Tuesday, November 30, 2021

anticoagulation after WATCHMAN device

Q; 64 years old male with a longstanding history of atrial fibrillation is admitted to ICU after WATCHMAN DEVICE implantation. Patient anticoagulation should be stopped onwards? 

A) True 

B) False 


 WATCHMAN device is a percutaneous closure of Left Atrial Appendage (LAA). It is advisable to continue anticoagulation for 6 weeks after the procedure with either warfarin (keeping INR 2-3) or direct oral anticoagulant (DOAC) plus daily aspirin (81 or 325 mg). 

If patient can't tolerate anticoagulation dual antiplatelet therapy (DAPT) should be kept on for one-six months (as per the clinician's discretion). Afterward, a patient can be managed only on daily aspirin. 

 It would be prudent to let the cardiology service manage the anticoagulation.



1. Pacha HM, Hritani R, Alraies MC. Antithrombotic Therapy After Percutaneous Left Atrial Appendage Occlusion Using the WATCHMAN Device. Ochsner J. 2018;18(3):193-194. doi:10.31486/toj.18.0012 

2. Bergmann MW, Betts TR, Sievert H, Schmidt B, Pokushalov E, Kische S, Schmitz T, Meincke F, Stein KM, Boersma LVA, Ince H. Safety and efficacy of early anticoagulation drug regimens after WATCHMAN left atrial appendage closure: three-month data from the EWOLUTION prospective, multicentre, monitored international WATCHMAN LAA closure registry. EuroIntervention. 2017 Sep 20;13(7):877-884. doi: 10.4244/EIJ-D-17-00042. PMID: 28606886.

3. Enomoto Y and et. al. Use of non-warfarin oral anticoagulants instead of warfarin during left atrial appendage closure with the Watchman device. Heart Rhythm. 2017 Jan;14(1):19-24. doi: 10.1016/j.hrthm.2016.10.020. Epub 2016 Oct 19. PMID: 27771552.

Monday, November 29, 2021

Edinburgh Depression Scale

 Q: 34 years old female with no significant past medical history is admitted to ICU with severe depression and suicidal ideation. Psychiatry service is called and details are given. Consultant asked you to obtain Edinburgh Depression Scale till they see the patient. In which particular situation Edinburgh Depression Scale is applied? (select one) 

A) death of a loved one

B) postnatal 

C) recent diagnosis of cancer 

D) unexpected divorce 

E) unexpected death of a living child 

 Answer: B

Edinburgh Depression Postnatal Scale (EDPS) is an easy 10 items questionnaire. It is particularly designed to determine the severity of disease in postnatal period. In doubtful cases, it may be repeated in 2 weeks. The maximum possible score is 30. The score of 20 shifts the severity to a severe zone. Obstetric complications such as fetal loss, postpartum hemorrhage, or low fetal birth weight may play a part. 

Caution: This scale is not meant for mothers with anxiety neuroses, phobias, or personality disorders. 

Scale is freely available on search engines: 


Authors request that: "Users may reproduce the scale without further permission providing they respect copyright by quoting the names of the authors, the title and the source of the paper in all reproduced copies."




1. Cox, J.L., Holden, J.M., and Sagovsky, R. 1987. Detection of postnatal depression: Development of the 10-item Edinburgh Postnatal Depression Scale. British Journal of Psychiatry 150:782-786 . 

2. K. L. Wisner, B. L. Parry, C. M. Piontek, Postpartum Depression N Engl J Med vol. 347, No 3, July 18, 2002, 194-199

Sunday, November 28, 2021


 Q: What are the two evaluations in the diagnosis of pulmonary embolism (PE) with bedside focus cardiac ultrasound (FoCUS)? 

Answer: Point Of Care Ultrasound (POCUS) and Focus Cardiac Ultrasound (FoCUS) has now become a standard of care in ICU management.

If the following two are demonstrated simultaneously on a patient, it almost confirms the diagnosis of PE:

  • ratio of the size of Right Ventricle (RV) and Left Ventricle (LV) more than 1:1 
  • a floating thrombus in the RA, RV, or a clot in transit
FoCUS has a good negative value in the assessment of PE. Other parameters which are looked into assessing PE are McConnell's sign, septal flattening, tricuspid regurgitation (TR), and tricuspid annular plane systolic excursion. 



1. Daley JI, Dwyer KH, Grunwald Z, Shaw DL, Stone MB, Schick A, Vrablik M, Kennedy Hall M, Hall J, Liteplo AS, Haney RM, Hun N, Liu R, Moore CL. Increased Sensitivity of Focused Cardiac Ultrasound for Pulmonary Embolism in Emergency Department Patients With Abnormal Vital Signs. Acad Emerg Med. 2019 Nov;26(11):1211-1220. doi: 10.1111/acem.13774. Epub 2019 Sep 27. PMID: 31562679.

2. Taylor RA, Davis J, Liu R, Gupta V, Dziura J, Moore CL. Point-of-care focused cardiac ultrasound for prediction of pulmonary embolism adverse outcomes. J Emerg Med. 2013 Sep;45(3):392-9. doi: 10.1016/j.jemermed.2013.04.014. Epub 2013 Jul 2. PMID: 23827166.

Saturday, November 27, 2021

Vesicular lesion at the tip of the nose

 Q; 52 years old male with history of renal insufficiency is recovering in ICU from community-acquired pneumonia. The patient develops zoster-like vesicular lesion at the tip and side of the nose. What's the underlying danger? 

Answer: Herpes zoster ophthalmicus (HZO) 

It is called Hutchinson's sign. Vesicular lesion at the tip or the side of nose highly correlates with involvement of the eye. This represents involvement of the nasociliary branch of ophthalmic division of trigeminal nerve, which innervates the globe of the eye. 

