CVP and bed level

Q: 68-year-old patient admitted with CHF. Now, with diuresis, the patient is clinically stable and ready for transfer to the floor. Patient's last CVP noted was 12. The patient's bed is raised to perform a portable chest x-ray. With elevation of the bed, CVP will? (select one)

A) Fall

B) Rise

C) No change

Answer: B

The CVP transducer and intravascular volume at the "zero" point act as a balance of fluids. If the transducer drops below zero (such as when the bed is elevated), CVP will rise. It's similar to a seesaw.

Bed up  - CVP falsely down

Bed down  - CVP falsely up

#hemodynamics

References:

1. Zhou J, Zuo X, Liu S, Chu M, Tian Y. [Discussion on the zero-calibration and the zero line in the measurement of central venous pressure and invasive arterial blood pressure]. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2023 Mar;35(3):316-320. Chinese. doi: 10.3760/cma.j.cn121430-20220926-00862. PMID: 36916347.

2. Lloyd-Donald P, Fujino M, Waldman B, Miles LF. Measurement and interpretation of central venous pressure: a narrative review. Anaesthesia. 2025 Sep;80(9):1093-1102. doi: 10.1111/anae.16633. Epub 2025 Jun 3. PMID: 40457939; PMCID: PMC12351226.

3. Figg KK, Nemergut EC. Error in central venous pressure measurement. Anesth Analg. 2009 Apr;108(4):1209-11. doi: 10.1213/ane.0b013e318196482c. PMID: 19299788.

Pentad of Graves' disease

Q: What is the pentad of Graves' disease?

Answer: A full-blown ideal Graves' disease usually consists of five features:

1. Hyperthyroidism
2. Goiter
3. Oorbitopathy
4. Dermopathy
5. Tachycardia

Other features may also be present, including heat intolerance, tremor, palpitations, anxiety, weight loss despite a normal or increased appetite, increased bowel frequency, and shortness of breath. Skin exam may have some remarkable and striking onycholysis, softening of the nails, hyperpigmentation, pruritus and hives, vitiligo, alopecia areata, and thinning of the hair.

A large number of patients may not have all of these features overtly. Diagnosis is based on clinical signs and symptoms and laboratory work-up.

Graves' disease, by definition, is an autoimmune disease. It is caused by thyroid-stimulating hormone (TSH, thyrotropin) receptor antibodies (TRAb) that activate the receptor, thereby stimulating thyroid hormone synthesis and secretion, as well as thyroid growth (diffuse goiter).

#endocrinology

#clinical-exam

References:

1. Toro-Tobon D, Stan MN. Graves’ Disease and the Manifestations of Thyrotoxicosis. [Updated 2024 Sep 24]. In: Feingold KR, Adler RA, Ahmed SF, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK285567/

2. Lee SY, Pearce EN. Hyperthyroidism: A Review. JAMA. 2023 Oct 17;330(15):1472-1483. doi: 10.1001/jama.2023.19052. PMID: 37847271; PMCID: PMC10873132.

3. Davies TF, Andersen S, Latif R, Nagayama Y, Barbesino G, Brito M, Eckstein AK, Stagnaro-Green A, Kahaly GJ. Graves' disease. Nat Rev Dis Primers. 2020 Jul 2;6(1):52. doi: 10.1038/s41572-020-0184-y. PMID: 32616746.

MOA of clopidogrel

Q: Clopidogrel (and other platelet P2Y12 receptor blockers) causes gastrointestinal bleed (GIB) due to its ulcerogenic characteristic.

A) True

B) False

Answer: B

Aspirin (ASA) and other nonsteroidal antiinflammatory drugs (NSAIDs) are directly ulcerogenic, but Platelet P2Y12 receptor blockers are not. They actually impair ulcer healing! This is the reason some experts believe in "GI-bleeders" only monotherapy with Platelet P2Y12 receptor blockers can be used.

In GI ulceration (caused by ASA, NSAIDs, or other causes), platelet aggregation leads to the release of platelet-derived growth factors, such as vascular endothelial growth factor (VEGF), which promote angiogenesis and endothelial cell proliferation, processes required for ulcer healing. Platelet P2Y12 receptor blockers prevent this healing.

#pharmacology

#cardiology

References:

1. Cryer B. Reducing the risks of gastrointestinal bleeding with antiplatelet therapies. N Engl J Med 2005; 352:287.

2. Ma L, Elliott SN, Cirino G, et al. Platelets modulate gastric ulcer healing: role of endostatin and vascular endothelial growth factor release. Proc Natl Acad Sci U S A 2001; 98:6470.

3. Waqas SA, Imran Z, Bilal AR, Ahmed S, Gaba H, Chew NWS, Greene SJ, Khan MS. Efficacy of clopidogrel monotherapy versus aspirin monotherapy after percutaneous coronary intervention. J Thromb Thrombolysis. 2025 Oct 10. doi: 10.1007/s11239-025-03185-0. Epub ahead of print. PMID: 41071255.

Total Bilirubin and CHF

Q:  Elevated total bilirubin is associated with increased risk of death in advanced Congestive Heart Failure (CHF).

A) True

B) False

Answer: A

At least four blood tests, either combined or alone, predict a worse outcome in advanced CHF.

• Rising serum creatinine
• Hyponatremia 
• Hypoalbuminemia 
• Elevated total bilirubin

Neurohormonal adaptations, reduced renal perfusion, increased renal venous pressure, and right ventricular dysfunction result in a lower Glomerular Filtration Rate (GFR) and higher blood urea nitrogen (BUN), both of which have been associated with increased mortality and worse prognosis in CHF. This may get complicated by high-dose diuresis for refractory volume overload. Renal compromise and volume overload result in hyponatremia, which itself is associated with worse outcomes in this population of patients. Once hypoalbuminemia goes at ≤3.4 mg/dL, also becomes a marker for poor prognosis. Hypoalbuminemia results from decreased liver synthesis, increased vascular permeability, increased degradation, and renal and gastrointestinal loss. 

