Steroids and KS

Q: Steroids _______________ Kaposi Sarcoma (KS)? - select one

A) exacerbates

B) suppresses 

Answer: A

Steroids may induce as well as exacerbate preexisting KS. This is true for HIV, transplant patients, autoimmune disorders, and lymphoproliferative diseases.

HIV patients are particularly at risk as steroid is frequently used in them for immune thrombocytopenia and Pneumocystis jirovecii pneumonia PJC - previous PCP). 

Fortunately, KS lesions regress on reduction or withdrawal of steroids.

Besides steroids, opportunistic infections have also been associated with the induction or exacerbation of preexisting KS due to high levels of proinflammatory cytokines.

#ID

References:

1. Fernández-Sánchez M, Iglesias MC, Ablanedo-Terrazas Y, Ormsby CE, Alvarado-de la Barrera C, Reyes-Terán G. Steroids are a risk factor for Kaposi's sarcoma-immune reconstitution inflammatory syndrome and mortality in HIV infection. AIDS. 2016 Mar 27;30(6):909-14. doi: 10.1097/QAD.0000000000000993. PMID: 26636923; PMCID: PMC4794188.

2. Trattner A, Hodak E, David M, Sandbank M. The appearance of Kaposi sarcoma during corticosteroid therapy. Cancer 1993; 72:1779.

3. Gill PS, Loureiro C, Bernstein-Singer M, et al. Clinical effect of glucocorticoids on Kaposi sarcoma related to the acquired immunodeficiency syndrome (AIDS). Ann Intern Med 1989; 110:937.

Proper handling of SV fluid analysis

Q: Mention at least one precaution that should be taken while evaluating crystals in synovial (SV) fluid analysis.

Answer: Talc-free gloves

Synovial fluid analysis is a delicate process that requires strict precautions when handling the specimen. Talc gloves are still the norm in many countries. Contamination of the slide with birefringent talc particles can make microscopic examination for pathogenetically important crystals difficult. A few other important precautions are:

• Aspiration under aseptic conditions
• Quick transfer of specimen to sterile tubes*
• As early as possible platation
• Avoid contamination of the synovial fluid sample with injectable corticosteroid 
• Either EDTA or heparinized tubes should be used for inflammatory joint fluids, which often contain high fibrinogen and fibrin

* Some experts directly place a drop of fresh synovial fluid on a slide with a cover slip and expedite viewing under a microscope in the lab.

#rheumatology

#pathology

References:

1. Dieppe P, Swan A. Identification of crystals in synovial fluid. Ann Rheum Dis 1999; 58:261.

2. Miller JM, Binnicker MJ, Campbell S, et al. A Guide to Utilization of the Microbiology Laboratory for Diagnosis of Infectious Diseases: 2018 Update by the Infectious Diseases Society of America and the American Society for Microbiology. Clin Infect Dis 2018; 67:e1.

3. Freemont AJ. Microscopic analysis of synovial fluid--the perfect diagnostic test? Ann Rheum Dis 1996; 55:695.

4. Graf SW, Buchbinder R, Zochling J, Whittle SL. The accuracy of methods for urate crystal detection in synovial fluid and the effect of sample handling: a systematic review. Clin Rheumatol 2013; 32:225.

Attrition Bias

Q: What is the usual threshold to be considered as a high rate of attrition in a Randomized Control Trial (RCT)? 

Answer: 20%

Attrition refers to participants dropping out of a study, which can occur in any medical study. Contrary to popular belief, it's not only the participants leaving the study, but it also includes patients who die or are lost to follow-up during the study. 

The authors are obliged to report the level of attrition so readers and critics can assess the validity and bias (attrition bias), and the effect on statistical power and confidence intervals of the (probably skewed) results. Attrition bias may overestimate the results. There is a high probability that participants who leave the study may differ from those who remain or survive during the study period.

A minor level, i.e., up to 5%, is expected in long-term studies, but >20% is considered high. Attrition may occur due to higher mortality, negative experiences, complicated protocols, side effects, logistical issues, relocations, and the length of the study.

#statistics

References:

1. Dumville JC, Torgerson DJ, Hewitt CE. Reporting attrition in randomised controlled trials. BMJ. 2006 Apr 22;332(7547):969-71. doi: 10.1136/bmj.332.7547.969. PMID: 16627519; PMCID: PMC1444839.

2. Nunan D, Aronson J, Bankhead C. Catalogue of bias: attrition bias. BMJ Evid Based Med. 2018 Feb;23(1):21-22. doi: 10.1136/ebmed-2017-110883. PMID: 29367321.

3. Rees JS, Somi S. A guide to the clinical management of attrition. Br Dent J. 2018 Mar 9;224(5):319-323. doi: 10.1038/sj.bdj.2018.169. Epub 2018 Mar 2. PMID: 29495028.

4. Linardon J. Rates of attrition and engagement in randomized controlled trials of mindfulness apps: Systematic review and meta-analysis. Behav Res Ther. 2023 Nov;170:104421. doi: 10.1016/j.brat.2023.104421. Epub 2023 Oct 14. PMID: 37862854.

In mitral valve IE

Q: Which of the leaflets is more prone to embolization in Mitral valve endocarditis (IE)? - select one

A) Anterior

B) Posterior

Answer: A

Vegetation characteristics, including location, play an important role in the risk of embolization in IE. The major risk factors are:

• vegetation size >10 mm 
• vegetation mobility
• vegetation on the anterior leaflet
• prior embolization
• infection with S. aureus, Streptococcus bovis, or fungus

Although cardiac surgical service should be consulted as soon as possible (ASAP!), the importance of starting antibiotics as early as possible is extremely vital, as the risk of embolization tends to decline rapidly after initiation of effective antimicrobial therapy, and becomes uncommon after a week of antibiotics.

#surgical-critical-care

#cardiology

#ID

References:

1. Yanagawa B, Pettersson GB, Habib G, et al. Surgical Management of Infective Endocarditis Complicated by Embolic Stroke: Practical Recommendations for Clinicians. Circulation 2016; 134:1280.

2. Mohananey D, Mohadjer A, Pettersson G, et al. Association of Vegetation Size With Embolic Risk in Patients With Infective Endocarditis: A Systematic Review and Meta-analysis. JAMA Intern Med 2018; 178:502.

3. Weber C, Marin-Cuartas M, Tugtekin SM, Diab M, Saha S, Akhyari P, Elderia A, Muench F, Petrov A, Aubin H, Misfeld M, Lichtenberg A, Hagl C, Doenst T, Matschke K, Borger MA, Wahlers T, Luehr M; Study Group “Clinical, Multicenter Project of Analysis of Infective Endocarditis in Germany” (CAMPAIGN). Aortic and Mitral Valve Endocarditis-Simply Left-Sided Endocarditis or Different Entities Requiring Individual Consideration?-Insights from the CAMPAIGN Database. J Clin Med. 2024 Sep 30;13(19):5841. doi: 10.3390/jcm13195841. PMID: 39407901; PMCID: PMC11477404.

