against better judgement…

the case.

a 62 year old female is bought into your ED following a high-speed MVA. She has driven her car into telegraph pole at ~ 80km/hr.

She is haemodynamically stable, with an unremarkable primary survey. Of note, she has an obvious seat-belt abrasion over her anterior chest with significant sternal tenderness on palpation.

This is her mobile CXR taken in the resus-bay….

mobile CXR

Clearly her chest x-ray is abnormal. Whilst it is a poor inspiratory film [& the patient is supine], there is an abnormal mediastinal contour which is markedly widened. The trachea is also deviated to the right side.

In the setting of a moderate deceleration mechanism, this raises the suspicion of a blunt aortic injury. She needs to get to CT quickly…

In the meantime;

  • Two large-bore IVs are sited
  • Fentanyl administered for analgesia
  • EFAST performed: difficult study 2* to habitus. Possible LUQ free fluid.

Within the next 10 minutes she is transported to radiology for a CT ‘pan scan’….

 

  • Small 16×6 mm focal traumatic aortic dissection of the inner curvature of the aorta ~1.5cm distal to the origin of the left subclavian artery.
    • No other intrathoracic injuries
  • Multiple (undisplaced) pelvic fractures.
    • Left sacral ala
    • Anterior column of left acetabulum
    • Left pubic bone
    • Left inferior pubic rami
  • No intraabdominal injuries.
  • CTB + C-spine reported as normal also.

So let’s have a closer look…

Dissection01    Dissection02

Marked Dissection

Marked dissection 2

… with a pulse rate of 66 per minute & a blood pressure of 172/98.

What are you going to do now ?!?

This is a trauma patient with a blunt aortic injury. Extrapolating from the non-traumatic aortic dissections, you recognise the importance of both heart rate and blood pressure control in this scenario however cannot help but question the role of β-blockers & vasodilators in a patient with pelvic fractures & an equivocal FAST scan.

Against better judgement you commence a sodium nitroprusside infusion…

TRAUMATIC AORTIC DISSECTION.

Blunt aortic injury is the second most common cause of death from blunt trauma following head injury.

The classic teaching of traumatic aortic injury is that it carries a dismal prognosis; that is 90% die at the scene and of the remaining 10%, 50% die within 24 hour and 90% will be dead within 4 months !! It is  It is important to recognise that this data originates from the 1950′s and now with the advent of endoluminal repairs one would expect better survival rates…

Current numbers suggest;

  • 50% of aortic injuries will rupture within 24 hours (~80% within the 1st week)
  • Overall mortality for those surviving to hospital evaluation is ~31%.

The most common location of injury is the aortic isthmus, accounting for 75-95% of cases. Whilst the aorta can be injured directly, there are several theories of various indirect forces resulting in aortic injury;

  • During deceleration the mobile heart & ascending aorta swing forward and can result in intimal tearing at the isthmus, where the descending aorta is fixed to the posterior chest wall.
  • Sudden rise in intraabdominal pressure creates a water-hammer effect within the aorta.
  • Osseous pinch results in entrapment of the aorta between the anterior chest wall & the vertebral column.
Aortic Isthmus. *adapted from http://en.wikipedia.org/wiki/Aorta

Aortic Isthmus.
*adapted from http://en.wikipedia.org/wiki/Aorta

Osseous pinch theory for Blunt Aortic Injury *adapted from "decode-medicine.blogspot.com.au"

Osseous pinch theory for Blunt Aortic Injury                                                                   *adapted from “decode-medicine.blogspot.com.au”

For more information on Aortic Dissection, especially clinical features, diagnostic tools and management - check out thebluntdissection – chest pain and… !!

WHEN SHOULD WE SUSPECT THIS INJURY ?

MECHANISM.

Blunt aortic injury most often occurs after sudden deceleration, typically motor vehicle accidents (72% from ‘head-on’ collisions). Other causes include;

  • motor cycle or aircraft crashes
    • especially unrestrained drivers or ejected passengers.
  • pedestrian vs car
  • falls (>10 feet, 3 meters)
  • crush or compression injury

CLINICAL FEATURES.

  • Chest (± back) pain
  • Dyspnoea
  • Hoarseness
  • 1st & 2nd rib fractures or sternal fracture
  • Multiple rib fractures (or flail chest)
  • Posterior displaced clavicle fracture
  • Brachial plexus injury
  • Palpable supraclavicular mass
  • Unexplained chest haematoma
  • Blood pressure differentials or pulse deficit

RADIOLOGICALLY (Chest Xray).

