Mechanism

Two theories explain the systemic symptoms seen in FES. The mechanical theory describes how intramedullary free fat is released into the venous circulation directly from the fracture site or from increased intramedullary pressure during an orthopedic procedure. The basis for the theory is that the fat particles produce mechanical obstruction. However, not all fat emboli translocated into the circulation are harmful. It is estimated that fat particles larger than 8 μm embolize (23-25). As they accumulate in the lungs, aggregates larger than 20 μm occlude the pulmonary vasculature (26). Particles 7-10 μm particles can cross pulmonary capillary beds to affect the skin, brain, and kidneys. On a larger scale, the embolized free fatty acids produce ischemia and the subsequent release of inflammatory markers (27). The mechanism of this systemic spread beyond the pulmonary capillaries is not well understood. Patients without a patent foramen ovale or proven pulmonary shunt develop FES (28). Interestingly enough, other patients with a large fat emboli burden in the pulmonary microvasculature have not progressed to FES (29). One possible explanation for this may be elevated right-sided pressures force pulmonary fat into systemic circulation (1).

The biochemical theory has also been proposed to explain the systemic organ damage. The mechanism describes that enzymatic degradation of fat particles in the blood stream brings about the release of free fatty acids (FFA) (30, 31). FFA and the toxic intermediaries then cause direct injury on the lung and other organs. The fact that many of the symptoms are seen much later than the initial injury would support the Biochemical Theory. This theory also has an obstructive component to it as it recognizes that large fat particles coalesce to obstruct pulmonary capillary beds (11).

Discussion

Fat emboli syndrome is a rare and difficult clinical diagnosis. Currently there is no diagnostic test for FES and even the reported incidence is quite variable. The wide clinical presentation of FES makes the diagnosis challenge, and classic pulmonary involvement does not always occur (31). Furthermore, the symptoms overlap with other illness such as infection, as it did in this patient who was initially thought to be septic. The delayed onset of symptoms may further confound its identification. Finally, the traditional criteria used to diagnosis FES are variable depending on which source is referenced. Case-in-point is the Lindque criteria which require the presence of a femur fracture. By this requirement the patient presented in this case would not have been diagnosed with FES as she presented with a pelvic fracture.

The patient in this case was likely suffering from undiagnosed FES from the time of her admission. Since it did not present in the classic fashion, her progressive respiratory failure and neurologic deterioration were incorrectly attributed to congestive heart failure and opioid administration.

In this patient, the diagnosis of FE was somewhat unexpected, although it was within the differential. For this case the implementation of bedside ultrasound proved critical to the correct diagnosis and subsequent outcome. Instead of following other possible diagnoses and treatment options such as sepsis in this tachycardic, hypotensive patient, supportive care was employed with the diagnosis of fat embolism in mind.

The use of ultrasound imaging is not well studied for the diagnosis of FES, however it may provide an additional tool for making this difficult diagnosis when the classic triad of rash, cardiopulmonary symptoms, and neurologic changes is not seen or is in doubt. When used to evaluate for cardiogenic causes of acute hypotension, bedside cardiac ultrasound may reveal findings suggestive of FES, as it did in this case.

Review of the literature (5-8) confirms similar echogenic findings from fat emboli as seen by TEE intraoperatively during orthopedic procedures. However, similar spheres can be seen in a number of other instances. Infusion of blood products, such as packed red blood cells, may create similar acoustic images. No blood products had been given to the patient at the time of the bedside ultrasound. Additionally cardiologists have traditionally used agitated saline to look for patent foramen ovale. This and air embolism after placement of a central venous catheter can both produce similar images. In this case the emboli were seen traveling through the inferior vena cava, inferior and distal to the right side of the heart. The right internal jugular catheter would not have showered air emboli to that location, additionally once these were seen circulating in the right ventricle, the first action performed was to ensure all ports on the central line were secure. Given that these hyperechoic spheres were present for hours, air emboli would be less likely to be the underlying etiology. The images were later seen during the formal cardiac echo, and again validated by the cardiologist as being consistent with fat emboli.

