Patients presenting with severe alcoholic hepatitis (Discriminant Function value ≥32) have high short-term mortality and may benefit from treatment with glucocorticoids.

Prednisolone is used as oppose to prednisone for 28 days (with taper).

 

WHY? Prednisone requires conversion to prednisolone (the active metabolite) in the liver. This process may be impaired in alcoholic hepatitis.

 

REFERENCES

  1.  Ramond MJ, Poynard T, Rueff B, Mathurin P, Theodore C, Chaput JC, Benhamou JP. A randomized trial of prednisolone in patients with severe alcoholic hepatitis. N Engl J Med 1992; 326:507. 
  2. Friedman SL, McQuaid KR, Grendell JH, et al. Current Diagnosis & Treatment in Gastroenterology, 2nd ed, McGraw-Hill Medical 2002.

Distinguishing between the coagulation abnormalities of liver disease vs. Disseminated intravascular coagulation (DIC) can be difficult as clinical and biochemical findings are similar.

However, Factor VIII levels are usually increased or normal in liver disease. 

Whereas, Factor VIII levels are decreased in DIC.

WHY? Factor VIII is produced in endothelial cells rather than the liver; hence it is not affected by the process of cirrhosis.

REFERENCES

  1. Senzolo M, Burra P, Cholongitas E, Burroughs AK. New insights into the coagulopathy of liver disease and liver transplantation. World J Gastroenterol. 2006;12(48):7725-36.
  2. Mammen EF. Coagulation abnormalities in liver disease. Hematol Oncol Clin North Am. 1992 Dec;6(6):1247-57.

Hoover’s sign refers to the paradoxical inspiratory retraction of the rib cage and lower intercostal

interspaces. Normally, the costal margin moves minimally during the regular respiratory cycle. However, if it does, it moves outward and upward.

It is commonly seen in COPD. However, it may also be seen in numerous other conditions (i.e congestive heart failure, asthma, severe pneumonia etc.)

It results from alterations in dynamics of diaphragmatic contraction due to hyperinflation, resulting in traction on the rib margins by the flattened diaphragm.

REFERENCES

  1. Klein M: Hoover sign and peripheral airways obstruction. JPediatr 1992, 120:495-496.
  2. Johnston, Chambless R et al. “The Hoover’s Sign of Pulmonary Disease: Molecular Basis and Clinical Relevance” Clinical and molecular allergy: CMA vol. 6 8. 5 Sep. 2008

Malar rash (also known as the “butterfly rash,”) is an acute manifestation of lupus (SLE) seen in over 50% of patients. It is a bilateral, erythematous maculopapular rash which spares the nasolabial folds. The rash will last anywhere from days to weeks, and it can be painful/ itchy. It is a photosensitivity phenomenon.

Suspected Mechanism: the nasolabial folds are a relatively UV protected surface and therefore less affected.

REFERENCES:

  1. Amre Nouh, Jodi Speiser, José Biller. Chapter 3 – Acquired neurocutaneous disorders. Handbook of Clinical Neurology. Volume 132, 2015, Pages 29-73
  2. Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology, 8e. Klaus Wolff, Richard Allen Johnson, Arturo P. Saavedra, Ellen K. Roh. THE SKIN IN IMMUNE, AUTOIMMUNE, AUTOINFLAMMATORY, AND RHEUMATIC DISORDERS.

Up to 40% of inferior wall Myocardial infarctions have associated right ventricular involvement. Venodilation and medications that decrease RV filling (i.e nitrates, diuretics) should be avoided.

WHY?

The right ventricle contains less myocardial tissue compared to the left ventricle. It is more dependent on adequate preload (Frank-Starling curve) to assure adequate cardiac function (CO). If there is damage to the right ventricle, preload reduction from nitrates/ diuresis could result in significant hypotension.

REFERENCES

  1. Albulushi A., et al. Acute right ventricular myocardial infarction. Expert Rev Cardiovasc Ther. 2018 Jul;16(7):455-464.
  2. Bouhuijzen LJ, Stoel MG. Inferior acute myocardial infarction with anterior ST-segment elevations. Neth Heart J. 2018 Oct;26(10):515-516.
Ventricular interdependence occurs when there is discordance. This results from the heart ventricles filling out of phase with one another. It is an important physiological manifestation of cardiac tamponade and constrictive pericarditis.

