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.

Modified Marshall Score

Q: In the Modified Marshall scoring system for organ dysfunction in acute pancreatitis, deterioration of which of the following organs is included? - select one

A) Gall Bladder

B) Liver

C) Pancrease

D) Kidney

E) Spleen

Answer: D

The Modified Marshall Score in acute pancreatitis objectively assesses the level of organ dysfunctions. It has three main components:

• PaO2/FiO2
• serum creatinine, and
• systolic blood pressure

 Clinical significance: Patients with worsening Modified Marshall scores for organ dysfunction may qualify for plasmapheresis, though the decision to perform plasmapheresis should be made in conjunction with other clinical and laboratory data.

#GI

#procedures

#scores

References:

1.  Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis - 2012: revisions of the Atlanta classification and definitions by international consensus. Gut 2013; 62:102. 

2. Ling CHY, Bond R, East S, Young R. Modified Marshall Score: An Underutilised Prognostication Tool for Acute Pancreatitis. Cureus. 2025 Nov 14;17(11):e96842. doi: 10.7759/cureus.96842. PMID: 41356937; PMCID: PMC12677363.

3. Hartmann J, Werge M, Schmidt PN, Hansen EF, Pedersen UG, Kristiansen KT, Gluud LL, Novovic S. Modified Marshall Score Predicts Mortality in Patients With Walled-off Pancreatic Necrosis Treated in an Intensive Care Unit. Pancreas. 2019 Oct;48(9):e68-e70. doi: 10.1097/MPA.0000000000001409. PMID: 31609936.

4. Abu Omar Y, Attar BM, Agrawal R, Randhawa T, Majeed M, Wang Y, Simons-Linares CR, Wang Y. Revised Marshall Score: A New Approach to Stratifying the Severity of Acute Pancreatitis. Dig Dis Sci. 2019 Dec;64(12):3610-3615. doi: 10.1007/s10620-019-05719-y. Epub 2019 Jul 8. PMID: 31286346.

pulmonary complication with Daptomycin infusion

Q: Which life-threatening pulmonary complication may happen with Daptomycin infusion?

Answer: Eosinophillic Pneumonia

According to the FDA report, seven cases of eosinophilic pneumonia were confirmed between 2004 and 2010. The seven confirmed cases were all aged 60 or older, and symptoms appeared within 2 weeks of therapy initiation.

To date, the scientific literature continues to report cases. 

#pharmacology

References:

1. Acute Eosinophilic Pneumonia Secondary to Daptomycin: A Report of Three Cases - Becky A. Miller, Alice Gray, Thomas W. LeBlanc, Daniel J. Sexton, Andrew R. Martin, and Thomas G. Slama - Clin Infect Dis. (2010) 50 (11): e63-e68.

2. Somoza-Cano FJ, Makadia A, Cruz-Peralta MP, Zakarna L, Demyda E, Al Armashi AR, Patell K, Altaqi B. Acute Eosinophilic Pneumonia Secondary to Daptomycin. Cureus. 2021 Nov 9;13(11):e19403. doi: 10.7759/cureus.19403. PMID: 34926005; PMCID: PMC8658045.

3. Di Lorenzo A, Rindi LV, Campogiani L, Imeneo A, Alessio G, Pace PG, Lodi A, Rossi B, Crea AMA, Vitale P, Kontogiannis D, Malagnino V, Andreoni M, Iannetta M, Sarmati L. Daptomycin-Induced Eosinophilic Pneumonia: A Case Report and Systematic Review. Chemotherapy. 2024;69(2):85-99. doi: 10.1159/000535190. Epub 2023 Nov 14. PMID: 37963447.

"ventricular interdependence" In cardiac tamponade

Q: What is "ventricular interdependence" In cardiac tamponade?

Answer: Distension of one ventricle alters the distensibility and filling pressure of the other

A less-discussed pathophysiology of cardiac tamponade is "ventricular interdependence," also known as "ventricular interaction," which plays an integral role in the decreased filling of the left ventricle during inspiration. As cardiac tamponade progresses, the effective compliance of the cardiac chambers is limited by pericardial stretch. This transmits the right ventricle's (RV) ensuing distension to the interventricular septum and causes the septum to bulge to the left, which is already underfilled due to a tight pericardium. This further reduces left ventricular compliance and exacerbates the reduction in left ventricular filling during inspiration. 

#hemodynamic

#cardiology

References:

1. Tiwari S, LeJemtel T, Finn M. Role of ventricular interdependence as an early echocardiographic sign of cardiac surgical postoperative pericardial tamponade. J La State Med Soc. 2012 Nov-Dec;164(6):336-9, 341-2. PMID: 23431677.