HZO is an ophthalmic emergency as it can threaten vision. It may be associated with hyperemic conjunctivitis, uveitis, episcleritis, or keratitis.



1. Tomkinson A, Roblin DG, Brown MJ. Hutchinson's sign and its importance in rhinology. Rhinology 1995; 33:180. 

2. Zaal MJ, Völker-Dieben HJ, D'Amaro J. Prognostic value of Hutchinson's sign in acute herpes zoster ophthalmicus. Graefes Arch Clin Exp Ophthalmol 2003; 241:187. 

3. Liesegang TJ. Herpes zoster ophthalmicus natural history, risk factors, clinical presentation, and morbidity. Ophthalmology 2008; 115:S3. 

4. Szeto SK, Chan TC, Wong RL, et al. Prevalence of Ocular Manifestations and Visual Outcomes in Patients With Herpes Zoster Ophthalmicus. Cornea 2017; 36:338.

Friday, November 26, 2021


 Q: At what level of International Normalized Ratio (INR), it would be prudent to add stress ulcer prophylaxis (SUP) in ICU patients? (select one)

A) > 1.5

B) > 2.0

Answer: A

There is a long list of risk factors which cause stress induced gastrointestinal (GI) bleed in ICU patients. Coagulopathy is high on the list. SUP is advisable if platelet count is less than 50,000/m3, INR above 1.5, or a partial thromboplastin time (PTT) > 2 times the control. 

Other major risk factors (but not limited to) are: 
  • Mechanical ventilation for more than 48 hours
  • Septic shock 
  • Renal failure (including CRRT)
  • Liver failure
  • History of peptic ulcer with H.Pylori -or history upper GI bleed
  • ECMO
  • Trauma
  • Burns (mostly over 35% of TBSA)  
  • Organ transplant
  • Anti-platelet drugs or drugs prone to cause GI bleed like NSAIDs
  • Steroids 



1. Cook DJ, Fuller HD, Guyatt GH, et al. Risk factors for gastrointestinal bleeding in critically ill patients. Canadian Critical Care Trials Group. N Engl J Med 1994; 330:377.

2. Ye Z & et.al - Gastrointestinal bleeding prophylaxis for critically ill patients: a clinical practice guideline. BMJ. 2020 Jan 6;368:l6722. doi: 10.1136/bmj.l6722. PMID: 31907223.

3. Quenot JP, Thiery N, Barbar S. When should stress ulcer prophylaxis be used in the ICU? Curr Opin Crit Care. 2009 Apr;15(2):139-43. doi: 10.1097/MCC.0b013e32832978e0. PMID: 19578324. 

4. PEPTIC Investigators for the Australian and New Zealand Intensive Care Society Clinical Trials Group, Alberta Health Services Critical Care Strategic Clinical Network, and the Irish Critical Care Trials Group, Young PJ & et. al - Effect of Stress Ulcer Prophylaxis With Proton Pump Inhibitors vs Histamine-2 Receptor Blockers on In-Hospital Mortality Among ICU Patients Receiving Invasive Mechanical Ventilation: The PEPTIC Randomized Clinical Trial. JAMA. 2020 Feb 18;323(7):616-626. doi: 10.1001/jama.2019.22190. PMID: 31950977; PMCID: PMC7029750.

Thursday, November 25, 2021

Wednesday, November 24, 2021

sense of smell

On olfaction (sense of smell)

One of the perks of COVID pandemic is the renewed interest in physical exam! It is widely reported that due to COVID, a patient may lose sense of taste and smell.

Olfaction is a test of first cranial nerve (CN I). It can be quickly tested by occluding one nostril with closed eyes and identify any common scent from the other nostril. Said that the proper evaluation of olfaction is itself a complicated science.

Said that, the proper evaluation of olfaction is itself a complicated science. There are three articles for further readings, below in the reference section.



 Further readings:

1. Kronenbuerger M, Pilgramm M. Olfactory Testing. [Updated 2020 Dec 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK565861/

2. Cain WS, Gent J, Catalanotto FA, Goodspeed RB. Clinical evaluation of olfaction. Am J Otolaryngol. 1983 Jul-Aug;4(4):252-6. doi: 10.1016/s0196-0709(83)80068-4. PMID: 6625103.

3. Reden J, Draf C, Frank RA, Hummel T. Comparison of clinical tests of olfactory function. Eur Arch Otorhinolaryngol. 2016 Apr;273(4):927-31. doi: 10.1007/s00405-015-3682-x. Epub 2015 Jun 7. PMID: 26050222.

Tuesday, November 23, 2021

atropine test

 Q: What is the physiological basis of using atropine in establishing brain death?

Answer: The dorsal motor vagal nucleus is in the medulla. Atropine works via this center and provides an assessment of caudal medullary function. This is one of the last functions which gets lost in brain death. Atropine provides a restricted assessment of brainstem function. 

The test is performed by giving 2-3 mg atropine intravenously. The test is considered positive (means brain is dead) if heart rate fails to increase by 3% compared with basal heart rate.

This excludes people with denervation like a previous heart transplant.



1. Hüttemann E, Schelenz C, Sakka SG, Reinhart K. Atropine test and circulatory arrest in the fossa posterior assessed by transcranial Doppler. Intensive Care Med. 2000 Apr;26(4):422-5. doi: 10.1007/s001340051176. PMID: 10872134. 

