eventration of the diaphragm

Q: Complete eventration of the hemidiaphragm usually happens on? - select one

A) left 

B) right

Answer: A

Diaphragmatic eventration is defined as a thinning of a portion or all of the diaphragmatic muscle by fibroelastic tissue.

For a not completely understood reason:

• Partial eventration mostly happens on the right hemidiaphragm 
• Complete eventration mostly happens on the left hemidiaphragm

Bilateral involvement is rare.

Clinically, it may cause tachypnea, palpitations, chest pain, chronic cough, recurrent pneumonia, dyspepsia, GERD, and epigastric pain.

#pulmonary

#radiology

References:

1. Groth SS, Andrade RS. Diaphragmatic eventration. Thorac Surg Clin. 2009 Nov;19(4):511-9. doi: 10.1016/j.thorsurg.2009.08.003. PMID: 20112634.

2. Mouroux J, Venissac N, Leo F, et al. Surgical treatment of diaphragmatic eventration using video-assisted thoracic surgery: a prospective study. Ann Thorac Surg 2005; 79:308.

Urea and Na

Q: Oral Urea tablets can be used in the treatment of? - select one

A) Hypernatremia

B) Hyponatremia

Answer: B

Although not widely used because of other modalities for treating hyponatremia, oral urea is one option for lowering sodium concentration. It is particularly useful in patients who require long-term treatment with Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH). It is popularly known as 'poor man's Vaptan.' It has shown its efficacy in acute cases also, such as on Intracranial Pressure (ICP) in Patients With Acute Brain Injury and Hyponatremia (reference# 4)

Urea is available as oral packets in the USA and can also be given via a nasogastric tube (NGT). The mechanism of action is via increasing the excretion of electrolyte-free water. The usual maintenance dose is 15 to 30 g/day.

#electrolytes

References:

1. Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Nephrol Dial Transplant 2014; 29 Suppl 2:i1.

2. Decaux G, Andres C, Gankam Kengne F, Soupart A. Treatment of euvolemic hyponatremia in the intensive care unit by urea. Crit Care 2010; 14:R184.

3. Soupart A, Coffernils M, Couturier B, et al. Efficacy and tolerance of urea compared with vaptans for long-term treatment of patients with SIADH. Clin J Am Soc Nephrol 2012; 7:742.

4. Annoni F, Fontana V, Brimioulle S, et al. Early Effects of Enteral Urea on Intracranial Pressure in Patients With Acute Brain Injury and Hyponatremia. J Neurosurg Anesthesiol 2016.

 

Clozapine and tobacco

Q: A 64-year-old male with only a past history of depression and smoking is admitted to the hospital for severe community-acquired pneumonia (CAP). His only home medication is clozapine. His dose for clozapine should be? - select one

A) decreased

B) increased

Answer: A

Clozapine has a complex relationship with smoking. Smokers require almost a twofold increase in dose. Once they are stable on a higher-than-usual dose, it needs to be tapered down when in a nonsmoking environment.

Another important aspect of chronic clozapine use is the risk of agranulocytosis and its strong anticholinergic, sedative, cardiac, and hypotensive properties, so any agents with these characteristics should be used with care. 

#pharmacology

#psychiatry

References:

1. Tsuda Y, Saruwatari J, Yasui-Furukori N. Meta-analysis: the effects of smoking on the disposition of two commonly used antipsychotic agents, olanzapine and clozapine. BMJ Open 2014; 4:e004216.

2. McEvoy JP, Freudenreich O, Wilson WH. Smoking and therapeutic response to clozapine in patients with schizophrenia. Biol Psychiatry. 1999 Jul 1;46(1):125-9. doi: 10.1016/s0006-3223(98)00377-1. PMID: 10394482.

3. Zeng L, Lv H, Li J, Xue R, Liu X, Zhou C, Yu H. Cigarette smoking, coffee consumption, alcohol intake, and clozapine metabolism: A Mendelian randomization study. Front Psychiatry. 2022 Sep 29;13:1002235. doi: 10.3389/fpsyt.2022.1002235. PMID: 36245885; PMCID: PMC9559606.

importance of paracentesis in SBP

Q: What's the importance of paracentesis in spontaneous bacterial peritonitis (SBP)?

Answer: Determination of mortality

As famously said for lungs: "the sun should never set on a parapneumonic effusion, " similarly, it is true for abdominal paracentesis in SBP, as mortality increases by 3.3 percent/hour of delay in performing a paracentesis in patients with SBP.

Overall, hospitalized patients with SBP who received delayed paracentesis (DP) had a 2.7-fold increased risk of mortality, adjusting for MELD score and renal dysfunction. Diagnostic paracentesis performed less than 12 hours from hospitalization in patients with cirrhosis and ascites has improved short-term survival.  

#procedures

References:

1. Kim JJ, Tsukamoto MM, Mathur AK, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis. Am J Gastroenterol 2014; 109:1436.

2. Sahn SA, Light RW. The sun should never set on a parapneumonic effusion. Chest. 1989 May;95(5):945-7. doi: 10.1378/chest.95.5.945. PMID: 2707086.

3. Harvey JJ, Prentice R, George J. Diagnostic and therapeutic abdominal paracentesis. Med J Aust. 2023 Jan 16;218(1):18-21. doi: 10.5694/mja2.51795. Epub 2022 Nov 30. PMID: 36450339; PMCID: PMC10099762.

BAT

Q: Which of the following has the highest likelihood ratio (LR) of Blunt Abdominal Trauma, popularly known as BAT? - select one

A) Abdominal distension 

B) Abdominal guarding

C) Hypotension  

D) Rebound tenderness 

E) Seatbelt sign

Answer: E

Of note, the most important pearl to remember during trauma evaluation of the abdomen is: "The absence of abdominal pain or tenderness does not rule out significant intra-abdominal injury."

A history and physical exam should be performed in detail. Interestingly, the seatbelt sign has the highest LR of probable underlying BAT. 

Seat Belt sign is followed by rebound tenderness, and in frequency down with hypotension, and abdominal distension. Abdominal guarding has the lowest LR in the above question for BAT.

Another important pearl to remember is that "the negative LR for the above signs, either alone or in combination, is low, which means that the absence of either sign does not exclude injury."

                                                     

Concomitant femur fracture can significantly distract the clinician from BAT, particularly in pedestrian trauma.

#trauma

References:

1. Nishijima DK, Simel DL, Wisner DH, Holmes JF. Does this adult patient have a blunt intra-abdominal injury? JAMA 2012; 307:1517.

2. Shreffler J, Smiley A, Schultz M, et al. Patients with Abrasion or Ecchymosis Seat Belt Sign Have High Risk for Abdominal Injury, but Initial Computed Tomography is 100% Sensitive. J Emerg Med 2020; 59:491.

3. Pourmand A, Terrebonne E, Shapovalov V, et al. Prevalence of intra-abdominal injury among patients with seatbelt signs, a systematic review and meta-analysis. Am J Emerg Med 2024; 76:199.

4. Agrawal A, Inamadar PI, Subrahmanyam BV. Seat belt sign and its significance. J Family Med Prim Care. 2013 Jul;2(3):288-90. doi: 10.4103/2249-4863.120769. PMID: 24479100; PMCID: PMC3902689.

cola colored urine

Q: What could be the underlying renal pathophysiology in cola or tea colored urine?

Answer: Possible glomerular bleeding

An astute physician can quickly differentiate glomerular and nonglomerular bleeding at first sight at the bedside.