2. Mohanan Nair KK, Gopalakrishnan A, Ganapathi S, Harikrishnan S, Valaparambil A, Tharakan J. Arterial Discordance in Cardiac Tamponade. J Invasive Cardiol. 2016 Oct;28(10):E124-E125. PMID: 27705896.

3. Alerhand S, Adrian RJ, Long B, Avila J. Pericardial tamponade: A comprehensive emergency medicine and echocardiography review. Am J Emerg Med. 2022 Aug;58:159-174. doi: 10.1016/j.ajem.2022.05.001. Epub 2022 May 6. PMID: 35696801.

Na in Posm formula

Q: While calculating Effective Plasma Osmolality, particularly in hyperosmotic hyperglycemic nonketotic state (HHNK), which of the sodium (Na) concentrations should be used? - select one

A) Actual measured plasma Na concentration

B) Corrected Na concentration

Answer: A

The formula for effective Plasma osmolality (Posm) is a useful method for diagnosing HHNK, where effective Posm is typically >320 mOsm/kg.

The formula is:

Effective Posm = [2 x Na (mEq/L)] + [glucose (mg/dL) ÷ 18]

The Na concentration used should be the actual measured plasma Na concentration, not the corrected Na concentration with high glucose.

#endocrinology

#electrolytes

#metabolism

References:

1. Rasouli M. Basic concepts and practical equations on osmolality: Biochemical approach. Clin Biochem. 2016 Aug;49(12):936-41. doi: 10.1016/j.clinbiochem.2016.06.001. Epub 2016 Jun 22. PMID: 27343561.

2. Fazekas AS, Funk GC, Klobassa DS, Rüther H, Ziegler I, Zander R, Semmelrock HJ. Evaluation of 36 formulas for calculating plasma osmolality. Intensive Care Med. 2013 Feb;39(2):302-8. doi: 10.1007/s00134-012-2691-0. Epub 2012 Oct 19. PMID: 23081685.

Etomidate and ICP

Q: Etomidate? - select one

A) decreases the intracranial pressure

B) increases the intracranial pressure 

  

Answer: A

  

Etomidate is a useful drug for neurologic patients, particularly those with Traumatic Brain Injury (TBI), because it tends to decrease Intra-Cranial Pressure (ICP) and to keep Cerebral Perfusion Pressure (CPP) unchanged or even improve it.

  

#procedures

#pharmacology

#neurology

#neurosurgery

  

  

References:

  

1. Moss E, Powell D, Gibson RM, McDowall DG. Effect of etomidate on intracranial pressure and cerebral perfusion pressure. Br J Anaesth. 1979 Apr;51(4):347-52. doi: 10.1093/bja/51.4.347. PMID: 465257.

  

2. Bramwell KJ, Haizlip J, Pribble C, VanDerHeyden TC, Witte M. The effect of etomidate on intracranial pressure and systemic blood pressure in pediatric patients with severe traumatic brain injury. Pediatr Emerg Care. 2006 Feb;22(2):90-3. doi: 10.1097/01.pec.0000199563.64264.3a. PMID: 16481923.

  

3. Modica PA, Tempelhoff R, Harris LW, Spitznagel EL. Prevention of intracranial hypertension at intubation with preservation of cerebral perfusion pressure during induction: cerebral protective effect of etomidate-induced burst suppression on EEG. J Neurosurg Anesthesiol. 1989 Jun;1(2):132-3. doi: 10.1097/00008506-198906000-00019. PMID: 15815265.

LIMA. RIMA and RA

Q: Which of the following arteries has the largest medial cross-sectional area? - select one

A) Left internal mammary artery (LIMA)

B) Radial artery (RA)

C) Right Internal Mammary Artery (RIMA)

Answer: B

Although the radial artery has a large medial cross-sectional area, it is used judiciously in coronary artery bypass surgery (CABG) because it is more prone to graft spasm. One in ten patients may experience it and require vasodilator agents, such as calcium channel blockers, immediately postoperatively. Additionally, many of these patients have underlying or impending renal failure, and the use of the radial artery as a graft may preclude the future construction of an arteriovenous graft (AVG) on the ipsilateral arm.

The Medial Cross-Sectional Area (mm²) of the Proximal Radial Artery is, on average, about 2.48, and that of the Distal Radial Artery is about 1.86. In comparison, the medial cross-sectional area (mm²) of the Left Internal Mammary Artery (LIMA) is, on average, about 0.54. Although, for technical reasons, the Right Internal Mammary Artery (RIMA) is used less frequently, it has a larger cross-sectional area than the LIMA, with an average of 0.67.

#surgical-critical-care

#cardiology

References:

1. Gaudino M, Benedetto U, Fremes S, et al. Radial-Artery or Saphenous-Vein Grafts in Coronary-Artery Bypass Surgery. N Engl J Med 2018; 378:2069.

