Serum Creatinine can be a deceptive surrogate during an acute kidney injury. It may lag behind acute onset renal failure and misrepresent the current degree of renal impairment.

RULE OF THUMB: During an AKI, a creatinine rise of 1-1.5mg/dL (88.4-132.6umol/L) per day is considered an anephric rise. It is the average expected rise in a person with a GFR of 0mL/minute.

Example: Cr rise of 1mg/dL to 2mg/dL is considered an “anephric rise”.

REFERENCES

  1. Chen, S. Retooling the Creatinine Clearance Equation to Estimate Kinetic GFR when the Plasma Creatinine Is Changing Acutely. JASN Jun 2013, 24 (6) 877-888; DOI: 10.1681/ASN.2012070653
  2. Appendix C: Tables, conversions and abbreviations. Nephrol Dial Transplant (2004) 19 [Suppl 2]: ii42–ii43DOI: 10.1093/ndt/gfh1030
Macrophage activation syndrome (MAS) is a life-threatening complication of rheumatic diseases (i.e SLE, Juvenile idiopathic arthritis, Adult onset Still’s disease).
Hemophagocytic lymphohistiocytosis (HLH) is an inherited disease, whereas secondary HLH is triggered by other diseases, including infections (i.e EBV, HSV, CMV), malignancy (i.e Lymphoma, Leukemia), and autoimmune diseases.
***Both can present with high-grade fever (>39C), hemorrhagic manifestations (DIC), hepatosplenomegaly and lymphadenopathy. BOTH require immediate and appropriate treatment.
REFERENCES
  1. Lerkvaleekul B, Vilaiyuk S. Macrophage activation syndrome: early diagnosis is key. Open Access Rheumatol. 2018;10:117–128. Published 2018 Aug 31. doi:10.2147/OARRR.S151013

After creation of a percutaneous tracheotomy site for prolonged ventilation, one of the immediate complications is accident decannulation.

Conventional practice is if the tracheotomy site is <7 days old, NOT to blindly re-insert the tracheotomy cannula. The risk is re-cannulation into a false tract (i.e anterior mediastinum). Immediate preparation for endo-tracheal intubation should be considered.

REFERENCES

  1. National Health Service. https://www.nhsggc.org.uk/about-us/professional-support-sites/shock-team/guidelines-for-care-of-patients-with-a-tracheostomy-tube/changing-a-tracheostomy-tube/
  2. White AC, Kher S, O’Connor HH. When to change a tracheostomy tube. Respir Care. 2010 Aug;55(8):1069-75.
Two systematic reviews have assessed the diagnostic accuracy of elements of the medical history, physical examination, or readily available tests in diagnosing HF in adults with undifferentiated dyspnea: 
____________________________________________________________________________
Many features increased the probability of heart failure, with the best feature for each category being the presence of:
(1) the chest radiograph showing pulmonary venous congestion (positive LR = 12.0; 95% CI, 6.8-21.0); 
(2) the sign of the third heart sound (S3) gallop (positive LR = 11; 95% CI, 4.9-25.0); 
(3) past history of heart failure (positive LR = 5.8; 95% confidence interval [CI], 4.1-8.0); 
(4) electrocardiogram showing atrial fibrillation (positive LR = 3.8; 95% CI, 1.7-8.8).
(5) the symptom of paroxysmal nocturnal dyspnea (positive LR = 2.6; 95% CI, 1.5-4.5); 
____________________________________________________________________________
Conversely, findings useful in excluding HF include, in decreasing order: 
  1. A low serum BNP proved to be the most useful test (serum B-type natriuretic peptide <100 pg/mL; negative LR = 0.11; 95% CI, 0.07-0.16).
  2. The chest radiograph not showing cardiomegaly (negative LR = 0.33; 95% CI, 0.23-0.48);
  3. The absence of a past history of heart failure (negative LR = 0.45; 95% CI, 0.38-0.53);
  4. The absence of symptom of dyspnea on exertion (negative LR = 0.48; 95% CI, 0.35-0.67);
  5. No Rales (negative LR = 0.51; 95% CI, 0.37-0.70)
  6. Lack of Any electrocardiogram abnormality (negative LR = 0.64; 95% CI, 0.47-0.88). 

