don’t jump the gun…

the case.

an elderly male is bought to ED following a high-speed motor vehicle accident having driven his car into a tree at ~100 km/h. He is complaining of severe chest pain & trouble breathing.

Primary survey: 

A. Patent & protected. C-spine immobilised.

B. RR 20. SaO2 99%. Symmetrical chest movement but reduced left-sided air entry. No subcutaneous emphysema.

C. P 100/min. BP 146/80. Warm & perfused. No active bleeding.

D. GCS 15. PEARL (4mm). Moving all 4 limbs.

E. Afebrile. BSL 8. Swollen, deformed LEFT ankle.

You perform your EFAST exam. (There is NO free-fluid in the abdomen & the pericardial view is normal).

2D lung ultrasound: Preservation of pleural sliding with presence of comet-tail artefact – ie. no pneumothorax.

M-mode ultrasound of right chest. Seashore sign present (ie. no pneumothorax).

M-mode ultrasound of right chest. Seashore sign present (ie. no pneumothorax).

2D lung ultrasound: Poorly visualised lung sliding. No comet-tail artefacts. Highly suspicious for pneumothorax.

M-mode ultrasound: Stratosphere (bar-code) sign suggestive of pneumothorax.

M-mode ultrasound: Stratosphere (bar-code) sign suggestive of pneumothorax.

Are you going to place a chest drain on this information ?

Do you get his CT first ??

Would would you do ???

Mobile CXR: marked left upper lobe opacification with distortion of the nearby mediastinal structures.

Mobile CXR: marked left upper lobe opacification with distortion of the nearby mediastinal structures.

This CXR could easily be explained by a traumatic blunt aortic injury, especially given the mechanism of action. The patients overall clinical picture & haemodynamic stability however, made this less likely.

It was at this point that the patients’ wife arrived to explain that he had recently been diagnosed with a left-sided lung cancer which was inoperable.

False positive pneumothorax

I have previously posted on FALSE POSITIVE FAST EXAMS with respect to the abdominal component of the study.

Firstly; some quick revision…
MAKING the DIAGNOSIS of PNEUMOTHORAX on ULTRASOUND.

Requires the following three steps.

  1. abolished lung sliding
  2. stratosphere (bar-code) sign on M-mode
  3. presence of a lung point

CAUSES of FALSE POSITIVE PNEUMOTHORAX.

  • Bullous lung disease
  • Main-stem bronchial intubation
  • Inflammatory adherence.
    • ARDS
    • Pleurodesis
  • Pulmonary contusion/consolidation
  • Atelectasis
  • Severe pulmonary fibrosis
  • Phrenic nerve palsy

Check out this great review on Ultrasound for Pneumothorax at R.E.B.E.L EM…

  1. Volpicelli, G., Elbarbary, M., Blaivas, M., Lichtenstein, D. A., Mathis, G., Kirkpatrick, A. W., et al. (2012). International evidence-based recommendations for point-of-care lung ultrasound. Intensive care medicine, 38(4), 577–591. doi:10.1007/s00134-012-2513-4
  2. Lichtenstein, D. A. (2014). Lung ultrasound in the critically ill. Annals of intensive care, 4(1), 1. doi:10.1186/2110-5820-4-1
  3. Zhang, M., Liu, Z.-H., Yang, J.-X., Gan, J.-X., Xu, S.-W., You, X.-D., & Jiang, G.-Y. (2006). Rapid detection of pneumothorax by ultrasonography in patients with multiple trauma. Critical care (London, England), 10(4), R112. doi:10.1186/cc5004
  4. Nandipati, K. C., Allamaneni, S., Kakarla, R., Wong, A., Richards, N., Satterfield, J., et al. (2011). Extended focused assessment with sonography for trauma (EFAST) in the diagnosis of pneumothorax: experience at a community based level I trauma center. Injury, 42(5), 511–514. doi:10.1016/j.injury.2010.01.105lhop
  5. Slater, A., Goodwin, M., Anderson, K. E., & Gleeson, F. V. (2006). COPD can mimic the appearance of pneumothorax on thoracic ultrasound. Chest, 129(3), 545–550. doi:10.1378/chest.129.3.545

don’t jump the gun…

the case.

an elderly male is bought to ED following a high-speed motor vehicle accident having driven his car into a tree at ~100 km/h. He is complaining of severe chest pain & trouble breathing.

