periodontitis in CAD

 Q: Radiographic bone loss in chronic periodontitis can be used as a risk factor for coronary artery disease (CAD) in? (select one) 

A) Younger patients 

B) Older patients

Answer: A

Radiologic bone loss in chronic periodontitis among men less than age 60 is found to carry a remarkable risk of coronary heart disease (CAD) with a hazard ratio (HR)  of 2.12, with a P-value for trend=0.02. This is from a large study comprising more than 1200 patients span over 24 years. Ths HR was adjusted for age, body mass index (BMI), smoking, alcohol intake, diabetes mellitus, fasting glucose, total cholesterol, high-density lipoprotein cholesterol, triglycerides, systolic and diastolic blood pressure, education, marital status, income, and occupation. Interestingly, this correlation was lost in men above 60 years of age. 

Loss of teeth at age less than 60 years of age also carried an HR of 1.61 for CAD, independent of confounders described above.

#cardiology

#dental-health

References:

1. Dietrich T, Jimenez M, Krall Kaye EA, et al. Age-dependent associations between chronic periodontitis/edentulism and risk of coronary heart disease. Circulation 2008; 117:1668. 

2. Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review. Ann Periodontol 2003; 8:38. 

3. Hung HC, Joshipura KJ, Colditz G, et al. The association between tooth loss and coronary heart disease in men and women. J Public Health Dent 2004; 64:209. 

4. Friedewald VE, Kornman KS, Beck JD, et al. The American Journal of Cardiology and Journal of Periodontology Editors' Consensus: periodontitis and atherosclerotic cardiovascular disease. Am J Cardiol 2009; 104:59. 

clindamycin excretion

 Q: Clindamycin is metabolized in the liver but should be adjusted for patients on dialysis? 

A) True

B) False

Answer: A

Clindamycin is an interesting antibiotic in the sense that it is metabolized in the liver and its active metabolite N-demethyl clindamycin is more active than clindamycin itself. This activated compound gets excreted via bile and kidney. This is an important concept. Clindamycin's dose needs to be adjusted for both liver and kidney insufficiencies. Clindamycin cannot be effectively removed via either peritoneal dialysis or hemodialysis.

#pharmacology

#ID

Reference:

Clindamycin: FDA access data: https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/050162s098s099lbl.pdf (Last accessed on February 26, 2021)

Reynolds pentad

 Q; Which of the following is not a part of Reynolds pentad? 

A) Fever 

B) Abdominal pain

C) Jaundice 

D) Tachypnea 

E) Hypotension

Answer: D

The classic presentation of acute cholangitis is Charcot's triad consists of fever, abdominal pain, and jaundice. In its severe form, it becomes a Reynolds pentad with the addition of hypotension and mental status change. These symptoms do not necessarily present all the time or correlate well with the severity of the disease e.g., people on chronic glucocorticoids may have had one or two symptoms. In the contrast, superimposed bacteremia or hepatic abscess may present a patient with more severe symptoms and with multiple system organ failure (MSOF) with shock. 

At the bedside, Reynold pentad may be demonstrated only less than 5 percent of the time (reference # 3).

#hepatology

References:

1. Mosler P. Diagnosis and management of acute cholangitis. Curr Gastroenterol Rep 2011; 13:166.

2. Rumsey S, Winders J, MacCormick AD. Diagnostic accuracy of Charcot's triad: a systematic review. ANZ J Surg. 2017 Apr;87(4):232-238. doi: 10.1111/ans.13907. Epub 2017 Feb 17. PMID: 28213923. 

3. Rosing DK, De Virgilio C, Nguyen AT, El Masry M, Kaji AH, Stabile BE. Cholangitis: analysis of admission prognostic indicators and outcomes. Am Surg. 2007 Oct;73(10):949-54. PMID: 17983054.

AAA - and diabetes

 Q: Diabetes mellitus has a protective effect in an expansion of the Aortic Abdominal Aneurysm (AAA)?

A) True

B) False

Answer: A

Diabetes mellitus has a negative association and appears to have a protective effect against the expansion of AAA. Diabetic patients have a 25 to 40 percent less chance of expansion of AAA when compared to patients without diabetes. This is due to increased arterial stiffness/atherosclerosis occurring in the aorta due to diabetes. Said that, despite this negative effect on expansion of AAA, it is unknown if this prevents the rupture. 

Interestingly, with the same mechanism there is a negative association between the history of coronary artery disease and AAA expansion.

#surgical-critical-care

References:

1. Bhak RH, Wininger M, Johnson GR, et al. Factors associated with small abdominal aortic aneurysm expansion rate. JAMA Surg 2015; 150:44.

2. Sweeting MJ, Thompson SG, Brown LC, et al. Meta-analysis of individual patient data to examine factors affecting growth and rupture of small abdominal aortic aneurysms. Br J Surg 2012; 99:655.