The ventricles experience impaired diastolic relaxation secondary the constrictive pericardium and are unable to fully expand. During inspiration, the right ventricle will fill and shift the interventricular septum to the left reducing its filling capacity. During expiration, the opposite will occur with the interventricular septum moving to the right.
REFERENCES
  1. Santamore WP, Dell’Italia LJ. Ventricular interdependence: significant left ventricular contributions to right ventricular systolic function. Prog Cardiovasc Dis. 1998 Jan-Feb;40(4):289-308.
The clot CAUSES Dead space; which does not cause hypoxia/hypoxemia on its own.
ALWAYS ASK ABOUT: 
  1. Resp Rate (PE creates dead space, reduced alveolar ventilation, CO2 increases and patient attempts to blow off CO2)
  2. Blood pressure (?Obstructive shock from large saddle PE)
  3. Tachycardia (Left heart trying to increase cardiac output because stroke volume low) 
Image Credit: Dr. Douglas Mckim, MD
Mechanisms by which a PE might cause Hypoxia/Hypoxemia:
  1. Significant V/q Mismatch
  2. Pain -> Splinting and atelectasis
  3. Inflammation causing infarction +/- superimposed pneumonia 
  4. Increased pulmonary vascular resistance; potentiating right heart strain and cardiac stunting if PFO present

REFERENCES

  1. Huet Y, Lemaire F, Brun-Buisson C, Knaus WA, Teisseire B, Payen D, Mathieu D. Hypoxemia in acute pulmonary embolism. Chest. 1985 Dec;88(6):829-36.
  2. Santolicandro A, Prediletto R, Fornai E, Formichi B, Begliomini E, Giannella-Neto A, Giuntini C. Mechanisms of hypoxemia and hypocapnia in pulmonary embolism. Am J Respir Crit Care Med. 1995 Jul;152(1):336-47.
  3. Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P, Bengel F, Brady AJ, Ferreira D, Janssens U, Klepetko W, Mayer E, Remy-Jardin M, Bassand JP. Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J. 2008 Sep;29(18):2276-315. 

It is common teaching to be judicious when interpreting the thoracentesis results of patients receiving diuretic therapy. It is stated, their pleural LDH will often be elevated and result in them being misclassified as exudative effusions when they are in fact transudative.

WHY?

Currently, the mechanism is not entirely clear, but proposed mechanisms include:

  • Lactate dehydrogenase (LDH) is an intracellular protein responsible for catalysing the conversion of lactate to pyruvic acid. It tends to leak during cellular injury or lysis.
  • Thus, any patient with repeated or bloody thoracentesis, the LDH may be elevated secondary to RBC lysis (blood) or local trauma from the thoracentesis; repeated attempts augmenting that damage.
  • LDH is primarily created by the liver, and in patients with CHF, hepatic congestion/ release upon diuresis may play a role in its elevation in pleural fluid.
  • Diuretics move water via diffusion; from the extravascular (pleural space) to the blood, leading to an increase in the protein and LDH concentration in the pleural cavity.

REFERENCES

  • Bielsa, J.M. Porcel, J. Castellote, et al. Solving the Light’s criteria misclassification rate of cardiac and hepatic transudates. Respirology, 17 (2012), pp. 721-726
  • Mitrouska I, Bouros D. The Trans-Exudative Pleural Effusion. CHEST, Volume 122, Issue 5, 1503 – 1505
  • Broaddus, V. Diuresis and transudative effusions—changing the rules of the game. The American Journal of Medicine, Volume 110 , Issue 9 , 732 – 735

Aspiration events have a gravity-based predilection, meaning the lobes/ lung segments in the most dependent positions are likely affected. Also, the right main bronchus has a larger luminal diameter and more vertical trajectory than the left main bronchus making it more susceptible to aspirated content.

Lobes of the lungs most likely to be affected by aspiration include:

Upright: The lower lobes (Right>Left)

Supine: Superior segments of the lower lobes (Right>Left) or posterior segment of the RIGHT upper lobe. This is typically in patients with altered LoC (i.e Alcoholics, Intubated patients etc.).  

REFERENCES:

  1. Kuhajda, Ivan et al. “Lung Abscess-Etiology, Diagnostic and Treatment Options.” Annals of Translational Medicine 3.13 (2015): 183. PMC. Web. 14 Sept. 2018.
  2. Kim M, Lee KY, Lee KW et-al. MDCT evaluation of foreign bodies and liquid aspiration pneumonia in adults. AJR Am J Roentgenol. 2008;190 (4): 907-15.
  3. Moreira Jda S, Camargo Jde J, Felicetti JC, et al. Lung abscess: analysis of 252 consecutive cases diagnosed between 1968 and 2004. J Bras Pneumol 2006;32:136-43.

As its name suggests, Monoarticular involves one joint.

Oligoarticular is defined as involving greater than one joint but less than 5 joints.

Polyarticular is defined as greater than or equal to 5 joints.

This pattern/ number of joint involvement is typically defined within the first 6 months of disease onset.

REFERENCES

  1. Macaubas C, Nguyen K, Milojevic D, Park JL, Mellins ED. Oligoarticular and polarticular JIA: epidemiology and pathogenesis. Nature reviews Rheumatology. 2009;5(11):616-626. doi:10.1038/nrrheum.2009.209.
  2. Lin YT, Wang CT, Gershwin ME, Chiang BL. The pathogenesis of oligoarticular/polyarticular vs systemic juvenile idiopathic arthritis. Autoimmun Rev. 2011 Jun;10(8):482-9. doi: 10.1016/j.autrev.2011.02.001. Epub 2011 Feb 12.