Cola or tea-colored or dark brown urine may indicate glomerular bleeding, in which prolonged transit time through the nephron in an acidic urine environment can result in the formation of methemoglobin, giving the urine a smoky brown, tea, or cola color.

Obviously, this is a first glance bedside observation at the bedside. Urine can still appear red or pink in glomerular bleeding if urine is not acidic, or transit time is too fast, but by default, as a rule of thumb, in gross hematuria -

• nonglomerular bleeding appears red or pink, and
• glomerular bleeding appears dark brown (cola colored)

Other caveats are false colorations due to dye, food, drugs, or underlying non-renal pathophysiologies such as rhabdomyolysis or hyperbilirubinemia.

#nephrology

References:

1. Stark A, Kanduri SR, Ramanand A, Rosenbloom S, Varghese V, Chalmers DR, Velez SA, Gonzalez-Fuentes C, Wickman TJ, Mohamed M, Shueib A, Zarm A, Lukitsch I, Velasco-Gonzalez C, Seltzer JR, Velez JCQ. Glomerular Hematuria for the Diagnosis of Glomerulonephritis. Glomerular Dis. 2025 Apr 10;5(1):206-218. doi: 10.1159/000545051. PMID: 40406196; PMCID: PMC12097761.

2. Rose BD. Pathophysiology of Renal Disease, 2nd ed, McGraw-Hill, New York 1987. p.10.

3. Hamadah AM, Gharaibeh K, Mara KC, Thompson KA, Lieske JC, Said S, Nasr SH, Leung N. Urinalysis for the diagnosis of glomerulonephritis: role of dysmorphic red blood cells. Nephrol Dial Transplant. 2018 Aug 1;33(8):1397-1403. doi: 10.1093/ndt/gfx274. PMID: 29156008.

Anbx in Ebola

Q: Patients with Ebola virus should be covered at least for? - select one

A) Gram-negative pathogens

B) Gram-positive pathogens

Answer: A

Prevention and isolation are foremost in the Ebola outbreak, and in case of infection, supportive treatment is the mainstay.

Two antibody-based therapies that have shown effectiveness for the Ebola virus.

1. Atoltivimab, maftivimab, and odesivimab (REGN-EB3) – It's a triple-monoclonal antibody (mAb) product. This combination of three mAbs targets three nonoverlapping epitopes on the Ebola virus surface glycoprotein, providing potent virus neutralization.

2. Ansuvimab (mAb114) – This mAb was originally isolated from a survivor of Ebola virus disease and found to neutralize the virus.

Although critical care patients should be covered with broad-spectrum antibiotics, gram-negative pathogens are more common in Ebola patients and should be covered. Said that empiric gram-positive therapy should be added as hospital-acquired pneumonia or CLABSI (Central Line Associated Blood Stream Infections) can have low thresholds to occur. 

#ID

References:

1. Kreuels B, Wichmann D, Emmerich P, et al. A case of severe Ebola virus infection complicated by gram-negative septicemia. N Engl J Med 2014; 371:2394.

2. Misasi J, Sullivan NJ. Immunotherapeutic strategies to target vulnerabilities in the Ebolavirus glycoprotein. Immunity 2021; 54:412.

3. Rayaprolu V, Fulton BO, Rafique A, et al. Structure of the Inmazeb cocktail and resistance to Ebola virus escape. Cell Host Microbe 2023; 31:260.

THAM

Q: THAM should ideally be infused through central line.

A) True

B) False

Answer: A

THAM stands for Tromethamine (tris-hydroxymethyl aminomethane. Other less popular names are TRIS and trometamol. Although now rarely used, THAM is a viable option in mixed metabolic and respiratory acidosis, as it has two advantages over "bicarb" (H2CO3).

• no sodium load
• no generation of CO2, or may even reduce it

Unfortunately, it is not widely and commercially available, and many institutions prepare their own THAM.

Mechanism of action: THAM is an amino alcohol that buffers hydrogen ions by virtue of its amine (NH2) moiety (pKa = 7.7) via the following two reactions

1.  THAM-NH2 + H+  →  THAM-NH3+
2.  THAM-NH2 + H2O + CO2  →  THAM-NH3+ + HCO3-

The final product is the protonated form of THAM, which requires either a functioning kidney or dialysis. When given via peripheral IV line, extravasation may cause tissue necrosis. Central line is preferred.

#acid-base

References:

1. Nahas GG, Sutin KM, Fermon C, et al. Guidelines for the treatment of acidaemia with THAM. Drugs 1998; 55:191.

2. Kallet RH, Jasmer RM, Luce JM, et al. The treatment of acidosis in acute lung injury with tris-hydroxymethyl aminomethane (THAM). Am J Respir Crit Care Med 2000; 161:1149.

3. Weber T, Tschernich H, Sitzwohl C, et al. Tromethamine buffer modifies the depressant effect of permissive hypercapnia on myocardial contractility in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2000; 162:1361.

4. Holmdahl MH, Wiklund L, Wetterberg T, et al. The place of THAM in the management of acidemia in clinical practice. Acta Anaesthesiol Scand 2000; 44:524.

5. Radosevich MA, Wieruszewski PM, Wittwer ED. Tris-Hydroxymethyl Aminomethane in Critically Ill Adults: A Systematic Review. Anesth Analg 2023; 137:1007.

cyproheptadine in serotonin syndrome

Q: 42 years old female is admitted to the ICU with probable serotonin syndrome. Cyproheptadine has been initiated. Cyproheptadine is a? - select one

A) histamine-1 receptor agonist

B) histamine-1 receptor antagonist 

Answer: B

Although cyproheptadine continues to have a debatable role in serotonin syndrome (SS) - see reference #3 -, it is universally used as it has relatively benign side effects, such as sedation (which is actually desired in SS), and hypotension, which can be relatively managed easily. Cyproheptadine has three properties. It is a:

• histamine-1 receptor antagonist 
• nonspecific 5-HT1A and 5-HT2A antagonistic (two subtypes of serotonin receptors)
• though weak, but has needed anticholinergic activity

#neurology

#pharmacology

References:

1. Graudins A, Stearman A, Chan B. Treatment of the serotonin syndrome with cyproheptadine. J Emerg Med 1998; 16:615.

2. Prakash S, Patel H, Kumar S, Shah CS. Cyproheptadine in serotonin syndrome: A retrospective study. J Family Med Prim Care. 2024 Apr;13(4):1340-1346. doi: 10.4103/jfmpc.jfmpc_652_23. Epub 2024 Apr 22. PMID: 38827706; PMCID: PMC11142004.

3. Nguyen H, Pan A, Smollin C, Cantrell LF, Kearney T. An 11-year retrospective review of cyproheptadine use in serotonin syndrome cases reported to the California Poison Control System. J Clin Pharm Ther. 2019 Apr;44(2):327-334. doi: 10.1111/jcpt.12796. Epub 2019 Jan 16. PMID: 30650197.

Mushroom-shaped RBCs

Q: Mushroom-shaped Red Blood Cells (RBCs) signify what?

Answer: Oxidative stress

During the COVID-19 pandemic, Mushroom-shaped RBCs, also known as fish-shaped cells or pincer cells, became a widely used term. They can also be associated with anisocytosis, spherocytes, stomatocytes, and polychromasia. 