2. Iacò AL, Teodori G, Di Giammarco G, et al. Radial artery for myocardial revascularization: long-term clinical and angiographic results. Ann Thorac Surg 2001; 72:464.

3. Nappi F, Bellomo F, Nappi P, Chello C, Iervolino A, Chello M, Acar C. The Use of Radial Artery for CABG: An Update. Biomed Res Int. 2021 Apr 7;2021:5528006. doi: 10.1155/2021/5528006. PMID: 33928147; PMCID: PMC8049807.

4. Gaudino M, Tondi P, Benedetto U, Milazzo V, Flore R, Glieca F, Ponziani FR, Luciani N, Girardi LN, Crea F, Massetti M. Radial Artery as a Coronary Artery Bypass Conduit: 20-Year Results. J Am Coll Cardiol. 2016 Aug 9;68(6):603-610. doi: 10.1016/j.jacc.2016.05.062. PMID: 27491903.

APS and INR

Q: In patients with Anti-Phospholipid Syndrome (APS), PT/INR can be? - select one

A) falsely elevated

B) falsely lowered

Answer: A

Many patients with APS may have prolonged baseline PT/INR values. This is due to the effect of lupus anticoagulant. This is an in vitro artifact. 

This effect is further enhanced in aPTT measurement. Ideally, these patients should be monitored during anticoagulation therapy using alternative assays rather than standard PT and INR, such as an alternative thromboplastin reagent. 

The hematology service should be consulted, and the lab should be notified in such instances.

#rheumatology

#hematology

References:

1. Kasthuri RS, Roubey RA. Warfarin and the antiphospholipid syndrome: does one size fit all? Arthritis Rheum 2007; 57:1346.

2. Tripodi A, de Laat B, Wahl D, et al. Monitoring patients with the lupus anticoagulant while treated with vitamin K antagonists: communication from the SSC of the ISTH. J Thromb Haemost 2016; 14:2304.

3. Robert A, Le Querrec A, Delahousse B, et al. Control of oral anticoagulation in patients with the antiphospholipid syndrome--influence of the lupus anticoagulant on International Normalized Ratio. Groupe Méthodologie en Hémostase du Groupe d'Etudes sur l'Hémostases et la Thrombose. Thromb Haemost 1998; 80:99.

4. Tripodi A, Chantarangkul V, Clerici M, et al. Laboratory control of oral anticoagulant treatment by the INR system in patients with the antiphospholipid syndrome and lupus anticoagulant. Results of a collaborative study involving nine commercial thromboplastins. Br J Haematol 2001; 115:672.

Green tea and liver failure

Case: 38 years old female is admitted to the ICU with jaundice, fever, hypotension, and elevated liver enzymes. Patient has no past medical history, but a mildly higher BMI of 26. Approximately 6 months ago, the patient began intermittent fasting to lose weight and consuming green tea 8-10 times per day.

Discussion: The extracts of green tea are technically called Camellia sinensis L. and contain catechin polyphenols. It is usually harmless and may be beneficial when consumed in moderation. In higher doses, i.e., more than a gram per day, can be toxic, particularly to the liver. The risk of toxicity is higher in chronic users. Unfortunately, extracts are used and sold over the counter in many other weight-loss products without the buyer's awareness. Overconsumption causes catechin exposure and hepatic injury. 

Three major factors affecting are genetic predisposition, female gender, and fasting. Hepatic injury is usually hepatocellular, but can be mixed with cholestatic presentations. 

Fortunately, liver injury is reversible with discontinuation of the product.

#toxicity

References:

1. Gurley BJ, McGill MR, Koturbash I. Hepatotoxicity due to herbal dietary supplements: Past, present and the future. Food Chem Toxicol 2022; 169:113445.

Molinari M, Watt KD, Kruszyna T, et al. Acute liver failure induced by green tea extracts: case report and review of the literature. Liver Transpl 2006; 12:1892.

Oketch-Rabah HA, Roe AL, Rider CV, et al. United States Pharmacopeia (USP) comprehensive review of the hepatotoxicity of green tea extracts. Toxicol Rep 2020; 7:386.

Galati G, Lin A, Sultan AM, O'Brien PJ. Cellular and in vivo hepatotoxicity caused by green tea phenolic acids and catechins. Free Radic Biol Med 2006; 40:570.

GFR, steroids and reliable test

Q: Systemic Glucocorticoids usually increase plasma creatinine. Which other test can be performed to estimate the actual glomerular filtration rate (GFR)?

Answer: Serum cystatin C 

Systemic glucocorticoids usually increase plasma creatinine. Although it may not increase GFR, it may yield an inaccurate estimate, as many GFR formulae use Creatinine.