To our knowledge this is the first case report of critical care bedside echocardiography (BE), assisting with the diagnosis of fat emboli syndrome. This is in contrast to TEE which has been used to diagnose FE and presumed FES in hemodynamically unstable patients in the operating room (5-8).

BE is attractive as it requires less training than TEE and can be repeated at the bedside as the clinical picture changes. By itself BE cannot differentiate FE from FES, but since the practitioner using it is presumably familiar with the patient’s condition, it can be used to augment the diagnosis when other findings are also suggestive of FE.

It has been suggested that a basic level of expertise in bedside echocardiography can be achieved by the non-cardiologist in as little as 12 hours of didactic and hands-on teaching. Given this amount of training, the novice ultrasonographer should be able to identify severe left or right ventricular failure, pericardial effusions, regional wall motion abnormalities, gross valvular abnormalities, and volume status by assessing the size and collapsibility of the inferior vena cava (32-37). Potentially, based on this case, the list could include FE with FES in the correct clinical context, pending further clinical validation.

In conclusion, this is the first reported case of bedside ultrasonography assisting in the diagnosis of FES in the ICU. The case illustrates the diagnostic challenge of FE and FES and also highlights the potential utility of bedside ultrasonography as a diagnostic tool.

References

1. Akhtar S. Fat Embolism. Anesthesiology Clinics. 2009;27:533-50. [CrossRef] [PubMed] 
2. Gitin TA, Seidel T, Cera PJ, Glidewell OJ, Smith JL. Pulmonary microvascular fat: The significance? Critical Care Medicine. 1993;21(5):673-7. [CrossRef] [PubMed] 
3. Raza SS, Noheria A, Kesman RL. 21-year-old man with chest pain, respiratory distress, and altered mental status. Mayo Clin Proc. 2011;86(5):e29-e32. [CrossRef] [PubMed]
4. Capan LM, Miller SM, Patel KP. Fat embolism. Anesthesiol Clin North America. 1993;11:25–54.
5. Shine TS, Feinglass NG, Leone BJ, Murray PM. Transesophageal echocardiography for detection of propagating, massive emboli during prosthetic hip fracture surgery. Iowa Orthop J. 2010;30:211-4. [PubMed] 
6. Heinrich H, Kremer P, Winter H, Wörsdorfer O, Ahnefeld FW. Transesophageal 2-dimensional echocardiography in hip endoprostheses. Anaesthesist. 1985;34(3):118-23. [PubMed] 
7. Pell AC, Christie J, Keating JF, Sutherland GR. The detection of fat embolism by transoesophageal echocardiography during reamed intramedullary nailing. A study of 24 patients with femoral and tibialfractures. J Bone Joint Surg Br 1993; 75:921-5. [PubMed]
8. Christie J, Robinson CM, Pell AC, McBirnie J, Burnett R. Transcardiac echocardiography during invasive intramedullary procedures. J BoneJoint Surg Br 1995;77:450-5. [PubMed]
9. Pazell JA, Peltier LF. Experience with sixty-three patients with fat embolism. Surg Gynecol Obstet 1972;135(1):77–80. [PubMed] 
10. Gossling HR, Pellegrini VD Jr. Fat embolism syndrome: a review of the pathophysiology and physiological basis of treatment. Clin Orthop Relat Res. 1982;165:68–82. [PubMed] 
11. Shaikh N, Parchani A, Bhat V, Kattren MA. Fat embolism syndrome: Clinical and imaging considerations: Case report and review of literature. Indian J Crit Care Med. 2008;12(1):32-6. [CrossRef] [PubMed]
12. Butteriss DJ, Mahad D, Soh C, Walls T, Weir D, Birchall D. Reversible cytotoxic cerebral edema incerebral fat embolism. AJNR Am J Neuroradiol. 2006;27(3):620-3. [PubMed]
13. Nandi R, Krishna HM, Shetty N. Fat embolism syndrome presenting as sudden loss of consciousness. J Anaesthesiol Clin Pharmacol. 2010;26(4):549-50. [Pubmed]
14. Adams CB. The retinal manifestations of fat embolism. Injury. 1971;2(3):221-4. [CrossRef]
15. Mellor A, Soni N. Fat embolism. Anaesthesia. 2001;56:145-54. [CrossRef]
16. Bulger EM, Smith DG, Maier RV, Jurkovich GJ. Fat embolism syndrome. A 10-year review. Arch Surg. 1997;132:435-9. [CrossRef] [PubMed]  