Advanced CHF results in congestive hepatopathy due to Right-sided failure, which often accompanies left-sided failure. Abnormalities in serum aminotransferase levels, serum alkaline phosphatase, and total bilirubin are given, and elevated total bilirubin is associated with increased risk of death in HF.

#cardiology

#clinical-medicine

References:

1. Filippatos G, Rossi J, Lloyd-Jones DM, et al. Prognostic value of blood urea nitrogen in patients hospitalized with worsening heart failure: insights from the Acute and Chronic Therapeutic Impact of a Vasopressin Antagonist in Chronic Heart Failure (ACTIV in CHF) study. J Card Fail 2007; 13:360.

2. Klein L, Massie BM, Leimberger JD, et al. Admission or changes in renal function during hospitalization for worsening heart failure predict postdischarge survival: results from the Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF). Circ Heart Fail 2008; 1:25.

3. Uthamalingam S, Kandala J, Daley M, et al. Serum albumin and mortality in acutely decompensated heart failure. Am Heart J 2010; 160:1149.

4. Allen LA, Felker GM, Pocock S, et al. Liver function abnormalities and outcome in patients with chronic heart failure: data from the Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity (CHARM) program. Eur J Heart Fail 2009; 11:170.

An anti-hypertensive in scorpion envenomination

Q: Which of the following anti-hypertensives is found to be of benefit in scorpion envenomation?

A) Amlodipine

B) Losartan

C) Metoprolol

D) Hydrochlorothiazide

E) Prazosin

Answer: E

Antivenom for scorpion bites is not readily available, and when available, it is usually species-specific. It is almost an art to know the right venom for the right scorpion species. Interestingly, a simple antihypertensive, prazosin, has been found to be of value in Grade II* or higher scorpion envenomation, particularly with Hottentotta (Mesobuthus) species. It may reduce the risk of death from scorpion envenomation from 25 percent to almost nil. Also, it may expedite the recovery by preventing cardiogenic pulmonary edema. 

Due to its relatively few side effects, it is recommended as an adjuvant treatment in almost all venomations, including those involving Androctonus, Buthus, Leiurus, or Tityus species. Prazosin works by mitigating excessive catecholamine release and progression to cardiotoxicity! The recommended prazosin dose is 0.5 mg every three hours until systemic toxicity resolves.

#toxicity

* There are four grades, as per escalation of toxicity severity

References:

1. Bawaskar HS, Bawaskar PH. Scorpion sting: update. J Assoc Physicians India 2012; 60:46.

2. Gupta V. Prazosin: a pharmacological antidote for scorpion envenomation. J Trop Pediatr 2006; 52:150.

3. Al-Asmari AK, Al-Seif AA, Hassen MA, Abdulmaksood NA. Role of prazosin on cardiovascular manifestations and pulmonary edema following severe scorpion stings in Saudi Arabia. Saudi Med J 2008; 29:299.

Acute scrotal pain (but not a torsion)

Case: A 19-year-old male is admitted to the ICU with severe scrotal pain. Ultrasound reports read marked edema of the scrotal skin and contents with intact vascular flow in the testes, and acute torsion is ruled out. Patient reports having been told in childhood that he has some kind of vascular disease, but he does not remember. 

Answer: Immunoglobulin A (IgA) vasculitis

Acute scrotal pain can be the presenting symptom of IgA vasculitis, also known as Henoch-Schönlein purpura. Although the scrotum is mostly involved, the ureter, bladder, prostate, testicle, and peniscan also be affected.

IgA vasculitis is a systemic vasculitis characterized by a tetrad of:

• Palpable purpura in patients with neither thrombocytopenia nor coagulopathy
• Arthritis/arthralgia
• Abdominal pain (+/- GI bleed)
• Kidney disease

It is usually a disease of children, but adults may be affected too. The differential diagnosis for torsion is hard to make solely on clinical exam. Ultrasound is the key, and is usually described as given in the question. Another clue to the diagnosis is its seasonal preference! It occurs primarily in the fall, winter, and spring but rarely in the summer. Probable explanations are its association with infections, mostly URI by Streptococcus. Besides infections such as RSV, influenza, and norovirus, vaccinations and insect bites have also been the cause. Other associations have also been described, such as familial Mediterranean fever.

Treatment is usually supportive and involves treating the underlying cause. In severe cases, steroids or immunosuppressants can be used.

#urology

References:

1. Dalpiaz A, Schwamb R, Miao Y, et al. Urological Manifestations of Henoch-Schonlein Purpura: A Review. Curr Urol 2015; 8:66.

2. Balslev T. [Schoenlein-Henoch syndrome with acute scrotal condition simulating torsion of the testis]. Ugeskr Laeger 1990; 152:678.

3. Buscatti IM, Abrão HM, Kozu K, et al. Characterization of scrotal involvement in children and adolescents with IgA vasculitis. Adv Rheumatol 2018; 58:38.

4. Parums DV. A Review of IgA Vasculitis (Henoch-Schönlein Purpura) Past, Present, and Future. Med Sci Monit. 2024 Jan 28;30:e943912. doi: 10.12659/MSM.943912. PMID: 38281080; PMCID: PMC10832303.

Rx of phantom limb pain

Q: Gabapentin is considered a standard of care treatment for phantom limb pain after upper or lower extremity amputation due to its high effectiveness.

A) True

B) False

Answer: B

Unfortunately, despite being well-known in the literature after limb amputations, the etiology of phantom limb pain is poorly understood, and so far, no standard of treatment has been agreed upon. Various modalities can be tried, and treatment should be case-by-case, depending on each patient's responsiveness. There is weak evidence that the use of preemptive epidural anesthesia may reduce the incidence and severity of phantom pain. 