3. Salomaa V, Riley W, Kark JD, et al. Non-insulin-dependent diabetes mellitus and fasting glucose and insulin concentrations are associated with arterial stiffness indexes. The ARIC Study. Atherosclerosis Risk in Communities Study. Circulation 1995; 91:1432. 

4. Takagi H, Umemoto T, ALICE (All-Literature Investigation of Cardiovascular Evidence) Group. Coronary artery disease and abdominal aortic aneurysm growth. Vasc Med 2016; 21:199.

DOACs

 Q: Which of the following is not a direct oral anticoagulant (DOAC)? (select one) 

A) Rivaroxaban 

B) Apixaban 

C) Edoxaban 

D) Betrixaban

E) dronedarone

Answer; E

The objective of the above question is to highlight the mechanism of Direct Oral Anticoagulants. 

All of the DOACs end in "Xa-ban" - "Ban Factor Xa"!! They all directly bind directly to factor Xa. These drugs are direct factor Xa inhibitors and prevent factor Xa from cleaving prothrombin to thrombin.

They are different from warfarin as they are non-vitamin K antagonist oral anticoagulants. 

Dronedarone (Multaq) is a non-iodine based antiarrhythmic used in the treatment of atrial fibrillation or atrial flutter (choice E).

#pharmacology

#cardiology

References:

1. Barnes GD, Ageno W, Ansell J, et al. Recommendation on the nomenclature for oral anticoagulants: communication from the SSC of the ISTH. J Thromb Haemost 2015; 13:1154. 

2. Schwarb H, Tsakiris DA. New Direct Oral Anticoagulants (DOAC) and Their Use Today. Dent J (Basel). 2016;4(1):5. Published 2016 Mar 11. doi:10.3390/dj4010005

T4 in myxedema coma

 Q: In myxedema coma, a loading dose of T4 should be avoided to decrease the risk of arrhythmias?

A) True

B) False

Answer: B

There are two strategies to administer intravenous T4 in myxedema coma 

• 100 mcg daily without a loading dose 
• 500 mcg loading dose followed by 100 mcg daily 

Evidence (though weak) tends to favor the strategy with loading dose to show the lower mortality. The risk of arrhythmias with loading dose is preferred to be accepted in view of very high mortality (up to 50%) of myxedema coma.

#endocrinology

References:

1. Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism: prepared by the american thyroid association task force on thyroid hormone replacement. Thyroid 2014; 24:1670.

2. Rodríguez I, Fluiters E, Pérez-Méndez LF, et al. Factors associated with mortality of patients with myxoedema coma: prospective study in 11 cases treated in a single institution. J Endocrinol 2004; 180:347.

BLUE and FALLS protocol

 Q: What are the BLUE and FALLS protocols in respiratory failure?

Answer: 

Ultrasound in emergency (BLUE) and fluid administration limited by lung sonography (FALLS) are systemic and algorithmic approaches to perform thoracic ultrasound in acute respiratory failure. They examine well-defined points on both sides of the thorax i.e., anterior, lateral, and posterolateral. They are easy bedside procedures but powerful tool to determine the etiology of respiratory failure. BLUE protocol, if performed properly, is found to be 90% accurate to diagnose pneumonia, CHF, COPD, asthma, PE, and pneumothorax. 

They can be performed together. They look for five main processes: 

 1. Normal lung surface 

•  bat sign 
• lung sliding A-lines 

 2. Pleural effusions 

•  quad sign 
• sinusoid sign 

 3. Lung consolidations 

•  fractal 
•  tissue-like sign 

 4. Interestial syndrome

•  lung rockets 

 5. Pneumothorax 

• stratosphere sign
• lung point 

#procedures

References:

1. Lichtenstein DA. BLUE-protocol and FALLS-protocol: two applications of lung ultrasound in the critically ill. Chest. 2015 Jun;147(6):1659-1670. doi: 10.1378/chest.14-1313. PMID: 26033127. 

2. Lichtenstein D. Lung ultrasound in the critically ill. Curr Opin Crit Care 2014; 20:315.

Telavancin

 Q: Telavancin should be used with caution in? (select one) 

A) Renal insufficiency 

B) Hepatic insufficiency

Answer: A

The objective of this question is to introduce readers to novel antibiotics that are used only in dire situations. Telavancin is a glycopeptide antibiotic approved by FDA for the Methicillin-resistant Staphylococcus aureus (MRSA), in Healthcare-Associated Pneumonia (HAP) and Ventilator-Associated Pneumonia (VAP). Telavancin is not the first line of antibiotics and should be used when alternative agents such as vancomycin and linezolid cannot be used. 

FDA has a black box warning for a patients who have impaired renal function. It has shown increased mortality in renally impaired patients. Renal function needs to be monitored while patients are receiving Telavancin. Also, it should be avoided in pregnancy as it may cause fetal teratogenic effects.

