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Ultrasound of the Month

Ultrasound of the Month

USOM I:

Critical Care and Electrolytes

73 y/o F w/ hx of hyperlipidemia, IDDM, and prior smoking hx presents with her daughter reporting weakness in the setting of 1 week of nausea and vomiting.  She is also reporting difficulty with motor functions including walking and picking up objects such as the morning paper and her afternoon teacup.  Her exam is significant for global weakness and ataxia, however the pt is noted to be conversing normally with her daughter in the room.

Basic metabolic panel: Na+ 105, K+ 3.2, Cl 98, CO2 18, BUN 35, Cr 1.5, Glu 200
Complete blood count: wbc 8, hct 33, hbg 11.5, plt 150
Remaining labs are pending

What’s the diagnosis and what treatment do you want to initiate?

Hyponatremia; first treatment is to DO NOTHING and obtain additional labs to determine the etiology of the hyponatremia (hypovolemic hyponatremia, euvolemic hyponatremia, hypervolemic hyponatremia, SIADH, medication related (thiazides), drugs (ecstasy), psychogenic polydipsia, potomania, etc…).  You first need to determine the etiology of the hyponatremia and if you initiate treatment before obtaining these labs then it’ll make it difficult to determine the cause.  Also, initiating aggressive treatment turns off ADH and can lead to massive over diuresis, which can cause a sharp rise in serum sodium levels and potentially result in osmotic demyelination (i.e. locked-in syndrome, severe neurologic morbidity, death). Lastly, normal saline can actually worsen the hyponatremia in a patient with SIADH, therefore the etiology of the electrolyte abnormality needs to be elucidated BEFORE treatment.  This is especially true in asymptomatic patients.  If a patient is presenting with severe neurologic symptoms, then the risks/benefits need to be assessed when considering treatment.

Labs to send: serum osm, urine UA, urine electrolytes (Na, K), urine osm; other useful labs: serum uric acid, TSH/cortisol, urine urea, urine uric acid, urine creatinine

To better establish the patient’s fluid status you perform the following ultrasound: Case 1 Ultrasound

Is the patient hypovolemic, euvolemic, or hypervolemic? How can you tell? 

Hypovolemic: The Inferior vena cava (IVC) is seen completely collapsing with respirations, which suggests a volume depleted state. The IVC should normally, in a euvolemic patient, collapse by about ~50% with respirations. An IVC that doesn't collapse at all with respirations is usually seen in a well-resuscitated patient OR fluid overloaded patient while an IVC that completely collapses suggests volume depletion. The parasternal long and parasternal short echocardiogram views shown display a hyper dynamic, tachycardic heart, which in the right clinical setting can indicate hypovolemia. (note, there is decent literature to support using IVC diameter to determine fluid states in conjunction with clinical status, however there isn't comparable data for a hyper-dynamic tachycardic heart, it's just an interesting finding that you might find, especially in patients suffering from septic or hemorrhagic shock).

The following labs return: Serum osmolality 256 mosmol/kg, urine sodium 10 meq/L, urine osmolality 400 mosmol/kg

Charge nurse calls: no beds are available in the hospital and none are anticipated to be ready until 7 AM (7 hours from now).

You decide to initiate treatment for this patient's condition. What do you give and what's your target goal?

The labs (and echocardiogram) above support the diagnosis of hypovolemia hyponatremia (serum osm < 280, urine Na+ < 20 suggesting the patient is dehydrated and the kidneys are attempting to retain sodium/water, and the urine osm isn't egregiously low which would have suggested severe malnutrition (beer potomania). Best course of action is to do nothing and fluid restrict, however if the patient is showing signs of severe neurologic dysfunction and boarding in the ED then you can consider correcting the Na+ SLOWLY. Different sources recommend different rates of correction, but it's better to be more conservative and never correct more than by 6 mmol/L in first 6 hours in the ED. If you find yourself boarding a hyponatremic patient beyond this initial correction, nephrology should be consulted to help guide care (of course, in an academic setting, you might be consulting nephrology from the beginning). The following equation can be used to predict the rise in Na+ based on the fluid initiated: Change in serum Na+ = infusate Na+ – serum Na+ / (total body water + 1) (Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med 2000; 342:1581). The infusate Na+ for 3% Na+ solution is 513 mmol/L and the infusate for NS is 154 mmol/L. To calculate total body water try MD calc: http://www.medcalc.com/tbw.html. The rate of infusion can be calculated based on the Na+ concentration chosen and the desired Na+ increase over a given time period.