They are strongly associated with oxidative stress in RBC physiology. It can also occur in iron deficiency, vitamin B12 or folate deficiency, hepatic insufficiency, hereditary elliptocytosis, MDS, myeloproliferative neoplasms, and acute leukemia.

#hematology

References:

1. Gérard D, Ben Brahim S, Lesesve JF, Perrin J. Are mushroom-shaped erythrocytes an indicator of COVID-19? Br J Haematol 2021; 192:230.

2. Robier C, Körber C, Quehenberger F, et al. The frequency of occurrence of fish-shaped red blood cells in different haematologic disorders. Clin Chem Lab Med 2018; 56:323.

3. Ford J. Red blood cell morphology. Int J Lab Hematol 2013; 35:351.

Emergent blood transfusion with Group O

Q: A 32-year-old male is admitted to the ICU with severe life-threatening shock after an esophageal variceal bleed. Emergency release of blood is ordered. The blood bank informed you that, unfortunately, no Group O, RhD-negative blood is available. Can Group O, RhD-positive blood be transfused?

A) Yes

B) No

Answer: A

In case of emergency, blood released from the bank is typically group O, RhD-negative. But in a situation like our patient in the above question, group O, RhD-positive RBC units can be used. It is popularly known as low-titer O-positive whole blood (LTO+WB). Many blood banks use this approach to preserve O-negative blood units for childbearing women in emergencies.

Also, patients with a confirmed ABO type on a current specimen can receive uncrossmatched, type-specific blood for emergency release. 

In all such situations, pRBC should be infused slowly, with close monitoring for signs of an acute hemolytic transfusion reaction, such as fever, chills, hypotension, hematuria, or chest or flank pain.

#hematology

References:

1. Chowdhury R, Williams BA, Williams S, Casey J. Quality improvement review of O positive blood in emergency transfusion. Transfusion. 2023 Oct;63(10):1841-1848. doi: 10.1111/trf.17537. Epub 2023 Sep 12. PMID: 37698202.

2. Flommersfeld S, Mand C, Kühne CA, Bein G, Ruchholtz S, Sachs UJ. Unmatched Type O RhD+ Red Blood Cells in Multiple Injured Patients. Transfus Med Hemother. 2018 May;45(3):158-161. doi: 10.1159/000485388. Epub 2018 Mar 7. PMID: 29928169; PMCID: PMC6006622.

3. Courcelles L, Pouplard M, Braun O, Streel C, Deneys V. Optimizing O red blood cell concentrate usage in the emergency department in the era of patient blood management. Hematol Transfus Cell Ther. 2024 Nov;46 Suppl 5(Suppl 5):S90-S96. doi: 10.1016/j.htct.2024.05.008. Epub 2024 Aug 21. PMID: 39183144; PMCID: PMC11670554.

four stages of Neurocysticercosis on neuro-imaging

Q: What are the four  stages of Neurocysticercosis on neuro-imaging?

Answer: There are 4 stages of the cyst itself while reviewing brain imaging

• First - Vesicular cyst. Note the well-defined scolex, minimal contrast enhancement, and mass effect.
• Second -  MRI of a colloidal cyst. Note ring enhancement, loss of the scolex, and perilesional edema.
• Third -  MRI of the nodular/granular stage. Note nodule with diffuse enhancement and no cystic component.
• Fourth - Non-contrast computed tomography showing multiple punctuate calcifications.

#ID

#radiology

References:

1. Lopes M, Ferreira M, Ramos I, Melo Freitas P. Neurocysticercosis: a contemporary presentation of the neuroimaging main stages. BMJ Case Rep. 2022 Feb 9;15(2):e247927. doi: 10.1136/bcr-2021-247927. PMID: 35140100; PMCID: PMC8830162.

2. Knott MV, Berke CN, Shah KH, Gurses ME, Bashti M, Lu VM, Ivan ME, Castro JG, Komotar RJ, Shah AH. Neurosurgical Approach to Neurocysticercosis in Adults: A Comprehensive Systematic Review of Clinical and Imaging Insights. Neurosurgery. 2025 Feb 21;97(2):281-297. doi: 10.1227/neu.0000000000003371. PMID: 39982074.

AKI after cardiac bypass

Q: Addition of mannitol to Cardio-pulmonary Bypass (CPB) in the OR reduce the risk of acute kidney injury (AKI) post cardiac surgery?

A) True

B) False

Answer: B

In the past, different modalities have been tried to decrease the risk of AKI post-cardiac surgery, including mannitol, furosemide, and low-dose dopamine (popularly known as renal dose dopamine), but none have been shown to protect against AKI post-bypass. The best approach to prevent AKI post-surgery is to maintain adequate 

• CPB pump flow
• Mean arterial pressure (MAP)
• Mixed Venous Oxygenation (SvO2), and 
• Arterial blood gases (ABGs)

Simultaneously, monitoring urine output to maintain at or above 0.5 mL/kg per hour is the best strategy. If urine output drops, quickly determine the cause by checking bladder catheter (aka Foley) placement, cardiac function, and possible development of aortic dissection via transesophageal echocardiography (TEE).

#surgical-critical-care

#cardiac-surgery

#cardiology

#nephrology

References:

1. junggren M, Sköld A, Dardashti A, Hyllén S. The use of mannitol in cardiopulmonary bypass prime solution-Prospective randomized double-blind clinical trial. Acta Anaesthesiol Scand 2019; 63:1298.

2. Bell S, Ross VC, Zealley KA, et al. Management of post-operative acute kidney injury. QJM 2017; 110:695.

3. Yang X, Zhu L, Pan H, Yang Y. Cardiopulmonary bypass associated acute kidney injury: better understanding and better prevention. Ren Fail. 2024 Dec;46(1):2331062. doi: 10.1080/0886022X.2024.2331062. Epub 2024 Mar 21. PMID: 38515271; PMCID: PMC10962309.

4. Chu H, Li S, Cao L, Xu G, Yang L, Ma C. Risk factors for acute kidney injury after coronary artery bypass graft surgery: a systematic review and meta-analysis. Front Med (Lausanne). 2026 Feb 24;13:1722801. doi: 10.3389/fmed.2026.1722801. PMID: 41816661; PMCID: PMC12971401.

DrawingTacrolimus Trough Level

Q: Which one precaution should be taken while drawing blood for Tacrolimus (FK506) level?

Answer: Tacrolimus can leach into plastic catheters.

In the immediate transplant period, Tacrolimus prophylaxis is initiated via intravenous (IV) infusion. Tacrolimus can leach into plastic catheters, so the Central Venous Catheter (CVC) lumen used to measure serum levels should be separate from the lumen through which tacrolimus is infused; otherwise, serum levels are likely to be falsely elevated.

Tacrolimus should be converted to the oral route whenever the patient can utilize the enteral route. Tacrolimus is almost completely metabolized in the liver, so the half-life of nine hours can be longer in liver insufficiency. 

#transplant

#pharmacology

#laboratory-medicine

References:

1. Hacker C, Verbeek M, Schneider H, Steimer W. Falsely elevated cyclosporin and tacrolimus concentrations over prolonged periods of time due to reversible adsorption to central venous catheters. Clin Chim Acta. 2014 Jun 10;433:62-8. doi: 10.1016/j.cca.2014.02.031. Epub 2014 Mar 11. PMID: 24631133.