Serum cystatin C is a biomarker that may provide a more accurate estimate. It is a protein produced by all cells, filtered by the kidneys, and then broken down; its blood level reflects kidney function. It is usually not affected by muscle mass, age, gender, or ethnicity. Cystatin C is preferable in older adults, obese patients, and those with poor nutrition.

#nephrology

#laboratory-medicine

References:

1. Andreev E, Koopman M, Arisz L. A rise in plasma creatinine that is not a sign of renal failure: which drugs can be responsible? J Intern Med 1999; 246:247.

2. Liang S, Shi M, Bai Y, et al. The effect of glucocorticoids on serum cystatin C in identifying acute kidney injury: a propensity-matched cohort study. BMC Nephrol 2020; 21:519.

3. Benoit SW, Ciccia EA, Devarajan P. Cystatin C as a biomarker of chronic kidney disease: latest developments. Expert Rev Mol Diagn. 2020 Oct;20(10):1019-1026. doi: 10.1080/14737159.2020.1768849. Epub 2020 May 25. PMID: 32450046; PMCID: PMC7657956.

PTA and airway

Q: A 42-year-old male is admitted to the ICU with a peritonsillar abscess (PTA). On exam, the patient is anxious, leaning forward, tripoding on the bedside table with head in a "sniffing position," drooling, suprasternal retractions, and respiratory distress. No stridor is present. Saturation is 98% on 2L NC Oxygen. On exam, deviation of the uvula to the opposite side is noted. What's your next step?

A) Intubate the patient STAT at the bedside

B) Call Emergent ENT consult and prepare for STAT OR-SUITE

C) Gave Broad-spectrum antibiotics, including anaerobes, STAT

D) Insert Central Line for anticipated IVF resuscitation

E) Insert an arterial line to obtain ABG

Answer: B

The patient has a compromised airway and appears to have an extremely difficult airway. Ideally, the patient should be intubated in the OR to deal with any complications. Additionally, if needed, Incision and Drainage (InD) can be performed simultaneously. 

Intubating at the bedside is not a prudent decision (choice A). If needed, and there is no luxury of time for OR, an extremely experienced anesthesiologist with a difficult airway cart backup should be called.

Securing the airway takes precedence over Antibiotics (choice C)

Making a patient lie in bed for central line insertion may compromise the airway (choice D). Patient is in the tripod and sniffing positions to maintain ventilation.

An arterial line can be inserted once the airway is secure (choice E).

#procedures

#ENT

#ID

#surgical-critical-care

References:

1. Ono K, Hirayama C, Ishii K, Okamoto Y, Hidaka H. Emergency airway management of patients with peritonsillar abscess. J Anesth. 2004;18(1):55-8. doi: 10.1007/s00540-003-0211-7. PMID: 14991479.

2. Beriault M, Green J, Hui A. Innovative airway management for peritonsillar abscess. Can J Anaesth. 2006 Jan;53(1):92-5. doi: 10.1007/BF03021533. PMID: 16371615.

COPD - GOLD criteria

Q: As per GOLD criteria, the definition of COPD requires airflow obstruction to be? - select one

A) Intermittent

B) Persistence

C) Progressive

Answer: B

As per The Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria from National Heart, Lung, and Blood Institute (NHLBI) and the World Health Organization (WHO), Chronic Obstructive Pulmonary Disease (COPD) is defined as a "heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnea, cough, expectoration, exacerbations) due to abnormalities of the airway (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction."

If airflow is intermittent (choice A), it does not meet the criteria for COPD. Also, it does not need to be, though it can be progressive (choice C). 

In summary, the three pillars of the diagnosis of COPD are:

• pulmonary symptoms 
• clinical context 
• Persistent airflow limitation despite acute bronchodilator treatment

#pulmonary

References:

1. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management and Prevention of Chronic Obstructive Pulmonary Disease: 2025 Report. www.goldcopd.org (Accessed on January 8, 2026).

2. Agustí A, Celli BR, Criner GJ, et al. Global Initiative for Chronic Obstructive Lung Disease 2023 Report: GOLD Executive Summary. Am J Respir Crit Care Med 2023; 207:819.

PVOD

Q: A 44-year-old male is getting transferred from the ICU to the rehabilitation center after 6 weeks of stay, where he was admitted for severe COVID-19 infection, requiring ECMO, which was successfully decannulated after 3 weeks, and now s/p tracheostomy and is off all drips. The patient also developed a complete loss of smell. Which methodology can be implemented in the rehabilitation center to restore olfactory function?

Answer: Olfactory training

Postviral olfactory dysfunction (PVOD) or postinfectious olfactory dysfunction (PIOD) became a well-known clinical entity since the COVID pandemic. Olfactory training has shown remarkable clinical improvement.