Primary survey: 

A. Patent & protected. C-spine immobilised.

B. RR 20. SaO2 99%. Symmetrical chest movement but reduced left-sided air entry. No subcutaneous emphysema.

C. P 100/min. BP 146/80. Warm & perfused. No active bleeding.

D. GCS 15. PEARL (4mm). Moving all 4 limbs.

E. Afebrile. BSL 8. Swollen, deformed LEFT ankle.

You perform your EFAST exam. (There is NO free-fluid in the abdomen & the pericardial view is normal).

2D lung ultrasound: Preservation of pleural sliding with presence of comet-tail artefact – ie. no pneumothorax.

M-mode ultrasound of right chest. Seashore sign present (ie. no pneumothorax).

M-mode ultrasound of right chest. Seashore sign present (ie. no pneumothorax).

2D lung ultrasound: Poorly visualised lung sliding. No comet-tail artefacts. Highly suspicious for pneumothorax.

M-mode ultrasound: Stratosphere (bar-code) sign suggestive of pneumothorax.

M-mode ultrasound: Stratosphere (bar-code) sign suggestive of pneumothorax.

Are you going to place a chest drain on this information ?

Do you get his CT first ??

Would would you do ???

Mobile CXR: marked left upper lobe opacification with distortion of the nearby mediastinal structures.

Mobile CXR: marked left upper lobe opacification with distortion of the nearby mediastinal structures.

This CXR could easily be explained by a traumatic blunt aortic injury, especially given the mechanism of action. The patients overall clinical picture & haemodynamic stability however, made this less likely.

It was at this point that the patients’ wife arrived to explain that he had recently been diagnosed with a left-sided lung cancer which was inoperable.

False positive pneumothorax

I have previously posted on FALSE POSITIVE FAST EXAMS with respect to the abdominal component of the study.

Firstly; some quick revision…
MAKING the DIAGNOSIS of PNEUMOTHORAX on ULTRASOUND.

Requires the following three steps.

  1. abolished lung sliding
  2. stratosphere (bar-code) sign on M-mode
  3. presence of a lung point

CAUSES of FALSE POSITIVE PNEUMOTHORAX.

  • Bullous lung disease
  • Main-stem bronchial intubation
  • Inflammatory adherence.
    • ARDS
    • Pleurodesis
  • Pulmonary contusion/consolidation
  • Atelectasis
  • Severe pulmonary fibrosis
  • Phrenic nerve palsy

Check out this great review on Ultrasound for Pneumothorax at R.E.B.E.L EM…

  1. Volpicelli, G., Elbarbary, M., Blaivas, M., Lichtenstein, D. A., Mathis, G., Kirkpatrick, A. W., et al. (2012). International evidence-based recommendations for point-of-care lung ultrasound. Intensive care medicine, 38(4), 577–591. doi:10.1007/s00134-012-2513-4
  2. Lichtenstein, D. A. (2014). Lung ultrasound in the critically ill. Annals of intensive care, 4(1), 1. doi:10.1186/2110-5820-4-1
  3. Zhang, M., Liu, Z.-H., Yang, J.-X., Gan, J.-X., Xu, S.-W., You, X.-D., & Jiang, G.-Y. (2006). Rapid detection of pneumothorax by ultrasonography in patients with multiple trauma. Critical care (London, England), 10(4), R112. doi:10.1186/cc5004
  4. Nandipati, K. C., Allamaneni, S., Kakarla, R., Wong, A., Richards, N., Satterfield, J., et al. (2011). Extended focused assessment with sonography for trauma (EFAST) in the diagnosis of pneumothorax: experience at a community based level I trauma center. Injury, 42(5), 511–514. doi:10.1016/j.injury.2010.01.105lhop
  5. Slater, A., Goodwin, M., Anderson, K. E., & Gleeson, F. V. (2006). COPD can mimic the appearance of pneumothorax on thoracic ultrasound. Chest, 129(3), 545–550. doi:10.1378/chest.129.3.545

going the wrong way…

the case.

56 year old male presents to ED with dyspnoea, cough and small-volume haemoptysis.

He has had gradually worsening orthopnoea & reduced exercise tolerance over the past two weeks which is associated with a non-productive cough. Three hours ago however, he became acutely unwell with the development of sharp, left-sided chest pain.