4. Cabezon G, Pulido P, López Díaz J, de Miguel-Álava M, Vilacosta I, García-Azorin D, Lozano A, Oña A, Arenillas JF, San Román JA. Embolic Events in Infective Endocarditis: A Comprehensive Review. Rev Cardiovasc Med. 2024 Mar 7;25(3):97. doi: 10.31083/j.rcm2503097. PMID: 39076945; PMCID: PMC11263858.

Nephrotoxins in AKI

Q: A 62-year-old patient with a past history of hypertension (HTN) and Diabetes Mellitus (DM) is admitted to the ICU with severe community-acquired pneumonia (CAP) and septic shock. Patient required intubation, and in the next 48 hours, went into Acute Kidney Injury (AKI). Which of his following medications should be discontinued? - select one

A) Angiotensin-converting enzyme (ACE) inhibitors

B) Sodium-glucose cotransporter 2 (SGLT2) inhibitors

C) Both A and B

Answer: C

In case of severe illness and AKI, all nephrotoxic meds, like nonsteroidal anti-inflammatory drugs (NSAIDs), should be stopped. Many of these patients are usually on ACE inhibitors, ARBs, and SGLT2 inhibitors - they all should be stopped. 

SGLT2 inhibitors are relatively new agents, and there remains limited understanding about their role. Although they have shown to reduce the rate of AKI, once AKI and severe hemodynamic instability ensues they should be stopped. To date, the scientific evidence is mixed, and the jury is still out on this! 

ACE inhibitors and ARBs, as well as SGLT2 inhibitors, alter the kidney's ability to autoregulate blood flow during AKI and reduce kidney perfusion. This results in exacerbation of hemodynamically mediated AKI. It is rarely appreciated that if ACE inhibitors or ARBs are discontinued in hospital-acquired AKI within the first 48 hours of admission, there is an overall statistically significant 30-day mortality. The only exception is scleroderma renal crisis. 

A few other harmful drugs in AKI that should be stopped are metformin and gabapentin. All renally excreted drugs should be dose-adjusted.

#nephrology

#pharmacology

#endocrinology

References:

1. Nie S, Li Y, Sun Y, et al. Discontinuation of Renin-Angiotensin System Inhibitors during Acute Kidney Injury Episode and All-Cause Mortality: Target Trial Emulation Studies. J Am Soc Nephrol 2025; 36:2410.

2. Nakao Y, Mori M, Mori Y, Bonventre JV. SGLT2 inhibitors and acute kidney injury. Nephrol Dial Transplant. 2026 Jan 30;41(2):243-254. doi: 10.1093/ndt/gfaf132. PMID: 40736512; PMCID: PMC12855603.

3. Dong Z, Mo W, Ling Z, Hou L, Deng T. Efficacy of SGLT2 inhibitors on acute kidney injury in patients with chronic kidney disease, cardiovascular disease, and type 2 diabetes: A meta-analysis. J Natl Med Assoc. 2025 Dec;117(6):458-469. doi: 10.1016/j.jnma.2025.08.110. Epub 2025 Sep 16. PMID: 40962701.

SUP in head trauma

Q: Why are patients with head trauma at increased risk for Gastrointestinal bleed (GIB) and require stress ulcer prophylaxis (SUP)?

Answer: The head trauma patients are usually pointed out in all review articles to be at high risk for GIB in the ICU. The data is decades old, but still applicable. This is due to the pathophysiology of high gastrin stimulation of parietal cells in patients with head trauma. Some clinicians put all ICU patients on SUP, but this practice is flawed and not evidence-based. This practice may expose patients with low or no risk of GIB in the ICU to the risk of nosocomial infections. That said, all patients with risk of stress-related GIB should be placed on SUP till risk exists. 

Discontinuation of SUP is also an important clinical decision for each patient and should be discussed every day.

# neurosurgery

#GI

#patient-safety

References:

1. Bowen JC, Fleming WH, Thompson JC. Increased gastrin release following penetrating central nervous system injury. Surgery 1974; 75:720.

2. Stremple JF, Molot MD, McNamara JJ, et al. Posttraumatic gastric bleeding: prospective gastric secretion composition. Arch Surg 1972; 105:177.

3. Watts CC, Clark K. Gastric acidity in the comatose patient. J Neurosurg 1969; 30:107.

4. McGraw C, Briscoe A, Reynolds C, Carrick M, Palacio CH, Waswick W, Miller A, Trujillo L, Bar-Or D. Outcomes of patients with traumatic brain injury after stress ulcer prophylaxis: a retrospective multicenter study. Trauma Surg Acute Care Open. 2024 Feb 23;9(1):e001285. doi: 10.1136/tsaco-2023-001285. PMID: 38410756; PMCID: PMC10895230.

5. Liu B, Liu S, Yin A, Siddiqi J. Risks and benefits of stress ulcer prophylaxis in adult neurocritical care patients: a systematic review and meta-analysis of randomized controlled trials. Crit Care. 2015 Nov 17;19:409. doi: 10.1186/s13054-015-1107-2. PMID: 26577436; PMCID: PMC4650140.

Defining Neutropenia

Q: Neutropenia is defined as an absolute neutrophil count (ANC) of less than? -select one

A) 500/microL

B) 1500/microL

Answer: B

Neutropenia is defined as an absolute neutrophil count (ANC) of less than 1500/microL. The formula to calculate ANC is 

ANC = WBC (cells/microL) x percent (PMNs + bands) ÷ 100

Where:

WBC = white blood cell count

PMNs = polymorphonuclear cells 

There are various online calculators available.

An ANC below 500 cells/L (choice B) does not define ANC, but at this level, the risk of infection is very high.

The general rule of thumb suggests that if ANC:

• 1000 to 1500/microL = No significant risk of infection; fever can be managed on an outpatient basis
• 500 to 999/microL = Some risk of infection; fever can occasionally be managed on an outpatient basis
• 200 to 499/microL = Significant risk of infection; fever should always be managed on an inpatient basis with parenteral antibiotics, despite few clinical signs of infection
• less than 200/microL = Very significant risk of infection; fever should always be managed on an inpatient basis with parenteral antibiotics, despite few or no clinical signs of infection

The objective of the above question is to identify the common mistakes clinicians make while defining neutropenia.

References:

1. Min KI, Byeon S. Diagnosis and management of neutropenia. Blood Res. 2025 May 26;60(1):30. doi: 10.1007/s44313-025-00079-1. PMID: 40418265; PMCID: PMC12106181.