Check serum sodium every hour.

Before initiating treatment, the patient begins to have a tonic-clonic seizure. What do you give?

The seizure is likely due to the hyponatremia, therefore rapid Na+ infusion is the best treatment: 100 cc of 3% Normal Saline, which increases Na+ by 2 mmol/L, given over 10 mins. Wait 10 mins, then give a second dose if they continue to seize. This can be given peripherally assuming you have a decent line. You can also give benzos concurrently, but not as effective in these hyponatremic seizures. Check the sodium level after these two doses before giving more, consult nephrology, and of course explore other etiologies of the patient's seizure.

64 y/o M with pmhx of CAD, prior PCI, presents with increasing dyspnea on exertion, fatigue, paroxysmal nocturnal dyspnea, and weight gain.  Over the last two days he has developed confusion and weakness.

You perform a bedside ultrasound, which reveals the following: Case 2 Ultrasound

What is the diagnosis and what ultrasound findings support this?

Congestive heart failure, fluid overload state: Pt has a decreased EF (ejection fraction) as evidenced by poor mitral valve excursion toward the septum in the parasternal long view and minimal left ventricular wall motion in the parasternal short axis.  There are several methods to determine ejection fraction including using EPSS, Stimpson method, etc…, but studies have shown that visual gestalt is just as effective and accurate (in experienced ED echocardiogram MD interpreters, granted).  In a normal EF, the mitral valve will slap against the septum (as seen best in the parasternal long view) and in severe EF, the mitral valve will hardly move as seen in this ECHO.  Ventricular wall motion is best seen in the parasternal short view as the entire circumferential wall can be visualized.  In this echo, the walls are barely moving, suggesting a severely depressed EF. 

This ultrasound also shows B-lines in the lungs, which are detected by using an abdominal probe placed longitudinally on the anterior chest at the mid-clavicular line around the 2nd – 4th intercostal spaces.  Generally, if there are >3 B-lines visualized ~7 mm apart between two ribs, then that is suggestive of pulmonary edema (Lichtenstein et al. A-Lines and B-Lines: lung ultrasound as a bedside tool for predicting pulmonary artery occlusion pressure in the critically ill.  Chest.  2009, Oct; 136(4):1014-20)

Lastly, this patient has a pleural effusion.  An abdominal probe is used on the right flank similar to evaluating the liver and kidney on a fast exam, but moved a bit more cephalad.  The liver and diaphragm are easily visualized and a clearly hypoechoic fluid collection is seen above the diaphragm within the pleural space. 

All these findings (decreased EF, pulmonary edema, pleural effusion) suggest that this patient has decompensated congestive heart failure and is fluid overloaded.

The lab calls to report a critical value on the patient’s vbg (corroborated on bmp) of a Na+ of 112 (new compared to prior labs)

What type of hyponatremia does this patient have (question 1 of case 1 lists a few of the possibilities)?  How do you want to do to treat the patient’s hyponatremia? 

Hypervolemia hyponatremia: CHF results in a fluid overload state but overall hypoperfusion of end organs such as the kidneys, resulting in fluid retention. Treatment for these patients is fluid restriction and ACE inhibitors, although those can be started inpatient and are generally used in refractory cases. The ACE will increase cardiac output and inhibit ADH, ACE also decreases renal water absorption….all beneficial effects in CHF patients with hyponatremia.

USOM II:

Trauma

Case 1: A 32 y/o M motorcyclist struck the side of a moving motor vehicle at high speed, was thrown 15 feet, and transiently lost consciousness per bystanders. Prehospital vital signs were as follows: P: 120, BP: 100/palpitation, SpO2: 95%, RR: 25, GCS 9/15.  In the Emergency Department, the patient was A&Ox3 with a GCS of 15 and labored respirations.  The patient reported left shoulder pain and shortness of breath.  Initial ED vitals: HR 125, RR 25-30, SpO2 97% RA, blood pressure nonpalp by automated cuff, with no radial pulses and faint femoral pulses.  The patient’s airway was intact and b/l breath sounds were present.  Providers noted mild anterior chest tenderness without ecchymosis or deformity.  A left shoulder joint dislocation was noted.  US performed:

What ultrasound exam was performed above and what are the significant findings?