17. Miller P, Prahlow JA. Autopsy diagnosis of fat emboli syndrome. Am J Forensic Med Pathol. 2011;32(3):291-9. [CrossRef] [PubMed] 
18. Gurd AR. Fat embolism: an aid to diagnosis. J Bone Joint Surg Br. 1970;52(4):732-7. [PubMed]
19. Gurd AR, Wilson RI. The fat embolism syndrome. J Bone Joint Surg Br 1974;56(3):408-16.
20. Weisz GM, Rang M, Salter RB. Posttraumatic fat embolism in children: review of the literature and of experience in the Hospital for Sick Children, Toronto. J Trauma. 1973;13:529-34. [CrossRef] [PubMed] 
21. Lindeque BG, Schoeman HS, Dommisse GF, Boeyens MC, Vlok AL. Fat embolism and the fat embolism syndrome. A double-blind therapeutic study. J Bone Joint Surg Br 1987;69(1):128-31. [PubMed] 
22. Schonfeld SA, Ploysongsang Y, DiLisio R, Crissman JD, Miller E, Hammerschmidt DE, Jacob HS. Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients. Ann Intern Med. 1983;99:438-43. [CrossRef] [PubMed] 
23. Pell AC, Hughes D, Keating J, Christie J, Busuttil A, Sutherland GR. Fulminating fat embolism syndrome caused by paradoxical embolism through a patent foramen ovale. N Engl J Med. 1993;329:926-9. [CrossRef] [PubMed] 
24. Argenziano M. The incidental finding of a patent foramen ovale during cardiac surgery: should it always be repaired? Anesth Analg. 2007;105:611-2. [CrossRef] [PubMed] 
25. Emson HE. Fat embolism studied in 100 patients dying after injury. J Clin Pathol. 1958;11(1):28-35. [CrossRef] [PubMed]
26. Batra P. The fat embolism syndrome. J Thorac Imaging. 1987;2(3):12–17. [CrossRef] [PubMed] 
27. Meyer N, Pennington WT, Dewitt D, Schmeling GJ. Isolated cerebral fat emboli syndrome in multiply injured patients: a review of three casesand the literature. J Trauma. 2007;63:1395-1402. [PubMed] 
28. Nijsten MW, Hamer JP, ten Duis HJ, Posma JL. Fat embolism and patent foramen ovale [letter]. Lancet 1989;1(8649):1271. [CrossRef]
29. Aoki N, Soma K, Shindo M, Kurosawa T, Ohwada T. Evaluation of potential fat emboli during placement of intramedullary nails after orthopedic fractures. Chest. 1998;113(1):178-81. [CrossRef] [PubMed] 
30. Talbot M, Schemitsch EH. Fat embolism syndrome: history, definition, epidemiology. Injury. 2006;37S:S3-S7. [CrossRef] [PubMed] 
31. Levy D. The fat embolism syndrome. A review. Clin Orthop Relat Res. 1990;261:281-6. [PubMed] 
32. Vignon P, Mücke F, Bellec F, Marin B, Croce J, Brouqui T, Palobart C, Senges P, Truffy C, Wachmann A, Dugard A, Amiel JB. Basic critical care echocardiography: Validation of a curriculum dedicated to noncardiologist residents. Crit Care Med. Apr 2011;39(4):636-42. [CrossRef] [PubMed] 
33. Vignon P, Dugard A, Abraham J, Belcour D, Gondran G, Pepino F, Marin B, François B, Gastinne H. Focused training for goal-oriented hand-held echocardiography performed by noncardiologist residents in the intensive care unit. Intensive Care Med. 2007;33(10):1795-99. [CrossRef] [PubMed] 
34. Manasia AR, Nagaraj HM, Kodali RB, Croft LB, Oropello JM, Kohli-Seth R, Leibowitz AB, DelGiudice R, Hufanda JF, Benjamin E, Goldman ME. Feasibility and potential clinical utility of goal-directed transthoracic echocardiography performed by noncardiologist intensivists using a small hand-carried device (SonoHeart) in critically ill patients. J Cardiothorac Vasc Anesth. 2005;19(2):155-9. [CrossRef] [PubMed] 
35. Melamed R, Sprenkle MD, Ulstad VK, Herzog CA, Leatherman JW. Assessment of left ventricular function by intensivists using hand-held echocardiography. Chest. Jun 2009;135(6):1416-20. [CrossRef] [PubMed] 
36. Vignon P, Chastagner C, François B, Martaillé JF, Normand S, Bonnivard M, Gastinne H. Diagnostic ability of hand-held echocardiography in ventilated critically ill patients. Crit Care. 2003;7(5):R84-91. [CrossRef] [PubMed]
37. Mayo PH, Beaulieu Y, Doelken P, Feller-Kopman D, Harrod C, Kaplan A, Oropello J, Vieillard-Baron A, Axler O, Lichtenstein D, Maury E, Slama M, Vignon P. American College of Chest Physicians/La Societe de Reanimation de Langue Francaise statement on competence in critical care ultrasonography. Chest. 2009;135(4):1050-60. [CrossRef] [PubMed]