#pharmacology

#ID

References:

1. Sandrock CE, Shorr AF. The role of telavancin in hospital-acquired pneumonia and ventilator-associated pneumonia. Clin Infect Dis 2015; 61 Suppl 2:S79. 

2. Rubinstein E, Lalani T, Corey GR, et al. Telavancin versus vancomycin for hospital-acquired pneumonia due to gram-positive pathogens. Clin Infect Dis 2011; 52:31. 

3. Corey GR, Kollef MH, Shorr AF, et al. Telavancin for hospital-acquired pneumonia: clinical response and 28-day survival. Antimicrob Agents Chemother 2014; 58:2030.

ABCD2 score

 Q: The ABCD2 score determines patients who are at high risk of ischemic stroke after Transient Ischemic Attack (TIA). Which of the following is not part of the score? (select one)

A) Age

B) Blood pressure

C) Clinical features

D) Days after symptoms

E) Diabetes

Answer: D

The ABCD2 score stands for

• Age
• Blood pressure
• Clinical features
• Duration of symptoms, and 
• Diabetes

It is a prognostic assessment tool. It is intended to identify patients at high risk of ischemic stroke after TIA. This is a very arbitrary calculator (available online) and experts disagree on its accuracy. The 2009 American Heart Association (AHA) and American Stroke Association (ASA) guidelines advise that it is reasonable to hospitalize patients with TIA who present within three days of symptoms and has any of the following criteria: 

•  ABCD2 score of ≥3 
•  ABCD2 score of 0-2 and uncertainty that the diagnostic workup can be completed within two days as an outpatient 
•  ABCD2 score of 0-2 and other evidence that the event was caused by focal ischemia

#neurology

References:

1. Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke 2009; 40:2276. 

2.Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet 2007; 369:283. 

3. Wardlaw JM, Brazzelli M, Chappell FM, et al. ABCD2 score and secondary stroke prevention: meta-analysis and effect per 1,000 patients triaged. Neurology 2015; 85:373. 

4. Sanders LM, Srikanth VK, Blacker DJ, et al. Performance of the ABCD2 score for stroke risk post TIA: meta-analysis and probability modeling. Neurology 2012; 79:971.

5. Stead LG, Suravaram S, Bellolio MF, et al. An assessment of the incremental value of the ABCD2 score in the emergency department evaluation of transient ischemic attack. Ann Emerg Med 2011; 57:46. 

Cefiderocol

 Q: Cefiderocol is which generation of cephalosporin? (select one) 

A) First 

B) Second 

C) Third 

D) Fourth 

E) None of the above 

 Answer: E 

Cefiderocol is a very unique cephalosporin and has been granted the status in none of so far developed five generations of cephalosporins. This is due to its novel mechanism of action that can overcome the effect of membrane permeability mutations when transporting across the outer membrane of the organism. Most of its activity is against multidrug-resistant gram-negative bacteria. It has poor gram-positive and anaerobic activity. It is used in the cases where culture grew multidrug-resistant P. aeruginosa, A. baumannii, Stenotrophomonas maltophilia, and Burkholderia cepacia.

#pharmacology

References:

1. Stevens RW, Clancy M. Compassionate Use of Cefiderocol in the Treatment of an Intraabdominal Infection Due to Multidrug-Resistant Pseudomonas aeruginosa: A Case Report. Pharmacotherapy 2019; 39:1113. 

2. Edgeworth JD, Merante D, Patel S, et al. Compassionate Use of Cefiderocol as Adjunctive Treatment of Native Aortic Valve Endocarditis Due to Extremely Drug-resistant Pseudomonas aeruginosa. Clin Infect Dis 2019; 68:1932. 

3. Cefiderocol. US Food and Drug Administration (FDA) approved product information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/209445s002lbl.pdf (Accessed on February 3, 2020).

IV K mix

 Q: Intravenous (IV) infusion of potassium should be given in mix with? (select one)

A) Dextrose

B) Saline

Answer: B

The effect of giving IV potassium in dextrose mix can be detrimental. A dose of 20 mEq/L of potassium given in dextrose mix can cause a transient drop of potassium of 0.2 to 1.4 mEq/L. This may bear consequences in cardiac patients with arrhythmia, first demonstrated almost 60 years ago (reference # 2). This is due to the endogenous insulin released in response to a carbohydrate load. 

A similar impact can be seen in patients with underlying poor nutrition who gets high carbohydrate load via tube feeding, which is one of the manifestations of the refeeding syndrome.

#endocrinology

#electrolytes

References:

1. Gennari FJ. Hypokalemia. N Engl J Med 1998; 339:451. 

2. KUNIN AS, SURAWICZ B, SIMS EA. Decrease in serum potassium concentrations and appearance of cardiac arrhythmias during infusion of potassium with glucose in potassium-depleted patients. N Engl J Med 1962; 266:228. 