2. Han A, Jo AJ, Kwon H, Kim YH, Lee J, Huh KH, Lee KW, Park JB, Jang E, Park SC, Lee J, Lee J, Kim Y, Soliman M, Min S. Optimum tacrolimus trough levels for enhanced graft survival and safety in kidney transplantation: a retrospective multicenter real-world evidence study. Int J Surg. 2024 Oct 1;110(10):6711-6722. doi: 10.1097/JS9.0000000000001800. PMID: 38884261; PMCID: PMC11486932.

3. Yin S, Song T, Jiang Y, Li X, Fan Y, Lin T. Tacrolimus Trough Level at the First Month May Predict Renal Transplantation Outcomes Among Living Chinese Kidney Transplant Patients: A Propensity Score-Matched Analysis. Ther Drug Monit. 2019 Jun;41(3):308-316. doi: 10.1097/FTD.0000000000000593. PMID: 31083041; PMCID: PMC6553958.

Dig in pregnancy

Q: Digoxin is contraindicated in pregnancy?

A) Yes

B) No

Answer: B 

Digoxin is one of the unique medicines that is given to the mother for fetal cardiac indications. It crosses the placenta without causing fetal harm or teratogenicity. Moreover, it can be used in lactation for maternal cardiac indications.

It is mostly used to treat sustained fetal tachyarrhythmias, such as supraventricular tachycardia (SVT) and atrial flutter, and to prevent hydrops fetalis.

#ob-gyn

#pharmacology

#pediatrics

#cardiology

References:

1. Hauptman PJ, Kelly RA. Digitalis. Circulation 1999; 99:1265.

2. Wang C, Zhao L, Shao S, Yu H, Zhou S, Li Y, Zhu Q, Liu X, Duan H, Liu H, Hua Y, Zhou K. Transplacental digoxin treatment for fetal supraventricular arrhythmias: Insights from Chinese fetuses. Chin Med J (Engl). 2025 Jun 20;138(12):1499-1501. doi: 10.1097/CM9.0000000000003583. Epub 2025 Apr 9. PMID: 40204513; PMCID: PMC12180843.

3. Soyka LF. Digoxin: placental transfer, effects on the fetus, and therapeutic use in the newborn. Clin Perinatol. 1975 Mar;2(1):23-35. PMID: 1102216.

catamenial epilepsy

Q: Catamenial epilepsy occurs more frequently in which phase of the menstrual cycle?

A) early 

B) mid

C) late

Answer: C

Catamenial epilepsy can best be predicted by keeping a seizure diary. In a regular menstrual cycle, estrogen levels peak during mid-cycle (without conception) and drop just before the onset of menses. During this period, most seizure clusters are reported. Although a periovulatory seizure may occur. 

Standard treatment of seizures should be sufficient.

Use of Clobazam during the vulnerable phase of the menstrual cycle has shown some promise. 20 to 30 mg of Clobazam per day for 10 days during the high-risk phase of the menstrual cycle has been found to be effective. Intermittent lorazepam may also be used in the vulnerable period.

Some experts recommend the use of an adjunctive continuous estrogen-progestin contraceptive as hormonal prophylaxis for catamenial epilepsy, though evidence is weak for such practice. Other recommended treatments, but with very limited data, are acetazolamide, gonadotropin analogs, and neurosteroids (ganaxolone).

#neurology

#ob-gyn

References:

1. Herzog AG, Fowler KM, Sperling MR, et al. Variation of seizure frequency with ovulatory status of menstrual cycles. Epilepsia 2011; 52:1843.

2. Maguire MJ, Nevitt SJ. Treatments for seizures in catamenial (menstrual-related) epilepsy. Cochrane Database Syst Rev 2021; 9:CD013225.

3. Herzog AG, Fowler KM, Smithson SD, et al. Progesterone vs placebo therapy for women with epilepsy: A randomized clinical trial. Neurology 2012; 78:1959.

4. Feely M, Calvert R, Gibson J. Clobazam in catamenial epilepsy. A model for evaluating anticonvulsants. Lancet 1982; 2:71.

5. Ansell B, Clarke E. Acetazolamide in Treatment of Epilepsy. Br Med J 1956; 1:650.

6. Reddy DS. Neurosteroid replacement therapy for catamenial epilepsy, postpartum depression and neuroendocrine disorders in women. J Neuroendocrinol 2022; 34:e13028.

PP and Carbs

Q: A high-carbohydrate load is recommended in patients who present with hypokalemic Periodic paralysis (PP), including thyrotoxic PP.

A) True

B) False

Answer: B

PP attacks in hypokalemic thyrotoxic patients result from increased release of epinephrine or insulin, causing intracellular potassium shifts and low serum potassium levels. Known inciting events are:

• strenuous physical activity
• stress
• high-carbohydrate load (answer for above Q)
• cold exposure
• infection
• alcohol intake
• pulse corticosteroid therapy
• beta-2 adrenergic bronchodilator 
• menses 
• exogenous epinephrine or insulin
• acetazolamide
• thyroid supplements 

#electrolytes

References:

1. Hsieh MJ, Lyu RK, Chang WN, et al. Hypokalemic thyrotoxic periodic paralysis: clinical characteristics and predictors of recurrent paralytic attacks. Eur J Neurol 2008; 15:559.

2. Qing G, Zakaria WNA, Rom FZM, Nik WNFHW, Zulkeflee HA, Rahim SNA. Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms. Endocrinol Metab (Seoul). 2025 Dec;40(6):821-829. doi: 10.3803/EnM.2025.2554. Epub 2025 Dec 11. PMID: 41376301; PMCID: PMC12765881.

3. Chang CC, Cheng CJ, Sung CC, et al. A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants. Eur J Endocrinol 2013; 169:529.

MH and gender

Q: Malignant Hyperthermia (MH) is disproportionally high in? - select one

A) males

B) females

Answer: A

The male-to-female ratio for MH is 2:1. The obvious explanation is the likely higher skeletal mass in males, though it does not fully account for the high prevalence in males. Moreover, children less than 19 years of age are more prone to develop MH.

#anesthesia

References:

1. Brady JE, Sun LS, Rosenberg H, Li G. Prevalence of malignant hyperthermia due to anesthesia in New York State, 2001-2005. Anesth Analg 2009; 109:1162.

2. Larach MG, Gronert GA, Allen GC, et al. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006. Anesth Analg 2010; 110:498.

3. Rosenberg H, Davis M, James D, et al. Malignant hyperthermia. Orphanet J Rare Dis 2007; 2:21.

4. Rosenberg H, Pollock N, Schiemann A, Bulger T, Stowell K. Malignant hyperthermia: a review. Orphanet J Rare Dis. 2015 Aug 4;10:93. doi: 10.1186/s13023-015-0310-1. PMID: 26238698; PMCID: PMC4524368.

Metronidazole and disulfiram-like reactions.

Q: Metronidazole should be avoided with alcohol intake as it may cause disulfiram-like reactions.

A) True

B) False

Answer: B

Although it was once believed that metronidazole could cause disulfiram-like reactions with ETOH, this was based on a few weak reports. Evidence failed to prove any such association. The United States Centers for Disease Control and Prevention (CDC) Sexually Transmitted Infection Guidelines in 2021 removed abstaining from alcohol while taking metronidazole.

Metronidazole does not inhibit alcohol metabolism in the liver or increase blood acetaldehyde production, the basis for disulfiram-like reactions. It is suggested that metronidazole and ethanol both, independently, increase brain serotonin levels, potentially giving an impression of disulfiram-like reactions.