The typical training protocol endorsed by the clinical Olfactory Working Group consists of deep sniffing of at least four distinct odors for 10 seconds, twice daily, for at least 12 weeks. The odorants used are distinct and strong. For aesthetic reasons, scents may include rose, lemon, clove, eucalyptus, cinnamon, vanilla, or orange. Supervising service can provide "smell training kits" with instructions.

Hoping that repeated olfactory stimulation will promote olfactory neuron regeneration or the creation of new synaptic connections.

Adjuvant treatment is budesonide nasal irrigations. 

#ENT

References:

1. Kattar N, Do TM, Unis GD, et al. Olfactory Training for Postviral Olfactory Dysfunction: Systematic Review and Meta-analysis. Otolaryngol Head Neck Surg 2021; 164:244.

2. Hura N, Xie DX, Choby GW, et al. Treatment of post-viral olfactory dysfunction: an evidence-based review with recommendations. Int Forum Allergy Rhinol 2020; 10:1065.

3. Fletcher ML, Chen WR. Neural correlates of olfactory learning: Critical role of centrifugal neuromodulation. Learn Mem 2010; 17:561.

4. Addison AB, Wong B, Ahmed T, et al. Clinical Olfactory Working Group consensus statement on the treatment of postinfectious olfactory dysfunction. J Allergy Clin Immunol 2021; 147:1704.

Semaglutide and substance abuse

Q: Semaglutide, a GLP-1 receptor agonist, can be used as an adjuvant treatment for substance abuse disorder.

A) True

B) False

Answer: A

Although reports are mostly anecdotal and evidence is weak, Semaglutide, a glucagon-like peptide 1 (GLP-1) receptor agonist, has shown some benefit in reducing craving for psychoactive substances, including tobacco and ETOH. Also, it has shown to be associated with a lower rate of developing cannabis use disorder, particularly in patients who are obese and have type 2 diabetes, and are already on this medication.

#toxicology

#pharmacology

#endocrine

References:

1. Wang W, Volkow ND, Berger NA, et al. Association of semaglutide with reduced incidence and relapse of cannabis use disorder in real-world populations: a retrospective cohort study. Mol Psychiatry 2024; 29:2587.

2. Hendershot CS, Bremmer MP, Paladino MB, Kostantinis G, Gilmore TA, Sullivan NR, Tow AC, Dermody SS, Prince MA, Jordan R, McKee SA, Fletcher PJ, Claus ED, Klein KR. Once-Weekly Semaglutide in Adults With Alcohol Use Disorder: A Randomized Clinical Trial. JAMA Psychiatry. 2025 Apr 1;82(4):395-405. doi: 10.1001/jamapsychiatry.2024.4789. PMID: 39937469; PMCID: PMC11822619.

3. Wang W, Volkow ND, Berger NA, Davis PB, Kaelber DC, Xu R. Association of Semaglutide With Tobacco Use Disorder in Patients With Type 2 Diabetes : Target Trial Emulation Using Real-World Data. Ann Intern Med. 2024 Aug;177(8):1016-1027. doi: 10.7326/M23-2718. Epub 2024 Jul 30. PMID: 39074369; PMCID: PMC12721465.

Rx in WN virus

Q: Which of the following has not shown any benefit in the treatment of West Nile (WN) infection?

A) Corticosteroids 

B) Intravenous immunoglobulin

C) Interferon

D) Ribavirin 

Answer: D

The mainstay of treatment in WN virus infection is supportive care.

WN virus is known to cause acute flaccidity, paralysis, and opsoclonus-myoclonus-ataxia. Despite weak evidence, corticosteroids (choice A) inhibit the proinflammatory mediators that may contribute to the nervous system's clinical signs. 

Intravenous immunoglobulin (IVIG) - choice B - is particularly effective in patients with humoral deficiencies.

Similarly, interferon therapy (choice C), despite limited data, has shown a trend toward benefit in WN infection when other modalities fail and can be used as a last resort.

Although Ribavirin (choice D) has demonstrated in vitro activity against the WN virus, it has failed to show any benefit in vivo and, in fact, has shown to cause harm.

#ID

#pharmacology

#neurology

References:

1. Pyrgos V, Younus F. High-dose steroids in the management of acute flaccid paralysis due to West Nile virus infection. Scand J Infect Dis 2004; 36:509.

2. Leis AA, Sinclair DJ. Lazarus Effect of High Dose Corticosteroids in a Patient With West Nile Virus Encephalitis: A Coincidence or a Clue? Front Med (Lausanne) 2019; 6:81.

3. Colaneri M, Lissandrin R, Calia M, et al. The WEST Study: A Retrospective and Multicentric Study on the Impact of Steroid Therapy in West Nile Encephalitis. Open Forum Infect Dis 2023; 10:ofad092.