3. Fuentebella J, Kerner JA. Refeeding syndrome. Pediatr Clin North Am 2009; 56:1201.

Types of MI

 Q: Myocardial Infarction (MI) due to mismatch between oxygen supply and demand is? (select one) 

A) Type 1 

B) Type 2 

C) Type 3 

D) Type 4  

E) Type 5 

 Answer: B

The Joint Task Force of the European Society of Cardiology, American College of Cardiology Foundation, the American Heart Association, and the World Heart Federation (ESC/ACCF/AHA/WHF) has proposed a clinical classification of MI according to assumed proximate cause of myocardial ischemia 

Type 1: MI due to acute atherothrombotic coronary artery disease and usually precipitated by atherosclerotic plaque disruption (rupture or erosion). 

Type 2: MI because of a mismatch between oxygen supply and demand. 

Type 3: Patients with MI based on EKG or ventricular fibrillation, and unexpected death before biomarkers can be detected. 

Type 4a: MI associated with percutaneous coronary intervention (PCI).

Type 4b: A subcategory of PCI-related MI, which is due to stent/scaffold thrombosis. 

Type 5: MI in relation to Coronary artery bypass graft (CABG) surgery.

The objective of this question is to broadly introduce the types of MI. For further reading access the reference below.

#cardiology

Reference:

Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol 2018; 72:2231.

Octreotide effect in variceal bleed

 Q: Out of the following which of the octreotide effect is most responsible for decreasing portal pressure in the variceal gastrointestinal (GI) bleed? (select one)

A) Portal venous inflow 

B) Portal pressures 

C) Azygos flow 

D) Intravariceal pressures

Answer: C

During the management of variceal GI bleed, the effect of intravenous (IV) octreotide bolus is instant within seconds with a decrease in portal venous inflow, portal pressures, azygos flow, and intra-variceal pressures. Out of all these, the most beneficial and consistent effect comes from the decrease in collateral flow via azygos flow. Although this effect lasts temporarily but with continuous infusion after IV bolus, it is hoped that hemostasis can be achieved and maintained, although tachyphylaxis is rapid. 

Octreotide also increases the mean arterial pressure. Another secondary effect of octreotide is to postprandially inhibit the release of glucagon and other hormones that have roles in mediating the increase in mesenteric blood flow. It also helps to keep portal hemodynamics maintained via somatostatin receptors activation to avoid rebound in portal pressures during recovering phase with reversal of hypovolemia. This is the reason to continue IV infusion for at least 48-72 hours after bolus to see the maximum benefit.

#GI

#pharmacology

References:

1. Escorsell A, Bandi JC, Andreu V, et al. Desensitization to the effects of intravenous octreotide in cirrhotic patients with portal hypertension. Gastroenterology 2001; 120:161. 

2. McCormick PA, Biagini MR, Dick R, et al. Octreotide inhibits the meal-induced increases in the portal venous pressure of cirrhotic patients with portal hypertension: a double-blind, placebo-controlled study. Hepatology 1992; 16:1180. 

3. Ludwig D, Schädel S, Brüning A, et al. 48-hour hemodynamic effects of octreotide on postprandial splanchnic hyperemia in patients with liver cirrhosis and portal hypertension: double-blind, placebo-controlled study. Dig Dis Sci 2000; 45:1019.

Risk factors after hernia repair

 Q: 62 years old female is admitted to ICU with septic shock. Patient was found to have a mesh infection with her previous ventral wall hernia repair. Name few risk factors for infections after hernia repair?

Answer: Hernia repair is usually an uncomplicated surgery. At the same time, there is a long list of risk factors for its complications. The objective of this question is to mention some of the risk factors: 

• Old age
• Obesity 
• Low serum albumin 
• Diabetes 
• Smoking
• Immunosuppression 
• Chronic steroid use
• CHF
• Underlying COPD
• ASA score >3 
• History of  MRSA infection
• Emergency procedure 
• Prolonged operative time 
• Enterotomy or bowel resection done during repair
• Perioperative blood transfusion 
• Use of mesh to repair large ventral hernia defects >10 cm

#surgical-critical-care

References:

1. Finan KR, Vick CC, Kiefe CI, et al. Predictors of wound infection in ventral hernia repair. Am J Surg 2005; 190:676. 

2. Mavros MN, Athanasiou S, Alexiou VG, et al. Risk factors for mesh-related infections after hernia repair surgery: a meta-analysis of cohort studies. World J Surg 2011; 35:2389. 

3. Stremitzer S, Bachleitner-Hofmann T, Gradl B, et al. Mesh graft infection following abdominal hernia repair: risk factor evaluation and strategies of mesh graft preservation. A retrospective analysis of 476 operations. World J Surg 2010; 34:1702. 