Other modalities which can be tried are:

• ketamine
• calcitonin
• gabapentin
• amitriptyline
• mexiletine
• botulinum neurotoxin A, 
• mirror therapy
• virtual reality
• peripheral nerve stimulation
• incorporating sensory feedback from a specialized prosthetic
• target muscle reinnervation (TMR)

Phantom limb pain is a diagnosis of exclusion. It is a complex process, and patients describe various sensations like burning, aching, or electric-type pain in the amputated limb. Before labelling as phantom limb pain, ischemia, infection, neuroma, and pressure-related wounds should be ruled out.

#surgical-critical-care

#pain

References:

1. Karanikolas M, Aretha D, Tsolakis I, et al. Optimized perioperative analgesia reduces chronic phantom limb pain intensity, prevalence, and frequency: a prospective, randomized, clinical trial. Anesthesiology 2011; 114:1144.

2. Limakatso K, Bedwell GJ, Madden VJ, Parker R. The prevalence and risk factors for phantom limb pain in people with amputations: A systematic review and meta-analysis. PLoS One 2020; 15:e0240431.

3. Rutledge T, Velez D, Depp C, et al. A Virtual Reality Intervention for the Treatment of Phantom Limb Pain: Development and Feasibility Results. Pain Med 2019; 20:2051.

4. Bowen JB, Ruter D, Wee C, et al. Targeted Muscle Reinnervation Technique in Below-Knee Amputation. Plast Reconstr Surg 2019; 143:309.

Hyperkalemia, trimethoprim and anti-hypertensives

Q: 72-year-old male with a history of hypertension presented to the ER with dizziness. Patient found to have arrhythmias on tele-monitor. The lab showed hyperkalemia with 6.9 mEq/L. Wife reports starting on antibiotics for his chronic prostatitis about 2 weeks ago. Which drug interactions are suspected?

Answer: — Few common anti-hypertensives - and trimethoprim-sulfamethoxazole

Often ignored in the outpatient setting is the very low threshold of trimethoprim-sulfamethoxazole, popularly known as Bactrim, to cause hyperkalemia. Even without drug interaction, Trim-sulf can cause hyperkalemia, even in a conventional dose, though the risk is also dose-dependent. The trimethoprim component is responsible for hyperkalemia. Risk gets even higher if the patient is already on meds prone to cause hyperkalemia, like ACE inhibitors, ARBs, NSAIDs, beta-adrenergic blockers, or potassium-sparing diuretics. Also, obese people are at higher risk, as Trim-Sulf. is lipophilic. Plasma potassium concentration can change by a mean of 1.2 mEq/L within a week, even without any interaction or kidney impairment.

The mechanism of action is closure of the epithelial sodium channels in the collecting tubule. Also, note that ammonia production is inhibited in hyperkalemia, causing type 4 renal tubular acidosis (RTA).

Fortunately, all effects are reversible with discontinuation of the drug.

#pharmacology

References:

Velázquez H, Perazella MA, Wright FS, Ellison DH. Renal mechanism of trimethoprim-induced hyperkalemia. Ann Intern Med 1993; 119:296.

Perazella MA, Mahnensmith RL. Trimethoprim-sulfamethoxazole: hyperkalemia is an important complication regardless of dose. Clin Nephrol 1996; 46:187.

Weir MA, Juurlink DN, Gomes T, et al. Beta-blockers, trimethoprim-sulfamethoxazole, and the risk of hyperkalemia requiring hospitalization in the elderly: a nested case-control study. Clin J Am Soc Nephrol 2010; 5:1544.

Antoniou T, Gomes T, Juurlink DN, et al. Trimethoprim-sulfamethoxazole-induced hyperkalemia in patients receiving inhibitors of the renin-angiotensin system: a population-based study. Arch Intern Med 2010; 170:1045.

ESR in MAS/HLH

Q: Highly elevated Erythrocyte Sedimentation Rate (ESR) is expected in adults' Still's disease and Macrophage Activation Syndrome (MAS), and is a good biomarker to follow for the severity of the disease.

A) True

B) False

Answer: B

Contrary to what is expected, ESR in both adults' Still's disease and MAS is not a good biomarker. It may be even normal or lower than expected due to low or normal levels of haptoglobin and fibrinogen.

MAS is a subtype of hemophagocytic lymphohistiocytosis (HLH) and may occur in systemic rheumatic disease. It may occur in Still's disease, and is a leading cause of mortality. MAS and HLH are essentially hyperinflammatory states, commonly known as "cytokine storm," and are characterized by fever, hepatosplenomegaly, hyperferritinemia, hypertriglyceridemia, cytopenias, transaminitis, and CNS symptoms.

It is also proposed that MAS/HLH in Still's disease is likely due to infection in the setting of immunosuppression or to reactivation of latent viruses. 

#rheumatology

#immunology

References:

1. Wang R, Li T, Ye S, et al. Macrophage activation syndrome associated with adult-onset Still's disease: a multicenter retrospective analysis. Clin Rheumatol 2020; 39:2379.

2.Bae CB, Jung JY, Kim HA, Suh CH. Reactive hemophagocytic syndrome in adult-onset Still disease: clinical features, predictive factors, and prognosis in 21 patients. Medicine (Baltimore) 2015; 94:e451.

3. Javaux C, El-Jammal T, Neau PA, et al. Detection and Prediction of Macrophage Activation Syndrome in Still's Disease. J Clin Med 2021;11.

TXA in burn

Q: What is the 20:40 rule for the use of Tranexamic acid (TXA) in burn patients who require surgical excisions?

Answer: 

Evidence supports the use of TXA for patients who require burn wound excisions. It potentially reduces blood loss and transfusion requirements.

