SQ unf-Heparin in pregnancy

Case: 32-year-old newly pregnant patient admitted to the ICU with Pulmonary Embolism, and now getting discharged. The clinician decided to keep her on unfractionated heparin with a dose of 5000 units every 12 hours. As the pregnancy progresses, the dose of unfractionated heparin should be increased proportionally.

A) True

B) False

Answer: A

The unfractionated heparin dose should be increased as pregnancy progresses, as Heparin prescription is weight-based. A general rule of thumb is every 12 hours dose of:

• 5000 to 7500 units in the first trimester
• 7500 to 10,000 units in the second trimester
• 10,000 units in the third trimester

That said, clinical judgment and close monitoring of bleeding risks are required.

#ob-gyn

#hematology

References:

1. American College of Obstetricians and Gynecologists' Committee on Practice Bulletins—Obstetrics. ACOG Practice Bulletin No. 196: Thromboembolism in Pregnancy. Obstet Gynecol 2018; 132:e1. Reaffirmed 2022.

2. Barbour LA. Current concepts of anticoagulant therapy in pregnancy. Obstet Gynecol Clin North Am 1997; 24:499.

3. Mok T, Nguyen AV, Kwan L, et al. Prophylactic Unfractionated Heparin in Antepartum Hospitalizations: A Randomized Controlled Trial. Obstet Gynecol 2024; 144:118.

Bromocriptine treatment in PPCM

Q: The cardiology team decided to start Bromocriptine for a postpartum cardiomyopathy patient. Which one other intervention should be considered with bromocriptine?

Answer: Anticoagulation

Although bromocriptine or antiprolactin therapy is not yet a standard of care in PPCM, many experts have used it based on clinical judgment, on the premise that prolactin potentiates PPCM. So far, the evidence is very weak, though.

Bromocriptine is thrombogenic, and anticoagulation is warranted.

The recommended dose is 2.5 mg once daily for at least one week in uncomplicated cases. In those with LVEF less than 25 percent and/or in shock, 2.5 mg twice daily for two weeks, then 2.5 mg once daily for six weeks. It may also improve right ventricular function.

Cabergoline can be substituted if bromocriptine is not available.

#cardiology

#pharmacology

References:

1. Hilfiker-Kleiner D, Haghikia A, Berliner D, et al. Bromocriptine for the treatment of peripartum cardiomyopathy: a multicentre randomized study. Eur Heart J 2017; 38:2671.

2. van der Meer P, van Essen BJ, Viljoen C, et al. Bromocriptine treatment and outcomes in peripartum cardiomyopathy: the EORP PPCM registry. Eur Heart J 2025; 46:1017.

3. Attachaipanich T, Attachaipanich S, Kaewboot K. Efficacy and safety of bromocriptine in peripartum cardiomyopathy: A systematic review and meta-analysis. Int J Cardiol 2025; 427:133105.

4. Tremblay-Gravel M, Marquis-Gravel G, Avram R, et al. The effect of bromocriptine on left ventricular functional recovery in peripartum cardiomyopathy: insights from the BRO-HF retrospective cohort study. ESC Heart Fail 2019; 6:27.

5. Haghikia A, Schwab J, Vogel-Claussen J, et al. Bromocriptine treatment in patients with peripartum cardiomyopathy and right ventricular dysfunction. Clin Res Cardiol 2019; 108:290.

6. Maurel C, Abhay K, Schaeffer A, Lange F, Castot A, Melon E. Acute thrombotic accident in the postpartum period in a patient receiving bromocriptine. Crit Care Med. 1990 Oct;18(10):1180-1. doi: 10.1097/00003246-199010000-00026. PMID: 2209050.

Clinical exam in acute opioid toxicity

Q: Which of the following is a more reliable sign of acute opioid toxicity? - select one

A) Depressed mental status

B) Decreased respiratory rate

C) Miotic pupils

Answer: B

In acute opioid toxicity, pupils are expected to be constricted, but they can be normal or even larger. It also depends on the type of opioid, like meperidine, overdose tends to present with normal pupils. The co-ingestion of sympathomimetics or antimuscarinics can cause pupils to be larger on exam. In comparison, a decreased respiratory rate of less than 12 by manual counting on the best side is a better toxicity of acute opioid toxicity.