2. Machado C. Diagnosis of brain death. Neurol Int. 2010;2(1):e2. Published 2010 Jun 21. doi:10.4081/ni.2010.e2

Monday, November 22, 2021

ETOH in ethylene Glycol toxicity

 Q: ETOH can be given orally in Ethylene Glycol toxicity?

A) Yes

B) No

Answer: A

Although Fomepizole is now the standard treatment for ethylene glycol toxicity, ETOH is still a viable treatment. 

ETOH/distilled spirits (40 to 50% volume/volume) should be diluted to a 20 percent solution and can be given via oral or via nasogastric tube at 5 mL/kg of a 20 percent solution to raise serum concentrations by 100 mg/dL. It should be continued as 0.5 mL/kg/hour for the maintenance dose.



1. Sasanami M, Yamada T, Obara T, Nakao A, Naito H. Oral Ethanol Treatment for Ethylene Glycol Intoxication. Cureus. 2020;12(12):e12268. Published 2020 Dec 25. doi:10.7759/cureus.12268 

2. Achappa B, Madi D, Kanchan T, Kishanlal NK. Treatment of Ethylene Glycol Poisoning with Oral Ethyl Alcohol. Case Rep Med. 2019 Jan 30;2019:7985917. doi: 10.1155/2019/7985917. PMID: 30838047; PMCID: PMC6374870.

Sunday, November 21, 2021

AKI with drug interactions

 Case: 54 years old male with past medical history only significant for hypertension (HTN) stable over years with lisinopril, brought to ED with mental status change. The patient is found to be in Acute Kidney Failure. History is negative for any recreational drug abuse, though wife acknowledges he was in a motor vehicle accident (MVA) 8 weeks ago and was lately using over-the-counter pain killers. Which drug interaction is suspected to cause his AKF?

Answer: nonsteroidal anti-inflammatory drug (NSAID) and angiotensin-converting enzyme (ACE) inhibitors

The objective of this question is to identify the risk factors which can quickly culminate in renal injury. One of the biggest risk factors is the drug-interaction. Over-use of NSAID itself is one of the leading causes of Acute Kidney Injury (AKI) and the risk multiplies when combined with other drugs or clinical conditions. AKI due to NSAID gets exacerbated when used with diuretics, CHF, nephrotic syndrome, cirrhosis, hypercalcemia, ACE inhibitors, angiotensin receptor blockers (ARBs), or calcineurin inhibitors (CNIs). 

The AKI due to NSAID is dose-dependent, and usually reversible when NSAID is discontinued.



1.  Huerta C, Castellsague J, Varas-Lorenzo C, García Rodríguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis 2005; 45:531. 

2. Lapi F, Azoulay L, Yin H, et al. Concurrent use of diuretics, angiotensin converting enzyme inhibitors, and angiotensin receptor blockers with non-steroidal anti-inflammatory drugs and risk of acute kidney injury: nested case-control study. BMJ 2013; 346:e8525. 

3. Delzer LM, Golightly LK, Kiser TH, et al. Calcineurin Inhibitor and Nonsteroidal Anti-inflammatory Drug Interaction: Implications of Changes in Renal Function Associated With Concurrent Use. J Clin Pharmacol 2018; 58:1443.

Saturday, November 20, 2021

abscesses in complicated acute diverticulitis

 Q: In complicated acute diverticulitis, abscesses are classified as small and large depending on size. The cutoff is? (select one)

A) more than 2 cm 

B) more than 4 cm 

Answer: B

Abscess formation is common in complicated acute diverticulitis. Depending on the size, the invasive vs non-invasive approach can be decided. Abscess size above 5 cm has a higher rate of complication. Given that a more aggressive approach is needed for sizes above 4 cm. 

In smaller abscesses antibiotics is usually sufficient. Percutaneous drainage of diverticular abscesses should be strongly considered if the size is at or above 4 cm, though the American Society of Colon and Rectal Surgeons (ASCRS) recommends percutaneous drainage at or above 3 cm. Drainage catheter can be left till output is minimal. Catheter sinograms can be performed periodically as well as serial CT scans to evaluate the resolution.

In severe cases, open surgery may be needed.




1. Hall J, Hardiman K, Lee S, et al. The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Treatment of Left-Sided Colonic Diverticulitis. Dis Colon Rectum 2020; 63:728. 

2. Gregersen R, Mortensen LQ, Burcharth J, et al. Treatment of patients with acute colonic diverticulitis complicated by abscess formation: A systematic review. Int J Surg 2016; 35:201. 

3. Francis NK, Sylla P, Abou-Khalil M, et al. EAES and SAGES 2018 consensus conference on acute diverticulitis management: evidence-based recommendations for clinical practice. Surg Endosc 2019; 33:2726. 

4. Siewert B, Tye G, Kruskal J, et al. Impact of CT-guided drainage in the treatment of diverticular abscesses: size matters. AJR Am J Roentgenol 2006; 186:680. 

5. Gaertner WB, Willis DJ, Madoff RD, et al. Percutaneous drainage of colonic diverticular abscess: is colon resection necessary? Dis Colon Rectum 2013; 56:622.

Friday, November 19, 2021

Vitamin K and CAD

 Q: What role Vitamin K plays in coronary vessels?

Answer: Vitamin K plays many essential roles in the human body. Some of these roles are less known. Overall, it plays four major roles in the human body 

  1. It is necessary for the activation of coagulation factors VII, IX, X, and prothrombin. 
  2. It is required for the activation of proteins C and S 
  3. It helps in bone mineralization and prevents osteoporosis
  4. It helps to prevent coronary vascular calcification

An active form of Matrix Gla protein plays an essential part in preventing coronary vascular calcification. It requires Vitamin K for its carboxylation. Decrease matrix Gla protein activity leads to vascular calcification and may lead to coronary artery disease (CAD).