# pharmacology

References:

1. Visapää JP, Tillonen JS, Kaihovaara PS, Salaspuro MP. Lack of disulfiram-like reaction with metronidazole and ethanol. Ann Pharmacother 2002; 36:971.

2. Tillonen J, Väkeväinen S, Salaspuro V, et al. Metronidazole increases intracolonic but not peripheral blood acetaldehyde in chronic ethanol-treated rats. Alcohol Clin Exp Res 2000; 24:570.

3. Karamanakos PN, Panteli ES, Marselos M. Comment on 'Can Metronidazole Cause a Disulfiram-Like Reaction? A Case-Control Study Propensity Matched By Age, Sex and Ethanol. WMJ 2024; 123:3.

4. Workowski KA, Bachmann LH, Chan PA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep 2021; 70:1.

5. Feldman R, Jaszczenski R. Can Metronidazole Cause a Disulfiram-Like Reaction? A Case-Control Study Propensity Matched by Age, Sex, and Ethanol Concentration. WMJ 2023; 122:171.

Acute HIV on PrEP

Q: What's the caveat of diagnosing HIV in patients who are using pre-exposure prophylaxis (PrEP) for HIV?

Answer: Unreliable clinical signs and routine HIV screening test

Patients who are on pre-exposure prophylaxis (PrEP) due to their lifestyle may not develop full-blown acute HIV symptoms on initial contraction, but may have mild symptoms called pauci-symptomatic acute HIV. Cardinal acute HIV symptoms such as fever and rash are usually absent, and there may be no pharyngitis or diarrhea. To make things more complicated, routine HIV screening with the antigen/antibody test may not be reliable. Diagnosis can be made by history, exposure, keeping a high clinical suspicion, and HIV RNA as the screening tool.

#ID

References:

1. Landovitz RJ, Delany-Moretlwe S, Fogel JM, et al. Features of HIV Infection in the Context of Long-Acting Cabotegravir Preexposure Prophylaxis. N Engl J Med 2024; 391:1253.

2. Moschese D, Lazzarin S, Colombo ML, Caruso F, Giacomelli A, Antinori S, Gori A. Breakthrough Acute HIV Infections among Pre-Exposure Prophylaxis Users with High Adherence: A Narrative Review. Viruses. 2024 Jun 12;16(6):951. doi: 10.3390/v16060951. PMID: 38932243; PMCID: PMC11209220.

3. Elliott T, Sanders EJ, Doherty M, Ndung'u T, Cohen M, Patel P, Cairns G, Rutstein SE, Ananworanich J, Brown C, Fidler S. Challenges of HIV diagnosis and management in the context of pre-exposure prophylaxis (PrEP), post-exposure prophylaxis (PEP), test and start and acute HIV infection: a scoping review. J Int AIDS Soc. 2019 Dec;22(12):e25419. doi: 10.1002/jia2.25419. PMID: 31850686; PMCID: PMC6918508.

Calcium and Dengue Virus

Q: Dengue virus infection causes? - select one

A) hypercalcemia

B) hypocalcemia 

Answer: B

Most of the treatment for the Dengue virus during all three phases of the Dengue virus, i.e., early, critical, and recovery phase, is essentially supportive. One of the unique features of the Dengue virus is hypocalcemia, and its cause is still not well understood. That said, it is significant, as the level of hypocalcemia correlates with the severity of illness. Its clinical significance can be understood from the perspective that, in resource-limited countries where the dengue virus is common, and labs may not be readily available, calcium should be replaced empirically, correlating clinically with the level of shock.

Development of seizures or arrhythmia due to hypocalcemia predicts poor outcome and requires constant monitoring and replacement, particularly in the critical phase. IV calcium gluconate is preferred. Replacement of calcium also helps restore the coagulation defects, a cardinal feature of Dengue virus infection.

#ID

References;

1. Pourzangiabadi M, Najafi H, Fallah A, Goudarzi A, Pouladi I. Dengue virus: Etiology, epidemiology, pathobiology, and developments in diagnosis and control - A comprehensive review. Infect Genet Evol. 2025 Jan;127:105710. doi: 10.1016/j.meegid.2024.105710. Epub 2024 Dec 26. PMID: 39732271.

2. Shivanthan MC, Rajapakse S. Dengue and calcium. Int J Crit Illn Inj Sci 2014; 4:314.

3. Constantine GR, Rajapakse S, Ranasinghe P, et al. Hypocalcemia is associated with disease severity in patients with dengue. J Infect Dev Ctries 2014; 8:1205.

PAS

Q: 38 years old G5P2 female at 36 weeks of pregnancy is admitted to the ICU for high-risk delivery. She was found to have a placenta growing through the uterine wall and invading the urinary bladder. By definition, she has? - select one

A) Placenta accreta

B) Placenta increta 

C) Placenta percreta 

Answer: C

Although Placenta Accreta Spectrum (PAS) is an umbrella term for an abnormal trophoblast adherence to or into the myometrium, scar tissue, and sometimes to or beyond the serosa. At delivery, the placenta may not spontaneously separate, and iatrogenic removal may cause massive hemorrhage, which may require emergent hysterectomy. The highest risk factor for PAS is a placenta previa after a prior cesarean birth.

PAS has three grades:

• Placenta accreta  – Anchoring placental villi attach to the myometrium (rather than decidua)
• Placenta increta – Anchoring placental villi penetrate into the myometrium
• Placenta percreta – Anchoring placental villi penetrate through the myometrium to the uterine serosa or adjacent organ

#ob-gyn

References:

1. Jauniaux E, Ayres-de-Campos D, Langhoff-Roos J, et al. FIGO classification for the clinical diagnosis of placenta accreta spectrum disorders. Int J Gynaecol Obstet 2019; 146:20.

2. Society of Gynecologic Oncology; American College of Obstetricians and Gynecologists and the Society for Maternal–Fetal Medicine; Cahill AG, Beigi R, Heine RP, Silver RM, Wax JR. Placenta Accreta Spectrum. Am J Obstet Gynecol. 2018 Dec;219(6):B2-B16. doi: 10.1016/j.ajog.2018.09.042. PMID: 30471891.

3. O'Connor D, Berndl A. Placenta percreta. CMAJ. 2018 Feb 12;190(6):E168. doi: 10.1503/cmaj.171411. PMID: 29440338; PMCID: PMC5809218.

iron concentration in high exercise training

Q: High-intensity athletic workout may cause iron deficiency due to loss of iron in sweat.

A) True

B) False

Answer: A

A liter of sweat causes 0.6 mg of Iron (Fe) loss! Iron deficiency may be seen in some high-intensity athletes. Other contributing factors for iron deficiency in athletics, besides loss in sweat, are:

• Reduced iron intake
• Occult GI blood loss
• Traumatic hemolysis

#hematology

References:

1. McMahon LF Jr, Ryan MJ, Larson D, Fisher RL. Occult gastrointestinal blood loss in marathon runners. Ann Intern Med 1984; 100:846.

2. Coates A, Mountjoy M, Burr J. Incidence of Iron Deficiency and Iron Deficient Anemia in Elite Runners and Triathletes. Clin J Sport Med 2017; 27:493.

3. DeRuisseau KC, Cheuvront SN, Haymes EM, Sharp RG. Sweat iron and zinc losses during prolonged exercise. Int J Sport Nutr Exerc Metab. 2002 Dec;12(4):428-37. doi: 10.1123/ijsnem.12.4.428. PMID: 12500986.