  • Widened mediastinum (>8cm)
  • Mediastinal/chest width ratio > 0.38
  • Obscured aortic knob
  • Depressed left main bronchus
  • Large haemothorax
  • Opacification of aorto-pulmonary window
  • Widened paratracheal & paraspinous stripes
  • Left apical cap
  • NG tube deviation
  • Others;
    • 1st or 2nd rib fractures
    • Multiple rib fractures
    • Sternal fracture
    • Posteriorly displaced clavicle fracture

MANAGEMENT.

Once the diagnosis is made, treatment must be timed properly. Whilst immediate operative repair used to be the rule, several studies now support a delayed repair with tight haemodynamic control especially with coexisting traumatic injuries such as head injury, exsanguinating bleeding, pelvic injuries or lung injury. The following table highlights this decision process;

adapted from TRAUMA.org

adapted from TRAUMA.org

In the unstable patient, management focuses on concomitant resuscitation whilst detecting and correcting the underlying cause of haemorrhage. It is important however, to avoid over resuscitation.

ASSOCIATED INJURIES.

Associated injuries

MEDICAL THERAPY.

Careful, meticulous blood pressure control is mandatory until definitive surgical repair can be performed. If operative repair is delayed, then systolic blood pressure should be corrected to 100-120 mmHg.

Whilst there are many feasible ways of doing this (depending on available medications & local practices), the key is to avoid rebound tachycardia which can increase shear stress on the intimal flap (ie. lowering the dP/dT). Therefore beta-blockers are often utilised with the vasodilator agent (eg. esmolol + nitroprusside), aiming for a pulse rate of 60 per minute.

SURGICAL vs ENDOVASCULAR REPAIR.

Open surgical repair is usually indicated for;

  • Haemodynamic instability
  • Large-volume haemorrhage from chest tubes
  • Contrast extravasation on CT (or rapidly expanding mediastinal haematoma)
  • Penetrating aortic injury

Endovascular repair has documented benefits such as reduced blood loss, minimally invasive approach, allowance for neuroprotective positioning and reduction in rates of paraplegia. A significant limitation at present is, if the aortic injury occurs adjacent to a sharp bend the graft may provide poor apposition and risks device collapse. Proximity to the left subclavian artery can also result in ischaemia and care must be taken in those with a dominant left vertebral circulation.

… with the nitroprusside infusion trickling in her blood pressure gradually drifts down to 120 mmHg systolic !! Interestingly her pulse rate does not budge & you wonder if she is pre-morbidly beta-blocked. This was not clarified at the time due to language barrier.

Behind the scenes, arrangements are made with Interventional Radiology and Vascular Surgery to proceed to the angiography suite.

Here are her images…

Angio01    Post stent

Following an uneventful procedure, she is transferred to Intensive Care for ongoing observation and tight blood pressure control.

Here is her CXR on day 2…

day 2 CXR

She continues to make a slow but steady recovery….

  1. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
  2. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
  3. Parmley, L. F., et al. (1958). Nonpenetrating traumatic injury of the aorta. Circulation, 17(6), 1086–1101. doi:10.1161/01.CIR.17.6.1086
  4. Dosios, T. J., Salemis, N., Angouras, D., & Nonas, E. (2000). Blunt and penetrating trauma of the thoracic aorta and aortic arch branches: an autopsy study. The Journal of Trauma: Injury, Infection, and Critical Care, 49(4), 696–703.
  5. Reed KC & Curtis LA. Aortic Emergencies – Part II: Abdominal Aneurysms And Aortic Trauma. Emergency Medicine Practice. 2006; Volume 8, Number 3.
  6. Nagy, K., Fabian, T., Rodman, G., Fulda, G., Rodriguez, A., & Mirvis, S. (2000, June). Guidelines for the diagnosis and management of blunt aortic injury: an EAST Practice Management Guidelines Work Group. The Journal of Trauma: Injury, Infection, and Critical Care48(6): 1128-43.
  7. Fabian TC, Davis KA, Gavant ML,et al. Prospective study of blunt aortic injury: helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg. 1998;227:666-76
  8. Traumatic Aortic Injury – trauma.org

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