2. Patel S. Calculated decisions: Absolute neutrophil count. Emerg Med Pract. 2018 Jan 2;20(Suppl 1):1-2. PMID: 29323858.

3. Al-Gwaiz LA, Babay HH. The diagnostic value of absolute neutrophil count, band count and morphologic changes of neutrophils in predicting bacterial infections. Med Princ Pract. 2007;16(5):344-7. doi: 10.1159/000104806. PMID: 17709921.

ICS and voice

Q: Inhaled glucocorticoids (ICS) may cause dysphonia.

A) True

B) False

Answer: A

Unfortunately, dysphonia manifested as a hoarse voice is common among patients who use long-term ICS. It occurs due to laryngeal myopathy, leading to incomplete closure or bowing of the vocal cords during adduction. Other contributing factors are mucosal irritation and frequent laryngeal candidiasis. Fortunately, it is reversible on discontinuation of ICS.

Strategies to keep dysphonia to a minimum are using the lowest ICS dose, using drugs known to cause the least dysphonia, and adjusting technique to decrease laryngeal deposition.

#pulmonary

#pharmacology

References:

1. Roland NJ, Bhalla RK, Earis J. The local side effects of inhaled corticosteroids: current understanding and review of the literature. Chest 2004; 126:213.

2. Buhl R. Local oropharyngeal side effects of inhaled corticosteroids in patients with asthma. Allergy 2006; 61:518.

3. Galván CA, Guarderas JC. Practical considerations for dysphonia caused by inhaled corticosteroids. Mayo Clin Proc 2012; 87:901.

4. Rachelefsky GS, Liao Y, Faruqi R. Impact of inhaled corticosteroid-induced oropharyngeal adverse events: results from a meta-analysis. Ann Allergy Asthma Immunol 2007; 98:225.

Asthma and ACE-I

Q: Asthma patients are more prone to get cough from Angiotensin Converting Enzyme inhibitor (ACE-I).

A) True

B) False

Answer: B

Patients with asthma are not at high risk of developing additional cough, but they may experience increased bronchospasm, so it's still a watchful situation!

A dry hacking cough associated with ACE-I therapy remained an enigma for clinicians. For some reason, females are affected more. It resolves with discontinuation but may recur when challenged with the same ACE-I or a different name. A genetic component is highly suspected.

Interestingly, nonsteroidal antiinflammatory drugs (NSAIDs) and aspirin have shown to decrease or improve the tendency of cough due to ACE-I, but they come with the risk of hyperkalemia, particularly in patients with renal insufficiency.

#pharmacology

#toxicology

#pulmonary

References:

1. Wood R. Bronchospasm and cough as adverse reactions to the ACE inhibitors captopril, enalapril and lisinopril. A controlled retrospective cohort study. Br J Clin Pharmacol 1995; 39:265.

2. Lunde H, Hedner T, Samuelsson O, et al. Dyspnoea, asthma, and bronchospasm in relation to treatment with angiotensin converting enzyme inhibitors. BMJ 1994; 308:18.

3. Tenenbaum A, Grossman E, Shemesh J, et al. Intermediate but not low doses of aspirin can suppress angiotensin-converting enzyme inhibitor-induced cough. Am J Hypertens 2000; 13:776.

4. Ghouse J, Tragante V, Muhammad A, et al. Polygenic risk score for ACE-inhibitor-associated cough based on the discovery of new genetic loci. Eur Heart J 2022; 43:4707.

Indium Scan vs Gallium scan

Q: What is the difference between an Indium Scan and a Gallium scan?

Answer: The indium scan is a procedure in which WBCs (neutrophils) are removed from the patient, tagged with the radioisotope Indium-111, and then injected back into the patient. The tagged leukocytes subsequently enhance areas of relatively new infection, where live neutrophils are still rapidly and actively localizing.

A gallium scan has an advantage over the indium scan because gallium binds to neutrophil membranes, even after neutrophil death. This makes gallium more broadly sensitive, allowing it to localize to other sources of fever, such as chronic infections and tumors.

#nuclear-medicine

#ID

References:

1. Lewis SS, Cox GM, Stout JE. Clinical utility of indium 111-labeled white blood cell scintigraphy for evaluation of suspected infection. Open Forum Infect Dis. 2014 Sep 17;1(2):ofu089. doi: 10.1093/ofid/ofu089. PMID: 25734155; PMCID: PMC4281781.

2. Merkel KD, Brown ML, Dewanjee MK, Fitzgerald RH Jr. Comparison of indium-labeled-leukocyte imaging with sequential technetium-gallium scanning in the diagnosis of low-grade musculoskeletal sepsis. A prospective study. J Bone Joint Surg Am. 1985 Mar;67(3):465-76. PMID: 3919029.

3. Dittrich RP, De Jesus O. Gallium Scan. 2022 Dec 26. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. PMID: 33620825.

End-Tidal CO2

Q: Why its called "End-Tidal" CO2?

Answer: It's the point in the respiratory cycle where CO2 is at the highest level (End of the tide)

There are five phases of respiration when it comes to end-tidal Co2 analysis

1. Dead space ventilation
2. Ascending expiratory phase
3. Alveolar Plateau
4. End-tidal CO2
5. Descending inspiratory phase

These five phases are marked in the pic as

A - B: Dead space ventilation

B - C: Ascending expiratory phase

C - D: Alveolar Plateau

D: End-tidal CO2 (highest)

D - E: Descending inspiratory phase

#pulmonary

#procedures

References:

1. Krauss B, Deykin A, Lam A, et al. Capnogram shape in obstructive lung disease. Anesth Analg 2005; 100:884. Copyright © 2005 Lippincott Williams & Wilkins.

2. Zwerneman K. End-tidal carbon dioxide monitoring: a VITAL sign worth watching. Crit Care Nurs Clin North Am. 2006 Jun;18(2):217-25, xi. doi: 10.1016/j.ccell.2006.02.002. PMID: 16728308.

3. Benumof JL. Abnormal end-tidal CO2 waveforms. Can J Anaesth. 2003 Aug-Sep;50(7):754. doi: 10.1007/BF03018728. PMID: 12944461.

Bronchial Sleeve Resection

Q: What is sleeve resection of the lung?

Answer: A sleeve resection is a kind of maximum lung/tissue-sparing surgery, or an alternative to a pneumonectomy. This procedure is performed by removing a lobe containing a target lesion (mostly a tumor) with a portion of the lobar bronchus to an uninvolved lobe. The remaining bronchus to the uninvolved lobe is anastomosed to the remaining proximal airway.