4. Ousley J, Baucom RB, Stewart MK, et al. Previous Methicillin-Resistant Staphylococcus aureus Infection Independent of Body Site Increases Odds of Surgical Site Infection after Ventral Hernia Repair. J Am Coll Surg 2015; 221:470.

MALA prognostic factors

  Q: All of the following are found to be correlated to mortality in Metformin Associated Lactic Acidosis (MALA) EXCEPT? (select one)

A) Lower PH  

B) High lactate 

C) Increase INR 

D) Metformin level 

E) High associated comorbidities 

 Answer: D 

MALA carries a high mortality, up to 50 percent despite the best available treatment. From the available case-series, it appears that deteriorated liver function manifested by high INR is the best predictor of mortality in MALA (choice C). 

There are conflicting reports regarding correlation of death with level of lactic acidosis in PH (Choices A and B). 

Interestingly, most studies failed to show any correlation between absolute metformin level and mortality in MALA (choice D). 

It is assumed that the sicker the patient at baseline, the lower would be the chances of survival (choice E).

#toxicology

#endocrinology

#pharmacology

References: 

1. Vecchio S, Giampreti A, Petrolini VM, et al. Metformin accumulation: lactic acidosis and high plasmatic metformin levels in a retrospective case series of 66 patients on chronic therapy. Clin Toxicol (Phila) 2014; 52:129. 

2. Lalau JD, Race JM. Lactic acidosis in metformin-treated patients. Prognostic value of arterial lactate levels and plasma metformin concentrations. Drug Saf 1999; 20:377. 

3. Seidowsky A, Nseir S, Houdret N, Fourrier F. Metformin-associated lactic acidosis: a prognostic and therapeutic study. Crit Care Med 2009; 37:2191. 

4.  Dell'Aglio DM, Perino LJ, Kazzi Z, et al. Acute metformin overdose: examining serum pH, lactate level, and metformin concentrations in survivors versus nonsurvivors: a systematic review of the literature. Ann Emerg Med 2009; 54:818.

Clindamycin side-effects

 Q: One of the side-effects of intravenous (IV) Clindamycin is cardiac arrest? 

A) True

B) False

Answer: True

Although gastrointestinal (GI) side effects such as diarrhea and C. difficile colitis are well known, but clindamycin also has a high tendency to cause a generalized allergic reaction. Maculopapular rash, drug fever, eosinophilia, and erythema multiforme are very common. Sweet syndrome, urticaria, Stevens-Johnson alike syndrome, delayed-type hypersensitivity reactions are also described. 

One of the dreaded side-effects of clindamycin is hemodynamic collapse and cardiac arrest. This mostly occurs with rapid  IV infusion. Clindamycin should be given diluted with a slow infusion.

#pharmacology

References:

Aucoin P, Beckner RR, Gantz NM. Clindamycin-induced cardiac arrest. South Med J. 1982 Jun;75(6):768. doi: 10.1097/00007611-198206000-00041. PMID: 7089634.

ACE-I in renal artery stenosis

 Q: Angiotensin-converting enzyme inhibitors (ACE-I) should not be given to all of the following patients EXCEPT? (select one) 

A) previous lip swelling

B) previous unexpected drop in blood pressure 

C) known unilateral renal artery stenosis 

D) previous Acute Kidney failure from ACE-I 

  * previous is equivalent with use of ACE-I

 Answer: C

The objective of this question is to clarify the point that ACE-I is contraindicated in only bilateral renal artery stenosis. Actually, it is beneficial in unilateral renal artery stenosis. 

Another myth to avoid is ACE-I in any level of kidney dysfunction, which is not true. Patients who are candidates for its use due to left ventricular dysfunction can be prescribed for its mortality benefit up to serum creatinine above 3 mg/dL. Also, it can be used in patients who are already on dialysis.

#nephrology

#pharmacology

References:

1. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from AAVS/SVS, CAI, SVMB, SIR, and the ACC/AHA Task Force on Practice Guidelines: endorsed by the AACPR, NHLBI, SVN, TISC, and VDF. Circulation 2006; 113:e463. 

2.  Frances CD, Noguchi H, Massie BM, et al. Are we inhibited? Renal insufficiency should not preclude the use of ACE inhibitors for patients with myocardial infarction and depressed left ventricular function. Arch Intern Med 2000; 160:2645. 

3. Evans M, Carrero JJ, Szummer K, et al. Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers in Myocardial Infarction Patients With Renal Dysfunction. J Am Coll Cardiol 2016; 67:1687.