• Patients who require over 20% TBSA of burn wound excisions are usually given a gram bolus of TXA
• Patients who require over 40% TBSA of burn wound excisions are usually given a gram bolus of TXA, followed by a 1-gram drip over eight hours

Topical TXA, with or without epinephrine, can also be used during surgery, depending on the surgeon's preference.

*Total Body Surface Area

#burn

#surgical-critical-care

References:

1. Tapking C, Hundeshagen G, Kirchner M, Fischer S, Kneser U, Bliesener B. Tranexamic acid reduced blood transfusions in acute burn surgery: A retrospective case-controlled trial. Burns. 2022 May;48(3):522-528. doi: 10.1016/j.burns.2022.03.002. Epub 2022 Mar 16. PMID: 35339324.

2. Fijany AJ, Givechian KB, Zago I, et al. Tranexamic acid in burn surgery: A systematic review and meta-analysis. Burns 2023; 49:1249.

3. Hesamirostami M, Ramezanpour E, Asadpour-Sorkhkolaee H, Jamali A, Amini M, Moghaddam MR. The effect of tranexamic acid on blood loss after surgical excision in burn patients. Burns. 2025 Dec;51(9):107682. doi: 10.1016/j.burns.2025.107682. Epub 2025 Aug 25. PMID: 41109167.

Oral valganciclovir and ganciclovir

Q: Valganciclovir gets converted to ganciclovir in? - select one

A) Intestinal wall

B) Kidney

C) Vessel (endothelium)

D) Stomach (Gastric acid)

Answer: A

Valganciclovir is an L-valyl ester of ganciclovir. It is taken orally, represents a major advance in the treatment of cytomegalovirus (CMV) infection, and is widely favored over ganciclovir. It's absolute bioavailability as ganciclovir from valganciclovir tablets, when taken with food, is about 60 percent.

After oral administration, it is rapidly hydrolyzed to ganciclovir in the intestinal wall and liver.

#pharmacology

#ID

References:

1. Cvetković RS, Wellington K. Valganciclovir: a review of its use in the management of CMV infection and disease in immunocompromised patients. Drugs 2005; 65:859.

2. Curran M, Noble S. Valganciclovir. Drugs. 2001;61(8):1145-50 ; discussion 1151-2. doi: 10.2165/00003495-200161080-00013. PMID: 11465875.

3. Suganuma E, Sakata H, Adachi N, Asanuma S, Furuichi M, Uejima Y, Sato S, Abe T, Matsumoto D, Takahashi R, Yamamoto S, Kawano Y, Arai T, Oh-Ishi T. Efficacy, safety, and pharmacokinetics of oral valganciclovir in patients with congenital cytomegalovirus infection. J Infect Chemother. 2021 Feb;27(2):185-191. doi: 10.1016/j.jiac.2020.08.019. Epub 2020 Sep 6. PMID: 32907793.

Hydrocortisone and Mineralocorticoid activity

Q: What is the ratio of Mineralocorticoid: Glucocorticoid activity in hydrocortisone? - select one

A) 1:1

B) 1:2

C) 1:3

D) 1:4

Answer: A

Hydrocortisone continues to be the favored drug in ICUs for stress dose steroids in sepsis and other clinical situations where adrenal insufficiency is suspected. This is due to a 1:1 ratio of mineralocorticoid: glucocorticoid activity.

Dexamethasone has the least, rather negligible, mineralocorticoid activity.

#pharmacology

#endocrinology

References:

1. Ekman B, Quinkler M, Zhang P, Isidori AM, Murray RD, Wahlberg J; EU-AIR investigators. Mineralocorticoid effects of fludrocortisone and hydrocortisone in primary adrenal insufficiency: EU-AIR patient data. J Endocrinol Invest. 2025 Oct;48(10):2381-2392. doi: 10.1007/s40618-025-02657-7. Epub 2025 Sep 6. PMID: 40913682; PMCID: PMC12518465.

2. Venkatesh B, Cohen J. Hydrocortisone in Vasodilatory Shock. Crit Care Clin. 2019 Apr;35(2):263-275. doi: 10.1016/j.ccc.2018.11.005. Epub 2019 Jan 28. PMID: 30784608.

3. Sattar NA, Gaw A. Mineralocorticoid effects of high dose hydrocortisone. BMJ. 1995 Jul 22;311(6999):260. doi: 10.1136/bmj.311.6999.260b. PMID: 7627063; PMCID: PMC2550311.

Basophilic stippling

Q: Basophilic stippling can be seen in all of the following EXCEPT? - select one

A) Hb C / Hb SC disease

B) Thalassemia

C) Alcohol abuse

D) Lead poisoning

E) Hereditary pyrimidine 5'-nucleotidase deficiency

Answer: A

The objective of this question is to continue to emphasize the basic teachings learned in early medical school to apply at the bedside later as a clinician! The slide-preparation training in early lab classes in med school remains highly relevant in practice later on.

Basophilic stippling refers to blue granules of various sizes dispersed throughout the RBC cytoplasm. They are actually precipitated ribosomes. They can be seen in thalassemia, excess alcohol use, lead and heavy metal poisoning, and in hereditary pyrimidine 5'-nucleotidase deficiency.

Hb C disease or Hb SC disease usually has hemoglobin crystals, especially if the blood sample has become dehydrated before the peripheral smear is made. The crystals are usually hexagonal or rhomboid in shape.

#hematology

#pathology

References:

1. Munoz J, Guo Y. Basophilic stippling: a lead to the diagnosis. Blood. 2011 Nov 17;118(20):5370. doi: 10.1182/blood-2010-12-320911. Erratum in: Blood. 2014 Jan 9;123(2):302. PMID: 22204026.

2. Cheson BD, Rom WN, Webber RC. Basophilic stippling of red blood cells: a nonspecific finding of multiple etiology. Am J Ind Med. 1984;5(4):327-34. doi: 10.1002/ajim.4700050409. PMID: 6202140.