1. Beulens JW, Bots ML, Atsma F, et al. High dietary menaquinone intake is associated with reduced coronary calcification. Atherosclerosis 2009; 203:489. 

2. Shioi A, Morioka T, Shoji T, Emoto M. The Inhibitory Roles of Vitamin K in Progression of Vascular Calcification. Nutrients. 2020;12(2):583. Published 2020 Feb 23. doi:10.3390/nu12020583

3. Shea MK, O'Donnell CJ, Hoffmann U, Dallal GE, Dawson-Hughes B, Ordovas JM, Price PA, Williamson MK, Booth SL. Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr. 2009 Jun;89(6):1799-807. doi: 10.3945/ajcn.2008.27338. Epub 2009 Apr 22. PMID: 19386744; PMCID: PMC2682995.

Thursday, November 18, 2021

Vanco and different disease states

 Q: Inflammation of meninges _________________ the penetration of Vancomycin in Cerebrospinal Fluid (CSF)  (select one)

A) increases

B) decreases

Answer: A

Although vancomycin has limited penetration in CSF, it gets improved when the meninges are inflamed. This makes vancomycin a good choice in MRSA meningitis. Although some experts argue this claim. Daptomycin does not have this advantage. 

The objective of this question is to highlight the complex pharmacokinetics of commonly used drugs in ICU under various clinical conditions - like, diabetic patients do not respond well to vancomycin due to compromised soft tissue penetration. Also, contrary to popular belief, the penetration of vancomycin in lung tissues is limited. It requires four times higher serum levels to penetrate the lung tissues.



1. Taheri M, Dadashzadeh S, Shokouhi S, Ebrahimzadeh K, Sadeghi M, Sahraei Z. Administration of Vancomycin at High Doses in Patients with Post Neurosurgical Meningitis: A Comprehensive Comparison between Continuous Infusion and Intermittent Infusion. Iran J Pharm Res. 2018;17(Suppl2):195-205. 

2. Roman Mounier & et. al World Neurosurgery Is First-Line Vancomycin Still the Best Option to Treat Staphylococcus Health Care–Associated Meningitis? World Neurosurgery Volume 99, March 2017, Pages 812.e1-812.e5 

3. Skhirtladze K, Hutschala D, Fleck T, et al. Impaired target site penetration of vancomycin in diabetic patients following cardiac surgery. Antimicrob Agents Chemother 2006; 50:1372. 

4. Cruciani M, Gatti G, Lazzarini L, et al. Penetration of vancomycin into human lung tissue. J Antimicrob Chemother 1996; 38:865.

Wednesday, November 17, 2021


 Q: Midodrine causes? (select one)

A) arterial constriction 
B) venous constriction 
C) arterial and venous constrictions

Answer: C

Midodrine is an alpha agonist which causes both arterial and venous constrictions. It has many properties which makes it a desirable drug to use in ICU as an adjuvant treatment for refractory hypotension. Midodrine has no direct effect on heart rate and is rapidly absorbed from the GI tract. It reaches a peak plasma concentration in about 30 minutes and does not cross the blood-brain barrier. 

Dose should not exceed above 40 mg/day.



1. Rizvi MS, Trivedi V, Nasim F, Lin E, Kashyap R, Andrijasevic N, Gajic O. Trends in Use of Midodrine in the ICU: A Single-Center Retrospective Case Series. Crit Care Med. 2018 Jul;46(7):e628-e633. doi: 10.1097/CCM.0000000000003121. PMID: 29613861.

2. Anstey MH, Wibrow B, Thevathasan T, et al. Midodrine as adjunctive support for treatment of refractory hypotension in the intensive care unit: a multicenter, randomized, placebo controlled trial (the MIDAS trial). BMC Anesthesiol. 2017;17(1):47. Published 2017 Mar 21. doi:10.1186/s12871-017-0339-x

3. Parsaik AK, Singh B, Altayar O, et al. Midodrine for orthostatic hypotension: a systematic review and meta-analysis of clinical trials. J Gen Intern Med 2013; 28:1496. 

4. Low PA, Gilden JL, Freeman R, et al. Efficacy of midodrine vs placebo in neurogenic orthostatic hypotension. A randomized, double-blind multicenter study. Midodrine Study Group. JAMA 1997; 277:1046.

Tuesday, November 16, 2021

Open globe eye injury

 Q; What are the three big "NOs" in the early management of patients with open globe eye trauma?

Answer: It is important to recognize the basic classification of eye injury into three big categories.

  • Open globe 
  • Closed globe 
  • Periocular 

When it comes to open globe eye injury, three Big Nos are 

  1. No pressure to the eyeball (no tonometry exam) 
  2. No eye drops (eg fluorescein) 
  3. No removal of any foreign bodies
An eye surgeon should be called at the earliest convenience.



1. Ritson JE, Welch J. The management of open globe eye injuries: a discussion of the classification, diagnosis and management of open globe eye injuries. J R Nav Med Serv. 2013;99(3):127-30. PMID: 24511795.

2. Colby K. Management of open globe injuries. Int Ophthalmol Clin. 1999 Winter;39(1):59-69. doi: 10.1097/00004397-199903910-00008. PMID: 10083907. 

3. Xia T, Bauza A, Soni NG, Zarbin MA, Langer PD, Bhagat N. Surgical Management and Outcome of Open Globe Injuries with Posterior Segment Complications: A 10-Year Review. Semin Ophthalmol. 2018;33(3):351-356. doi: 10.1080/08820538.2016.1242634. Epub 2016 Dec 14. PMID: 27960623.

