A liver in the lung

65-yo female with COPD presents to the ED severely distressed and dyspneic. Oxygen saturation 70%. Breathing frequency 45/min. Obstructive breath sounds with spread rhonchi. The patient is heavily dependent on accessory respiratory muscles. 120BPM. BP 100/70. Afebrile. COPD with acute exacerbation is suspected. Corticosteroids, bronchodilators and oxygen are administered. A bloodgas shows PCO2 retention and respiratory acidosis. Vitals slightly improved but oxygen saturation is not adequate. Higher levels of oxygen therapy will cause carbon dioxid narcosis. BIPAP is started with progressive improvement. Bedside ultrasound:

Left lateral thoracic- and upper abdominal view plus zoom. Significant for consolidations and hence a high suspicion of severe pneumonia/pneumosepsis. Fluids and antibiotics are administered. Bloodpanel returns showing Lactate 4,5, CRP 200 and WBC 18 with a left shift. A central venous catheter is placed.

The patient is taken to the ICU where a new bedside ultrasound is done. Consolidations are again visualized. In addition the following is seen.

What do you think? Please comment below. All intercostal spaces look the same. The pleura is statically prolapsed intercostally. My guess:the intercostal muscles have been through a marathon of strain. Currently flaccid and off-loaded by a well-deserved non-invasive ventilation. Additionally we see a flattened diaphragm which signifies severe COPD/emphysema.

Three days into treatment inflammatory parameters and oxygen saturation have been improved and NIV discontinued.

Left lateralt thoracic- and upper abdominal view. Interestingly enough the consolidation has changed. What we see now is an air bronchogram/hepatization of the lung which simply means that the lung takes on the appearance of a liver. The bronchi appear white. Causes may vary, but in short it implies lung consolidation or atelectasis. In contrast to chest x-ray, ultrasound can divided air bronchograms into either static with no movement in the bronchi or to dynamic with movement in the bronchi (see youtube). The dynamic form has a very high specificity and positiv predictive value for pneumonia. In our case the air bronchogram is static but the clinical scenario implies an infectious process.

Furthermore the intercostal space and pleura seem to have normalized.

References
1. The dynamic air bronchogram. A lung ultrasound sign of alveolar consolidation ruling out atelectasis. 2009. Lichtenstein D, Mezière G, Seitz J.
2. Radiopaedia.orgAir bronchogram
3. Introduction to Bedside Ultrasound: Volume 1 by Matthew Dawson och Mike Mallin (free at Itunes)

Ultrasound saves lives! #2

A 55 yo woman lost consciousness at home. When the ambulance arrived she was pale, BP 70/40 with an irregular heart rhythm and ventricular frequency varying between 20 and 40 BPM. The ECG was sent through the “cloud” and the cardiologist on call ordered fluids and atropine. Upon arrival in the ED the patient was very ill, giving the impression of imminent cardiac failure. Diaphoretic, somnolent, BP 100/60 with an unchanged heart rate and frequency. The past medical history was significant for chronic kidney disease, pre-dialysis. Priority number one was to attach the defibrillator plates. Number two – an ECG.

Regular rhythm? P-waves present? QRS width? QTc? ST-segments and T-waves?

It seems to be some kind of a nodal escape rhythm. What about the ultrasound? UnFortunately you’ll have to use your fantasy on this one. I’ll be faster with the trigger finger next time. Imagine a gorgeous ejection fraction, the best one you’ve seen. The problem was that the ventricular rhythm was irregular, frequency low and successively getting lower by the minute. The impressions was that there was a failure of the SA-node, AV-node and other escape foci. Last swan dance.

Any electrolyte disorder that springs to mind?

The blodgas rightfully showed a potassium of 8, pH 7, creatinine 640 (6.8mg/dL), lactate 5.5, Base excess -20, pCO2 10.4, sodium 132. Not completely unexpected. Full measures were taken. Membrane-stabilizing calcium IV without any ECG improvements. Sodium bicarbonate, insulin/glucose and salbutamol nebulization followed. An isoprenalin-drip was started. The result?

Rising potassium and lactate. Dropping heart rate.