On examination he is febrile, clammy & diaphoretic. He is tachycardic [120/min] & hypotensive [84/50mmHg] with a pan-systolic murmur at his apex. Auscultation of his chest reveals bilateral [right>>left] coarse crackles.

  • Sepsis.
    • Pneumonia
    • Infective endocarditis
    • other…
  • Pulmonary embolism
  • Cardiogenic shock
    • AMI
    • Mitral regurgitation
    • Pericardial effusion
  • Aortic dissection

CXR - admission

Predominate right sided infiltrates, particularly perihilar & right-upper lobe.

You take your trust ultrasound to the bedside, keeping in mind the FALLS protocol…

Screening ECHO:

PLAX, PSAX + subcostal views: LV appears hyperdynamic (even a bit empty) with reasonable contractility.  

Lung Ultrasound:

Lung ultrasound demonstrating numerous B-lines. These were asymmetric (R>>L) and more marked in right upper lobe; suggestive of pulmonary oedema.

Focused Apical Four Chamber:

So…. What are you seeing ?!?!

In the A4C view the posterior mitral leaflet is seen to be prolapsing into the left atrium.

acute mitral regurgitation

A4C image demonstrating mitral valve prolapse with the posterior mitral leaflet billowing into the left-atrium.

Acute mitral regurgitation.

A true surgical emergency, however accurate & timely diagnosis can be difficult.

CAUSES.

  • Chordae or papillary muscle rupture
  • Endocarditis with valve destruction
  • Myocardial ischaemia
  • Acute rheumatic fever with carditis
  • Acute cardiomyopathy
  • Annular dilation with poor coaptation of leaflets
  • Prosthetic valve dysfunction.

CLINICALLY.

The majority of patients with acute mitral regurgitation will present with dyspnoea, haemodynamic instability & symptoms of shock [weakness, dizziness & altered mental state]. Symptoms may also reflect the underlying pathogenesis of the acute regurgitation, however most patients will have no prior history of cardiac disease.

A subset of patients with acute mitral regurgitation may present solely with new-onset dyspnoea & may be diagnosed as a non-cardiac respiratory failure.

The murmur of acute MR is often only a faint systolic murmur, rather than the classic holosystolic heard in chronic MR. This is a result of the rapid equilibration of ventricular & atrial pressures during systole.

ACUTE VS CHRONIC SEVERE REGURGITATION.

Acute vs Chronic MR, acute mitral regurgitation

Comparison of findings in acute & chronic mitral regurgitation. Adapted from Stout & Verrier (3).

CXR findings in Mitral Regurgitation.

  • Typically demonstrates a normal-sized heart with features of pulmonary oedema.
  • Interestingly, [and rarely] acute MR may direct regurgitant flow into a single pulmonary vein resulting in oedema most prominently in that lung segment. This is often [& easily] confused with pneumonia !
acute mitral regurgitation

Unilateral pulmonary oedema. A result of a lateralising MR jet regurgitating into a single pulmonary view. Image courtesy of Attias et al.

ECHO findings in Acute MR.

  • Normal LV size & function
  • Vena contracta >7 mm
  • Decreased aortic valve opening
  • Disrupted mitral valve apparatus
  • Systolic reversal of pulmonary vein flow
  • Vegetation &/or perforation
  • Wall motion abnormalities [ischaemia]

MANAGEMENT.

Surgical = urgent valvuloplasty !!

Medical = support patient prior to valvuloplasty !!

  • Respiratory support:
    • BiPAP
    • Intubation & mechanical ventilation.
  • Haemodynamic support:
    • Cautious fluid administration
    • Vasopressors
    • Consideration for intra-aortic balloon pump counterpulsation.
  • Consider underlying causes especially acute coronary syndrome.
    • ?angiography ± stenting prior to OT.

With his haemodynamics heading in the wrong direction, our patient is admitted to Intensive Care for ongoing vasopressor support and intermittent bursts of non-invasive ventilation.

Formal ECHO:
” Severe prolapse of posterior mitral leaflet. Normal LV size and systolic function”.

Taken to theatre on Day 10 of admission for mitral valve annuloplasty repair. Ruptured chordae found and repaired.

Here is his post-operative CXR….

CXR - postop

Post-op mitral valve repair. Note the sub-diaphragmatic gas, a result of an accidental intraoperative diaphragmatic injury.

He continues to do well.