4. Saran T, Zawadka M, Chmiel S, Mazur A. Sweat iron concentration during 4-week exercise training. Ann Agric Environ Med. 2018 Sep 25;25(3):500-503. doi: 10.26444/aaem/78787. Epub 2017 Nov 15. PMID: 30260183.

CCB overdose

Q: Hemodialysis should be instituted as early as possible in a Calcium Channel Blocker (CCB) overdose.

A) True

B) False

Answer: B

CCBs are highly protein-bound, so extracorporeal removal via hemodialysis or Continuous Renal Replacement Therapy (CRRT) is usually not effective. Said that it may help in case acute kidney injury or severe acidosis ensues, it can be added as an adjuvant therapy. Extracorporeal membrane oxygenation (ECMO) should be considered early if standard-of-care therapies show no evidence of effectiveness. 

Major components of CCB overdose are:

• Atropine for symptomatic bradycardia
• Intravenous calcium
• Calcium infusion with close monitoring of ionized calcium.
• Glucagon 
• Vasopressors (norepinephrine is preferred)
• Insulin and glucose with monitoring of possible hypokalemia
• Methylene blue 
• High-dose cyanocobalamin

# toxicity

References:

1. Wong A, Hoffman RS, Walsh SJ, et al. Extracorporeal treatment for calcium channel blocker poisoning: systematic review and recommendations from the EXTRIP workgroup. Clin Toxicol (Phila) 2021; 59:361.

2. Slamowitz A, Sweberg T, Labgold K, Nickerson T. Extracorporeal Membrane Oxygenation for Calcium Channel Blocker Intoxication: A Multicenter Retrospective Registry Review. ASAIO J. 2025 Oct 31. doi: 10.1097/MAT.0000000000002593. Epub ahead of print. PMID: 41168146.

3. Saha BK, Bonnier A, Chong W. Rapid reversal of vasoplegia with methylene blue in calcium channel blocker poisoning. Afr J Emerg Med 2020; 10:284.

Hyperalbuminemia and calcium

Q: Hyperalbuminemia can cause hypercalcemia.

A) True

B) False

Answer: A

Although it is very well known that hypoalbuminemia can cause hypocalcemia and various formulae have been invented, it is less emphasized that the reverse is also true, meaning hyperalbuminemia can lead to hypercalcemia. The most common reason is extracellular volume depletion. Another well-recognized clinical scenario is the widespread use of high-protein powders among athletes and 'gym-goers', which may increase serum calcium. It occurs mostly when more than 2 g of protein per kg of body weight per day is consumed.

Said that many experts believe that, just as hypoalbuminemia and hypocalcemia are related and require correction, the same phenomenon applies to hyperalbuminemia and hypercalcemia. The best clinical practice should be to measure ionized calcium.

#electrolytes

References:

1. DENT CE. Some problems of hyperparathyroidism. Br Med J 1962; 2:1419.

2. Mutlu EA, Keshavarzian A, Mutlu GM. Hyperalbuminemia and elevated transaminases associated with high-protein diet. Scand J Gastroenterol 2006; 41:759.

On ESR

Q: Erythrocyte Sedimentation Rate (ESR) in patients with sickle cell disease is expected to be spuriously? - select one

A) high

B) low

Answer: B

As ESR gets affected by changes in red cell shape or number, including sickle cell disease, anisocytosis, spherocytosis, acanthocytosis, microcytosis, and polycythemia, it can be spuriously low, particularly in sickle cell disease. Other conditions which may result in falsely low ESR are:

• extremely high serum bile salt levels 
• CHF
• Hypofibrinogenemia 
• high-dose glucocorticoids
• high-dose salicylate therapy
• IL-6 inhibitors 
• biopsy-proven giant cell arteritis
• statins 
• nonsteroidal antiinflammatory drugs (NSAIDs) 
• light alcohol consumption 
• clotting of the blood sample 
• delay in testing of greater than two hours
• low room temperature
• Short ESR tube

One of the most paradoxical situations is having "declining ESR" during a "cytokine storm," when it is expected to rise. This is because low fibrinogen levels are characteristic of macrophage activation syndrome (MAS), also called acquired hemophagocytic lymphohistiocytosis, which causes consumptive coagulopathy, including fibrinogen degradation and decreased fibrinogen synthesis, both of which are main drivers of the ESR.

#hematology

#inflammatory-markers

References:

1.  Jurado RL. Why shouldn't we determine the erythrocyte sedimentation rate? Clin Infect Dis 2001; 33:548.

2. Lawrence C, Fabry ME. Erythrocyte sedimentation rate during steady state and painful crisis in sickle cell anemia. Am J Med 1986; 81:801.

3. Brigden ML. Clinical utility of the erythrocyte sedimentation rate. Am Fam Physician 1999; 60:1443.

Gaisböck Syndrome

Q: What is Gaisböck's syndrome?

Answer: A version of relative polycythemia.

 Gaisböck's syndrome is also called stress or spurious polycythemia, as it is classically described as erythrocytosis in tense/anxious patients. The components of the syndrome are:

• Anxiety
• Hypertension (HTN)
• No evidence of splenomegaly, and 
• Evidence of reduced plasma volume

Many of these patients are on a diuretic for HTN treatment, and are smokers to alleviate their anxiety. These factors contribute to the syndrome.

Many experts argue against the existence of this syndrome as a specific entity (see reference # 4)

#hematology

References:

1. Manal N, Rizvi M, Nugent K. Gaisbock Syndrome: A Review of Contemporary Studies, Pathogenesis, Complications, and Possible Treatment. Cardiol Rev. 2023 Sep-Oct 01;31(5):247-251. doi: 10.1097/CRD.0000000000000443. Epub 2022 Feb 7. PMID: 35148535.

2. LAWRENCE JH, BERLIN NI. Relative polycythemia; the polycythemia of stress. Yale J Biol Med 1952; 24:498.

3. Krishnamoorthy P, Gopalakrishnan A, Mittal V, Kalla A, Slipczuk L, Rangaswami J, Figueredo VM, Messerli FH. Gaisböck syndrome (polycythemia and hypertension) revisited: results from the national inpatient sample database. J Hypertens. 2018 Dec;36(12):2420-2424. doi: 10.1097/HJH.0000000000001805. PMID: 29847483.

4. Brown SM, Gilbert HS, Krauss S, Wasserman LR. Spurious (relative) polycythemia: a nonexistent disease. Am J Med 1971; 50:200.

DBP with age

Q: Overall, Diastolic Blood Pressure (DBP) tends to increase with age.

A) True

B) False

Answer: B

Various factors contribute to the decrease in diastolic pressure with age, particularly after age 55. The aorta starts to stiffen, reducing its elastic reservoir capacity. This causes more blood to be ejected with each stroke during systole, reducing the blood volume in the aorta at the onset of diastole. Overall, systemic vessels exhibit diminished elastic recoil, leading to a fall in diastolic pressure with age. This phenomenon is universal across the board, including normotensive and hypertensive patients.

#hemodynamics

References:

1. Franklin SS, Gustin W 4th, Wong ND, et al. Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation 1997; 96:308.

2. Folkow B. Structure and function of the arteries in hypertension. Am Heart J 1987; 114:938.

RLS and BZRA

Case: A 74-year-old male with no major history, except for restless legs syndrome (RLS), is admitted to the ICU for community-acquired pneumonia. Patient is now recovering. The patient requested medicine for his insomnia in the ICU, and the resident prescribed zolpidem. Patient found to have hyperactive delirium in the early part of the next morning.