Lactic acidosis leads to rising extracellular potassium and vice versa. Like a dead fish turns its belly up, drifting away in loneliness, the mitral valve made a grand final agonal motion whereupon the gracious magic vanished. Seconds felt like minutes. A swirl of spontaneous contrast began making its presence. True ultrasound-witnessed asystole. What do the guidelines say? Compressions/ventilations/Adrenalin?

Based on the ultrasound and the appreciation of the hearts capabilities, the decision was made to try an alternative treatment modality. With continuous ultrasound observation, the external pacing function was started on the defibrillator. Note that part of the pacing-electricity was transmitted to the operator :) (Don’t try this at home kids)

Eureka! Time to pacing was of utmost importance. Any further delays and the race would have been lost. Followup blodgas showed improvement on all values. But why now? Most probably the cardiac output, previously deranged, now managed to deliver the drugs to the systemic circulation. The patient was dialyzed and had a temporary transvenous pacemaker implanted. She was discharged from the ICU after three days without any further complications. Neurological sequela? Nada.

Focus on the snake & miss the scorpion

47-year-old woman seeking due to acute / subacute onset dyspnea.
Past medical history significant for rectal cancer with metastasis to liver, lungs and brain. Previously hospitalized due to severe left sided pleural fluid.
Current vitalsigns: Sat 91% on 2L oxygen, p.90, BP 115/70. The journal shows a habitual BP of 140/70. Clinical examination reveals absent leftsided breath sounds and dull percussion.

Spine-sign, well-defined diaphragm and the absence of curtain-effect indicates a large amount of pleural fluid. A fluid gap is also seen apically. But was this the entire truth? One would expect a gradual onset dyspnea in this setting.

The right ventricle, located adjacent to the liver, seems overloaded basally. Inferior vena cava (IVC) seems plethoric (dilated with poor respiratory variation) signifying increased central venous pressure (CVP). What happens to the right ventricle if preload / returnvolume is increased? Ask the patient to take a deep breath. This generally also improves the subcostal image quality. Alternatively, try passive leg raise.

The basal part of the right ventricle is considerably dilated while the apex is hyperdynamic. Known as McConnell’s sign, it may indicate massive or submassive pulmonary embolism. But the question is if large amounts of unilateralt pleural fluid can induce respiratory variations in right ventricular load. A quick review of the literature comes back empty.
A left-sided pleural chest tube was set up and 1000cc of clear-red liquid drain after which the drainage was stopped. This was followed up by 500cc / 4hrs to avoid complications such as reexpansion-related pulmonary edema. The patient experienced immediate symptomatic relief and was admitted for further treatment. Sat 94%, p.80 and BP 120/70.
After a total of 2.5L fluid was drained, the patient noted a swelling of the lower extremities. Ultrasound showed bilateral DVT in common femoral veins. Pending thoracic CT according to LE protocol, a new cardiac echo was performed.

McConnell’s sign is accentuated by inspiration.
Central right-sided pulmonary embolism. In view of the brain metastasis, a reduced dose low molecular weight heparin was instituted BID.

One may ask if the CT is really necessary in this case. Bilateral DVT was already diagnosed and thus the indication for LMWH present. However, it was still deemed reasonable to perform the CT since the diagnosis was not quite clear and it may affect duration of treatment with anticoagulation.

Easy to get confused by bad TIP(S)

50-year-old man who a week earlier had a transjugular intrahepatic portosystemic shunt (TIPS) installed. Currently admitted due to altered mental status. The TIPS seems to be patent. The liver looks normal in size with a smooth margin. A small fluid gap is seen subcapsularly just below the diaphragm.

The portal vein, a gateway between two capillary beds, is formed by the union of veins from the gastrointestinal tract, spleen and pancreas. Disorders of drainage to, from, or in the liver may lead to portal vein hypertension which may result in varice formation, ascites, splenomegaly, and all of its complications. The most common cause of portal vein hypertension is liver cirrhosis and scartissueformation which result in partial blockage of blood flow passing through the liver. When the portal vein pressure goes up, compensatory shunts are formed from the capillaries connecting the hepatic veins, bypassing the liver first pass metabolism. Elevated systemic nitrogen levels ensue. Hepatic encephalopathy in this setting can occur due to increased nitrogen levels, electrolyte and acid-base disorders, infections, drugs-induced or due to worsening liver failure.