4. Planitzer CB, Modrof J, Kreil TR. West Nile virus neutralization by US plasma-derived immunoglobulin products. J Infect Dis 2007; 196:435.

5. Kalil AC, Devetten MP, Singh S, et al. Use of interferon-alpha in patients with West Nile encephalitis: report of 2 cases. Clin Infect Dis 2005; 40:764.

6. Chowers MY, Lang R, Nassar F, et al. Clinical characteristics of the West Nile fever outbreak, Israel, 2000. Emerg Infect Dis 2001; 7:675.

IBD and decrease AP

Q: 38 years old male with a long-standing history of Inflammatory Bowel Disease (IBD) presented with Right Upper Quadrant (RUQ) pain and suspicion of acute cholecystitis. Serum alkaline phosphatase (AP) is reported to be low, although ultrasound and clinical signs are highly consistent with the diagnosis. What could be the reason for decreased serum alkaline phosphatase in IBD?

Answer: Zinc Deficiency

Patients, particularly those with Crohn's disease, are at high risk of decreased serum zinc concentrations. Additionally, serum zinc levels depend on albumin. Total-body zinc deficiency is associated with reduced serum alkaline phosphatase levels; alkaline phosphatase is a zinc-containing metalloenzyme. 

Overall, patients with zinc deficiency have a higher risk of hospitalization, surgical procedures, and other complications.

IBD patients tend to have clinically significant zinc deficiency, particularly with excessive losses due to ostomies, fistulas, or profuse diarrhea. Additionally, during the active inflammatory state of IBD, there is zinc malabsorption via increased losses of endogenous zinc stores on the one hand and intestinal epithelial sloughing and disruption of reabsorption on the other.

Interestingly, zinc supplementation is found to improve chronic diarrhea in these patients. Some experts suggest supraphysiologic zinc replacement.

#GI

#vitamins-elements

#surgical-critical-care

References:

1. McClain C, Soutor C, Zieve L. Zinc deficiency: a complication of Crohn's disease. Gastroenterology 1980; 78:272.

2. Siva S, Rubin DT, Gulotta G, et al. Zinc Deficiency is Associated with Poor Clinical Outcomes in Patients with Inflammatory Bowel Disease. Inflamm Bowel Dis 2017; 23:152.

3. Sturniolo GC, Di Leo V, Ferronato A, et al. Zinc supplementation tightens "leaky gut" in Crohn's disease. Inflamm Bowel Dis 2001; 7:94.

4. Naber TH, Baadenhuysen H, Jansen JB, van den Hamer CJ, van den Broek W. Serum alkaline phosphatase activity during zinc deficiency and long-term inflammatory stress. Clin Chim Acta. 1996 May 30;249(1-2):109-27. doi: 10.1016/0009-8981(96)06281-x. PMID: 8737596.

Pathophysiology of orthostatic hypotension

Q: In a normal individual, orthostatic hypotension results in diastolic blood pressure to? - select one

A) fall

B) rise

Answer: B

The objective of this question is to understand the complex pathophysiology behind orthostatic hypotension. In a normal individual, a sudden change in posture to an upright position may pull up to a litre of blood in the lower extremities. Also, underestimated the pooling of blood in the splanchnic circulation during such instances. In such an event, venous return rapidly decreases, reducing ventricular filling and cardiac output. This provokes a compensatory neurological reflex, the baroreflex, which increases sympathetic and reduces parasympathetic outflow.

Overall effect is a rise in peripheral vascular resistance, venous return, and cardiac output, and so stabilizing the blood pressure via a slight fall in systolic blood pressure of about 5-10 mmHg, but an increase in diastolic blood pressure of almost similar value. Overall, heart rate increases by 10-25 beats per minute.

Failure at any stage of this compensatory mechanism causes exaggerated clinical signs of orthostatic hypotension.

#hemodynamic

#cardiology

References:

1. Magkas N, Tsioufis C, Thomopoulos C, Dilaveris P, Georgiopoulos G, Sanidas E, Papademetriou V, Tousoulis D. Orthostatic hypotension: From pathophysiology to clinical applications and therapeutic considerations. J Clin Hypertens (Greenwich). 2019 May;21(5):546-554. doi: 10.1111/jch.13521. Epub 2019 Mar 22. PMID: 30900378; PMCID: PMC8030387.

2. Freeman R, Abuzinadah AR, Gibbons C, Jones P, Miglis MG, Sinn DI. Orthostatic Hypotension: JACC State-of-the-Art Review. J Am Coll Cardiol. 2018 Sep 11;72(11):1294-1309. doi: 10.1016/j.jacc.2018.05.079. PMID: 30190008.