Discussion: As commonly said, restless legs syndrome and insomnia go hand in hand; most patients with RLS require some kind of pharmaceutical support for their insomnia. Precautions should be taken to prescribe selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), or antihistamines, as they can exacerbate RLS.

Particular care should be exercised in prescribing BZRAs (Benzodiazepine Receptor Agonists) such as zolpidem, as they increase the incidence of complex sleep-related behaviors.

Further readings/References:

1. Park YM, Shin HW. Zolpidem Induced Sleep-related Eating and Complex Behaviors in a Patient with Obstructive Sleep Apnea and Restless Legs Syndrome. Clin Psychopharmacol Neurosci. 2016 Aug 31;14(3):299-301. doi: 10.9758/cpn.2016.14.3.299. PMID: 27489385; PMCID: PMC4977817.

2. Mittal N, Mittal R, Gupta MC. Zolpidem for Insomnia: A Double-Edged Sword. A Systematic Literature Review on Zolpidem-Induced Complex Sleep Behaviors. Indian J Psychol Med. 2021 Sep;43(5):373-381. doi: 10.1177/0253717621992372. Epub 2021 Mar 9. PMID: 34584301; PMCID: PMC8450729.

3. Winkelman JW, Wipper B. Restless Legs Syndrome: A Review. JAMA. 2026 Feb 24;335(8):703-714. doi: 10.1001/jama.2025.23247. PMID: 41563785.

ART and CVS

Q: Antiretroviral therapy (ART) in HIV patients increases the risk of cardiovascular disease.

A) True

B) False

Answer: B

Although in the past it was believed and was partially true that abacavir and most protease inhibitors are associated with an increased risk of Myocardial Infarction (MI), overall, most antiretroviral therapy (ART) regimens do not increase the risk of MI. Instead, HIV infection itself accelerates atherosclerosis and the incidence of coronary artery disease (CAD). The rate of MI is higher in patients with HIV compared with patients without HIV who are matched for age and gender. 

Lower CD4 cell counts and higher HIV RNA levels have been found to be associated with increased MI risk.

#ID

#pharmacology

Reference:

Eyawo O, Brockman G, Goldsmith CH, et al. Risk of myocardial infarction among people living with HIV: an updated systematic review and meta-analysis. BMJ Open 2019; 9:e02587

Albumin and CIP

Q: Low serum albumin is a risk factor for Critical Illness Polyneuropathy (CIP).

A) True

B) False

Answer: A

CIP is commonly seen in patients who stay in the ICU for more than a week or two. Some of the known risk factors are:

• severe sepsis 
• severe systemic inflammatory response syndrome (SIRS)
• persistently elevated blood glucose
• low serum albumin 
• use of neuro-muscular blockade

Use of steroids is found to be more associated with Critical Illness Myopathy (CIM), though most patients in the ICU have a combined CIM and CIP.

#neurology

#icu-course

References:

1. Witt NJ, Zochodne DW, Bolton CF, et al. Peripheral nerve function in sepsis and multiple organ failure. Chest 1991; 99:176.

2. Zhou C, Wu L, Ni F, Ji W, Wu J, Zhang H. Critical illness polyneuropathy and myopathy: a systematic review. Neural Regen Res. 2014 Jan 1;9(1):101-10. doi: 10.4103/1673-5374.125337. PMID: 25206749; PMCID: PMC4146320.

3. Bednarík J, Vondracek P, Dusek L, Moravcova E, Cundrle I. Risk factors for critical illness polyneuromyopathy. J Neurol. 2005 Mar;252(3):343-51. doi: 10.1007/s00415-005-0654-x. Epub 2005 Mar 30. PMID: 15791390.

4. Atrash AK, de Vasconcellos K. Low albumin levels are associated with mortality in the critically ill: A retrospective observational study in a multidisciplinary intensive care unit. South Afr J Crit Care. 2020 Dec 1;36(2):10.7196/SAJCC.2020.v36i2.422. doi: 10.7196/SAJCC.2020.v36i2.422. PMID: 35493283; PMCID: PMC9045521.

Parovirus 19 fetal severe anemia

Q: A 24-year-old female with 22 weeks of pregnancy is admitted to the ICU with severe symptoms of Parvovirus 19, confirmed with a high IgM titer but a negative IgG titer. There is a severe fetal anemia, and thrombocytopenia is suspected. How should the blood transfusion be given? -select one

A) Slow Intravenous 

B) Intrauterine

C) Plasmapheresis

Answer: B

Usually, a fetus can handle mild to moderate anemia without any major intervention. Severe fetal anemia can lead to hydrops fetalis. Noninvasive methods to detect fetal anemia are:

• Doppler middle cerebral artery (MCA) peak systolic velocity (PSV), and 
• ductus venosus velocity  

Invasively, cord blood sampling can be performed via percutaneous umbilical venous sampling, but is reserved for suspected severe cases requiring intervention.

Interesting, blood transfusions in such situations are given directly via intrauterine. Intrauterine transfusion is possible only after 18 weeks of pregnancy due to the small vessel size prior to it.

The authors of this question highly encouraged students to review reference #4 below.

#Ob-gyn

References:

1. Fairley CK, Smoleniec JS, Caul OE, Miller E. Observational study of effect of intrauterine transfusions on outcome of fetal hydrops after parvovirus B19 infection. Lancet 1995; 346:1335.

2. Rodis JF, Borgida AF, Wilson M, et al. Management of parvovirus infection in pregnancy and outcomes of hydrops: a survey of members of the Society of Perinatal Obstetricians. Am J Obstet Gynecol 1998; 179:985.

3. von Kaisenberg CS, Jonat W. Fetal parvovirus B19 infection. Ultrasound Obstet Gynecol 2001; 18:280.

4. Devlieger R, Vergote S, Van den Eede E, Haenen K, Lewi L. Intrauterine transfusion: Best practices, techniques, and evolving trends. Best Pract Res Clin Obstet Gynaecol. 2026 Feb;104:102686. doi: 10.1016/j.bpobgyn.2025.102686. Epub 2025 Nov 20. PMID: 41289715.

NPPE - MOA

Case: 22 years old atheletic male went through a non-complicated appendectomy under general anesthesia. Patient became agitated on weaning sedation and started biting on the endotracheal tube (ETT). The patient was extubated, but on extubation developed severe pulmonary edema with desaturation. Patient recovered well with supplemental oxygen, non-invasive positive pressure ventilation (NIPPV), diuresis, and infusion of Dexmedetomidine, and was eventually extubated without complications. Why is post-extubation pulmonary edema called negative pressure pulmonary edema (NPPE)?

Answer: Post-extubation pulmonary edema is a common phenomenon in the PACU/ICU if a patient forcibly inhales against a closed glottis. This is also known as the Mueller or reverse Valsalva maneuver. This phenomenon occurs post-extubation due to laryngospasm, pharyngeal obstruction, or biting of the endotracheal tube during extubation. 

Conventional teaching holds that it occurs immediately, though this is not entirely true; a delayed NPPE has been reported up to 12 hours after extubation. People with obesity, short neck, obstructive sleep apnea, or acromegaly are at the highest risk, followed by young, healthy, athletic adults.