Antidepressant Discontinuation Syndrome

Q: Which of the following is usually not present in the antidepressant discontinuation syndrome? - select one

A) Chills without fever

B) Rhinorrhea

C) Electric shock-like sensations

D) Vivid dreams

E) Pupillary dilation

Answer: E

The antidepressant discontinuation syndrome may cause new-onset somatic and neuropsychiatric symptoms. Importantly, discontinuation symptoms differ from any adverse effects that occurred during active treatment with the antidepressant. These symptoms include:

• Dizziness
• Headache
• Insomnia
• Irritability
• Nausea/vomiting
• Agitation
• Anxiety
• Chills without fever (choice A)
• Diaphoresis
• Dysphoria
• Fatigue
• Lethargy
• Myalgias
• Rhinorrhea (choice B)
• Paresthesias
• Electric shock-like sensations (choice C)
• Tremor
• Vivid dreams (choice D)
• Anorexia 
• Loss of balance 
• Cognitive impairment
• Crying spells
• Dry mouth 
• Hypertension 
• Hypomania and mania
• Psychosis (with auditory and/or visual hallucinations
• Sexual dysfunction 
• Suicidal ideation
• Tinnitus 

Pupillary dilation occurs in opioid withdrawal but not in antidepressant discontinuation syndrome.

#psychiatry

#pharmacology

References:

1. Fornaro M, Cattaneo CI, De Berardis D, Ressico FV, Martinotti G, Vieta E. Antidepressant discontinuation syndrome: A state-of-the-art clinical review. Eur Neuropsychopharmacol. 2023 Jan;66:1-10. doi: 10.1016/j.euroneuro.2022.10.005. Epub 2022 Nov 4. PMID: 36345093.

2. Gabriel M, Sharma V. Antidepressant discontinuation syndrome. CMAJ. 2017 May 29;189(21):E747. doi: 10.1503/cmaj.160991. PMID: 28554948; PMCID: PMC5449237.

3. Kalfas M, Tsapekos D, Butler M, McCutcheon RA, Pillinger T, Strawbridge R, Bhat BB, Haddad PM, Cowen PJ, Howes OD, Joyce DW, Nutt DJ, Baldwin DS, Pariante CM, Lewis G, Young AH, Lewis G, Hayes JF, Jauhar S. Incidence and Nature of Antidepressant Discontinuation Symptoms: A Systematic Review and Meta-Analysis. JAMA Psychiatry. 2025 Sep 1;82(9):896-904. doi: 10.1001/jamapsychiatry.2025.1362. Erratum in: JAMA Psychiatry. 2025 Nov 1;82(11):1153. doi: 10.1001/jamapsychiatry.2025.2398. PMID: 40632531; PMCID: PMC12242823.

VQI prohibitive risk

Q: What is a prohibitive risk in vascular surgery?

Answer: Patients with high mortality where less invasive intervention is preferred 

There are a few risk calculators to estimate the risk of perioperative vascular morbidity and mortality. The updated guidelines from the Society for Vascular Surgery (SVS) endorse the use of a scoring system based on data from the Vascular Study Group of New England, part of the National Vascular Quality Initiative (VQI). 

Per the VQI risk calculator, there are four risk categories: low, moderate, high, and prohibitive.

There have been further sub-group categories, such as 

• Respiratory Risk Groups (RAE): Low, Intermediate-Low, Intermediate-High, and High.
• Cardiac Risk Index (VQI CRI): Predicts myocardial infarction based on pre-operative patient characteristics and procedure type (CEA, EVAR, INFRA, SUPRA, OAAA).
• Frailty Assessment (VQI-FS): Uses seven variables (CHF, renal impairment, COPD, non-home dwelling, non-ambulatory, anemia, underweight) to predict 9-month mortality.
• Adverse Outcomes Categories (General): Used in research, these include 1-year follow-up, 30-day mortality, composite perioperative adverse events, and 12-month mortality.

Calculators are available at: https://www.vqi.org/

#surgical-critical-care

References:

1. Chaikof EL, Dalman RL, Eskandari MK, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg 2018; 67:2.

2. Cronenwett JL, Kraiss LW, Cambria RP. The Society for Vascular Surgery Vascular Quality Initiative. J Vasc Surg. 2012 May;55(5):1529-37. doi: 10.1016/j.jvs.2012.03.016. PMID: 22542349.

3. Bertges DJ, Neal D, Schanzer A, Scali ST, Goodney PP, Eldrup-Jorgensen J, Cronenwett JL; Vascular Quality Initiative. The Vascular Quality Initiative Cardiac Risk Index for prediction of myocardial infarction after vascular surgery. J Vasc Surg. 2016 Nov;64(5):1411-1421.e4. doi: 10.1016/j.jvs.2016.04.045. Epub 2016 Jul 19. PMID: 27449347; PMCID: PMC5079798.

HILI and Causality Assessment Tools

Q: In case of suspected herb-induced liver injury (HILI), different causality assessment models may help in differential diagnosis of such products.

A) True

B) False

Answer: B

Different causality assessment models have been developed for the assessment of Drug-Induced Liver Injury (DILI), which include:

• Roussel Uclaf Causality Assessment Method (RUCAM)
• Drug-Induced Liver Injury Network (DILIN) Causality Scoring System 
• Maria and Victorino scale 
• Naranjo scale

Unfortunately, none provides a good assessment of HILI due to product variability and contamination.

HILI due to herbal and dietary supplements (HDS) requires the following elements to be satisfied:

• Exposure must precede the onset of liver injury* 
• Underlying liver disease should be excluded^
• Injury may improve when the HDS is stopped 

* Although the latent period is highly variable

^ In some cases, injury may initially worsen for days or weeks, and in cases of acute liver failure, declining liver biochemical tests may indicate deterioration rather than improvement

#hepatology

References:

Hayashi PH. Causality assessment in drug-induced liver injury. Semin Liver Dis 2009; 29:348.