Bradycardia or hypotension from histamine release may occur, but it can't predict opioid toxicity unless the history is very clear. Similarly, normal capnography or hypothermia should not be relied on too much.

Mental status can range from coma to euphoria. The occurrence of a seizure should raise the possibility of tapentadol, tramadol, or meperidine overdose.

Hypoxia and traumatic brain injury (TBI) can be the cause, result, or simultaneously occurring features and require prompt address.

#toxicity

References:

1. Fahmy NR, Sunder N, Soter NA. Role of histamine in the hemodynamic and plasma catecholamine responses to morphine. Clin Pharmacol Ther 1983; 33:615.

3. Viglino D, Bourez D, Collomb-Muret R, et al. Noninvasive End Tidal CO2 Is Unhelpful in the Prediction of Complications in Deliberate Drug Poisoning. Ann Emerg Med 2016; 68:62.

4. Palkovic B, Marchenko V, Zuperku EJ, Stuth EAE, Stucke AG. Multi-Level Regulation of Opioid-Induced Respiratory Depression. Physiology (Bethesda). 2020 Nov 1;35(6):391-404. doi: 10.1152/physiol.00015.2020. PMID: 33052772; PMCID: PMC7864237.

COPD - cardinal symptoms

Q: The presence of two out of three cardinal symptoms of COPD exacerbation helps to justify? - select one

A) Start antibiotics

B) Admit to hospital

C) Start IV steroids

D) Order chest X-ray

E) perform bronchoscopy

Answer: A

The three cardinal symptoms of COPD exacerbation are:

• Increased dyspnea
• Increased sputum volume/viscosity
• Increased sputum purulence

The presence of 2 out of 3 cardinal symptoms is a clinical indication for empiric antibiotic therapy; otherwise, antibiotics can be held off to balance the fine line between minimizing resistance and stewardship. The only other justification for starting antibiotics is radiographic or microbiologic evidence of pulmonary infection. That said, antibiotic initiation in COPD exacerbations remains a clinical decision based on the clinician's judgment. Various algorithms and guidelines have been described.

Admitting to the hospital (choice B) depends on the severity and clinical deterioration of the symptoms. Oral steroids and IV steroids (choice C) usually have similar efficacy. Getting C-X-ray (choice D) or performing 'bronch' (choice E) depends solely on the indications and suspicion of infections.

#pulmonary

#stewardship

References:

1. Sethi S, Murphy TF. Acute exacerbations of chronic bronchitis: New developments concerning microbiology and pathophysiology--impact on approaches to risk stratification and therapy. Infect Dis Clin N Am 2004; 18:861.

2. Vollenweider DJ, Frei A, Steurer-Stey CA, Garcia-Aymerich J, Puhan MA. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2018 Oct 29;10(10):CD010257. doi: 10.1002/14651858.CD010257.pub2. PMID: 30371937; PMCID: PMC6517133.

3. Balser E, Neher JO, Safranek S, Taraday J. Clinical inquiries: When are antibiotics indicated for acute COPD exacerbations? J Fam Pract. 2006 Dec;55(12):1079-80. PMID: 17137546.

4. Laue J, Reierth E, Melbye H. When should acute exacerbations of COPD be treated with systemic corticosteroids and antibiotics in primary care: a systematic review of current COPD guidelines. NPJ Prim Care Respir Med. 2015 Feb 19;25:15002. doi: 10.1038/npjpcrm.2015.2. PMID: 25695630; PMCID: PMC4373494.

Acidic PH of pleural fluid

Q: All of the following pathologies will cause pleural fluid acidosis EXCEPT? - select one

A) Malignancy

B) Tuberculosis

C) Urinothorax 

D) Misplaced central line

E) urease-splitting organisms 

Answer: E

Pleural effusion analysis remains an integral part of the differential diagnosis in most of the pulmonary pathologies with pleural effusion. Identifying the pH of pleural fluid is a valuable way to narrow down the cause of the underlying disease. Pleural fluid acidosis, particularly if combined with low glucose, is a given complicated parapneumonic pleural effusion or empyema, proven otherwise, EXCEPT for urease-splitting organisms such as Proteus species, which usually cause a spuriously elevated pleural PH.