  1. Boehmeke, T., & Doliva, R. (2006). Pocket Atlas of Echocardiography. Clinical sciences. Thieme.
  2. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
  3. Stout, K. K., & Verrier, E. D. (2009). Acute valvular regurgitation. Circulation, 119(25), 3232–3241. doi:10.1161/CIRCULATIONAHA.108.782292
  4. Mokadam, N. A., Stout, K. K., & Verrier, E. D. (2011). Management of acute regurgitation in left-sided cardiac valves. Texas Heart Institute journal / from the Texas Heart Institute of St. Luke“s Episcopal Hospital, Texas Children”s Hospital, 38(1), 9–19.
  5. Reynolds, H. R., & Hochman, J. S. (2008). Cardiogenic Shock: Current Concepts and Improving Outcomes. Circulation, 117(5), 686–697. doi:10.1161/CIRCULATIONAHA.106.613596
  6. Hanson, E. W., Neerhut, R. K., & Lynch, C. (1996). Mitral valve prolapse. Anesthesiology, 85(1), 178–195.
  7. Sutton, M. S. J. (2002). Mitral Valve Prolapse Prevalence and Complications: An Ongoing Dialogue. Circulation, 106(11), 1305–1307. doi:10.1161/01.CIR.0000031759.92250.F3
  8. Gilbert, B. W., Schatz, R. A., VonRamm, O. T., Behar, V. S., & Kisslo, J. A. (1976). Mitral valve prolapse. Two-dimensional echocardiographic and angiographic correlation. Circulation, 54(5), 716–723. doi:10.1161/01.CIR.54.5.716
  9. Raman, S., & Pipavath, S. (2009). Images in clinical medicine. Asymmetric edema of the upper lung due to mitral valvular dysfunction. The New England journal of medicine, 361(5), e6. doi:10.1056/NEJMicm0801147
  10. Attias, D., Mansencal, N., Auvert, B., Vieillard-Baron, A., Delos, A., Lacombe, P., et al. (2010). Prevalence, Characteristics, and Outcomes of Patients Presenting With Cardiogenic Unilateral Pulmonary Edema. Circulation, 122(11), 1109–1115. doi:10.1161/CIRCULATIONAHA.109.934950
  11. Roach, J. M., Stajduhar, K. C., & Torrington, K. G. (1993). Right upper lobe pulmonary edema caused by acute mitral regurgitation. Diagnosis by transesophageal echocardiography. Chest, 103(4), 1286–1288.
  12. Sudden Cardiogenic Shock – Dr Smith’s ECG Blog. April 2014.

the long way round…

the case.

a 52 year old male presents to your Emergency Department with more than 24 hours of typical sounding, retrosternal chest pain.

He has a prior history of ischaemic heart disease & an LAD stent placed 3 years earlier.

On examination:
Pale & clammy.
P 136/min, BP 104/60 mmHg, SaO2 92% (RA).
RR 30 with slight bilateral crackles.

This is his ECG…

Wrap around LAD lesion

  •  Rate:
    • 138 bpm.
  • Rhythm.
    • Sinus.
  • Axis.
    • Normal [+40*].
  • Intervals.
    • PR ~ 160msec.
    • QRS ~ 80msec.
    • QTc ~ 380msec.
  • Segments.
    • Widespread ST elevation;
      • “Tombstone” STE V1-4 [max ~5mm] w/ associated Q-waves.
      • Concave-up STE V5-6 + lead I
      • Concave-up STE [1-2mm] in inferior leads [II, III + aVF].
    • ST-depression in aVR ~1.5mm.
    • PR segments.
      • Depressed in III + aVF
      • ?subtle elevation in aVR

Interpretation.

Widespread ST-segment elevation consistent with acute anterior “tombstone” ST-elevation myocardial infarction meeting reperfusion criteria.

  • Prior Hx of LAD stent + presence of anterior Q-waves ?stent thrombosis
  • Inferior ST-segment elevation.
    • ?wrap around LAD
    • ???associated pericarditis.

The presence of tachycardia, basal crackles and borderline hypotension is concerning for early cardiogenic shock.

This patient warrants early Cardiology involvement and prompt transfer for PCI.

Left ventriculogram:

  • Ejection fraction ~ 49%
  • Regional wall motion abnormalities:
    • Anterolateral akinesis
    • Apical akinesis
    • Inferior hypokinesis

Angiogram:

Left coronary…

100% mid-LAD occlusion → successfully stented [see below]

Occluded mid-LAD.