Chalasani NP, Maddur H, Russo MW, et al. ACG Clinical Guideline: Diagnosis and Management of Idiosyncratic Drug-Induced Liver Injury. Am J Gastroenterol 2021; 116:878.

Hayashi PH, Lucena MI, Fontana RJ. RECAM: A New and Improved, Computerized Causality Assessment Tool for DILI Diagnosis. Am J Gastroenterol 2022; 117:1387.

St John's Wort and Clopidogrel

Q: 54 years old Asian male, recently discharged from the hospital after cardiac intervention due to an acute myocardial infarction, and on Dual Antiplatelet Therapy (DAPT), presented with severe upper GI bleed. Patient reports depressive mental health issue after his 'heart attack', and starts taking herbal medicines to feel better. Which widely used non-prescription drug should be suspected?

Answer: St. John's wort

The botanical name of St. John's Wort is Hypericum Perforatum. It is one of the most widely used herbal antidepressants worldwide. In the United States, an estimated 4.4 million adults are using it. It is particularly very popular in Eastern and Asian cultures. Frequently, its use goes unreported. 

St. John's wort increases the activity of clopidogrel by inducing CYP P450 enzymes, and can put patients at higher risk of bleeding. The objective of this question is to highlight patients' education on the risk of over-the-counter (OTC) and non-prescription herbal products when they are on life-saving drugs.

But here is the curveball: Some physicians use it in patients who are non-responders to clopidogrel to enhance its activity! The authors of this question would advise against such an adventure.

#pharmacology

#cardiology

References:

1. Monteiro MD, Dias ACP, Costa D, Almeida-Dias A, Criado MB. Hypericum perforatum and Its Potential Antiplatelet Effect. Healthcare (Basel). 2022 Sep 15;10(9):1774. doi: 10.3390/healthcare10091774. PMID: 36141386; PMCID: PMC9498564.

2. Trana C, Toth G, Wijns W, Barbato E. St. John's Wort in patients non-responders to clopidogrel undergoing percutaneous coronary intervention: a single-center randomized open-label trial (St. John's Trial). J Cardiovasc Transl Res. 2013 Jun;6(3):411-4. doi: 10.1007/s12265-013-9455-2. Epub 2013 Mar 6. PMID: 23463297.

3. Lau WC, Welch TD, Shields T, Rubenfire M, Tantry US, Gurbel PA. The effect of St John's Wort on the pharmacodynamic response of clopidogrel in hyporesponsive volunteers and patients: increased platelet inhibition by enhancement of CYP3A4 metabolic activity. J Cardiovasc Pharmacol. 2011 Jan;57(1):86-93. doi: 10.1097/FJC.0b013e3181ffe8d0. PMID: 20980920.

Trivia: St. John's wort plant is named after John the Baptist. The plant blooms around the feast of St. John the Baptist in late June.

Dexmedetomidine and Shivering

Q: Dexmedetomidine can __________ shivering. - Select one

A) exacerbate

B) suppress

Answer: B

Shivering is a common problem in the ICU, particularly post-op patients. Forced-air warming system (Bair Hugger), sedation, meperidine, and occasionally neuromuscular blocking agents (NMBAs) are used.

Dexmedetomidine is less commonly used for this indication, although it can effectively suppress shivering; the patient should be monitored for hypotension and bradycardia.

#surgical-critical-care

References:

1. Shokri M, Bakhtiari Z, Kargar B, Hajialigol A. The Effect of Intravenous Dexmedetomidine During Surgery in the Prevention of Shivering After General Anesthesia in Patients Undergoing Spinal Surgery: A Randomized Clinical Trial. Anesth Pain Med. 2025 May 18;15(2):e159077. doi: 10.5812/aapm-159077. PMID: 40717905; PMCID: PMC12297032.

2. Nesioonpour S, Bayat S, Ghomeishi A, Behaeen K, Savaie M, Ahmadzadeh A. Effect of Intravenous Dexmedetomidine on Shivering in Cesarean Section under Intrathecal Anesthesia: Randomized Clinical Trial. Anesth Pain Med. 2022 Jun 19;12(3):e122735. doi: 10.5812/aapm-122735. PMID: 36818484; PMCID: PMC9923329.

3. Callaway CW, Elmer J, Guyette FX, et al. Dexmedetomidine Reduces Shivering during Mild Hypothermia in Waking Subjects. PLoS One 2015; 10:e0129709.

Death Rattle

Q: An eye drop can help minimize the death rattle.

A) True

B) False

Answer: A

Patients in the end-of-life process lose their ability to clear oral secretions. As air moves over secretions that have pooled in the respiratory tract, the resulting turbulence produces noisy ventilation, known as a death rattle. This can be of great psychological distress to the family, though it does not usually affect the patient.

1% Atropine ophthalmic drops given sublingually can help to minimize the death rattle. The onset of action is about 30 minutes, and it can be given every 2 hours PRN.

Other treatments are:

• Scopolamine patch placed behind the ear once every three days
• Benadryl 25-100 mg every 4 to 6 hours PRN 
• Glycopyrrolate- 400 mcg SC every 8 hours PRN

#palliative-care

#end-of life-care

References:

1. McEvoy T. Atropine: Terminal Respiratory Secretions. Hosp Pharm. 2016 Jan;51(1):39-41. doi: 10.1310/hpj5101-39. Epub 2016 Jan 1. PMID: 38745721; PMCID: PMC11089618.

2. Shinjo T, Okada M. Atropine eyedrops for death rattle in a terminal cancer patient. J Palliat Med. 2013 Feb;16(2):212-3. doi: 10.1089/jpm.2011.0537. Epub 2012 Jun 29. PMID: 22747099.