The video demonstrates an eFAST (Expanded Focused Assessment with Sonography in Trauma).  This study incorporates both the abdominal FAST exam with a thoracic exam to evaluate for hemo- or pneumothorax.  The FAST in this case reveals hypoechoic fluid in the RUQ view (Morrison’s Pouch), which is the most sensitive view in a FAST to identify intraperitoneal fluid (#1).

FAST

How effective is the FAST exam?  What is the sensitivity and specificity?

The FAST is an integral component of a trauma evaluation and per ATLS protocol should be performed after the completion of the primary survey. The FAST has variable sensitivities for the detection of intraperitoneal fluid (63-100%), but excellent specificity (95-100%). Approximately ~500-600 cc of fluid is necessary to yield a positive exam (#2, #3).

In the setting of blunt trauma, a positive FAST should elicit high suspicion for intraperitoneal bleeding. If the FAST is negative, but the patient remains hypotensive or unstable, additional investigation is indicated (i.e. computed tomography or exploratory laparotomy).

Case 2: The same patient above presents to your trauma bay:
What is the finding on this EFAST?  How effective is ultrasound in detecting this pathology?

This patient has a pneumothorax. The hyperechoic linear line between the two rib shadows represents the pleura. In the previous case, one observes sliding between the visceral and parietal pleuras, a normal finding. The absence of lung sliding between pleural layers in this case reflects extrapulmonic air in the thorax, which is a pneumothorax. Ultrasound has a higher sensitivity than CXR in detecting pneumothorax (98.1% vs. 75.5%; #4).

PTX

Case 3: Same motorcycle patient presents and the following ultrasound is performed:
What condition is seen on this eFAST?

Pericardial effusion with evidence of both clot and fresh hemopericardium.

FAST

What’s the epidemiology and mechanism of this type of injury?

Hemopericardium in blunt trauma is relatively rare and is generally due to rupture of a free wall of the heart (right atrium 8-65%, right ventricle 17-32%, left atrium 8-15%, left ventricle 0-31%; #5). This injury carries a high mortality and only 5% of patients with blunt cardiac injury and hemodynamic instability survive to hospital admission (#6). This injury typically results from massive anterior thoracic forces, such as those in a motor vehicle collision. The injury mechanism often leads to a multi-system trauma in these patients and one may also observe other associated thoracic injuries such as sternal or rib fractures, pneumothorax, hemothorax, and pulmonary or cardiac contusions.

What is the sensitivity and specificity of transthoracic ultrasound in the detection of hemopericardium?

Sensitivity = 96% and specificity = 98% (#7).

What is the management of the patient above?

The patient presents with tamponade physiology and his injuries require immediate intervention. A stable patient with this injury should be taken directly to the OR for thoracotomy and definitive repair of the cardiac wall rupture. If the patient becomes hemodynamically unstable, then an ED thoracotomy may be considered. In patients with this injury who are hemodynamically stable (including low but stable blood pressure values), a pericardiocentesis may be considered. The drainage catheter would drain extra-cardiac volume and relieve the tamponade until more definitive care is possible.

What’s your airway management for this patient? 

If the patient should manifest distress or deteriorating mental status, endotracheal intubation may be indicated. However, intubation could be dangerous for this patient, as positive intra-thoracic pressure (as occurs in mechanical ventilation) may severely reduce cardiac filling and lead to cardiovascular collapse. As such, intubation should ideally occur in the controlled environment of the operating suite.