The other causes of acidic pleural effusion are all the other choices in the question, i.e., malignancy, tuberculosis, urinothorax, misplaced central venous catheter infusing isotonic saline, along with rheumatoid pleuritis and lupus pleuritis.

Putting pleural fluid analysis in context with the history and other findings almost always led clinicians to the right diagnosis.

#procedures

#pulmonary

#laboratory-analysis

References:

1. Pine JR, Hollman JL. Elevated pleural fluid pH in Proteus mirabilis empyema. Chest 1983; 84:109.

2. Sahn SA. State of the art. The pleura. Am Rev Respir Dis 1988; 138:184.

3. Houston MC. Pleural fluid pH: diagnostic, therapeutic, and prognostic value. Am J Surg. 1987 Sep;154(3):333-7. doi: 10.1016/0002-9610(89)90623-5. PMID: 3307471.

4. Bowmaster SM, Merrill AE, Manning NL, Wilson JS, Gross TJ. Improving Pleural Fluid pH Accuracy: A Quality Improvement Initiative. J Appl Lab Med. 2025 Nov 4;10(6):1593-1599. doi: 10.1093/jalm/jfaf118. PMID: 40891251.

Abdominal pain with bowel wall edema

Q: A 68-year-old male whose blood pressure medicines have recently been changed presented to the Emergency Room with severe colicky abdominal pain associated with nausea and vomiting. CT of the abdomen showed bowel wall edema. Acute care surgery was consulted for possible "ex-lap", but the only advice offered was to discontinue his home BP medicine. Which anti-hypertensive is highly suspected? - Select one

A) ACE inhibitor

B) Beta-Blocker

C) Calcium Channel Blocker 

D) Diuretic (Furosemide)

E) Vasodilator (hydralazine)

Answer: A

The objective of this question is to emphasize that well-known angioedema associated with ACE-I is not limited to the face, lips, mouth, throat, larynx, uvula, but also the extremities, genitalia, and bowel wall are also common. Appearance of bowel wall edema on abdominal computed tomography (CT) or ultrasound, including in POCUS, when combined with history and symptoms, can avoid undue further workup or even unneeded "exploratory laparotomy". Elderly patients are more prone to bowel wall angioedema.

#surgical-critical-care

#GI

#pharmacology

References:

1. Dobbels P, Van Overbeke L, Vanbeckevoort D, Hiele M. Acute abdomen due to intestinal angioedema induced by ACE inhibitors: not so rare? Acta Gastroenterol Belg 2009; 72:455.

2. Chase MP, Fiarman GS, Scholz FJ, MacDermott RP. Angioedema of the small bowel due to an angiotensin-converting enzyme inhibitor. J Clin Gastroenterol 2000; 31:254.

3. Arakawa M, Murata Y, Rikimaru Y, Sasaki Y. Drug-induced isolated visceral angioneurotic edema. Intern Med 2005; 44:975.

Meatal Care and CAUTI

Q: In the ICU, using antibacterial urethral lubricants at the meatal site prevents catheter-related urinary tract infections (CAUTIs).

A) True

B) False

Answer: B

Applying disinfectants or antibacterial urethral lubricants at the meatal site does not prevent CAUTI and may instead lead to the development of resistant bacteria at the meatus. Cleansing the peri-urethral area with soap and water during daily bathing is adequate to prevent CAUTI.

#ID

#ICU-care

References:

1. Koskeroglu N, Durmaz G, Bahar M, et al. The role of meatal disinfection in preventing catheter-related bacteriuria in an intensive care unit: a pilot study in Turkey. J Hosp Infect 2004; 56:236.

2. Willson M, Wilde M, Webb ML, et al. Nursing interventions to reduce the risk of catheter-associated urinary tract infection: part 2: staff education, monitoring, and care techniques. J Wound Ostomy Continence Nurs 2009; 36:137.

3. . Classen DC, Larsen RA, Burke JP, et al. Daily meatal care for prevention of catheter-associated bacteriuria: results using frequent applications of polyantibiotic cream. Infect Control Hosp Epidemiol 1991; 12:157.