#pulmonary

#surgical-critical-care

References:

1. Deslauriers J, Mehran RJ, Guimont C, Brisson J. Staging and management of lung cancer: sleeve resection. World J Surg. 1993 Nov-Dec;17(6):712-8. doi: 10.1007/BF01659080. PMID: 8109107.

2. Suzuki K. Extended Sleeve Resection for Lung Cancer. Thorac Surg Clin. 2018 Aug;28(3):291-297. doi: 10.1016/j.thorsurg.2018.03.004. PMID: 30054066.

3. Duan J, Cai H, Huang W, Lin L, Wu L, Fan J. Bronchial Sleeve Resection with Complete Pulmonary Preservation: A Single-Center Experience. Cancer Manag Res. 2020 Dec 16;12:12975-12982. doi: 10.2147/CMAR.S286934. PMID: 33364843; PMCID: PMC7751305.

Ventilator mode and sleep in ICU

Q; Which of the ventilator modes has so far shown that it causes more sleep disturbances in the ICU patients? - select one

A) Assist Controlled (AC)

B) Pressure Controlled (PC)

C) Synchronized Intermittent Mandatory Ventilation (SIMV)

Answer: B

Although the data is not robust and the evidence is weak, PC mode has so far shown to cause most sleep disturbances in the ICU. Unfortunately, sedation is not equivalent to a normal sleep cycle in ICU patients.

AC mode is widely believed to be easiest for the patient because it has the least impact on the patient's contribution to ventilation.

Although intensivists are hopeful that future data will show greater promise for other modes, such as Adaptive Support Ventilation (ASV) or Neurally adjusted ventilatory assist (NAVA).

#ventilators

#sleep

References:

1. Parthasarathy S, Tobin MJ. Effect of ventilator mode on sleep quality in critically ill patients. Am J Respir Crit Care Med 2002; 166:1423.

2. Cabello B, Thille AW, Drouot X, et al. Sleep quality in mechanically ventilated patients: comparison of three ventilatory modes. Crit Care Med 2008; 36:1749.

3. Locihová H, Žiaková K. The effects of mechanical ventilation on the quality of sleep of hospitalised patients in the Intensive Care Unit. Rom J Anaesth Intensive Care. 2018 Apr;25(1):61-72. doi: 10.21454/rjaic.7518.251.ven. PMID: 29756065; PMCID: PMC5931186.

Paradoxical Effect of Acetazolamide in the Kidneys and Lungs

Acetazolamide is a carbonic anhydrase inhibitor and is frequently used to treat hypercarbia and metabolic alkalosis. Acetazolamide affects three major organs of the body: the brain, lungs, and kidneys. It is imperative to understand the paradoxical effect of acetazolamide in kidneys and lungs.

In the kidneys, acetazolamide increases hydrogen ion retention and bicarbonate excretion, causing metabolic acidosis over several hours. This also has a secondary effect: metabolic acidosis further increases respiratory drive.

In the lungs, acetazolamide blocks the reciprocal conversion of bicarbonate to CO2 in pulmonary capillaries and impairs the lungs' ability to excrete the CO2. The intended effect is to increase minute ventilation and thereby reduce hypercarbia. But the patients who are not able to increase their ventilation, like patients on ventilators, and, to make it worse, on neuromuscular blockade, may have further deterioration in hypercarbia.

Clinical significance: In the ICU, acetazolamide may 'fire back' if the patient's kidneys are not working well and the patient is on a ventilator. Therefore, it should be used with much greater caution.

Centrally, acetazolamide blocks the CO2 conversion to bicarbonate in tissue capillaries and acutely raises the local tissue partial pressure of carbon dioxide (PCO2). This locally elevated PCO2 and lower pH in the brain increase the central ventilatory drive and lower PaCO2. This central effect, combined with its pulmonary effect, makes acetazolamide an effective prophylactic and therapeutic agent for acute and chronic mountain sickness in healthy individuals.

#pulmonary

#acid-base

References:

1. Swenson ER, Hughes JM. Effects of acute and chronic acetazolamide on resting ventilation and ventilatory responses in men. J Appl Physiol (1985) 1993; 74:230.

2. Richalet JP, Rivera M, Bouchet P, et al. Acetazolamide: a treatment for chronic mountain sickness. Am J Respir Crit Care Med 2005; 172:1427.

3. Alkhuzaee FS, Aldardeer NF, Althobaiti OA, Aljuaid AS, Alshehri AM. Acetazolamide for the Management of Diuretic-Induced Chloride Depletion Alkalosis: A Systematic Review. J Clin Med. 2025 Feb 7;14(4):1041. doi: 10.3390/jcm14041041. PMID: 40004571; PMCID: PMC11857046.

4. Van Berkel MA, Elefritz JL. Evaluating off-label uses of acetazolamide. Am J Health Syst Pharm. 2018 Apr 15;75(8):524-531. doi: 10.2146/ajhp170279. PMID: 29626002.

Wrist BP

Q: Blood Pressure (BP) taken at the wrist level is usually? - select one

A) falsely elevated

B) falsely lowered

Answer: A

Measuring non-invasive BP at the radial artery, i.e., wrist level, is not desirable, though it may be necessary in a few patients, such as those with axillary lymph node resection.

BP at wrist level is falsely elevated due to the hydrostatic pressure related to the lower position of the wrist relative to the heart. Additionally, the relatively small-diameter vessels in older adults are calcified and exhibit reduced elastance. Although BP can be measured with the wrist at heart level, wrist flexion may interfere with sensor positioning.

Wrist BP measurement requires equipment specifically designed for wrist BP, and devices used for brachial BP measurement should not be used.

#hemodynamics

References:

1. Muntner P, Shimbo D, Carey RM, et al. Measurement of Blood Pressure in Humans: A Scientific Statement From the American Heart Association. Hypertension 2019; 73:e35.

2. Palatini P, Asmar R, O'Brien E, et al. Recommendations for blood pressure measurement in large arms in research and clinical practice: position paper of the European society of hypertension working group on blood pressure monitoring and cardiovascular variability. J Hypertens 2020; 38:1244.

3. Zweiker R, Schumacher M, Fruhwald FM, Watzinger N, Klein W. Comparison of wrist blood pressure measurement with conventional sphygmomanometry at a cardiology outpatient clinic. J Hypertens. 2000 Aug;18(8):1013-8. doi: 10.1097/00004872-200018080-00004. PMID: 10953991.

chloride in adrenal insufficiency

Q: Patients with adrenal insufficiency tend to have? - select one

A) Hyperchloremia

B) Hypochloremia

Answer: A

Adrenal insufficiency, as defined by mineralocorticoid deficiency, causes hyperkalemia and hyperchloremic acidosis. 

Mechanism of action: The loss of aldosterone reduces hydrogen ion excretion in the renal collecting duct, leading to hyperchloremic normal anion gap metabolic acidosis. 