Reference as: Summerfield DT, Cawcutt K, Van Demark R, Ritter MJ. Fat embolism syndrome: improved diagnosis through the use of bedside echocardiography. Southwest J Pulm Crit Care. 2013;7(4):255-64. doi: http://dx.doi.org/10.13175/swjpcc109-13 PDF

Refractory Cardiogenic Shock

Bhupinder Natt, MD (bnatt@deptofmed.arizona.edu)

Tauseef Afaq Siddiqi, MD (tsiddiqi@deptofmed.arizona.edu)

Jarrod Mosier, MD (jmosier@aemrc.arizona.edu)

Yuval Raz, MD (yraz@deptofmed.arizona.edu)

Department of Medicine, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, University of Arizona, Tucson, AZ

Abstract

We present a case of refractory cardiogenic shock secondary to myxedema crises that was treated successfully with thyroid hormone replacement.

Case Presentation

History of Present Illness

A 62-year-old woman with past medical history significant only for hypothyroidism was seen in the emergency department (ED) after a fall at home. On further evaluation, the patient’s husband reported history consistent with deteriorating mental function as evident by speech alteration, inability to operate home appliances like the coffeemaker and gradually worsening generalized weakness. She was recently seen at an outside hospital the week previous to this admission and given a prescription for furosemide for pedal edema.

ED evaluation showed her to be lethargic, disoriented with progressively deteriorating mentation, with hypothermia and bradycardia. Her progressive decline in mentation led to endotracheal intubation for airway protection. The patient was started on vasopressors due to post-intubation hypotension and transferred to the Medical Intensive Care Unit (MICU).

Vitals and Physical Exam

Vitals upon presentation to ED: Temperature 29^o Celsius; Heart Rate 42 bpm; Blood Pressuren107/79 mm Hg; Respiratory Rate 14/min; SpO2 97 % on Room Air.

Vitals upon arrival in MICU: Temperature of 29^o Celsius; Heart Rate 43 bpm; Blood Pressure 111/57 mmHg; Respiratory Rate of 10/min; SpO2 100% on mechanical ventilation;

Neurologically, she was sedated with no obvious localizing signs. Skin exam revealed a sutured scalp lesion and scattered abrasion on arms. Cardiopulmonary exam was significant only for bradycardia, which was determined to be sinus rhythm by the electrocardiogram (EKG). Other system examination was significant only for 2+ non-pitting edema of upper and lower extremities.