Occluded mid-LAD.

Right coronary…

Despite the inferior changes, the RCA was pristine.

Wrap around LAD.

ECG. 

  • Simultaneous ST-segment elevation in the precordial and inferior leads.

In the presence of anterior STEMI, the amount of ST depression in the inferior leads is typically predictive of a more proximal LAD lesion. Even in the presence of a wrap-around LAD (ie. with inferior wall transmural ischaemia), almost all LAD occlusion proximal to D1 is show inferior ST depression.

A more distally occluded LAD is thought to be a prerequisite for isoelectric inferior ST-segments.

Additional ECG findings suggestive of a wrap-around LAD include ST-depression in lead III (with a positive T-wave) associated with ST-elevation in aVL.

Anatomically.

  • Occurs due to an occlusion of a variant “type III” LAD.
  • This wraps around the cardiac apex, supplying both the anterior and [partial] inferior walls of the left ventricle.
Left anterior descending anatomy. Reference (3)

Left anterior descending anatomy. Reference (3)

In our patients’ case;

Wraparound LAD

Wraparound LAD (labelled)

For more examples of wrap around LAD lesions check out the following from Dr Smith’s ECG Blog;

  1. 24 yo woman with chest pain: Is this STEMI? Pericarditis?
  2. Pericarditis, or Anterior STEMI? The QRS proves it.Hyperacute T-waves, with a Twist
  3. Hyperacute T-waves, with a Twist.

Interestingly, the combination of anterior and inferior ST-segment elevation appears to be associated with limited AMI size and better preserved LV function (when compared to anterior STEMIs with either isoelectric or depressed inferior ST segments).

Mind the gap…

the case.

a 29-year old female with a past history of anorexia nervosa, polycystic ovarian syndrome, chronic back pain and analgesic abuse presents to the Emergency Department.  She describes 3 days of bilateral ankle and facial swelling.  She tells you that she has been taking ‘lots of painkillers’ for her back pain.

On examination she appears well.  Her physical examination is only remarkable for perioribtal and bilateral ankle oedema.

Common causes:

  • Cardiac.
    • Systolic dysfunction
    • Diastolic dysfunction
    • Cor pulmonale
  • Vascular.
    • Deep vein thrombosis
    • Chronic venous insufficiency
  • Renal.
    • Nephrotic syndrome
    • Renal failure
  • Hepatic.
    • Cirrhosis
  • Pregnancy.

Not-so-common causes:

  • Cardiac:
    • Pericardial effusion
    • Constrictive pericarditis
    • Tricuspid regurgitation
  • Obstructive sleep apnoea
  • Protein-losing enteropathy
  • Lymphoedema
  • Hypothyroidism / Myxoedema
  • Medication-induced:
    • Calcium-channel blockers
    • Steroids
    • NSAIDS
    • Monoxidine
    • Gabapentin / pregabalin
    • Thiazolidinediones

Initial VBG

  • Primary metabolic acidosis.
    • pH 7.01, HCO3 9, BE -22. pCO2 33.
  • Expected CO2.
    • [HCO3 x 1.5] +8  (±2) – Winter’s formula
    • [9x 1.5] +8
    • 21.5 (±2)
    • Incomplete respiratory compensation or concomitant/additional respiratory acidosis.
  • Anion gap.
    • Na – [Cl - HCO3]
    • 138 – [120 + 9]
    • 9 - ie. normal.
  • Delta ratio.
    • [AG - 12 / 24 - HCO3]
    • [ 9-12 / 24 - 9 ]
    • 3 / 15
    • 0.2 ~ pure NAGMA.
  • Hyperchloraemia.
    • Likely contributing to the non-gap acidosis.
  • Normokalaemia.
    • In the setting of severe metabolic acidosis, this however likely represents marked whole-body depletion.
    • With expectation that this will fall with correction of acidosis, this requires early replacement & serial rechecks.
  • Moderate renal impairment.
    • Urea 16.4, Creatinine 164.
    • ?acute vs chronic
    • May be contributing to (1) acidosis via uraemia & (2) the patients oedematous state !!

Interpretation.

Life-threatening, non-anion gap metabolic acidosis with incomplete respiratory compensation (or concomitant respiratory acidosis).