References

1) Rozycki, G.S.; Ochsner, M.G.; Feliciano, D.V.; et al. Early Detection of hemoperitoneum by ultrasound examination of the right upper quadrant: a multicenter study. J Trauma. 45(1998), pp. 878-883
2) Patel, Riherd. Focused assessment with sonography for trauma: methods, accuracy, and indications. Surg Clin N Am 91 (2011); 195-207.
3) http://www.uptodate.com/contents/emergency-ultrasound-in-adults-with-abdominal-and-thoracic-trauma
4) Blaivas, Ml Lyon, M; Sandeep, D. Prospective comparison of supine chest radiography an bedside ultrasound for the diagnosis of traumatic pneumothorax. Academic Emergency Medicine. Vol 12, Issue 9, Sep 2005; 844-849
5) Schultz, J.M.; Trunkey, D.D. Blunt Cardiac Injury. Crit Care Clin. 2004; 20(1):57-70
6) Fedaker, et al. Fatal traumatic heart wounds: Review of 160 autopsy cases. Isr Med Assoc J. 2005;7 498-501 7) Mandavia D.P.; Hoffner R.J.; Mahaney K.; Henderson S.O. Bedside echocardiography by Emergency Physicians. Ann Emerg Med. 2001;38(4):377

USOM III:

Cardiac Critical Care

58 y/o F w/ hx of HTN, DM, GERD, family hx of CAD, recent stress echo 2 months ago with no notable ischemic changes or wall motion abnormalities, presents with 2-3 hours of gradual onset, dull epigastric pain radiating to her right shoulder associated with nausea.  You perform a bedside ultrasound:

Which of the following EKG’s likely belongs to this patient?

EKG

EKG

EKG

The echocardiogram shown has a wall motion defect in the anterior-septal distribution. Therefore, EKG 2, with ST elevations in V1-V3 in the anterior-septal leads, would likely be the corresponding EKG. It was helpful to know that the patient had a normal echocardiogram recently and that the wall motion abnormality noted was likely due to a recent ischemic event or development of coronary artery stenosis and inducible ischemia. This is essentially what cardiologists are looking for on a dobumatine stress echo: wall motion abnormalities during stress indicating potential reversible ischemia. In this case, the wall motion abnormality is likely due to a myocardial infarction given the EKG findings and the patient likely needs an interventional cardiologist for PCI. Check out the image below depicting wall locations on an echocardiogram:

USOM Wall Echo

Want to learn more about wall motion abnormalities?

Check out the Mike and Matt Ultrasound Podcast on WMA’s

What is the ejection fraction of the above echo?

Moderately reduced: 40-50%

This patient just had a negative dobutamine stress echo 2 months ago and is now having a myocardial infarction. What's the sensitivity and specificity of a stress test?

Sensitivity = 67%; Specificity = 72% (per the ACC/AHA practice guidelines). Imaging modalities are generally considered slightly superior to exercise testing, but they are essentially comparable studies once the multitude of variables are taken into account. These tests are meant to detect lesions that induce ischemia during exercise (>70% stenotic lesions) and do not detect moderate lesions (~50%). These moderate lesions are at greatest risk of rupture leading to an acute thrombotic event and subsequent myocardial infarction. Therefore, one must consider a stress test as a useful tool in detecting coronary artery disease, but certainly not the end-all-be-all of a patient's risk of having a cardiac event.

80 y/o M w/ a pmhx of HLD presents with chest pain and shortness of breath that began while shoveling snow.  The chest pain is described as substernal, pressure-like pain that is non-radiating and gradually worsening.  On exam, the patient appears in a moderate amount of distress, diaphoretic, cool to the touch, and is mildly confused.  The EMS truck that brought the patient in did not have a working 12-lead, but did note a blood pressure of 70/40 in the field.  In the trauma bay, the patient has the following vitals: BP 86/49, pulse 95, temp 93.5 F, RR 32, SpO2 95%.  The patient is not followed at your hospital and there are no prior EKGs or records.  An EKG is obtained and you perform a bedside echo:

Which of the following EKG’s likely corresponds with the above Echo?  What is the patient’s ejection fraction?  Refer to the echo wall map as shown in the previous case to help you:

USOM Wall Echo

EKG

EKG

EKG

The patient is likely suffering from an inferior wall MI. The EF is severely low (20-30%), which makes evaluation of focal wall motion abnormalities a bit more difficult, but you'll notice in the parasternal short view a clearly akinetic inferior wall compared to a kinetic (perhaps hypokinetic) lateral wall. EKG 2 displays ST elevations in the inferior leads II, III, aVF and assuming that the inferior wall akinesis is new would likely be the presenting EKG in the trauma bay.