PESI

Q: In the Full Pulmonary Embolism (PE) Severity Index (PESI), which gender is included? (select one) 

 A) Male 
B) Female 


 Answer: Male

Contrary to popular belief that females are more prone to getting more severe pulmonary embolism, males are found to have a higher risk of more severe PE. 

The full PESI comprises 11 identified points, which were subsequently reduced to 6.

1. Age
2. Male
3. History of cancer
4. Heart failure
5. Chronic lung disease
6. Pulse ≥110/min
7. Systolic blood pressure 
8. Respiratory rate
9. Temperature 
10. Altered mental status
11. Arterial oxygen saturation 

Simplified pulmonary embolism severity index (sPESI)

1. Clinical feature
2. Age >80 years
3. History of cancer
4. Chronic cardiopulmonary disease
5. Pulse ≥110/min
6. Systolic blood pressure <100 mmHg
7. Arterial oxygen saturation 

Many online calculators are available to score PESI

#pulmonary

#hemodynamic

#vascular

 
References: 

1. Aujesky D, Obrosky DS, Stone RA, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med 2005; 172:1041. 

2. Jiménez D, Aujesky D, Moores L, et al. Simplification of the pulmonary embolism severity index for prognostication in patients with acute symptomatic pulmonary embolism. Arch Intern Med 2010; 170:1383.

3. Hassine M, Kallala MY, Mahjoub M, Boussaada M, Bouchahda N, Gamra H. Embolie pulmonaire: indice de sévérité de l’embolie pulmonaire (ISEP) score et facteurs prédictifs de mortalité [Pulmonary embolism: the Pulmonary Embolism Severity Index (PESI) score and mortality predictors]. Pan Afr Med J. 2023 May 19;45:48. French. doi: 10.11604/pamj.2023.45.48.39031. PMID: 37575526; PMCID: PMC10422038.

MALA and metformin level

Q: A serum metformin level usually correlates with the severity of the poisoning, known as MALA (Metformin Associated Lactic Acidosis).

A) True

B) False

Answer: B

Serum metformin level is usually not ordered during suspected MALA for two reasons. First, it takes several days to report the level. Second, serum metformin concentrations typically do not correlate with the severity of toxicity or patient outcomes; however, a caveat of 'treatment bias' may be present, as by the time the level is reported, patients may be treated differently across institutions based solely on clinical signs and suspicion. Additionally, associated factors, such as renal insufficiency, may have played a role.

That said, some experts still advocate obtaining a serum metformin level, as it has a good negative predictive value. An undetectable metformin concentration basically rules out MALA.

#toxicity

#pharmacology

#acid-base

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. 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.

3. Kajbaf F, De Broe ME, Lalau JD. Therapeutic Concentrations of Metformin: A Systematic Review. Clin Pharmacokinet 2016; 55:439.

Anti-GBM - Rx

Q: A 52-year-old male presented to the Emergency Department (ED) with hemoptysis and a creatinine level of 6.2 mg/dL. There is a high degree of suspicion for the Anti-glomerular basement membrane (anti-GBM) disease, also known as Goodpasture syndrome. What is the first line of treatment?

A) Immunosuppressive therapy

B) Plasmapheresis

C) Plasmapheresis plus immunosuppressive therapy

Answer: C

The initial management of anti-GBM disease plays an essential role in immediate and long-term survival. The treatment is two-pronged:

• Plasmapheresis removes circulating anti-GBM antibodies and other inflammatory mediators, and 
• Immunosuppressive agents minimize new antibody formation

#rheumatology

#pulmonary

#nephrology

References:

1. McAdoo SP, Pusey CD. Anti-glomerular basement membrane disease-treatment standard. Nephrol Dial Transplant. 2025 Dec 23;41(1):42-54. doi: 10.1093/ndt/gfaf190. PMID: 40973182; PMCID: PMC12722177.

2. Bharati J, Jhaveri KD, Salama AD, Oni L. Anti-Glomerular Basement Membrane Disease: Recent Updates. Adv Kidney Dis Health. 2024 May;31(3):206-215. doi: 10.1053/j.akdh.2024.04.007. PMID: 39004460.

3. Taylor DM, Yehia M, Simpson IJ, et al. Anti-glomerular basement membrane disease in Auckland. Intern Med J 2012; 42:672.

4. Canney M, O'Hara PV, McEvoy CM, et al. Spatial and Temporal Clustering of Anti-Glomerular Basement Membrane Disease. Clin J Am Soc Nephrol 2016; 11:1392.