Systemic endotoxins and mastication

Q: Mastication ____________ the release of bacterial endotoxins of oral origin into the bloodstream. (select one)

A) decreases

B) increases

Answer: B

Oral health is highly associated with cardiovascular and cerebrovascular risk, with a hazard ratio of 2.12 in men less than 60 years of age, even after adjustment for known cardiovascular disease risk factors. Chronic periodontitis with radiographic bone loss is a significant risk factor.

The probable mechanism is chronic systemic inflammation. Interestingly, mastication has shown intermittent bacteremia and release of bacterial endotoxins of oral origin into the bloodstream, particularly in patients with poor oral health.

#dental

#cardiology

References: 

1. Chen F, Song Y, Li W, et al. Association between periodontitis and mortality of patients with cardiovascular diseases: A cohort study based on NHANES. J Periodontol 2024; 95:175.

2. Petrenya N, Hopstock LA, Holde GE, et al. Relationship between periodontitis and risk of cardiovascular disease: Insights from the Tromsø Study. J Periodontol 2022; 93:1353.

3. Geerts SO, Nys M, De MP, et al. Systemic release of endotoxins induced by gentle mastication: association with periodontitis severity. J Periodontol 2002; 73:73.

Ketamine-induced sclerosing cholangitis

Case: 72-year-old male ventilated in ICU after severe community-acquired pneumonia has been sedated on Ketamine infusion. On the fifth day of infusion, the patient's alkaline phosphatase is markedly elevated, and a liver ultrasound is negative for calculi or acalculous cholecystitis. What's the probable diagnosis?

Answer: Ketamine induced sclerosing cholangitis

In the last few years, ketamine has become widely popular in ICUs as a sedative agent. Less appreciated is ketamine induced sclerosing cholangitis and liver injury, particularly in ventilated patients who may require prolonged sedation, as it appears to be a dose-dependent effect. Ketamine infusion may be associated with sclerosing cholangitis, jaundice, decompensated cirrhosis, and even fatal acute liver failure (ALF).

#toxicity

#pharmacology

References:

1. Keta-Cov research group. Electronic address: vincent.mallet@aphp.fr, Keta-Cov research group. Intravenous ketamine and progressive cholangiopathy in COVID-19 patients. J Hepatol 2021; 74:1243.

2. de Tymowski C, Dépret F, Dudoignon E, et al. Ketamine-induced cholangiopathy in ARDS patients. Intensive Care Med 2021; 47:1173.

3. Vanrusselt A, Nijs J, Van den Bergh L, Schoofs N, Smets S, Strybol D, Rappaport A. Ketamine-induced sclerosing cholangitis: a case series. Acta Gastroenterol Belg. 2025 Jul-Sep;88(3):271-276. doi: 10.51821/88.3.13914. PMID: 41083171.

feeding in prone position

Q: Patients should not be fed in prone positioning, and tube feeding should be stopped.

A) True

B) False

Answer: B

Conventionally, it was thought that in the prone position, the chances of aspiration or emesis go high, but tube feeding in the prone position is safe, particularly if placed post-pyloric. The only precaution needed is to keep the patient's head in a slightly elevated position (about 25 degrees). 

Said that high residual volumes should be monitored. Adjuvant use of Prokinetic agents (like erythromycin) is helpful.

#nutrition

#pulmonary

References:

1. Reignier J, Thenoz-Jost N, Fiancette M, et al. Early enteral nutrition in mechanically ventilated patients in the prone position. Crit Care Med 2004; 32:94.

2. Saez de la Fuente I, Saez de la Fuente J, Quintana Estelles MD, et al. Enteral Nutrition in Patients Receiving Mechanical Ventilation in a Prone Position. JPEN J Parenter Enteral Nutr 2016; 40:250.

3. Reignier J, Dimet J, Martin-Lefevre L, et al. Before-after study of a standardized ICU protocol for early enteral feeding in patients turned in the prone position. Clin Nutr 2010; 29:210.

4. Linn DD, Beckett RD, Foellinger K. Administration of enteral nutrition to adult patients in the prone position. Intensive Crit Care Nurs 2015; 31:38.

absolute contraindications for laparoscopic cholecystectomy.

Q: Advanced cirrhosis with portal hypertension is an absolute contraindication for laparoscopic cholecystectomy.