Other imbalances that may occur

• Hyponatremia 
• hypercalcemia (though rare)
• hypoglycemia

#electrolytes

#endocrinology

References:

1. Sagar N, Lohiya S. A Comprehensive Review of Chloride Management in Critically Ill Patients. Cureus. 2024 Mar 6;16(3):e55625. doi: 10.7759/cureus.55625. PMID: 38586759; PMCID: PMC10995984.

2. Kromah F, Tyroch A, McLean S, Hughes H, Flavin N, Lee S. Relative adrenal insufficiency in the critical care setting: debunking the classic myth. World J Surg. 2011 Aug;35(8):1818-23. doi: 10.1007/s00268-011-1126-3. PMID: 21533963; PMCID: PMC7101698.

3. Fries C, Fenske W. Elektrolytentgleisungen unter endokrinologischen Gesichtspunkten [An Endocrinological Perspective on Electrolyte Imbalances]. Dtsch Med Wochenschr. 2025 Aug;150(15):883-889. German. doi: 10.1055/a-2318-7580. Epub 2025 Jul 21. PMID: 40690933.

Nimodipine prophylaxis in aneurysmal subarachnoid hemorrhage

Q: Why, despite no convincing angiographic evidence of nimodipine's effect on Subarachnoid Hemorrhage (SAH), does it continue to be the standard of care in SAH?

Answer: Although it is true that so far Nimodipine failed to show any concrete evidence of objective improvement of either angiographic or symptomatic vasospasm in SAH, it is considered essential, and not using it, a malpractice, in SAH management. This is because nimodipine likely dilates small arteries that are not visible on angiograms.

Other beneficial effects of nimodipine are due to the combination of:

• reduction of calcium-dependent excitotoxicity
• diminished platelet aggregation
• inhibition of ischemia triggered by red blood cell products

#neurology

#neurosurgery

#pharmacology

References:

1. Barker FG 2nd, Ogilvy CS. Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis. J Neurosurg 1996; 84:405.

2. Dayyani M, Sadeghirad B, Grotta JC, et al. Prophylactic Therapies for Morbidity and Mortality After Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Network Meta-Analysis of Randomized Trials. Stroke 2022; 53:1993.

3. Bellapart J, Laupland KB, Malacova E, Roberts JA, Paratz J. Nimodipine prophylaxis in aneurysmal subarachnoid hemorrhage, a question of tradition or evidence: A scoping review. J Clin Neurosci. 2024 May;123:91-99. doi: 10.1016/j.jocn.2024.03.016. Epub 2024 Apr 1. PMID: 38564967.

4. Hao G, Chu G, Pan P, Han Y, Ai Y, Shi Z, Liang G. Clinical effectiveness of nimodipine for the prevention of poor outcome after aneurysmal subarachnoid hemorrhage: A systematic review and meta-analysis. Front Neurol. 2022 Sep 21;13:982498. doi: 10.3389/fneur.2022.982498. PMID: 36212656; PMCID: PMC9533126.

Fenoldopam

Q: A 64-year-old male with a past medical history of hypertension, diabetes mellitus, hyperlipidemia, and stage-3 renal insufficiency is admitted to the ICU with hypertensive crises. The intensivist picked Fenoldopam infusion. What is the added advantage of Fenoldopam in this patient?

Answer: It either maintains or increases kidney perfusion

Although Fenoldopam is not commonly used as an antihypertensive infusion in ICUs, it offers several advantages. It is a peripherally acting dopamine-1 receptor agonist that maintains or increases renal perfusion while controlling hypertension. It has shown to increase glomerular filtration rate (GFR), urine output, and sodium excretion.

Dose-wise, it is usually initiated at 0.1 mcg/kg/min and titrated at 15-minute intervals to a maximum of 1.6 mcg/kg/min. If needed can be titrated up to 2.0 mcg/kg/minute. It is very unlikely to cause any real toxicity, though it is contraindicated in glaucoma, and caution should be applied in patients with sulpha allergy, as it is premixed in a solution containing sodium metabisulfite.

# hemodynamics

#nephrology

#pharmacology

References:

1. Murphy MB, Murray C, Shorten GD. Fenoldopam: a selective peripheral dopamine-receptor agonist for the treatment of severe hypertension. N Engl J Med 2001; 345:1548.

2. White WB, Halley SE. Comparative renal effects of intravenous administration of fenoldopam mesylate and sodium nitroprusside in patients with severe hypertension. Arch Intern Med 1989; 149:870.

3. Shusterman NH, Elliott WJ, White WB. Fenoldopam, but not nitroprusside, improves renal function in severely hypertensive patients with impaired renal function. Am J Med 1993; 95:161.

Removal of stylet during intubation

Q: What's the best time to remove the stylet from the Endotracheal Tube (ETT) while intubating the patient? - select one

A) Once the tip of the ETT has passed the vocal cords

B) After the ETT is fully inserted inside the trachea

Answer: A

An inexperienced operator usually keeps the stylet in the ETT till the tube is fully inserted and set in the trachea. This approach may cause injury or obstruct the passage of the tube beyond the vocal cords. 

Ideally, once the tip of the ETT has passed the vocal cords, the operator should pause and ask the staff next to remove the stylet while maintaining a firm hold on the tube and a clear view of the ETT and the glottis.

#procedures

References/further reading:

1. Higgs A, McGrath BA, Goddard C, Rangasami J, Suntharalingam G, Gale R, Cook TM; Difficult Airway Society; Intensive Care Society; Faculty of Intensive Care Medicine; Royal College of Anaesthetists. Guidelines for the management of tracheal intubation in critically ill adults. Br J Anaesth. 2018 Feb;120(2):323-352. doi: 10.1016/j.bja.2017.10.021. Epub 2017 Nov 26. PMID: 29406182.

2. DeMasi SC, Casey JD, Semler MW. Evidence-based Emergency Tracheal Intubation. Am J Respir Crit Care Med. 2025 Jul;211(7):1156-1164. doi: 10.1164/rccm.202411-2165CI. PMID: 40238943; PMCID: PMC12264701.

3. Long B, Gottlieb M. Emergency medicine updates: Endotracheal intubation. Am J Emerg Med. 2024 Nov;85:108-116. doi: 10.1016/j.ajem.2024.08.042. Epub 2024 Sep 3. PMID: 39255682.

On FFP

Q: One unit of Fresh Frozen Plasma (FFP) is the plasma taken from a unit of whole blood. How quickly should it be frozen after collection?

Answer: within eight hours of collection.

Each unit of FFP contains approximately 225-250 ml of plasma derived from a single unit of whole blood. It is stored frozen at -18° C or colder to preserve all coagulation factors. FFP is thawed in a 37° C (waterbath) upon request (20-30 minutes) and can be stored after thawing for up to 24 hours at 1-6° C. FFP doesn't require crossmatching.