Monday, November 15, 2021

Fever, hyperthermia, and hyperpyrexia

Fever, hyperthermia, and hyperpyrexia

It is important to understand that by definition fever, hyperthermia, and hyperpyrexia are three different entities 

Fever: Fever is a rise in core body temperature in which the set-point in the hypothalamus shifts upward from the normothermia to the febrile levels. It leads to vasoconstriction, resulting in blood divergence from periphery to the internal organs.

 Hyperthermia: This is the pathophysiology in heat stroke syndromes, metabolic dysregulations, and drugs/agents interfering with thermoregulation. The thermoregulatory center stays at normothermic levels. Body temperature increases to uncontrolled level and overrides the ability of the body to lose heat. In contrast to fever, hyperthermia can quickly become fatal. 

Hyperpyrexia: This term is used for extremely high fever (above 41.5°C). It is likely seen in brain hemorrhages.



1. Stitt JT. Fever versus hyperthermia. Fed Proc. 1979 Jan;38(1):39-43. PMID: 759237. 

2. Walter EJ, Hanna-Jumma S, Carraretto M, Forni L. The pathophysiological basis and consequences of fever. Crit Care. 2016;20(1):200. Published 2016 Jul 14. doi:10.1186/s13054-016-1375-5 

3. Hussein O, Torbey M. Hyperpyrexia as the Presenting Symptom of Intracranial Hypotension. Neurocrit Care. 2018 Jun;28(3):395-399. doi: 10.1007/s12028-017-0481-9. PMID: 29150776.

4. Singh IS, Hasday JD. Fever, hyperthermia and the heat shock response. Int J Hyperthermia. 2013 Aug;29(5):423-35. doi: 10.3109/02656736.2013.808766. Epub 2013 Jul 17. PMID: 23863046.

Sunday, November 14, 2021

DKA and chloride

 Q: Patients with Diabetes Ketoacidosis (DKA) may have? (select one)

A) pseudohypochloremia 

B) pseudohyperchloremia

Answer: B

Significant hyperlipidemia is common in DKA. This makes serum lactescent. Hyperlipidemia displaces water in plasma. Once plasma water phase fraction is below 93%, it can give an erroneous reading on electrolytes particularly sodium and chloride. Pseudohyponatremia is a well-known feature of DKA. In contrast, it may cause pseudohyperchloremia. 

Said that these effects are not universal and largely depend on the method used by the lab to test electrolytes. It would be prudent to discuss with labs prior to making any adjustment calculations. 

Salicylate and bromide poisonings are other well-known causes of pseudohyperchloremia.




1. Kaminska ES, Pourmotabbed G. Spurious laboratory values in diabetic ketoacidosis and hyperlipidemia. Am J Emerg Med 1993; 11:77. 

2. Graber ML, Quigg RJ, Stempsey WE, Weis S. Spurious hyperchloremia and decreased anion gap in hyperlipidemia. Ann Intern Med 1983; 98:607. 

3. Wiederkehr MR, Benevides R Jr, Santa Ana CA, Emmett M. Pseudohyperchloremia and Negative Anion Gap - Think Salicylate! Am J Med. 2021 Sep;134(9):1170-1174. doi: 10.1016/j.amjmed.2021.03.017. Epub 2021 Apr 20. PMID: 33864761. 

4. Danel VC, Saviuc PF, Hardy GA, Lafond JL, Mallaret MP. Bromide intoxication and pseudohyperchloremia. Ann Pharmacother. 2001 Mar;35(3):386-7. doi: 10.1345/aph.10156. PMID: 11261542.

Saturday, November 13, 2021

Shigella infection and clinical symptoms

 Q: 34 years old male after returning from a trip abroad is admitted to ICU with severe hypovolemic shock, fever, severe diarrhea, and blood-stained stools. Patient is diagnosed with Shigella infection.  If the patient is responding to antibiotics, how quickly clinical symptoms should improve? (select one)

A) 1 -2 days

B) 5-7 days

Answer: A

The objective of this question is to highlight the massive worldwide problem of high resistance to antibiotics in Shigella infection. Shigella can be treated with a wide range of antibiotics including ciprofloxacin, ceftriaxone, azithromycin, trimethoprim-sulfamethoxazole, and ampicillin. Said that resistance to all the classes is high due to rampant and widespread use of antibiotics for any travelers' diarrhea. Many times resistance is reported simultaneously to more than 3 classes of antibiotics. 

One effective way to establish antibiotic efficiency is to gauge improvement in clinical symptoms. If sensitive to prescribed antibiotic, clinical symptoms improve very quickly in shigella infection. 

Aggressive hydration continues to be the most important aspect in such severe diarrhea.




1. Centers for Disease Control and Prevention. National Antimicrobial Resistance Monitoring System for Enteric Bacteria (NARMS). NARMS Now: Human data, Shigella, 2018. Available at: https://wwwn.cdc.gov/narmsnow/ (Accessed on November 1, 2021).

2. Ranjbar R, Farahani A. Shigella: Antibiotic-Resistance Mechanisms And New Horizons For Treatment. Infect Drug Resist. 2019;12:3137-3167. Published 2019 Oct 7. doi:10.2147/IDR.S219755 

3. Puzari M, Sharma M, Chetia P. Emergence of antibiotic resistant Shigella species: A matter of concern. J Infect Public Health. 2018 Jul-Aug;11(4):451-454. doi: 10.1016/j.jiph.2017.09.025. Epub 2017 Oct 20. PMID: 29066021.

Friday, November 12, 2021

MM and encephalopathy

 Q: 59 years old male with recently diagnosed multiple myeloma (MM) is admitted to ICU with encephalopathy. Ammonia level is noted to be high. The most likely cause of encephalopathy in this patient is liver failure. 