REFERENCES:

  1. Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does This Dyspneic Patient in the Emergency Department Have Congestive Heart Failure? JAMA. 2005;294(15):1944–1956.

SYMPTOMS THAT RULE OUT  (Lowest -LR): 

The absence of pain of sudden onset substantively decreases the probability of dissection (negative LR, 0.3;95% CI, 0.2-0.5).

SYMPTOMS THAT RULE IN (Highest +LR): 

The presence of tearing or ripping pain (positive LR, 1.2-10.8) or pain that migrates (positive LR, 1.1-7.6) may prove useful.

 

FINDINGS THAT RULE IN (Highest +LR): 

Pulse deficits (positive LR, 5.7; 95% CI, 1.4-23.0) or focal neurological deficits (positive LR, 6.6-33.0)

FINDINGS THAT RULE OUT (Lowest -LR): 

A normal aorta and mediastinum on chest radiograph helps exclude the diagnosis (negative LR, 0.3; 95% CI,0.2-0.4) 

 

KEY POINT: No single test definitely rules in or out Aortic Dissection, so diagnostic imaging (CTA) will be necessary!

The presence or absence of a diastolic murmur is not useful (positive LR, 1.4; negative LR, 0.9)

 

REFERENCES

Klompas M. Does This Patient Have an Acute Thoracic Aortic Dissection? JAMA. 2002;287(17):2262–2272. doi:https://doi.org/10.1001/jama.287.17.2262

Nonalcoholic fatty liver disease (NAFLD) affects over 1/4th of the world’s population. It has become the leading cause of cirrhosis in developed western countries. NAFLD and NASH exist along a spectrum. 

NAFLD: Patients are usually asymptomatic and the condition is found incidentally. It is defined as:  >5% of hepatic steatosis in patients who do not consume excessive alcohol. They will not have hepatocellular injury (∼80% of patients have normal-range ALT levels).

Approximately 10–30% will progress to non-alcoholic steatohepatitis (NASH). Which is differentiated by inflammation and hepatocellular injury (elevated ALT>AST). Its the active form of NAFLD, with hepatic necro-inflammation and faster fibrosis progression.

Image Credit: Nature.com

REFERENCES

1) Dyson JK, Anstee QM, McPherson S. Non-alcoholic fatty liver disease: a practical approach to diagnosis and staging. Frontline Gastroenterology 2014;5:211-218.

2) Chalasani N, Younossi Z, Lavine JE, Charlton M, Cusi K, Rinella M, Harrison SA, Brunt EM, Sanyal AJ. The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018 Jan;67(1):328-357. doi: 10.1002/hep.29367. Epub 2017 Sep 29. 

Functions on the premise of mismatch in coronary perfusion after a vasodilator (e.g dipyridamole) is administered. 

HOW? The coronary vessels with disease burden are already maximally dilated, hence after the addition of the vasodilator, perfusion mismatch occurs as the healthier vessels dilate further.

False NEGATIVES:

  • Caffeine or theophylline can interact with dipyridamole.
  • Severe flow limiting triple vessel disease or LEFT main diseae (may both cause a balanced defect). 

CONTRAINDICATIONS:

  • Severe airway disease (COPD or Asthma)

BONUS: reversal agent to dipyridamole is amiophylline.

REFERENCES

  1. Driessen, Roel S et al. “Myocardial perfusion imaging with PET.” The international journal of cardiovascular imaging vol. 33,7 (2017): 1021-1031. doi:10.1007/s10554-017-1084-4
  2. Burrell S, MacDonald A. Artifacts and pitfalls in myocardial perfusion imaging. J Nucl Med Technol. 2006 Dec;34(4):193-211; quiz 212-4.

 

Often confused as the same syndrome, Hepatopulmonary syndrome and Portopulmonary hypertension are two distinct disease processes. Both are characterized as pulmonary vascular abnormalities in the context of liver disease.