Laboratory and Radiology Data

CBC: White Cell Count 8.4x1000/microL; Hemoglobin 9.5 g/dL; MCV 100 fL; Platelets 82x1000/microL.

Electrolytes and Metabolic Panel: Sodium 134 mMol/L; Potassium 4.2 mMol/L; Chloride 97 mMol/L; Bicarbonate 26 mMol/L; Urea Nitrogen 38 mg/dL; Creatinine 0.9 mg/dL. Glucose 78 mg/dL; Calcium 9.6 mg/dL.

Total Protein 6.3 g/dL; Albumin 3.7 g/dL; Bilirubin 0.7 mg/dL; Alkaline Phosphate 104 IU/L; ALT 72 IU/L; AST 158 IU/L; TSH 36.1 uIU/mL; Thyroxine 0.8 ng/dL; Free T3 1.2 pg/mL (Normal 2.4-4.2 pg/mL); Cortisol 20.3 mcg/dL.

ABG: pH 7.52; PaCO2 34; PaO2 166; HCO3 28; SaO2 97.6 % on 50% FiO2.

Urine Analysis: Negative.

Urine Drug Screen: Negative.

Chest X-Ray: Emphysematous changes with no acute cardiopulmonary process.

Non-contrast CT of the head and cervical spine: Unremarkable except scalp hematoma.

EKG at Presentation

MICU Course

After initial stabilization of blood pressure in ED; receiving four liters of intravenous fluids; and norepinephrine infusion at increasing doses, she was transferred to MICU. She required two more liters of crystalloids, vasopressin and increasing doses of norepinephrine, epinephrine, phenylephrine and dobutamine infusions. Corticosteroid was added for refractory shock. She also received first dose of broad-spectrum antimicrobials in ED.

Two hours after arrival to the MICU, seven hours post presentation to the ED; a Swan-Ganz pulmonary artery catheter was placed. The values obtained from the Swan-Ganz catheter are reported in table 1. 

These values were obtained seven hours into admission, while the patient was being actively rewarmed, treated with a total of six liters (L) of crystalloid solutions and on norepinephrine at 13 mcg/min and dobutamine at 5 mcg/kg/min.

The patient remained hypotensive and sequentially, within hours, multiple vasopressors and inotropic agents were required. Table 2 reports the vitals and values off the Swan-Ganz catheter 12 hours after initial placement, when the patient is being actively rewarmed, treated for close to 18 hours and while receiving intravenous epinephrine at 3 mcg/min, norepinephrine at 30 mcg/min, vasopressin a 0.03 units/min, phenylephrine at 150 mcg/min and dobutamine at 20 mcg/min. 

A formal 2-D echocardiogram was obtained which showed a global left ventricular dysfunction and hypokinesis with reduced ejection fraction of 35% and mildly reduced right ventricular dysfunction. No major valvular or pericardial pathology was noticed. Given the patient’s history and clinical features of hypothyroidism, a diagnosis of myxedema coma was made and treatment started with levothyroxine 125 mcg a day intravenously. Corticosteroids were discontinued due to concern of blockage of peripheral conversion of T4 to T3. T3 was unavailable in our city initially but was subsequently obtained and prescribed to our patient at 25 mcg of liothyronine three times a day. She responded very well to the treatment and was successfully weaned off all vasopressor support, liberated from mechanical ventilation on the fourth day and transferred out of the MICU on day five of admission. Limited repeat echocardiogram prior to transfer out of the MICU showed an ejection fraction of 65%.

Cultures, lumbar puncture and all imaging including brain MRI obtained during admission and MICU stay remained negative. A potential precipitating factor was not found and all empiric treatments were gradually withdrawn prior to the transfer out of MICU.

Retrospective history taking revealed patients’ non-compliance with levothyroxine treatment for the past 2 years. She had been given a dose of levothyroxine while she was admitted at the outside hospital the week previously leading to her relatively normal T4 level, suggesting inhibited peripheral conversion to T3 and thus the limited effect of intravenous levothyroxine initially. Surprisingly, despite the ordeal, she continued to refuse to take the medication once extubated and transferred to Medicine.