A) True

B) False

Answer:  B

The objective of this question is to highlight the fact that there are many other reasons besides liver insufficiency for hyperammonemia. Many of these causes are well known and many remain undiagnosed. It includes multiple myeloma, acute leukemia, infections, unmasked urea cycle defects in stressful situations, and drugs. 

Myeloma cell lines produce high ammonia, and chemotherapy resolves the pathology.



1. Kwan L, Wang C, Levitt L. Hyperammonemic encephalopathy in multiple myeloma. N Engl J Med 2002; 346:1674. 

2. Upadhyay R, Bleck TP, Busl KM. Hyperammonemia: What Urea-lly Need to Know: Case Report of Severe Noncirrhotic Hyperammonemic Encephalopathy and Review of the Literature. Case Rep Med. 2016;2016:8512721. 

3. Talamo G, Cavallo F, Zangari M, et al. Hyperammonemia and encephalopathy in patients with multiple myeloma. Am J Hematol 2007; 82:414.

Thursday, November 11, 2021

PV and AML

 Q: 74 years old male with a known history of Polycythemia Vera (PV) who has previous treatments with chemotherapy is admitted to ICU with community-acquired pneumonia - requiring intermittent BiPAP. Patient is also found to be in Acute Myeloid Leukemia (AML). AML with the history of PV usually signifies a good prognosis.

A) True

B) False

Answer: B

PV's transformation to AML bears a very poor prognosis. Two major risk factors in this regard are age above 70 years and previous treatments with cytoreductive agents except for hydroxyurea and interferon. The median survival of these patients is less than six months despite complete remission with AML treatment. 

These patients should be considered very early for allogeneic hematopoietic cell transplantation to avoid the fatal outcome.



1. Finazzi G, Caruso V, Marchioli R, et al. Acute leukemia in polycythemia vera: an analysis of 1638 patients enrolled in a prospective observational study. Blood 2005; 105:2664. 

2. Passamonti F, Rumi E, Arcaini L, et al. Leukemic transformation of polycythemia vera: a single center study of 23 patients. Cancer 2005; 104:1032. 

3. Tefferi A, Guglielmelli P, Larson DR, et al. Long-term survival and blast transformation in molecularly annotated essential thrombocythemia, polycythemia vera, and myelofibrosis. Blood 2014; 124:2507.

4. Gangat N, Strand J, Li CY, et al. Leucocytosis in polycythaemia vera predicts both inferior survival and leukaemic transformation. Br J Haematol 2007; 138:354.

Wednesday, November 10, 2021

GCA and TA

 Q: Renovascular hypertension is more common in? (select one) 

A) Giant Cell Arteritis (GCA) 

B) Takayasu Arteritis (TA) 

Answer: B

The objective of this question is to emphasize the significance of clinical signs as well as epidemiology in the differential diagnosis. Histopathologic, as well as radiographic features, are indistinguishable in GCA and TA. The two major establishing factors are age and clinical presentation. 

GCA almost always occurs after the age of 50 whereas TA almost always occurs at a younger age and never after the age of 40. Renovascular hypertension is common in TA but not a part of GCA. Conversely, vision loss due to anterior ischemic optic neuropathy does not occur in TA but is a cardinal feature of GCA.



Stamatis P. Giant Cell Arteritis versus Takayasu Arteritis: An Update. Mediterr J Rheumatol. 2020;31(2):174-182. Published 2020 Jun 30. doi:10.31138/mjr.31.2.174

Tuesday, November 9, 2021

Clinical aspect of Bradykinin-induced angioedema

 Q: Bradykinin-induced angioedema is usually associated with life-threatening bronchospasm? 

A) True 

B) False

Answer: B

The objective of this question is to highlight the clinical difference between mast-cell mediated and bradykinin-induced angioedema. In contrast to mast-cell mediated angioedema, bradykinin-induced angioedema is not associated with urticaria, bronchospasm, or any other signs of allergic reaction. Also, it is very hard to establish the cause or time frame. It has a prolonged course, developing over a day or so. Epinephrine is usually not required. 

The classic example of bradykinin-induced angioedema is an angiotensin-converting enzyme (ACE) inhibitor-induced angioedema, which is mostly confined to lips, tongue, and upper airway. The treatment is Fresh-Frozen Plasma (FFP) instead of epinephrine. ACE-I-induced angioedema may occur even after use for many years.



1. Obtułowicz K. Bradykinin-mediated angioedema. Pol Arch Med Wewn. 2016;126(1-2):76-85. doi: 10.20452/pamw.3273. PMID: 26842379.

2. Kostis WJ, Shetty M, Chowdhury YS, Kostis JB. ACE Inhibitor-Induced Angioedema: a Review. Curr Hypertens Rep. 2018 Jun 8;20(7):55. doi: 10.1007/s11906-018-0859-x. PMID: 29884969.

Monday, November 8, 2021

Alternative of flumazenil

 Q: If flumazenil is not available midazolam can be reversed with (select one) 

A) Aminophylline 

B) Remimazolam

Answer: A

Aminophylline has the ability to reverse both sedatives as well as the respiratory depressive effects of midazolam. The dose is 1-2 mg/kg intravenous over five minutes. It is not used as a first-line reversal agent as the effect can be partial and the drug has not been extensively studied. Also, it requires caution in patients with seizures, older age, heart and liver insufficiencies. Aminophylline has been used as a reversal agent for midazolam three decades ago and has seen some come back in newer literature.

Remimazolam is itself a new generation of short-acting benzodiazepine, and may worsen the effect of midazolam.