#hematology

References:

1. National Clinical Guideline Centre (UK). Blood Transfusion. London: National Institute for Health and Care Excellence (NICE); 2015 Nov. (NICE Guideline, No. 24.) 14, Fresh Frozen Plasma: thresholds and targets. Available from: https://www.ncbi.nlm.nih.gov/books/NBK338797/

2. Lauzier F, Cook D, Griffith L, Upton J, Crowther M. Fresh frozen plasma transfusion in critically ill patients. Crit Care Med. 2007 Jul;35(7):1655-9. doi: 10.1097/01.CCM.0000269370.59214.97. PMID: 17522577.

3. Ichikawa, J., Iba, T., Okazaki, R. et al. Hemostatic capability of ultrafiltrated fresh frozen plasma compared to cryoprecipitate. Sci Rep 13, 21579 (2023). https://doi.org/10.1038/s41598-023-48759-1

Cannabis and Asthma

Q: Cannabis (Marijuana) makes asthma? - select one

A) better

B) exacerbate

Answer: B

The objective of this question is to highlight the fact that cannabis tends to cause bronchospasm, wheezing, and chest tightness. It can be a trigger for potentially fatal status asthmaticus.

Unfortunately, some internet as well as medical literature describes cannabis as a bronchodilator, but that should not be promoted for the benefit of society.

#toxicity

#pulmonary

References:

1. Malvi A, Khatib MN, Balaraman AK, Roopashree R, Kaur M, Srivastava M, Barwal A, Siva Prasad GV, Rajput P, Syed R, Sharma G, Kumar S, Singh MP, Bushi G, Chilakam N, Pandey S, Brar M, Mehta R, Sah S, Gaidhane AM, Shabil M, Daniel AS. Cannabis consumption and risk of asthma: a systematic review and meta-analysis. BMC Pulm Med. 2025 Jan 29;25(1):48. doi: 10.1186/s12890-025-03516-0. PMID: 39881272; PMCID: PMC11780798.

2. Sule-Saa S, Hein PP, Sackey JA, Pinkrah D, Towfig M, Akella A, Kotei R, DiCasoli R, Sherazi A, Panigrahi K. The Effect of Cannabis Use Disorder on Mortality and Other Outcomes in Asthma: A Nationwide Analysis (2016-2021). Cureus. 2025 Oct 20;17(10):e94969. doi: 10.7759/cureus.94969. PMID: 41281008; PMCID: PMC12631705.

3. Rustagi AS, Jeffers AM, Graham FJ, Cohen BE, Slatore CG, Byers AL, Glantz SA, Keyhani S. Inhaled Cannabis, Asthma, and Chronic Obstructive Pulmonary Disease: A Population-Based Cross-Sectional Study of n = 379,049. J Gen Intern Med. 2025 Sep 4:10.1007/s11606-025-09833-8. doi: 10.1007/s11606-025-09833-8. Epub ahead of print. PMID: 40906010; PMCID: PMC12681257.

Tricks for intractable hiccups

 Q: Which 2 relatively non-pharmacologic tricks can work in intractable hiccups in the ICU?

Answer:

1. Give 2 ml Nebulised 0.9% saline over 5 minutes. It helps to relieve hiccups by pharyngeal stimulation.

2. Give Peppermint Water. Peppermint water helps by relaxing the lower oesophageal sphincter.

#ICU-care

#GI

Reference:

1. Twycross R, Wilcock A. - Symptom Management in Advanced Cancer. 3rd Edt. Radcliffe Medical Press. 2008

2. Rouse S, Wodziak M. Intractable Hiccups. Curr Neurol Neurosci Rep. 2018 Jun 22;18(8):51. doi: 10.1007/s11910-018-0856-0. PMID: 29934880. 

3. Kishi Y, Nakawaga M, Inumaru A, Nambu M, Sakaguchi M, Murabata M, Matsuoka M, Kako J. Interventions for Hiccups in Adults: A Scoping Review of Western and Eastern Approaches. Palliat Med Rep. 2025 Apr 17;6(1):171-178. doi: 10.1089/pmr.2024.0109. PMID: 40308713; PMCID: PMC12040553.

C/I of Magnesium in Eclampsia

Q: Mention at least one disease where Magnesium is contraindicated in eclampsia?

Answer: Myasthenia gravis

High-dose magnesium has remained the standard of care for eclampsia over the decades, and under time pressure, it is difficult to recall magnesium's contraindications, particularly in patients with a history of myasthenia gravis. Magnesium can precipitate a severe myasthenic crisis.

Similarly, magnesium should be used with caution in the following situations:

• Severe renal failure (lack of excretion)
• Severe Coronary Artery Disease (CAD)
• Heart blocks
• Myocardial disease
• Hypocalcemia (exacerbates the situation)

#ob-gyn

#electrolytes

References:

1. Lake AJ, Al Khabbaz A, Keeney R. Severe Preeclampsia in the Setting of Myasthenia Gravis. Case Rep Obstet Gynecol. 2017;2017:9204930. doi: 10.1155/2017/9204930. Epub 2017 Feb 9. PMID: 28280642; PMCID: PMC5322431.

2. Smith JM, Lowe RF, Fullerton J, Currie SM, Harris L, Felker-Kantor E. An integrative review of the side effects related to the use of magnesium sulfate for pre-eclampsia and eclampsia management. BMC Pregnancy Childbirth. 2013 Feb 5;13:34. doi: 10.1186/1471-2393-13-34. PMID: 23383864; PMCID: PMC3570392.

3. Abdulhadi B, Agarwal M. The Unusual Suspect: Hypocalcemia in Preeclampsia After Magnesium Infusion. J Endocr Soc. 2021 May 3;5(Suppl 1):A227. doi: 10.1210/jendso/bvab048.461. PMCID: PMC8089210.

Eye and Semaglutide

Q: Ischemic optic neuropathy due to semaglutide is?

A) reversible

B) irreversible

Answer: B

The last decade has seen a tremendous rise in the use of Glucagon-like peptide 1 (GLP-1)-based therapies, which include GLP-1 receptor agonists, dual-acting GLP-1 and glucose-dependent insulinotropic polypeptide [GIP] receptor agonists. Unfortunately, the improper use of semaglutide has skyrocketed due to its property of quick weight loss.

Non-arteritic ischemic optic neuropathy (NAION) is a dreaded side effect of semaglutide, as it causes irreversible vision loss. Any patient who experiences worsening vision while taking semaglutide should discontinue it and consult their physician immediately.