Discussion

A myxedema crisis is an extreme and life-threatening form of hypothyroidism that requires prompt diagnosis and treatment. Mortality rate has been reported as high as 60% despite appropriate diagnosis and management (1,2). Infections and discontinuation of thyroid supplements are the major precipitating factors. Other precipitants include hypothermia, gastrointestinal bleeding, congestive heart failure, cerebrovascular accident, metabolic disturbance and sedative drugs (3).

Myxedema crises manifests by involving multiple organ systems. Hypothermia can be profound and is usually the first sign of myxedema coma. Neuropsychiatric manifestations include confusion, lethargy, coma, psychosis (myxedema madness), and seizures. Respiratory depression is common likely due to depressed hypoxic and hypercapnic respiratory drive. Edema (myxedema) involving upper airways contributes to acute respiratory failure. Reduced intestinal motility leads to constipation, paralytic ileus and mega colon. Urine retention from bladder atony can be seen. Reduced glomerular filtration and reduced water excretion leads to hyponatremia, a consistent finding in myxedema crises.

Cardiovascular effects of myxedema crises include conduction abnormalities, reduced contractility, cardiomegaly and pericardial effusion. Sinus bradycardia, low voltage complexes, bundle branch blocks, complete heart blocks, and nonspecific ST-T changes in electrocardiogram have been reported. Prolonged QT interval and polymorphic ventricular tachycardia has been described as well (4). Depressed cardiac contractility leads to low stroke volume and cardiac output. Animal studies have documented that hypothyroidism leads to cardiomegaly from cardiac atrophy, impaired myocardial blood flow and loss of arterioles resulting in severe systolic dysfunction (5).

These cardiogenic effects of hypothyroid state leading to depressed ionotropy and chronotropy with compensatory vasoconstriction are believed to be a result of low intracellular T3. The hypothyroid heart attempts to perform by better coupling of ATP to contractile events until a precipitating event disrupts this fine balance (6). This resultant de-compensation leads to hypotension and cardiogenic shock that may not respond to vasopressors alone until thyroid hormone replacement is given.

Treatment usually involves intensive care admission with cardiopulmonary support, aggressive fluid and electrolyte management, treatment of underlying and precipitating factors and thyroid hormone replacement. Intravenous T4 is the most commonly used preparation as intestinal absorption may not be reliable. In severe illness, the conversion of T4 to T3 by 5’-monodeiodinase is impaired. Intravenous T3 preparation should be used. Improved cardiac function is reported in 24 hours when T3 replacement is used and it may take up to a week to notice beneficial effects with T4 replacement alone (7).

References

1. Mathew V, Misgar RA, Ghosh S, Mukhopadhyay P, Roychowdhury P, Pandit K, Mukhopadhyay S, Chowdhury S. Myxedema Coma: a new look into an old crisis. J Thyroid Res. 2011:493462.[CrossRef] [PubMed]
2. Wartofsky L, Myxedema Coma, Endocrinol Metab Clin N Am. 2006; 35(4): 687-98. [CrossRef][PubMed]
3. Brent GA, Davies TF. Hypothyroidism and thyroiditis. In: Melmed S, Polonsky KS, Reed P, Kronenberg HM, eds. Williams Textbook of Endocrinology. Philadelphia, PA: WB Saunders, 2008.
4. Schenck JB, Rizvi AA, Lin T. Severe primary hypothyroidism manifesting with torsades de pointes. Am J Med Sci. 2006 Mar; 331(3): 154-6. [CrossRef] [PubMed] 
5. Tang YD, Kuzman JA, Said S, Anderson BE, Wang X, Gerdes AM. Low thyroid function leads to cardiac atrophy with chamber dilatation, impaired myocardial blood flow, loss of arterioles, and severe systolic dysfunction. Circulation. 2005;112(20):3122-30. [CrossRef] [PubMed]
6. W. M. Wiersinga. Hypothyroidism and myxedema coma. In: Jameson JL, Legroot LJ, eds. Endocrinology: Adult and Pediatric. Philadelphia, PA: Saunders Elseiever, 6th edition, 2010:1607-22.
7. MacKerrow SD, Osborn LA, Levy H, Eaton RP, Economou P. Myxedema associated cardiogenic shock treated with intravenous triiodothyronine. Ann Int Med. 1992;117:1014-5. [CrossRef][PubMed] 