1. Aghabiklooei A, Sangsefidi J. The effects of intravenous aminophylline on level of consciousness in acute intentional benzodiazepines poisoning in comparison to flumazenil. Hum Exp Toxicol 2017; 36:311. 

2. Bonfiglio MF, Fisher-Katz LE, Saltis LM, et al. A pilot pharmacokinetic-pharmacodynamic study of benzodiazepine antagonism by flumazenil and aminophylline. Pharmacotherapy 1996; 16:1166. 

3. Sibai AN, Sibai AM, Baraka A. Comparison of flumazenil with aminophylline to antagonize midazolam in elderly patients. Br J Anaesth 1991; 66:591. Gallen JS. Aminophylline reversal of midazolam sedation. Anesth Analg 1989; 69:268.

Sunday, November 7, 2021

TOA in older patients

 Q: 64 years old postmenopausal woman presented with abdominal pain and sepsis-like picture. CT scan of abdomen raises high suspicion of Tubo-Ovarian abscess (TOA). What is the biggest concern? 

 Answer: Malignancy

Age plays an important role in the causality of TOA. Premenopausal patients develop TOA mostly due to Pelvic Inflammatory Disease (PID). TOA in postmenopausal women raises a strong suspicion of underlying malignancy. These patients should be strongly considered for full staging procedure besides treatment of TOA with antibiotics and/or drainage of the abscess.

If surgery is performed it requires an experienced surgeon who can explore the abdomen and pelvis fully to evaluate for metastatic disease and staging for cancer.




Protopapas AG, Diakomanolis ES, Milingos SD, et al. Tubo-ovarian abscesses in postmenopausal women: gynecological malignancy until proven otherwise? Eur J Obstet Gynecol Reprod Biol 2004; 114:203.

Saturday, November 6, 2021

Sch and MG

 Q: Succinylcholine (SCh) dose in myasthenia gravis should be? (select one) 

A) higher than calculated dose 

B) lower than calculated dose 

C) It should not be used in myasthenia gravis

Answer: A

In general, it is advisable to overestimate the dose of succinylcholine. The dose of SCh should be calculated based on total body weight, including obese and pregnant patients. Higher dose gives a better level of paralysis without much higher risk. If a dose is underestimated, it may leave the patient partially unparalysed. 

This also holds true for patients with myasthenia gravis (MG). SCh can be used safely in MG, and require about 25 percent higher dose. The usual dose of SCh is 1.5 mg/kg of total body weight. In patients with MG it should be increased to 2 mg/kg. MG patients are partially resistant to SCh and require a higher dose to appropriately stimulate the remaining acetylcholine receptors.




1. Naguib M, Samarkandi AH, El-Din ME, et al. The dose of succinylcholine required for excellent endotracheal intubating conditions. Anesth Analg 2006; 102:151. 

2. Guay J, Grenier Y, Varin F. Clinical pharmacokinetics of neuromuscular relaxants in pregnancy. Clin Pharmacokinet 1998; 34:483. 

3. Patanwala AE, Sakles JC. Effect of patient weight on first pass success and neuromuscular blocking agent dosing for rapid sequence intubation in the emergency department. Emerg Med J 2017; 34:739. 

4. Levitan R. Safety of succinylcholine in myasthenia gravis. Ann Emerg Med 2005; 45:225.

Friday, November 5, 2021

Remdesivir and LFT

 Q: 48 years old male is admitted to ICU with newly diagnosed COVID-19. Remdesivir has been initiated. On Day 3 his liver enzymes appears to be elevated. What is the usual recommended point where remdesivir should be discontinued if liver enzymes continue to rise?

Answer: About 10 folds 

Remdesivir has become a mainstay of treatment in COVID-19 hospitalized patients. FDA now approved its use for any inpatient above the age of 12 irrespective of disease severity. It is recommended to be stopped if a patient get discharged before the completion of the course. The dose is 200 mg IV on day one followed by 100 mg for a total of 5 days. A clinician may decide to continue it beyond 5 days if the patient is still sick. 

Its side effect includes renal and hepatic insufficiencies. Some elevation in liver enzymes is expected but the drug should be stopped if alanine aminotransferase (ALT) rises more than 10 times above the normal lab limit.





1. Zampino R, Mele F, Florio LL, et al. Liver injury in remdesivir-treated COVID-19 patients. Hepatol Int. 2020;14(5):881-883. doi:10.1007/s12072-020-10077-3

2. van Laar SA, de Boer MGJ, Gombert-Handoko KB, Guchelaar HJ, Zwaveling J; LUMC-Covid-19 research group. Liver and kidney function in patients with Covid-19 treated with remdesivir. Br J Clin Pharmacol. 2021 Nov;87(11):4450-4454. doi: 10.1111/bcp.14831. Epub 2021 May 4. PMID: 33763917; PMCID: PMC8251044.

3. Montastruc F, Thuriot S, Durrieu G. Hepatic Disorders With the Use of Remdesivir for Coronavirus 2019. Clin Gastroenterol Hepatol. 2020 Nov;18(12):2835-2836. doi: 10.1016/j.cgh.2020.07.050. Epub 2020 Jul 25. PMID: 32721580; PMCID: PMC7381904.