The correct term is negative pressure pulmonary edema, which refers to a non-cardiac form of pulmonary edema resulting from the development of negative interstitial pressure around the capillaries, drawing intravascular fluid into the interstitial space.

#procedure

#pulmonary

References:

1. Mulkey Z, Yarbrough S, Guerra D, et al. Postextubation pulmonary edema: a case series and review. Respir Med 2008; 102:1659.

2. Holmes JR, Hensinger RN, Wojtys EW. Postoperative pulmonary edema in young, athletic adults. Am J Sports Med 1991; 19:365.

3. Tsai PH, Wang JH, Huang SC, Lin YK, Lam CF. Characterizing post-extubation negative pressure pulmonary edema in the operating room-a retrospective matched case-control study. Perioper Med (Lond). 2018 Dec 6;7:28. doi: 10.1186/s13741-018-0107-6. PMID: 30534363; PMCID: PMC6282297.

PG

Q: A 43-year-old male with an established history of ulcerative colitis is admitted to the ICU with Lower GI bleed requiring transfusion. On physical exam, chronic ulceration was noted on the lower extremity and diagnosed as Pyoderma gangrenosum (PG). PG, as the name suggests, is an infectious process causing gangrene.

A) True

B) False

Answer: B

Pyoderma gangrenosum (PG) is a misnomer as it is neither an infectious nor a gangrenous condition! The probability of this misnomer arises from its striking, infectious-like appearance.

PG is a neutrophilic dermatosis that presents as an inflammatory, ulcerative skin disorder. The most common presentation of PG is an inflammatory papule or pustule that progresses to a painful ulcer with a violaceous, undermined border and a purulent base. It may also present with bullous, vegetative, peristomal, and extracutaneous lesions.

Clinical Significance: It has high association with an underlying systemic diseases like inflammatory bowel disease, hematologic disorders, and arthritis.

#dermatology

References:

1. Maverakis E, Marzano AV, Le ST, Callen JP, Brüggen MC, Guenova E, Dissemond J, Shinkai K, Langan SM. Pyoderma gangrenosum. Nat Rev Dis Primers. 2020 Oct 8;6(1):81. doi: 10.1038/s41572-020-0213-x. PMID: 33033263.

2. Łyko M, Ryguła A, Kowalski M, Karska J, Jankowska-Konsur A. The Pathophysiology and Treatment of Pyoderma Gangrenosum-Current Options and New Perspectives. Int J Mol Sci. 2024 Feb 19;25(4):2440. doi: 10.3390/ijms25042440. PMID: 38397117; PMCID: PMC10889749.

3. Moltrasio C, Romagnuolo M, Tavoletti G, Maronese CA, Marzano AV. Pyoderma gangrenosum: pathogenetic mechanisms and their implications for treatment. Semin Immunopathol. 2025 Oct 23;47(1):38. doi: 10.1007/s00281-025-01064-7. PMID: 41128863; PMCID: PMC12549756.

iNO and organ dysfunction

Q: Prolonged use of inhaled Nitric Oxide (iNO) is intended to cause more of? - select one

A) Kidney dysfunction

B) liver dysfunction

Answer: A

Prolonged use of iNO beyond 5-7 days may increase the risk of acute kidney injury (AKI). This inference is drawn primarily from trials of its use in patients with ARDS and after cardiac surgery. 

An interesting paradox is the finding that short-term use (24 hours post-surgery) of iNO in patients who require prolonged cardiopulmonary bypass may have a protective effect for AKI. This short-term benefit is due to the fact that, in prolonged bypass cases, increased hemolysis raises plasma levels of free oxyhemoglobin, which binds and depletes endogenous NO, leading to vasoconstriction, impaired tissue perfusion, and inflammation (reference #3).

#cardiovascular

#nephrology

References:

1. Ruan SY, Huang TM, Wu HY, et al. Inhaled nitric oxide therapy and risk of renal dysfunction: a systematic review and meta-analysis of randomized trials. Crit Care 2015; 19:137.

2. Gebistorf F, Karam O, Wetterslev J, Afshari A. Inhaled nitric oxide for acute respiratory distress syndrome (ARDS) in children and adults. Cochrane Database Syst Rev 2016; :CD002787.

3. Lei C, Berra L, Rezoagli E, et al. Nitric Oxide Decreases Acute Kidney Injury and Stage 3 Chronic Kidney Disease after Cardiac Surgery. Am J Respir Crit Care Med 2018; 198:1279.

The time-relationship of 'osmolal gap' and 'Anion gap' in toxic alcohols

Q: In Methanol and Ethylene Glycol toxicity, the time-relationship of 'osmolal gap' and 'Anion gap' is inversely proportional.

A) True

B) False

Answer: A

After ingestion of Methanol and Ethylene Glycol, the osmolal gap continues to drop as the alcohols are metabolized, while the anion gap rises. The following graph best describes the relationship.

#toxicity

References:

1. Kraut JA, Mullins ME. Toxic Alcohols. N Engl J Med. 2018 Jan 18;378(3):270-280. doi: 10.1056/NEJMra1615295. Erratum in: N Engl J Med. 2019 Jan 10;380(2):202. doi: 10.1056/NEJMx180046. PMID: 29342392.

2. Gallagher N, Edwards FJ. The Diagnosis and Management of Toxic Alcohol Poisoning in the Emergency Department: A Review Article. Adv J Emerg Med. 2019 May 22;3(3):e28. doi: 10.22114/ajem.v0i0.153. PMID: 31410405; PMCID: PMC6683589.

Clinical features of infective endocarditis

Q: A 52-year-old male with a history of End Stage Renal Disease (ESRD) is admitted to the ICU with suspected infective endocarditis (IE). On clinical exam found to have Janeway lesions. Janeway lesions are more common in? - select one

A) acute IE

B) subacute IE

Answer: A

Clinical exam in IE plays an important role. Three hallmark characteristic findings, though relatively uncommon, are highly suggestive of IE:

• Janeway lesions
• Osler nodes 
• Roth spots 

Janeway lesions are nontender erythematous macules on the palms and soles. Histologically, they are microabscesses with neutrophil infiltration of capillaries. Janeway lesions are more common in acute than subacute IE. 

In contrast, Osler nodes and Roth spots occur over a protracted time course of endocarditis. These two entities are sequelae of microthromboembolic occlusion, leading to localized immune-mediated vasculitis. Osler nodes, in contrast to Janeway lesions, are tender and subcutaneous (SQ) violaceous nodules mostly on the pads of the fingers and toes, and may also occur on the thenar and hypothenar eminences. Interestingly, tenderness begins a few days before the nodule appears. Roth spots are exudative, edematous, hemorrhagic lesions of the retina with pale centers.

#physical-exam

#ID

References:

1. Saccente M, Cobbs CG. Clinical approach to infective endocarditis. Cardiol Clin. 1996 Aug;14(3):351-62. doi: 10.1016/s0733-8651(05)70289-7. PMID: 8853130.

2. Loughrey PB, Armstrong D, Lockhart CJ. Classical eye signs in bacterial endocarditis. QJM 2015; 108:909.

3. Abdelgawad H, Azab S, Abdel-Hay MA, Almaghraby A. Clinical features and outcomes of infective endocarditis: a single-centre experience. Cardiovasc J Afr. 2023 May-Jun 23;34(2):82-88. doi: 10.5830/CVJA-2022-027. Epub 2022 Aug 3. PMID: 35924572; PMCID: PMC10512034.