Reference as: Natt B, Siddiqi TA, Mosier J, Raz Y. Refractory cardiogenic shock. Southwest J Pulm Crit Care. 2013;7(4):246-50. doi: http://dx.doi.org/10.13175/swjpcc098-13 PDF

Ultrasound for Critical Care Physicians: Right Diagnosis, Wrong Place

The patient was a 76 year old man, with a history of a prosthetic aortic valve (aortic stenosis) and chronic myelogenous leukemia.  He presented with fever and cough, and was found to have pneumonia with Klebsiella pneumonia cultured from a BAL. However, he also had persistent Enterococcus faecalis bacteremia and a new 3/6 diastolic murmur. 

An ultrasound of the heart was performed (Figures 1 and 2).

Figure 1. Parasternal long axis view of the heart.

Figure 2. Four chamber view of the heart.

Which of the following is the likely diagnosis?

1. Aortic dissection
2. Aortic valve endocarditis
3. Displacement of the aortic valve
4. Mitral valve endocarditis
5. Tricuspid endocarditis

Reference as: Raschke RA. Ultrasound for critical care physicians: right diagnosis, wrong place. Southwest J Pulm Crit Care. 2013;7(4):232-5. doi: http://dx.doi.org/10.13175/swjpcc123-13 PDF

October 2013 Critical Care Case of the Month: Slow to Respond

Michael P. Mohning, MD

Pulmonary Sciences and Critical Care Medicine

University of Colorado Hospital

Denver, CO

History of Present Illness

A 66-year-old woman presents with confusion and lower extremity edema. She was brought to the emergency department by her family after 2-3 days of increasing confusion.  She has fatigue and a dry non-productive cough but denies shortness of breath, chest pain, fevers or chills. She had a decrease in oral intake and constipation for several days.

PMH, SH, FH

Five months ago, she was admitted to a hospital for community acquired pneumonia and hyponatremia. She is a never smoker, and doesn’t use alcohol.

There is no significant family history.

Medications

• Omega 3 fatty acids
• Multivitamins

Physical Examination

Temperature 36.1° C, blood pressure 106/61 mm Hg, heart rate 72 beats/min, respiratory rate 15 breaths/min, oxygen saturation 90% on room air.

She was confused, and oriented to self only.  She had facial edema.  Cardiac exam was normal. Pulmonary findings include rales at the lung bases. Her abdomen was non-tender, with active bowel sounds. She had 1+  lower extremity edema, no rashes, and delayed relaxation of reflexes.

Laboratory

She was anemic with hematocrit of 32%, hemoglobin 11 g/dL and WBC 5,000. Serum sodium is low at 118 meq/L, anion gap was normal at 9 and potassium and calcium levels were normal. Albumin is low at 3.2 g/dL. Remaining liver function, blood glucose and creatinine are normal. EKG shows no T wave inversions or ST segment elevation.

Radiography

Chest x-ray is shown in figure 1.

 

Figure 1. Admission PA (Panel A) and lateral (Panel B) chest x-ray.

Which best describes the chest-x-ray?

1. Bilateral interstitial infiltrates
2. Enlarged cardiac silhouette
3. Hyperexpanded lungs
4. Poor inspiratory effort
5. Pulmonary edema

Reference as: Mohning MP. October 2013 critical care case of the month: slow to respond. Southwest J Pulm Crit Care. 2013;7(4):214-20. doi: http://dx.doi.org/10.13175/swjpcc105-13 PDF

Ultrasound for Critical Care Physicians: Connecting Disparate Symptoms

An 18-year-old woman was recently diagnosed with non-ACTH-Mediated Cushing syndrome, now with a complaint of mild shortness of breath.