Azoles and pseudohyperaldosteronism

Q: Which of the following azoles may cause pseudohyperaldosteronism? - select one

A) Fluconazole

B) Voriconazole

C) Isavuconazole

D) Itraconazole 

Answer: D

Itraconazole and posaconazole are two azoles known to cause pseudohyperaldosteronism with its triad of

• severe hypokalemia
• hypertension, and
• metabolic alkalosis

Itraconazole is also known to cause congestive heart failure, and all azoles are known to cause hepatotoxicity.

#pharmacology

#endocrinology

References:

1. Kuriakose K, Nesbitt WJ, Greene M, Harris B. Posaconazole-Induced Pseudohyperaldosteronism. Antimicrob Agents Chemother 2018; 62.

2. Brandi SL, Feltoft CL, Serup J, Eldrup E. Pseudohyperaldosteroism during itraconazole treatment: a hitherto neglected clinically significant side effect. BMJ Case Rep. 2021 Jun 18;14(6):e243191. doi: 10.1136/bcr-2021-243191. PMID: 34144953; PMCID: PMC8215247.

3. Katharina R. Beck, Lucija Telisman, Chris J. van Koppen, George R. Thompson III, Alex Odermatt - Molecular mechanisms of posaconazole- and itraconazole-induced pseudohyperaldosteronism and assessment of other systemically used azole antifungals - The Journal of Steroid Biochemistry and Molecular Biology, Volume 199, May 2020, 105605. Link: https://www.sciencedirect.com/science/article/abs/pii/S0960076019306958

Patient height and PES

Q: Which of the following is a risk factor for post-extubation stridor (PES)? - select one

A) High ratio of patient height (in mm) to ETT diameter (in mm)

B) Small ratio of patient height (in mm) to ETT diameter (in mm)

Answer: B

Post-extubation stridor is a common occurrence in the ICU. Various risk factors have been identified. One of the less discussed risk factors is:

A small ratio of patient height (in mm) to ETT diameter (in mm)

Some other well-known factors are:

• Prolonged intubation
• Old age
• Large ETT 
• Elevated APACHE score
• Low GCS score 
• Traumatic intubation
• Female gender
• Previous pulmonary history
• Excessive tube mobility due to insufficient fixation

#ventilators

#pulmonary

#procedures

References:

1. Maury E, Guglielminotti J, Alzieu M, et al. How to identify patients with no risk for postextubation stridor? J Crit Care 2004; 19:23.

2. Wittekamp BH, van Mook WN, Tjan DH, et al. Clinical review: post-extubation laryngeal edema and extubation failure in critically ill adult patients. Crit Care 2009; 13:233.

3. Shinohara M, Iwashita M, Abe T, Takeuchi I. Association between post-extubation upper airway obstruction symptoms and airway size measured by computed tomography: a single-center observational study. BMC Emerg Med. 2022 Mar 31;22(1):55. doi: 10.1186/s12873-022-00615-7. PMID: 35361111; PMCID: PMC8974026.

4. Sunil Rathore, Adam Bates, Lawrence Nolan, Trevena Anton, Mckay Jarman, and Gwendolyn Lynch - Neurology - Neurocritical Care: Procedures - Identifying Post-extubation Stridor (PES) Risk Factors in a Neurocritical Care Population (P2-2.002) - April 9, 2024 issue 102 (7_supplement_1) 5689 https://doi.org/10.1212/WNL.0000000000205984

Vision in HELPP

Q: A 28-year-old female is admitted to the ICU with HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets). Delivery was planned. The patient began reporting bilateral blurring of vision. What could be your concern?

Answer: Retinal detachment

Retinal detachment is an unusual but very well-documented complication of severe preeclampsia and patients with HELLP syndrome. An emergent ophthalmic consultation should be obtained in conjunction with the planned delivery.

#ob-gyn

# ophthalmology

#hepatology

Reference:

1. Teodoru CA, Tudor C, Cerghedean-Florea ME, Dura H, Tănăsescu C, Roman MD, Hașegan A, Munteanu M, Popa C, Vică ML, Matei HV, Stanca H. Bilateral Serous Retinal Detachment as a Complication of HELLP Syndrome. Diagnostics (Basel). 2023 Apr 26;13(9):1548. doi: 10.3390/diagnostics13091548. PMID: 37174940; PMCID: PMC10178147.

2. Vigil-De Gracia P, Ortega-Paz L. Retinal detachment in association with pre-eclampsia, eclampsia, and HELLP syndrome. Int J Gynaecol Obstet. 2011 Sep;114(3):223-5. doi: 10.1016/j.ijgo.2011.04.003. Epub 2011 Jun 29. PMID: 21719013.

3. Li M, Qu J. Exudative retinal detachment and hypertensive choroidopathy in a patient with suspected HELLP syndrome: a case report. BMC Ophthalmol. 2025 Jul 1;25(1):353. doi: 10.1186/s12886-025-04176-8. PMID: 40597840; PMCID: PMC12210448.