3. Lokker ME, van Zuylen L, van der Rijt CC, van der Heide A. Prevalence, impact, and treatment of death rattle: a systematic review. J Pain Symptom Manage. 2014 Jan;47(1):105-22. doi: 10.1016/j.jpainsymman.2013.03.011. Epub 2013 Jun 18. PMID: 23790419.

A note on intermittent sigh in mechanical ventilation

Intermittent sigh is rarely used in the ICU during mechanical ventilation. In fact, many trainees do not even know about it! Also, not all ventilator brands can deliver intermittent sigh.

Intermittent sigh is a maneuver of delivering a deep breath once every few minutes. Theoretically, it was practiced under the assumption that it would maintain lung volume, avoid atelectasis, and improve lung compliance. After ARDS network trials showing that low tidal volumes (TV) are lung-protective, intermittent sigh eventually becomes obsolete, given that such high breaths, even once every few minutes or after 6-8 breaths, may cause volutrauma. 

But in 2021, Mauri T. et al. showed that it is at least not harmful and can be considered in selected patients with limited, controlled lower-volume. Oxygenation was improved, whereas tidal volume, respiratory rate, and corrected minute ventilation were lower over the first 7 days from randomization in the sigh vs no-sigh group. Though there was no significant difference in terms of mortality and ventilator-free days for the sigh vs no-sigh group. 

Albert RK et al. in 2023 reported a potentially favourable reduction in 28-day mortality. As a secondary outcome, patients randomized to sighs had 28-day mortality of 11.6% (30/259) vs 17.6% (46/261).

This may be an area still untapped in 'vent. management' and may need further exploration.

#Mechanical-ventilation

#pulmonary

References:

1. Mauri T, Foti G, Fornari C, et al. Sigh in Patients With Acute Hypoxemic Respiratory Failure and ARDS: The PROTECTION Pilot Randomized Clinical Trial. Chest 2021; 159:1426.

2. Albert RK, Jurkovich GJ, Connett J, et al. Sigh Ventilation in Patients With Trauma: The SiVent Randomized Clinical Trial. JAMA 2023; 330:1982.

'poor man test' for septic arthritis

Q: What is the 'poor man's test' for septic arthritis?

Answer: Measuring the strength of synovial fluid leukocyte esterase in the urine "dipstick" test

It is an art to practice Medicine in a resource-limited country(RLC)! Septic arthritis is more common in RLCs. 

Exotic tests like polymerase chain reaction (PCR) or matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectometry may not be available at many places. Aspirating synovial fluid and measuring the strength of synovial fluid leukocyte esterase using a simple urine "dipstick" test, usually available in units/wards, can guide a clinician in initiating antibiotics.

Ideally, synovial fluid and blood cultures x2 should be obtained before starting antibiotics, and synovial fluid should be sent for Gram stain, bacterial culture, white blood cell count with differential, and assessment of crystals (monosodium urate and calcium pyrophosphate crystal deposition) with a polarizing microscope.

Another tip is NOT to rely on synovial fluid glucose, lactate, or pH, as they are very unreliable in septic arthritis.

#ID

#procedures

References: 

1. Aslani H, Pasha Zanoosi MR, Navali AM. Urine Dipstick Leukocyte Esterase in the Rapid Diagnosis of Septic Arthritis. Arch Bone Jt Surg. 2022 Jan;10(1):38-44. doi: 10.22038/ABJS.2021.47573.2334. PMID: 35291247; PMCID: PMC8889425.

2. Mirghaderi P, Pahlevan-Fallahy MT, Mahmoudi J, Mortazavi SMJ. Determining the accuracy of the leukocyte esterase reagent strip test in the rapid diagnosis of adult septic arthritis. Adv Rheumatol. 2024 Aug 30;64(1):65. doi: 10.1186/s42358-024-00409-4. PMID: 39215379.

3. Dey M, Al-Attar M, Peruffo L, et al. Assessment and diagnosis of the acute hot joint: a systematic review and meta-analysis. Rheumatology (Oxford) 2023; 62:1740.

anisocoria

Case: A 22-year-old male is admitted to the ICU with exacerbation of asthma. The patient has been started on intravenous steroids and aerosolized bronchodilators. Medical student reports the finding of unilateral mydriasis (anisocoria).

Discussion: Pharmacologic pupillary changes are very common in the ICU. Commonly used drugs in the ICU may cause mydriasis. It occurs due to different drugs, either by stimulation of the sympathetic innervation of the dilator pupillae or inhibition of the parasympathetic innervation to the sphincter pupillae. These drugs include atropine, homatropine, phenylephrine, clonidine, and glycopyrrolate.

Aerosolized anticholinergic drugs (eg, ipratropium) administered through ventilator masks may produce unilateral mydriasis.

Pharmacologic mydriasis is, by definition, asymptomatic.

# ophthalmology

#pulmonary

#pharmacology

References:

1. Iosson N. Images in clinical medicine. Nebulizer-associated anisocoria. N Engl J Med 2006; 354:e8.

2. Lust K, Livingstone I. Nebulizer-induced anisocoria. Ann Intern Med 1998; 128:327.

3. Openshaw H. Unilateral mydriasis from ipratropium in transplant patients. Neurology 2006; 67:914.

SS in MDMA

Q: A 22-year-old female is admitted to the ICU with a clinical diagnosis of serotonin syndrome (SS) after being found having trismus and 'acting weird' at a dance club on Saturday night. Friends informed about ingesting 'ecstasy' prior to the party. Which concomitant drug is suspected to increase the risk of SS with ecstasy (MDMA)?

Answer: SSRI

Unfortunately, 3,4-methylenedioxymethamphetamine (MDMA), popularly known as ecstasy or Molly, is widely available in society. With the rise of use of Selective Serotonin Reuptake Inhibitors (SSRIs) in society, particularly among college-going students, the concurrent use of MDMA and SSRIs greatly increases the risk of SS. 