Her cardiac exam showed normal sinus rhythm at 84 beats per minute and blood pressure of 130/80 mmHg. Her mitral first heart sound was slightly accentuated, but the pulmonic sound was normal. Grade-I diastolic murmur was heard over the mitral area. Opening snap was absent. Lungs were clear and chest radiograph showed slight cardiomegaly. She had multiple freckles on his face and trunk and along the vermillion border of the lips.

An ultrasound of the heart was performed (Figure 1).

Figure 1. Four chamber view of the heart.

Which of the following is the likely diagnosis?

1. Brugada syndrome
2. Carney syndrome
3. Gotway syndrome
4. Jervell and Lange-Nielsen syndrome
5. Peutz-Jeghers syndrome

Reference as: Gotway MB. Ultrasound for critical care physicians: connecting disparate symptoms. Southwest J Pulm Crit Care. 2013;7(3):176-8. doi: http://dx.doi.org/10.13175/swjpcc122-13 PDF

September 2013 Critical Care Case of the Month: Revenge of the Pharaohs

Robert A. Raschke, MD

Elijah Poulos, MD

Banner Good Samaritan Regional Medical Center

Phoenix, AZ

History of Present Illness

The patient was a 68 year-old man, admitted to our ICU through the emergency room (ER) in July 2013 with suspected urinary tract origin sepsis.

The patient was evaluated in ER by the ICU team. He was in his usual state of general good health until he visited his primary care physician for what he felt was a left inguinal hernia, and underwent a prostate examination, four days previously. The patient associated this prostate examination with the onset of fevers and chills that began the next morning. He was seen in an urgent care center where he was told his urinalysis was normal, and antibiotics were not prescribed. Over the intervening 3 days, he suffered recurrent fevers, had vomited three times, and had one diarrheal bowel movement. Earlier on the day of presentation, he had been mowing his lawn (in >100° F environment) and had become a little dizzy. His wife, a retired nurse, finally convinced him to report to the ER.

He denied dysuria, urinary frequency or urgency, headache, sore throat, cough, or abdominal pain.

PMH, SH, FH

He had a prior history of hypertension, gastroesophageal reflux, gout and hypercholesterolemia. He drank alcohol about twice a month and did not smoke.

There was no family history of illnesses.

Medications

• Atorvastatin
• Allopurinol
• Hydrochlorothiazide
• Lisinopril
• Temazepam

Physical Exam

On ER triage, his temperature was 41.2° C, but vitals at the time of our initial examination were temp 38.2° C, HR 93 beats/min, BP 103/48 mm Hg, and respiratory rate 20 breaths/min. He was awake and alert, but made a few errors while relating his history – for instance, he initially answered yes when asked if he had a headache, then corrected himself and said no – he meant he had a fever. He was actively rigoring. HEENT exam was unrevealing. He had no lymphadenopathy. His lungs were clear. His abdomen was soft and nontender. He had a sliding left inguinal hernia that was not tender. None of his joints were acutely inflamed. His prostate was not enlarged or tender to palpation. He had no focal neurological deficits.

Laboratory

Pertinent laboratory values in the ER:

• WBC: 7.7 x10⁹/L
• Hematocrit: 38.4%
• Sodium: 131 me/L
• Potassium: 3.1 me/L
• BUN:28 g/dL
• Creatinine: 1.3 mg/dL
• Lactate: 2.1 mMol/L.

The rest of his admission labs and urinalysis were unremarkable.

Chest Radiography

His initial portable chest x-ray is shown in Figure 1.

Figure 1. Initial portable chest x-ray.

Which of the following is the likely cause of his fever?

1. Prostatitis exacerbated by digital rectal exam
2. Right middle lobe pneumonia
3. Urinary tract infection
4. All of the above
5. None of the above

Reference as: Raschke RA, Poulos E. September 2013 critical care case of the month: revenge of the pharaohs. Southwest J Pulm Crit Care. 2013;7(3):142-50. doi: http://dx.doi.org/10.13175/swjpcc104-13 PDF