You've diagnosed the patient with a myocardial infarction and established that he has severe cardiomyopathy, but what worrisome complication of acute MI is the patient also presenting with?

Cardiogenic Shock, which is a shock state caused by the inability of the heart to pump adequate volume leading to end-organ hypoperfusion and subsequent dysfunction, is most frequently caused by LV failure in the setting of an MI. It is the leading cause of death in patients' with AMI and carries an in-hospital mortality rate of ~50%. Classic clinical manifestations include hypotension, confusion, oliguria, cool 'clammy' skin, and respiratory distress due to pulmonary congestion.

Do these patients have an elevated systemic vascular resistance (SVR) or a reduced SVR?

In general, these patients will have an increased SVR as the physiological response to a low cardiac output and low stroke volume would be vasoconstriction of the peripheral vessels in order to increase perfusion. This unfortunately then leads to worsening end-organ dysfunction and decreased coronary artery flow leading to increased cardiac cell death and pump failure.

Some of these patients will actually have a decreased SVR. As shown in the SHOCK1 trial, which looked at 302 cases of cardiogenic shock, 54 patients (18%) actually had fever and 40 of these patients had positive blood cultures, therefore some of these patients may be presenting with sepsis as well. The teaching point here is to not close the book too quickly on these patients and always keep sepsis in the back of your head as an etiology or at least a component to the patient's symptoms.

What is your pressor of choice for this patient in cardiogenic shock?

Norepinephrine? Dopamine? Dobutamine? A study of 1679 patients who presented in any form of shock and were randomized to receive either dopamine or norepinephrine showed no difference in the survival benefit at day 282. However, patients who received dopamine did have more adverse events such as arrhythmias. This study also did show a very small survival benefit in the subset of patients who presented in cardiogenic shock (280 patients) when they received norepinephrine. Additionally, the ACC/AHA recommends norepinephrine in hypotensive patients complicated by AMI with SBP <70 mm Hg. Overall, the data isn't overwhelming for any one particular agent. If you'd like to read more on vasopressors, check out the following citation.3

What about Dobutamine?

Dobutamine is a β1-receptor agonist and weak β2-agonist and therefore produces positive inotropic and chronotropic effects, but also produces vasodilation. Dobutamine can cause tachycardia which increases myocardial O2 consumption. The vasodilatory and tachycardic effects of Dobutamine make it a poor choice as a single vasopressor for patients in severe, life-threatening cardiogenic shock. Dobutamine does have a role in patients in acute decompensated heart failure with normal/low normal blood pressures to increase stroke volume and cardiac output in an attempt to prevent circulatory collapse.

What other treatments should be initiated for this patient?

Although this patient is in cardiogenic shock, he is ALSO having a myocardial infarction. Therefore heparin gtt should be initiated and the patient should receive an ASA. Delay clopidogrel until consultation with cardiology as many of these patients will require surgical intervention / CABG. These patients will benefit from positive pressure ventilation in the form of CPAP/BIPAP or intubation if the patient is not protecting their airway. Clinical studies have shown that continuous positive airway pressure increases cardiac output in patients with left-sided heart failure.4 The SHOCK trial has shown that these patients have a survival benefit at 6-12 months if they undergo early interventional revascularization via either PCI or CABG, therefore the cath lab should be activated and the patient transferred once they are adequately stabilized. Many of these patients will then receive intra-aortic balloon counterpulsation (IABP) to temporarily improve their pump function. These patients will then likely head to the CCU where our PGY-2's will have the pleasure of managing them from here on out.

Should these patients be receiving fluids for their low blood pressure?

Assuming that this patient's shortness of breath is due to pulmonary edema, the fluids may exacerbate this problem. In patients with cardiogenic shock as a result of acute right heart failure, then fluids are the mainstay of therapy. In general, these patients present with an AMI (frequently an inferior MI) associated with hypotension, but with no evidence of pulmonary congestion (no rales, no SOB, normal CXR). If fluids don't improve their hemodynamics, then pressers may be initiated.

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