Causes of non-anion gap metabolic acidosis

Causes of non-anion gap metabolic acidosis

This can essentially be subdivided into three groups;

  1. Loss of base via kidney [eg. RTA]
  2. Loss of base via bowel [eg. diarrhoea]
  3. Gain of mineral acid [eg. HCl infusion]

URINARY ANION GAP [UAG].

  • = urinary anions – urinary cations.
  • = [Na+] + [K+] – [Cl-]

The urinary anion gap can help to differentiate between GIT and renal causes of a hyperchloraemic metabolic acidosis.

  • It provides a indirect index of urinary ammonium excretion.
  • Ammonium is positively charged so a rise in its urinary concentration (ie increased unmeasured cations) will cause a fall in UAG (as this is paralleled by an increase in Cl- excretion)
  • Principle idea: UAG ≈ concentration of ammonium [- unmeasured anions, which remains essentially constant]

NEGATIVE-UAG.

  • Loss of base via bowel - negGUTive !
  • ie. kidneys can respond by increasing ammonium excretion [to balance H+], ∴ reducing UAG.

POSITIVE-UAG.

  • Loss of base via kidney.
  • ie. the kidney is unable to increased ammonium excretion to balance H+.

Here is her URINE CHEMISTRY…

Urine chemistry demonstrating a raised urinary anion-gap

Urine chemistry demonstrating an elevated urinary anion-gap

  • UAG = [Na+] + [K+] – [Cl-]
  • = [87+16] – [54]
  • = 49 ∴ elevated !!

The on-call Renal Physician feels this is likely a case of distal renal tubular acidosis (dRTA) caused by her ibuprofen ingestion.  She is admitted to HDU and treated with IV bicarbonate and potassium replacement….

Renal tubular acidosis.

A group of disorders in which, due to either abnormal bicarbonate reabsorption (proximal) or hydrogen ion excretion (distal), results in development of a metabolic acidosis.

The basics.

  • Hyperchloraemic (non-anion gap) metabolic acidosis
  • Does not impair glomerular filtration
  • There are three major subgroups of RTA’s with different clinical characteristics;
    1. Distal (Type 1) RTA
    2. Proximal (Type 2) RTA
    3. Hypoaldosteronism (Type 4) RTA
Types of renal tubular acidosis

Features of subtypes of Renal Tubular Acidosis

Causes.

Type 1.

  • Idiopathic
  • Autoimmune diseases – Sjogren’s, SLE, rheumatoid arthritis, primary biliary cirrhosis, chronic active hepatitis, congenital adrenal hyperplasia
  • Calcium disorders - primary hyperparathyroidism, vitamin D toxicity, hypercalcaemic hyperthyroidism
  • Drugs/toxins – amphotericin B, lithium, toluene, amiloride, analgesic abuse
  • Renal - renal transplant rejection, medullary sponge kidney, obstructive + reflux uropathy

Type 2.

  • Associated with other proximal tubule defects
  • Fanconi syndrome
  • Heavy metals
  • Renal transplant, medullary cystic disease, recurrent nephrolithiasis
  • Chemotherapy
  • Amyloidosis

Type 4.

  • Adrenal insufficiency – Addison’s disease, hypoaldosteronism, congenital adrenal hyperplasia
  • Hyporeninaemia
  • Drugs – NSAIDs, ACE inhibitors, cyclosporin, amiloride, spironolactone, trimethoprim
  • Diabetes
  • Interstitial nephropathies – obstructive, medullary-cystic, drug-induced, transplant-rejection + AIDS nephropathy
  • Analgesic nephropathy.

Specific to this case…

There are multiple case reports of Ibuprofen causing a distal RTA, usually when taken in excessive doses.  Such doses are most commonly taken in combination analgesics that also contain codeine.  Although the mechanism is unknown it is postulated that it may involve inhibition of carbonic anhydrase.  It may be associated with marked hypokalaemia and hypokalaemic paralysis.

Management.

  • Treat the underlying cause / Remove the precipitant.
  • Correct the acidosis;
    • Alkali therapy [sodium bicarbonate]
      • DISTAL RTA ~ typically 1-4 mmol/kg/day !
      • PROXIMAL RTA requires very large quantities of alkali [up to 10-20 mmol/kg/day]
      • Ideally mixture of both Na+ & K+ salts.
    • Aims to provide adequate base to balance H+ production.
  • Correction of hypercalciuria.
  • Correct electrolytes.
    • Cautious potassium replacement.