 

Hepatopulmonary Syndrome (HPS): triad of vasodilatation (Intrapulmonary vascular dilatations), abnormal oxygenation (an elevated alveolar-arterial oxygen gradient) and liver disease (any degree of liver disease). *LOOK FOR: digital clubbing, cyanosis and spider angiomas.

 

Portopulmonary hypertension (POPH): vascular obstruction secondary to portal hypertension (varices, splenomegaly, thrombocytopenia, portal vein abnormalities) with concomitant pulmonary arterial hypertension (mean pulmonary artery pressure >25 mmHg at rest, mean pulmonary capillary wedge pressure <15 mmHg, and pulmonary vascular resistance (PVR) >3 Wood units.

 

REFERENCES:

1. Porres-Aguilar M, Altamirano JT, Torre-Delgadillo A, Charlton MR, Duarte-Rojo A. Portopulmonary hypertension and hepatopulmonary syndrome: a clinician-oriented overview. Eur Respir Rev. 2012 Sep 1;21(125):223-33. doi: 10.1183/09059180.00007211.

2. Gupta S, Krowka M J. Hepatopulmonary syndrome. CMAJ Feb 2018, 190 (8) E223; DOI: 10.1503/cmaj.170253

When a patient presents with DKA, it is important to try to elucidate the cause. An easy way to remember those causes are the 7 I’s of DKA:

  1. Infection: Look for potential infectious foci (pneumonia, bacteremia, UTI etc.).
  2. Ischemia: Such as ACS, critical limb ischemia or ischemic bowel.
  3. Intoxication: ETOH, MDMA, Cocaine, Methamphetamine etc. 
  4. Infraction/ Intolerance: Patient not taking their insulin. 
  5. Iatrogenic: Secondary to medications (i.e steroids) or surgeries.
  6. Initial Presentation: First time presentation typically in young children. 
  7. Impregnation: Increased metabolic demands of pregnancy make precipitate an episode of DKA.

*NOTE: These causes are also precipitants for Hyperosmolar Hyperglycemic State (HHS).

REFERENCES

  1. Umpierrez GE, Kitabchi AE. Diabetic ketoacidosis: risk factors and management strategies. Treat Endocrinol. 2003;2(2):95-108.

Alpha1 antitrypsin (α1 AT) deficiency is the only known genetic abnormality that leads to COPD; it accounts for less than 1% of COPD in the United States.

Typically:

  • Basilar-predominant hyperlucency on chest imaging -> early-onset emphysema (eg, before age 55).
  • Occurrence of emphysema in a non- or trivial-smoker, or a family history of liver or lung disease.

WHY? Unimpeded neutrophil elastase contributes to the alveolar destruction of emphysema.

NAMING (disease is inherited co-dominant)

Pi*MM– Normal

Pi*S (essentially normal; leading to a mild decrease in circulating A1-PI)

Pi*null– They do NOT make any alpha-1 antitrypsin. The rare null variants that are characterized by complete absence of AAT synthesis; does not cause liver disease.

Pi*MZ– heterozygous. Heterozygotes are not deemed to be at significant risk of developing emphysema.

PI*ZZ– Homozygotes for the severe deficiency allele Z. Most* but not all severely deficient individuals develop emphysema, risk for which is markedly increased by smoking. For liver disease, the lifetime risk is estimated to be approximately 40%.

Copyright: Craig TJ 2015.

*More than 95% of persons in the severely deficient category are homozygous for the Z allele, designated PiZZ.

REFERENCES

  1. Craig TJ. Suspecting and Testing for Alpha-1 Antitrypsin Deficiency-An Allergist’s and/or Immunologist’s Perspective. J Allergy Clin Immunol Pract. 2015 Jul-Aug;3(4):506-11. doi: 10.1016/j.jaip.2015.04.005. Epub 2015 May 29.
  2. Stoller JK, Aboussouan LS. A review of α1-antitrypsin deficiency. Am J Respir Crit Care Med. 2012;185:246–59.
  3. de Serres F, Blanco I. Role of alpha-1 antitrypsin in human health and disease. J Intern Med. 2014;276:311–35.