TIPS, a bridge between the portal vein and the hepatic veins, is an alternative therapy refractory portal vein hypertension, ascites and variceal bleeding. However, this increases the immediate postoperative risk of hepatic encephalopathy.

Misleading chest pain #1

30 year old man with acute onset chest pain two hours earlier. Radiation to the neck and left arm.

ECG shows ST-elevation V4-V6 with a hint of ST-elevation V2-V3. The morphology leans towards the convex, valley, side. Reciprocal ST depression might be suspected in limb lead III. The patient informs of a fever and diarrhea for the past three days.

Ultrasound of course:

Can you see the regional wall motion abnormality? The inferolateral part of the apex is affected. So how do we proceed? The history and age raises a suspicion of perimyocarditis, but STEMI must be excluded. An emergency percutaneous coronary angiography was performed and showed absolutely fine coronary artery. The first highly sensitive Troponin T 650. In conclusion myocarditis with localized inferolateral RWMA was diagnosed.

See also Amal Mattu’s approach on how to differ myocardial infarction from pericarditis by ECG.

http://ekgumem.tumblr.com/post/30868011279/ecg-findings-in-pericarditis-vs-stemi-episode

Creeping NSTEMI

35-year-old woman seeking due to exercise-induced chest pain for three days which has now transitioned into constant pain.

ECG on arrival shows ST depression v4-v6.

Repeat ECG after 15 minutes shows regression of the ST-depressions.

The patient has just performed a stress-ECG!

Can you see the regional wall motion abnormality (RWMA)?

In a stepwise fashion, evaluate each region. As a novice it might be difficult to distinguish RWMA from normal myocardium when looking at the heart as a whole. Feel free placing the mouse pointer over the endocardium to look for dynamic changes in the wall thickness. This is referred to as radial contraction.

Systematic review shows RWMA in the apex and the entire lateral wall.

NSTEMI treatment was instituted. Because of persistent chestpain PCI was performed two hours later showing total occlusion of the LCx.

The Whistleblower

It was a sunny July afternoon and time to wrap up for the day. A quick glance at the patient list however, and before you knew it I was taking a history.
Intermittent lower leg edema the last couple of months in a 40-or so woman. Physically active every day. No other complaints. No past medical history and no medication. A pinch of short stature and a pinch of overweight. Vital signs were ok. Lower extremities slender. All in all currently asymptomatic and seemingly well. This was a clear-cut case of thoracic aortic aneurysm involving the roots of the coronary arteries. Now all I had to do was convince the surgeon to perform a composite graft implantation.
A quick physical revealed a diastolic decrescendo murmur 2/6 at IC2-3 left parasternal. No rumbling, anterior mitral leaflet Austin-Flynt murmur over the apex, but it was good enough to justify a bedside echo. Lo and behold, a 6cm wide ascending thoracic aortic aneurysm with a mild aortic insufficiency.

But let’s drop the cool. Was this simply an ad-hoc finding? What was I looking for with the ultrasound? To make things clear, a diastolic murmur always warrants further diagnostics. But was the absent lower extremity edema related to the TAA? Perhaps it was, perhaps it wasn’t, perhaps it was hormones. Her neck was a bit short. Webbing of the neck springs to mind, and as such Noonan and Turner syndromes. Just as in Marfan-, Ehler-Danlos- and Loeys-Dietz syndromes, diseases effecting connective tissue, there is a relation to pathology of the aorta. Did I think of this? No. Upon focused history regarding chest pain, burried beneath a thick layer of anxiety, in the trunk of an old caaar, much was revealed. Onset, location, duration, character, alleviating- & aggravating factors, accessory symptom and radiating pain. First onset one year ago, 1-4 times a week, increasing in frequency lately. Episodes described as sudden in onset, retro sternal, stabbing chest pain radiating to the right arm and back. Aggravate by lifting boxes at work or while straining upon defecation, 5-10 minutes of duration, alleviated by rest.  Accessory symptom of dispnea while lying supine, alleviated by lying in lateralt decubitus. Compression of adjacent organs? She admitted to rationalizing the pain because there was no radiation to the left arm.

Boy oh boy was I worried. A young, vital woman in her prime with an intermittently symptomatic TAA and open heart surgery around the corner. I’ll leave you suspended in mid-air to appreciate the emotional limbo. Goal systolic BP < 120 until then.