Remifentanil

Q: Remifentanil is metabolized by? (select one)

A) Kidney

B) Liver

C) Plasma

D) Auto-degraded

Answer: C

Remifentanil is metabolized by plasma esterases to inactive metabolites. This describes its ultrashort duration of action. It has a rapid onset of action, within three minutes. As it is metabolized in the plasma, it does not accumulate in the body. Despite its remarkable properties it failed to find its place in ICU. It failed to show any advantage in comparison to fentanyl or hydromorphone to decrease delirium, days of mechanical ventilation, or ICU length of stay. Also, it quickly develops tachyphylaxis. It is expensive and causes rebound hyperalgesia.

#pharmacology

#pain-management

References:

1. Tan JA, Ho KM. Use of remifentanil as a sedative agent in critically ill adult patients: a meta-analysis. Anaesthesia 2009; 64:1342. 

2. Joly V, Richebe P, Guignard B, et al. Remifentanil-induced postoperative hyperalgesia and its prevention with small-dose ketamine. Anesthesiology 2005; 103:147. 

3. Guignard B, Bossard AE, Coste C, et al. Acute opioid tolerance: intraoperative remifentanil increases postoperative pain and morphine requirement. Anesthesiology 2000; 93:409.

Gender and QT interval

 Q;  Which gender tends to have a higher propensity to have a prolonged QT interval? (select one)

A) Males

B) Females

Answer: B

The 99th percentile of QTc value in an adult male has a QT interval on average of 470 milliseconds and an adult female of 480 milliseconds. This makes the female gender more prone to develop prolong QT-related arrhythmias. This also explains why females are more at risk of Torsades de Pointes (TdP) with sotalol and other commonly prescribed anti-arrhythmic drugs. Female sex is considered the highest risk factor for drug-induced TdP. 

The objective of the above question is to highlight the American Heart Association/American College of Cardiology (AHA/ACC) scientific statement on the prevention of TdP in hospital settings that a QTc over the 99th percentile should be considered abnormally prolonged.

#cardiology

References:

1. Drew BJ, Ackerman MJ, Funk M, et al. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation 2010; 121:1047. 

2. Lehmann MH, Hardy S, Archibald D, et al. Sex difference in risk of torsade de pointes with d,l-sotalol. Circulation 1996; 94:2535. 

3. Makkar RR, Fromm BS, Steinman RT, et al. Female gender as a risk factor for torsades de pointes associated with cardiovascular drugs. JAMA 1993; 270:2590. 

4. Drici MD, Clément N. Is gender a risk factor for adverse drug reactions? The example of drug-induced long QT syndrome. Drug Saf 2001; 24:575. 

Anion gap

 Q: The normal anion gap with use of ion-selective electrodes is? (select one)

A) 12 +/- 4 mEq/L 

B) 8 +/- 4 mEq/L 

C) 6 +/- 3 mEq/L

Answer: C

The objective of this question is to introduce to the readers that the anion gap value largely depends on lab instruments. It is even more relevant than adjusting for albumin level. Although, this is true that traditionally and still 12 +/- 4 mEq/L has been used as a normal anion gap but labs now mostly use ion-selective electrodes for measurement. The formula for the anion gap is Serum AG = Na - (Cl + HCO3), and this method reports higher serum chloride concentrations. 

It has been more than ever important to know the method and normal range reported by the specific lab.

#electrolytes

References:

1. Kraut JA, Nagami GT. The serum anion gap in the evaluation of acid-base disorders: what are its limitations and can its effectiveness be improved? Clin J Am Soc Nephrol 2013; 8:2018. 

2. Jurado RL, del Rio C, Nassar G, et al. Low anion gap. South Med J 1998; 91:624. 

3. Winter SD, Pearson JR, Gabow PA, et al. The fall of the serum anion gap. Arch Intern Med 1990; 150:311. 

4. Paulson WD, Roberts WL, Lurie AA, et al. Wide variation in serum anion gap measurements by chemistry analyzers. Am J Clin Pathol 1998; 110:735. 

5. Pratumvinit B, Lam L, Kongruttanachok N, et al. Anion gap reference intervals show instrument dependence and weak correlation with albumin levels. Clin Chim Acta 2020; 500:172.

IV Mg supplementation

 Q: Up to what percentage of administrated intravenous (IV) magnesium (Mg) is lost in urine? 

 Answer: 50% 

 IV supplementation of Mg is not a very efficacious route of replacement, though in ICU oral route is not feasible many times. The kidney is the major site of active magnesium transport in the human body. Whenever IV mg is infused it causes a transient elevation of plasma magnesium concentration. This leads to negative feedback and decreases reabsorption of Mg in the kidney's loop of Henle. Up to 50 percent of the administrated IV Mg gets excreted in the urine. Moreover, cells do not absorb Mg quickly. The serum Mg level does not adequately reflect the intracellular level. 

Oral supplementation is efficacious but in hospitalized patients, either this route may not be available or contributes to diarrhea.