  • Over the next 24 hours, the acid-base disturbance returns to essentially normal.
  • Unfortunately she signs herself out of hospital on Day 3 & is lost to follow-up….

  1. Bersten AD, Soni N. Oh’s Intensive Care Manual (6th edition), Butterworth-Heinemann 2009.
  2. Overview of renal tubular acidosis – UpToDate.com
  3. Rodríguez Soriano, J. (2002). Renal tubular acidosis: the clinical entity. Journal of the American Society of Nephrology : JASN, 13(8), 2160–2170. doi:10.1097/01.ASN.0000023430.92674.E5
  4. Ring, T., Frische, S., & Nielsen, S. (2005). Clinical review: Renal tubular acidosis–a physicochemical approach. Critical care (London, England), 9(6), 573–580. doi:10.1186/cc3802
  5. Ng, J. L., Morgan, D. J. R., Loh, N. K. M., Gan, S. K., Coleman, P. L., Ong, G. S. Y., & Prentice, D. (2011). Life-threatening hypokalaemia associated with ibuprofen-induced renal tubular acidosis. The Medical Journal of Australia, 194(6), 313–316.
  6. BMJ Best Practice: Assessment of Peripheral Oedema
  7. The Urinary Anion Gap – AnaesthesiaMCQ.com
  8. Acidosis in Kidney Disease - Paul Young’s Intensive Care Mind Maps 
  9. Renal Tubular Acidosis and Uraemic Acidosis – Life in the Fast Lane

Author: Jimmy Bliss
Web editing + additional writing: Chris Partyka

FALLS protocol…

Below is the main content discussed at an ultrasound workshop I ran this week at the Sydney HEMS Clinical Governance Day.

Whilst the bread & butter use of prehospital ultrasound would have to be an extended-FAST scan in the setting of trauma, I decided to focus more on utility of basic ECHO & lung ultrasound in the assessment of shocked medical patients.

A lot has been written about the RUSH protocol and its role in aiding the diagnosis of undifferentiated shock/hypotension. From my own experience (in initiating patient transfers, not conducting them), a source of shock is largely defined by the time an inter-hospital retrieval takes place (ie. abdominal aortic aneurysms excluded by history, examination or ED ultrasound).

When faced with the ongoing ED-based resuscitation of shocked patients (esp. those with septic shock & refractory hypotension), I find myself using a process similar to Lichtenstein’s FALLS protocol which I believe can be carried into the arena of retrieval medicine to guide ongoing therapy (and potentially alter outcomes).

The FALLS protocol.

This is a tool proposed to assist in the management of shocked patients, mainly by the use of lung ultrasound.

Firstly, it aims to exclude obstructive shock by

  1. Cardiac ECHO.
    • ?tamponade
    • ?massive pulmonary embolism with right heart strain
  2. Lung USS.
    • ?tension pneumothorax.

The second phase aims to assess volume status by exploiting ultrasound lung-artefact to detect interstitial syndrome (suggestive of extravascular lung water).

  1. B-Profile.
    • ie. cardiogenic shock – supported by distended, non-compressing inferior vena cava & the presence of pleural effusions.
    • alternatively; signals appropriate volume replacement & a trigger to start vasopressors to maintain blood pressure.
  2. A-Profile.
    • suggestive of hypovolaemic or distributive shock.
    • triggers further fluid administration.
FALLS Protocol - Lichtenstein, 2012.

FALLS Protocol – Lichtenstein, 2012.

Below are the images & ultrasound clips used in my presentation, demonstrating the significant findings at each stage of the protocol.

Early tamponade with RV diastolic collapse.

 

Massive pericardial effusion with obvious tamponade. Dx: Malignant effusion 2* to NSCLC.

 

Massive pericardial effusion with features of tamponade.
NB. the both right atrial and right ventricular diastolic collapse.

Pulse wave doppler measuring MV inlet velocities. ~25% variation through respiratory cycle suggests tamponade physiology.

Pulse wave doppler measuring MV inlet velocities. ~25% variation through respiratory cycle suggests tamponade physiology.

For more information on features of tamponade check out “Sequential sinister sightings…” !!