A) True

B) False

Answer: B

The objective of this question is to emphasize that there are very absolute contraindications to laparoscopic cholecystectomy 

• Inability to tolerate general anesthesia
• Peritonitis with hemodynamic compromise
• Refractory coagulopathy 

Previous extensive abdominal surgery, advanced cirrhosis with portal hypertension, active cholangitis, CHF, or compromised respiratory status - all are relative contraindications. Although it should be kept in mind that patients with poor reserve may not tolerate pneumoperitoneum and may have a higher likelihood of conversion to open operation.

#surgical-critical-care

#GI

References:

1. Keus F, Broeders IA, van Laarhoven CJ. Gallstone disease: Surgical aspects of symptomatic cholecystolithiasis and acute cholecystitis. Best Pract Res Clin Gastroenterol 2006; 20:1031.

2. Chin X, Mallika Arachchige S, Orbell-Smith J, Wysocki AP. Preoperative and Intraoperative Risk Factors for Conversion of Laparoscopic Cholecystectomy to Open Cholecystectomy: A Systematic Review of 30 Studies. Cureus 2023; 15:e47774.

3. Nathaniel J Soper, Preeti Malladi - Laparoscopic cholecystectomy - https://www.uptodate.com/contents/laparoscopic-cholecystectomy (last access: March 30, 2026) UpToDate®

Chiari and Chiari-like Malformations

Q: Chiari malformations by definition is _________________ displacement of the cerebellum. - select one

A) downward 

B) upward

Answer: A

Chiari malformations are a heterogeneous group of disorders characterized by anatomic anomalies of the cerebellum, brainstem, and craniocervical junction, with downward displacement of the cerebellum, either alone or with the lower medulla, into the spinal canal.

#neurology

# neurosurgery

References:

1. Sarnat HB. Disorders of segmentation of the neural tube: Chiari malformations. Handb Clin Neurol 2008; 87:89.

2. Schijman E. History, anatomic forms, and pathogenesis of Chiari I malformations. Childs Nerv Syst 2004; 20:323.

3. Sahuquillo J, Moncho D, Ferré A, López-Bermeo D, Sahuquillo-Muxi A, Poca MA. A Critical Update of the Classification of Chiari and Chiari-like Malformations. J Clin Med. 2023 Jul 11;12(14):4626. doi: 10.3390/jcm12144626. PMID: 37510741; PMCID: PMC10380265.

'Livedo reticularis' and 'livedo racemosa'

Q: What's the difference between 'Livedo reticularis' and 'Livedo racemosa'?

Answer: Although Livedo reticularis and Livedo racemosa have been used interchangeably, technically, there is a subtle difference between them. Both have a violaceous mottling or reticular pattern of the skin of the extremities, mostly legs, and usually with circles.

• In Livedo reticularis – the circles are usually unbroken
• In Livedo racemosa - the circles are usually broken

Livedo reticularis can be seen in many clinical situations, such as Raynaud's phenomenon and cold exposure. The finding is benign and reversible with rewarming. 

Livedo racemosa (though commonly referred to as livedo reticularis) occurs in vasculitis, occlusive vascular disease (athero-emboli or thrombosis), or antiphospholipid syndrome (APS). This can be a sign of an underlying devastating clinical process.

#rheumatology

#clinical-exam

References:

1. Choi E, Henkin S. Raynaud's phenomenon and related vasospastic disorders. Vasc Med 2021; 26:56.

2. Uthman IW, Khamashta MA. Livedo racemosa: a striking dermatological sign for the antiphospholipid syndrome. J Rheumatol 2006; 33:2379.

3. Sajjan VV, Lunge S, Swamy MB, Pandit AM. Livedo reticularis: A review of the literature. Indian Dermatol Online J. 2015 Sep-Oct;6(5):315-21. doi: 10.4103/2229-5178.164493. PMID: 26500860; PMCID: PMC4594389.

4. Pincelli MS, Echavarria AMJ, Criado PR, Marques GF, Morita TCAB, Valente NYS, de Carvalho JF. Livedo Racemosa: Clinical, Laboratory, and Histopathological Findings in 33 Patients. Int J Low Extrem Wounds. 2021 Mar;20(1):22-28. doi: 10.1177/1534734619896938. Epub 2020 Jan 29. PMID: 31996060.

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.