#electrolytes

References:

1. Seo JW, Park TJ. Magnesium metabolism. Electrolyte Blood Press. 2008;6(2):86-95. doi:10.5049/EBP.2008.6.2.86 

2. Judith Blaine, Michel Chonchol and Moshe Levi Renal Control of Calcium, Phosphate, and Magnesium Homeostasis CJASN July 2015, 10 (7) 1257-1272; DOI: https://doi.org/10.2215/CJN.09750913

V.fib in crush trauma victims

 Q: Trauma victims with crush injury may die of ventricular fibrillation on evacuation from the rubble. What is the reason behind such an acute event?

Answer:  Extremity reperfusion and hyperkalemia 

When a trapped extremity is released from the rubble at the disaster site, it causes immediate release of potassium from tissues and leads to acute severe hyperkalemia resulting in ventricular fibrillation. The objective of the above question is to emphasize the need to rapidly initiate non-potassium containing intravenous fluid (IVF), evaluation of EKG to determine peaked T waves, and any other treatment needed to counter this hyperkalemia. A massive load of calcium to counter this hyperkalemia is discouraged. Some experts advise prophylactic administration of oral potassium resin binders.

In the past tourniquets have been placed above crushed extremities to counter this acute release of potassium but evidence shows that it's not helpful rather may cause further damage to already ischemic tissues.

#trauma

#disaster

#mass-casualty

References:

1. Sever MS, Erek E, Vanholder R, et al. Lessons learned from the Marmara disaster: Time period under the rubble. Crit Care Med 2002; 30:2443.  

2. Sever MS, Vanholder R, Lameire N. Management of crush-related injuries after disasters. N Engl J Med 2006; 354:1052. 

3. Sever MS, Erek E, Vanholder R, et al. Serum potassium in the crush syndrome victims of the Marmara disaster. Clin Nephrol 2003; 59:326.

complicated grief

 Q: What is the difference between grief and mourning? 

Answer:

• Grief is a natural response that can manifest in any form such as thoughts, behaviors, or physiologic reactions. 
• Mourning is the process of adapting to a loss and integrating the grief associated with it.

End of life care is not only patients' requirement, it carries its toll on physicians as well. They are very frequently required to provide comfort to bereaved family members. One of the objectives of a clinician in such a situation is to prevent grief from generating into complex grief and allow mourning to incur.

Complicated grief is broadly defined as disabling and troubling thoughts, dysfunctional behaviors, dysregulated emotions, and/or serious psychosocial problems. Clinicians need to appreciate its unique existence besides other psychiatric issues (please see references below).

#palliative-care

#psychiatry

References:

1. Lobb EA, Kristjanson LJ, Aoun SM, et al. Predictors of complicated grief: a systematic review of empirical studies. Death Stud 2010; 34:673. 

2. Simon NM. Treating complicated grief. JAMA 2013; 310:416. 

3. Latham AE, Prigerson HG. Suicidality and bereavement: complicated grief as psychiatric disorder presenting greatest risk for suicidality. Suicide Life Threat Behav 2004; 34:350. 

4. Shear K, Shair H. Attachment, loss, and complicated grief. Dev Psychobiol 2005; 47:253.

Remdesivir in pregnancy

 Q: During COVID-19 treatment Remdesivir should be avoided in pregnancy? 

A) True 

B) False

Answer: B

Management in pregnancy is not much different than in any other patient with COVID-19, though extra caution is needed. So far experience in COVID-19 and with previous viruses in the past such as the Middle East respiratory syndrome (MERS), Ebola, and Marburg virus, remdesivir is found to be safe at any stage of pregnancy.

COVID-19 literature continues to evolve fast. Readers are advised to consult updated guidelines before making any clinical decision.

#ob-gyn

#COVID

#pharmacology

References:

1. Igbinosa I, Miller S, Bianco K, et al. Use of remdesivir for pregnant patients with severe novel coronavirus disease 2019. Am J Obstet Gynecol. 2020;223(5):768-770. doi:10.1016/j.ajog.2020.08.001 

2.  Sheahan TP, Sims AC, Graham RL, et al. Broad-spectrum antiviral GS-5734 inhibits both epidemic and zoonotic coronaviruses. Sci Transl Med 2017; 9. 

3. Mulangu S, Dodd LE, Davey RT Jr, et al. A Randomized, Controlled Trial of Ebola Virus Disease Therapeutics. N Engl J Med 2019; 381:2293. 

4. Burwick RM, Yawetz S, Stephenson KE, et al. Compassionate Use of Remdesivir in Pregnant Women with Severe Covid-19. Clin Infect Dis 2020.

hypothermia control

 Q: Heat is generated in human body by which set of two organs? (select one) 

A) heart and liver 

B) heart and lungs 

C) liver and lungs 

D) skin and lungs 

 E) skin and heart

Answer: A

Normally, the heat regulation in human body is balanced by four organs. 