# endocrinology

# ophthalmology

#pharmacology

References:

1. Grauslund J, Taha AA, Molander LD, et al. Once-weekly semaglutide doubles the five-year risk of nonarteritic anterior ischemic optic neuropathy in a Danish cohort of 424,152 persons with type 2 diabetes. Int J Retina Vitreous 2024; 10:97.

2. Hathaway JT, Shah MP, Hathaway DB, et al. Risk of Nonarteritic Anterior Ischemic Optic Neuropathy in Patients Prescribed Semaglutide. JAMA Ophthalmol 2024; 142:732.

3. Natividade GR, Spiazzi BF, Baumgarten MW, et al. Ocular Adverse Events With Semaglutide: A Systematic Review and Meta-Analysis. JAMA Ophthalmol 2025; 143:759.

Other labs in hyperthyroidism

Q; In patients with hyperthyroidism, serum total, low-density (LDL), and high-density lipoprotein (HDL) cholesterol tends to be? - select one

A) higher

B) lower

Answer: B

It is always interesting and a good clinical and academic exercise to look for nonspecific laboratory findings in patients with hyperthyroidism. These patients usually have

• lower total, LDL, and HDL cholesterol (due to high sympathathetic activity)
• increased red blood cell (RBC) mass*
• increased plasma volume*
• higher alkaline phosphatase level^
• higher osteocalcin concentrations^

*RBC mass is increased, but the plasma volume is even more increased, showing up as a normochromic, normocytic anemia

^ due to increased bone turnover

#endocrinology

#laboratory-medicine

References: 

1. O'Brien T, Katz K, Hodge D, et al. The effect of the treatment of hypothyroidism and hyperthyroidism on plasma lipids and apolipoproteins AI, AII and E. Clin Endocrinol (Oxf) 1997; 46:17.

2. Dorgalaleh A, Mahmoodi M, Varmaghani B, Kiani Node F, Saeeidi Kia O, Alizadeh Sh, Tabibian Sh, Bamedi T, Momeni M, Abbasian S, Kashani Khatib Z. Effect of thyroid dysfunctions on blood cell count and red blood cell indice. Iran J Ped Hematol Oncol. 2013;3(2):73-7. Epub 2013 Apr 22. PMID: 24575274; PMCID: PMC3915449.

3. Kumeda Y, Inaba M, Tahara H, Kurioka Y, Ishikawa T, Morii H, Nishizawa Y. Persistent increase in bone turnover in Graves' patients with subclinical hyperthyroidism. J Clin Endocrinol Metab. 2000 Nov;85(11):4157-61. doi: 10.1210/jcem.85.11.6979. PMID: 11095447.

Sildenafil and Heart

Q: Sildenafil may have an antiplatelet effect.

A) True

B) False

Answer: A

Sildenafil exerts its mild antianginal effect via four mechanisms:

• It lowers the systolic blood pressure by approximately 8-10 mmHg 
• Dilation of epicardial coronary arteries
• Improving endothelial dysfunction, and 
• Inhibiting platelet activation

That said, all patients with cardiovascular disease should use sildenafil after risk-stratification and under the care of a physician, as its vasodilatory effect can be detrimental in some patients, particularly with undiagnosed or underlying Aortic Stenosis (AS).

#cardiology

#pharmacology

References:

1. Levine GN, Steinke EE, Bakaeen FG, et al. Sexual activity and cardiovascular disease: a scientific statement from the American Heart Association. Circulation 2012; 125:1058.

2. Herrmann HC, Chang G, Klugherz BD, Mahoney PD. Hemodynamic effects of sildenafil in men with severe coronary artery disease. N Engl J Med 2000; 342:1622.

3. Halcox JP, Nour KR, Zalos G, et al. The effect of sildenafil on human vascular function, platelet activation, and myocardial ischemia. J Am Coll Cardiol 2002; 40:1232.

4. Mittleman MA, Maclure M, Glasser DB. Evaluation of acute risk for myocardial infarction in men treated with sildenafil citrate. Am J Cardiol 2005; 96:443.

OTC anti-diarrheal and dizzyness

Case: 32-year-old male, healthy male with no past medical history, presented to the Emergency Department (ED) with dizziness. On telemetry patient is found to be in wide-complex tachycardia. Patient recently returned from a three-week trip and reported using over-the-counter (OTC) anti-diarrheal multiple times a day during vacation for traveler's diarrhea. Which dug is suspected?

Answer: Loperamide 

Less well-known is the fact that Loperamide is an opioid that acts as a peripherally acting mu-opioid receptor agonist and rarely affects the central nervous system (CNS). It is an effective anti-diarrheal and usually safe, so the FDA approved it as an OTC medicine. 

Interestingly, in overdose, it loses specificity for the gastrointestinal (GI) tract. Potentially fatal side effects of overdose are QRS and QT interval prolongation and wide-complex tachycardia.

#pharmacology

#toxicity

References:

1. Eggleston W, Nacca N, Marraffa JM. Loperamide toxicokinetics: serum concentrations in the overdose setting. Clin Toxicol (Phila) 2015; 53:495.

2. Spinner HL, Lonardo NW, Mulamalla R, Stehlik J. Ventricular tachycardia associated with high-dose chronic loperamide use. Pharmacotherapy 2015; 35:234.

3. Wightman RS, Hoffman RS, Howland MA, et al. Not your regular high: cardiac dysrhythmias caused by loperamide. Clin Toxicol (Phila) 2016; 54:454.

4. Eggleston W, Clark KH, Marraffa JM. Loperamide Abuse Associated With Cardiac Dysrhythmia and Death. Ann Emerg Med 2017; 69:83.

Sleep Disturbances in ICU

Q: ICU patients, particularly older patients, who sleep more during the day than at night, tend to have greater cognitive impairment during Post-ICU recovery.

A) True

B) False

Answer: A

Preserving physiological sleep during hospitalization remains a challenge for clinicians. Pragmatically, none of the patients achieve a normal sleep pattern in the ICU due to various environmental and pharmacological factors, some of which can be modified and some of which remain non-negotiable. Preservation of the normal sleep cycle remains more challenging in older, sedated, and ventilated patients.

Good sedation is not equivalent to a normal sleep cycle. This can be best described as "atypical sleep" or "pathologic wakefulness", due to sleep fragmentation and the absence of rapid eye (REM) movement.

Although all patients experience sleep disturbance in Post-ICU recovery, the older patients remained at high risk, particularly those patients who slept more during the day than at night while they were in the ICU.

#sleep

#PICS

References:

1. Elliott R, McKinley S, Cistulli P, Fien M. Characterisation of sleep in intensive care using 24-hour polysomnography: an observational study. Crit Care 2013; 17:R46.

2. Sun T, Sun Y, Huang X, et al. Sleep and circadian rhythm disturbances in intensive care unit (ICU)-acquired delirium: a case-control study. J Int Med Res 2021; 49:300060521990502.