MDMA causes SS via stimulation of massive serotonin release. 

#toxicity

#pharmacology

References:

1. Mueller PD, Korey WS. Death by "ecstasy": the serotonin syndrome? Ann Emerg Med 1998; 32:377.

2. Singh AN, Catalan J. Rave drug (ecstasy) and selective serotonin reuptake inhibitor anti-depressants. Indian J Psychiatry. 2000 Apr;42(2):195-7. PMID: 21407935; PMCID: PMC2957712.

3. Dobry Y, Rice T, Sher L. Ecstasy use and serotonin syndrome: a neglected danger to adolescents and young adults prescribed selective serotonin reuptake inhibitors. Int J Adolesc Med Health. 2013;25(3):193-9. doi: 10.1515/ijamh-2013-0052. PMID: 24006318.

NSF and kidney

Q: Patients with a history of a kidney transplant are at risk for nephrogenic systemic fibrosis (NSF) when exposed to gadolinium-based contrast agents (GBCA).

A) True

B) False

Answer: B

Although NSF is a true dreaded complication of GBCA, in various ways, it has been blown out of proportion in clinical practice. Deciding to have GBCA during MRI for patients with kidney dysfunction is always based on clinical judgement for risks vs benefits. Few patients are definitely at high risk and require a nephrologist's consent. In descending order, risk is highest in:

• End-stage kidney disease (ESRD) patients on dialysis of any type
• Acute kidney injury (AKI) 
• eGFR less than 30 mL/min per 1.73 m2

One important point that is often missed is that although a single dose of GBCA can induce NSF, it's usually multiple, cumulative, or higher-than-usual doses of GBCA that are responsible for NSF.

Prior kidney transplant, hepatorenal syndrome, perioperative liver transplantation, exposure to lanthanum carbonate, high-dose erythropoietin treatment, metabolic acidosis, proinflammatory conditions, and elevated iron or phosphate levels were proposed in the past as risk factors for NSF but were found to be unproven.

#nephrology

#radiology

#dermatology

References:

1. Shabana WM, Cohan RH, Ellis JH, et al. Nephrogenic systemic fibrosis: a report of 29 cases. AJR Am J Roentgenol 2008; 190:736.

2. Prince MR, Zhang HL, Roditi GH, et al. Risk factors for NSF: a literature review. J Magn Reson Imaging 2009; 30:1298.

3. Abu-Alfa AK. Nephrogenic systemic fibrosis and gadolinium-based contrast agents. Adv Chronic Kidney Dis 2011; 18:188.

4. Malikova H. Nephrogenic systemic fibrosis: the end of the story? Quant Imaging Med Surg. 2019 Aug;9(8):1470-1474. doi: 10.21037/qims.2019.07.11. PMID: 31559176; PMCID: PMC6732068.

DD in alcohol poisoning

Q: 34 years old patient presents with known ingested alcohol at home. Which of the following toxins may cause cranial nerve palsies and tetany? - select one

A) Ethylene glycol 

B) Methanol 

Answer: A

There is usually no luxury of time in initiating alcohol management. History and clinical exam play a vital role in determining the actual type of alcohol toxicity, particularly if sophisticated, reliable, or fast labs are not available, like in free-standing Emergency Rooms (ERs) and Urgent Cares. 

Cranial nerve palsies and tetany are almost exclusively limited to ethylene glycol toxicity and occur due to oxalate-induced hypocalcemia.

Similarly, an afferent pupillary defect is almost always due to advanced methanol poisoning and demonstrates mydriasis, a retinal sheen (a glossy or metallic reflex) due to retinal edema, and hyperemia of the optic disk.

#toxicity

#physical-exam

#differential-diagnosis

References:

1. Cohen ET, Su MK, Biary R, Hoffman RS. Distinguishing between toxic alcohol ingestion vs alcoholic ketoacidosis: how can we tell the difference? Clin Toxicol (Phila). 2021 Aug;59(8):715-720. doi: 10.1080/15563650.2020.1865542. Epub 2021 Jan 21. PMID: 33475435.

2. Leth PM, Gregersen M. Ethylene glycol poisoning. Forensic Sci Int. 2005 Dec 20;155(2-3):179-84. doi: 10.1016/j.forsciint.2004.11.012. Epub 2005 Jan 21. PMID: 16226155.

3. Alrashed M, Aldeghaither NS, Almutairi SY, Almutairi M, Alghamdi A, Alqahtani T, Almojathel GH, Alnassar NA, Alghadeer SM, Alshehri A, Alnuhait M, Almohammed OA. The Perils of Methanol Exposure: Insights into Toxicity and Clinical Management. Toxics. 2024 Dec 20;12(12):924. doi: 10.3390/toxics12120924. PMID: 39771139; PMCID: PMC11728796.

Cutaneous Lesions

 

Steroids and KS

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

A) exacerbates

B) suppresses 

Answer: A

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

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

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

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

#ID

References:

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

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

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

Proper handling of SV fluid analysis

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

Answer: Talc-free gloves

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

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

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

#rheumatology

#pathology

References:

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

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

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

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

Attrition Bias

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

Answer: 20%

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

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

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

#statistics

References:

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

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

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

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

In mitral valve IE

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

A) Anterior

B) Posterior

Answer: A

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

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

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

#surgical-critical-care

#cardiology

#ID

References:

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

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

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

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

Nephrotoxins in AKI

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

A) Angiotensin-converting enzyme (ACE) inhibitors

B) Sodium-glucose cotransporter 2 (SGLT2) inhibitors

C) Both A and B

Answer: C

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

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

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

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

#nephrology

#pharmacology

#endocrinology

References:

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

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

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

SUP in head trauma

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

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

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

# neurosurgery

#GI

#patient-safety

References:

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

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

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

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

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