• Heat production = heart and liver (ongoing cellular metabolism) 
• Heat loss = skin and lungs (ongoing evaporation, radiation, conduction, and convection)

The human's capacity to balance the temperature through the above mechanism is very limited. Hypothalamus acts as a mediator to regulate body temperature at 37±0.5°C. In response to cold, hypothalamus takes over the system! and stimulates heat production. The overt obvious mechanism is to induce shivering. Covertly it increases thyroid, catecholamine, and adrenal activities. Also, it sympathetically mediates the vasoconstriction to peripheral tissues. 

If the environmental cold persists, shivering declines and stops around 32°C. At this point, human metabolism (production) and cardiac output start to cease.

#hypothermia

References:

1. Hanania NA, Zimmerman JL. Accidental hypothermia. Crit Care Clin 1999; 15:235. 

2. Lee-Chiong TL Jr, Stitt JT. Disorders of temperature regulation. Compr Ther 1995; 21:697. 

3. Brown DJ, Brugger H, Boyd J, Paal P. Accidental hypothermia. N Engl J Med 2012; 367:1930.

Insulin and potassium

 Q: Insulin overdose is a frequent cause of hypokalemia in ICU?

A) True

B) False

Answer: B

It is true that insulin is used in the immediate management of hyperkalemia but it rarely causes hypokalemia if given in excess. Although it may cause hypoglycemia. The objective of this question is to highlight the role of insulin in the treatment of hyperkalemia. 

 Insulin treats hyperkalemia by increasing the entry of potassium at two major sites i.e., skeletal muscles and hepatic cells. At the bedside, this trick may not work if a patient has liver insufficiency or low muscle mass, which frequently co-exists. The entry of potassium is by the increased activity of Na-K-ATPase pump due to insulin. This activity is further enhanced if the body receives exogenous insulin but it rarely causes hypokalemia even if the insulin dose is excessive (see reference # 2).

Despite the above fact, care should be taken in close monitoring of potassium during the management of Diabetic-Keto-Acidosis (DKA) and the associated clinical conditions.

#endocrinology

References:

1. Mount DB, Zandi-Nejad K. Disorders of potassium balance. In: Brenner and Rector's The Kidney, 8th ed, Brenner BM (Ed), WB Saunders Co, Philadelphia 2008. p.547. 

2. Bradberry SM, Vale JA. Disturbances of potassium homeostasis in poisoning. J Toxicol Clin Toxicol 1995; 33:295.

po vanc dose

 Q: High dose of oral vancomycin is more effective in cases of life-threatening severe clostridioides difficile infection? 

A) True 

B) False

 

Answer: B

Overall vancomycin is found to be more effective and shown to reduced 30-day mortality when compared with metronidazole in severe clostridioides difficile infection. Said that the outcome is similar between a standard dosing of vancomycin or higher dosing (125 mg vs 500 mg four times daily).

#ID

References:

1. Fekety R, Silva J, Kauffman C, et al. Treatment of antibiotic-associated Clostridium difficile colitis with oral vancomycin: comparison of two dosage regimens. Am J Med 1989; 86:15. 

2. Stevens VW, Nelson RE, Schwab-Daugherty EM, et al. Comparative Effectiveness of Vancomycin and Metronidazole for the Prevention of Recurrence and Death in Patients With Clostridium difficile Infection. JAMA Intern Med 2017; 177:546.

GI bleed and platelet transfusion

 Q: 52 years old male with a recent percutaneous coronary intervention (PCI)with drug-eluting stents and now on dual anti-platelet therapy (DAPT) with aspirin and clopidogrel developed gastrointestinal (GI) bleed, and now admitted in ICU. Platelet transfusion is indicated? 

A) True

B) False

Answer: B

Patients who are on chronic therapy of antiplatelet drugs such as aspirin or clopidogrel may develop GI bleed. Many clinicians may think that in such non-thrombocytopenic patients platelet transfusion should be of help due to dysfunctional platelets circulating in the system. However, the evidence failed to justify such transfusions. Actually, on the contrary, it may harm the patient. 

Some of these patients may have recent coronary artery stents and stopping these drugs may cause further harm. The patient's cardiologist should be taken on board to decide to stop or not to stop or how long to stop the antiplatelet drugs.

#GI

#cardiology

#hematology

References:

1. Zakko L, Rustagi T, Douglas M, Laine L. No Benefit From Platelet Transfusion for Gastrointestinal Bleeding in Patients Taking Antiplatelet Agents. Clin Gastroenterol Hepatol 2017; 15:46. 

2. ASGE Standards of Practice Committee, Anderson MA, Ben-Menachem T, et al. Management of antithrombotic agents for endoscopic procedures. Gastrointest Endosc 2009; 70:1060.