Submassive PE.
Severe dyspnoea with A-a gradient > 500 !! Normotensive, but elevated serum troponin.

 

Massive pulmonary embolism.
Elderly male with undifferentiated shock, hypoxia and abdominal pain.

Features of right ventricular strain in PE.

  1. RV:LV (end-diastolic diameter) > 0.9 – A4C or subcostal view.
  2. RV end-diastolic diameter > 30mm – PLAX or PSAX view.
  3. Hypokinetic RV free wall
  4. Tricuspid regurgitant jet velocity > 2.6m/s
  5. Paradoxical interventricular septal motion
  6. McConnell’s sign - akinesia of the RV-mid free wall with normal motion at the RV apex.

For further discussion on the role of thrombolysis in pulmonary embolism check out “Two in two days…

Normal lung sliding. Comet tails + A-line artefact present.

Normal lung ultrasound. Comet-tail artefact present with obvious A-lines.

Normal lung ultrasound. Comet-tail artefact present with obvious A-lines.

M-mode image. Sandy beach sign. No pneumothorax.

M-mode image. Sandy beach sign. No pneumothorax.

 

Pneumothorax present. No visible comet tails, no lung sliding.

M-mode ultrasound demonstrating a 'bar-code' sign, consistent with pneumothorax.

M-mode ultrasound demonstrating a ‘bar-code’ sign, consistent with pneumothorax.

 

Bilateral B-lines ['lung rockets'] consistent with pulmonary oedema/interstitial syndrome.

7 criteria for B-lines.

  1. There is a comet-tail, vertical artefact.
  2. Arises from the pleural line.
  3. Moves in concert with lung sliding.
  4. Does not fade.
  5. Well-defined, laser like.
  6. Hyperechoic.
  7. Obliterates the A-lines.

In the BLUE-protocol detection of interstitial syndrome to anterior chest, bilaterally (with lung-sliding) makes the diagnosis of haemodynamic pulmonary oedema with 97% Sn & 95% Sp.

Differential diagnoses of B-lines;

  • pulmonary contusion
  • pneumonia
  • pulmonary fibrosis

Bilateral A-lines with lung sliding.

 

The presence of A-profile in a shocked patient = a FALLS responder. This suggests a hypovolaemic or distributive contributor to shock & correlates with pulmonary artery occlusion pressures of < 18mmHg [Sp 93%, PPV 97%].

The protocol recommends further fluid boluses with serial assessment by lung-ultrasound, looking specifically for change from A-lines to B-lines. At this stage, vasopressors would be started.

FALLS protocol + lung ultrasound

  • Lichtenstein, D. A., & Mezière, G. A. (2008). Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest134(1), 117–125. doi:10.1378/chest.07-2800
  • Lichtenstein, D. (2013). FALLS-protocol: lung ultrasound in hemodynamic assessment of shock. Heart, lung and vessels, 5(3), 142–147.
  • Lichtenstein, D. A. (2014). Lung ultrasound in the critically ill. Annals of intensive care, 4(1), 1. doi:10.1186/2110-5820-4-1
  • Mount Sinai Emergency Medicine Ultrasound.

RUSH protocol.

ECHO for Pulmonary Embolism.

  • MD, S. D., et al. (2014). Right Ventricular Dilatation on Bedside Echocardiography Performed by Emergency Physicians Aids in the Diagnosis of Pulmonary Embolism. Annals of Emergency Medicine, 63(1), 16–24. doi:10.1016/j.annemergmed.2013.08.016
  • Rudski, L. G.., et al. (2010). Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography, 23(7), 685–713– quiz 786–8. doi:10.1016/j.echo.2010.05.010
  • Meyer, G., Vicaut, E., Danays, T., Agnelli, G., Becattini, C., Beyer-Westendorf, J., et al. (2014). Fibrinolysis for Patients with Intermediate-Risk Pulmonary Embolism. The New England journal of medicine, 370(15), 1402–1411. doi:10.1056/NEJMoa1302097
  • Sosland, R. P., & Gupta, K. (2008). Images in cardiovascular medicine: McConnell’s Sign. Circulation, 118(15), e517–8. doi:10.1161/CIRCULATIONAHA.107.746602
  • REBEL EM.

 

For a great bibliography on the evidence available for prehospital ultrasound, check out Cliff’s Resus.me.

Special thanks to Dr Justin Bowra for his assistance & advice with putting this together.