3. Altman MT, Knauert MP, Pisani MA. Sleep Disturbance after Hospitalization and Critical Illness: A Systematic Review. Ann Am Thorac Soc 2017; 14:1457.

4. Elías MN, Munro CL, Liang Z. Daytime-to-Nighttime Sleep Ratios and Cognitive Impairment in Older Intensive Care Unit Survivors. Am J Crit Care 2021; 30:e40.

Hypoxemia and Hyponatremia connection

With serum sodium concentration even with a little less than 130 mEq/L,  and subtle symptoms like nausea, vomiting, headache, or confusion - few subsets of patients like:

• Psychosis
• Marathon runners (or athletes)
• Recreational drug users, particularly ecstasy
• Women and children with acute postoperative hyponatremia
• Traumatic brain injury (TBI or intracranial hemorrhage (ICH)
• Recent intracranial surgery 
• Intracranial space-occupying lesion (like a tumor)

- are very prone to quickly develop seizures, respiratory arrest, and permanent or fatal brain damage.

To make things complicated, concurrent hypoxemia, from noncardiogenic pulmonary edema or hypoventilation, exacerbates the hyponatremia-induced cerebral edema. Timely intervention with elevation of the serum sodium concentration to 4 to 6 mEq/L may prevent impending brain herniation.

#neurology

#electrolytes

# neurosurgery

References:

1. Ayus JC, Varon J, Arieff AI. Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners. Ann Intern Med 2000; 132:711.

2. Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol 2009; 29:282.

3. Chawla A, Sterns RH, Nigwekar SU, Cappuccio JD. Mortality and serum sodium: do patients die from or with hyponatremia? Clin J Am Soc Nephrol 2011; 6:960.

4. Seethapathy H, Zhao S, Ouyang T, et al. Severe Hyponatremia Correction, Mortality, and Central Pontine Myelinolysis. NEJM Evid 2023; 2:EVIDoa2300107.

Hyperkalemia-induced Brugada pattern on EKG

Q: What is "hyperkalemic Brugada sign"?

Answer: Type I Brugada type change on EKG with hyperkalemia 

Frequently observed in ICU patients who are extremely acidotic and hyperkalemic, a type I Brugada pattern can be seen on EKG, with a pseudo-right bundle branch block and persistent "coved" ST-segment elevation in at least 2 precordial leads. This is known as the "hyperkalemic Brugada sign".

This should be differentiated from genetic Brugada syndrome by an absence of P waves, marked QRS widening, and/or an abnormal QRS axis. 

#cardiology

#electrolytes

#acidosis

References:

1. Littmann L, Monroe MH, Taylor L 3rd, Brearley WD Jr. The hyperkalemic Brugada sign. J Electrocardiol 2007; 40:53.

2. Doty B, Kim E, Phelps J, Akpunonu P. Pathophysiology of Hyperkalemia Presenting as Brugada Pattern on Electrocardiogram (ECG). Am J Case Rep. 2020 Jul 8;21:e923464. doi: 10.12659/AJCR.923464. PMID: 32636355; PMCID: PMC7370581.

3. Liu R, Chang Q. Hyperkalemia-induced Brugada pattern with electrical alternans. Ann Noninvasive Electrocardiol. 2013 Jan;18(1):95-8. doi: 10.1111/j.1542-474X.2012.00540.x. Epub 2012 Aug 13. PMID: 23347033; PMCID: PMC6932092.

findings in advSM

Q: In advanced systemic mastocytosis (advSM), impaired organ function will be described as? - select one

A) A findings

B) B findings 

C) C findings

Answer: C

There are five subtypes of SM:

• Indolent SM
• Smoldering SM
• Aggressive SM (ASM)
• Mast cell leukemia (MCL)
• SM with an associated hematologic/myeloid neoplasm (SM-AHN)

Last 3, i.e., ASM, MCL, and SM-AHN, are collectively referred to as advanced SM (advSM). 

B Findings - are defined as high disease burden or significant organ enlargement without organ dysfunction.

C Findings -  are defined as Impaired organ function due to mast cell infiltration.

#oncology-hematology

References:

1. Arber DA, Orazi A, Hasserjian RP, et al. International Consensus Classification of Myeloid Neoplasms and Acute Leukemias: integrating morphologic, clinical, and genomic data. Blood 2022; 140:1200.

2. Khoury JD, Solary E, Abla O, et al. The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Myeloid and Histiocytic/Dendritic Neoplasms. Leukemia 2022; 36:1703.

3. Pardanani A, Reichard K, Tefferi A. Advanced systemic mastocytosis-Revised classification, new drugs and how we treat. Br J Haematol. 2024 Feb;204(2):402-414. doi: 10.1111/bjh.19245. Epub 2023 Dec 6. PMID: 38054381.

4. Ustun C, Keklik Karadag F, Linden MA, Valent P, Akin C. Systemic mastocytosis: current status and challenges in 2024. Blood Adv. 2025 May 13;9(9):2048-2062. doi: 10.1182/bloodadvances.2024012612. PMID: 39853317; PMCID: PMC12052678.

CRAB in MM

Q: What is the "CRAB" of Multiple Myeloma (MM)?

Answer: 

"CRAB" is an acronym "CRAB" to remember the essential features of the spectrum of MM, which is a disease of infiltration of plasma cells into the bone or organs, and damage from immunoglobulin deposition. The "CRAB" stands for

• Calcium elevation
• Renal insufficiency
• Anemia, &
• Bone disease

MM is a disease of the older population, and may go undiagnosed for many years, and many times comes to attention when acute complications happen after many years, such as spinal cord compression, kidney failure, or hyperviscosity. 

Audience should be aware that CRAB is just an acronym, can be present in other diseases, and should not be used as a diagnostic criterion as MM can present with other features too.

#electrolytes

#nephrology

#bone-disease

#hematology

References:

1. Kyle RA, Gertz MA, Witzig TE, et al. Review of 1027 patients with newly diagnosed multiple myeloma. Mayo Clin Proc 2003; 78:21.

2. Nakaya A, Fujita S, Satake A, Nakanishi T, Azuma Y, Tsubokura Y, Hotta M, Yoshimura H, Ishii K, Ito T, Nomura S. Impact of CRAB Symptoms in Survival of Patients with Symptomatic Myeloma in Novel Agent Era. Hematol Rep. 2017 Feb 23;9(1):6887. doi: 10.4081/hr.2017.6887. PMID: 28286629; PMCID: PMC5337823.

3. Rajkumar SV. Evolving diagnostic criteria for multiple myeloma. Hematology Am Soc Hematol Educ Program. 2015;2015:272-8. doi: 10.1182/asheducation-2015.1.272. PMID: 26637733.