Thursday, November 4, 2021


 Q: 42 years old male with chronic and continuous use of cannabinoids is admitted to ICU with severe hypovolemic shock due to persistent vomiting. Patient has been to Emergency Department (ED) many times and has been diagnosed with Cyclic Vomiting Syndrome (CVS). What is the first line of drug for the treatment? (select one) 

A) dexamethasone 

B) metoclopramide 

C) naloxone 

D) sumatriptan 

E) ondansetron 


It has been shown that CVS and migraines have associated pathology. The new data shows that the prevalence of CVS is as common in adults as in children. Apart from migraine other associated pathologies are mitochondrial dysfunction, autonomic dysfunction, hypothalamic-pituitary-adrenal axis hyperreactivity, estrogen sensitivity (also known as catamenial CVS), long cannabis abuse [also known as — Cannabis hyperemesis syndrome (CHS)], sensitivity to chocolate, cheese, monosodium glutamate, and other food items. 

The only drugs shown to have the effect to abort CVS once symptoms set in are sumatriptan and aprepitant. Surprisingly, all other potent anti-emetics (Choice A, B, C, and E) have a limited role in aborting CVS.





1. Fleisher DR, Gornowicz B, Adams K, et al. Cyclic Vomiting Syndrome in 41 adults: the illness, the patients, and problems of management. BMC Med 2005; 3:20. 

2. Sagar RC, Sood R, Gracie DJ, et al. Cyclic vomiting syndrome is a prevalent and under-recognized condition in the gastroenterology outpatient clinic. Neurogastroenterol Motil 2018; 30. 

3. Aziz I, Palsson OS, Whitehead WE, et al. Epidemiology, Clinical Characteristics, and Associations for Rome IV Functional Nausea and Vomiting Disorders in Adults. Clin Gastroenterol Hepatol 2019; 17:878. 

4. Venkatesan T, Levinthal DJ, Tarbell SE, et al. Guidelines on management of cyclic vomiting syndrome in adults by the American Neurogastroenterology and Motility Society and the Cyclic Vomiting Syndrome Association. Neurogastroenterol Motil 2019; 31 Suppl 2:e13604.

Wednesday, November 3, 2021

SPS and Lung Ca

 Q: 58 years old male presented to ED with acute chest pain and shortness of breath (SOB). Chest-X-ray revealed spontaneous pneumothorax (SPS). Subsequent workup led to the diagnosis of cancer. SPS is more in (select one)

A) Primary lung tumor

B) Metastatic lung tumor

Answer: A

Although SPS can occur in either primary or metastatic lung cancer, it is more common in primary lung tumors. SPS occurs in lung cancer due to tumor necrosis, endobronchial obstruction, necrotizing cysts, pneumonia, and coexisting emphysema. 

Malignancies that metastasize to lungs cause necrotic cysts, resulting in SSP. The most common tumors are lymphoma, sarcoma, GI or GU adenocarcinoma, mesenchymal cystic hamartoma, pleuropulmonary blastoma, and angiosarcoma.




1. Choi YK, Kim KC. Spontaneous pneumothorax as the first manifestation of lung cancer: two case report. J Thorac Dis. 2015;7(8):E252-E254. doi:10.3978/j.issn.2072-1439.2015.07.31

2. Okada D, Koizumi K, Haraguchi S, Kawamoto M, Mikami I, Tanaka S. Pneumothorax manifesting primary lung cancer. Jpn J Thorac Cardiovasc Surg. 2002 Mar;50(3):133-6. doi: 10.1007/BF02913477. PMID: 11968723. 

3. Steinhäuslin CA, Cuttat JF. Spontaneous pneumothorax. A complication of lung cancer? Chest. 1985 Nov;88(5):709-13. doi: 10.1378/chest.88.5.709. PMID: 2996838.

Tuesday, November 2, 2021

PE with T therapy

 Q: 64 years old health-conscious man is admitted to ICU with Pulmonary Embolism (PE). Few weeks ago, patient was started on Testosterone therapy after his insistence to increase his prowess at the gym. Which of the underlying disease need to be ruled out?

Answer: Thrombophilia-hypofibrinolysis 

Unfortunately, in the last few years, there is an epidemic of exogenous Testosterone replacement even in normal healthy individuals. Multiple studies are now showing increased prevalence of ICU admissions due to Deep Venous Thrombosis (DVT) and PE in otherwise healthy patients. ICU clinicians need to rule out such inappropriate use.

There are two major causes described for thromboembolism in patients who have been treated with exogenous testosterone therapy. 1) Erythrocytosis 2) Thrombophilia-hypofibrinolysis. 

Testosterone should be stopped if hematocrit is above 54 percent. Most patients with underlying but undiagnosed thrombophilia-hypofibrinolysis develop DVT and PE within three months of starting the therapy. There is a complex interaction between familial and acquired thrombophilia and exogenous hormone use.



1. Ponce OJ, Spencer-Bonilla G, Alvarez-Villalobos N, et al. The efficacy and adverse events of testosterone replacement therapy in hypogonadal men: A systematic review and meta-analysis of randomized, placebo-controlled trials. 

2. J Clin Endocrinol Metab 2018. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2018; 103:1715. 

3. Glueck CJ, Goldenberg N, Wang P. Testosterone Therapy, Thrombophilia, Venous Thromboembolism, and Thrombotic Events. J Clin Med. 2018 Dec 21;8(1):11. doi: 10.3390/jcm8010011. PMID: 30577621; PMCID: PMC6352146.

4. Glueck CJ, Goldenberg N, Wang P. Thromboembolism peaking 3 months after starting testosterone therapy: testosterone-thrombophilia interactions. J Investig Med. 2018 Apr;66(4):733-738. doi: 10.1136/jim-2017-000637. Epub 2017 Dec 15. PMID: 29248890.

Monday, November 1, 2021

P wave in Sinus Tachycardia

 Q: In Sinus Tachycardia, the P wave is inverted (negative) in lead? (select one)

A) I 

B) II 

C) aVL 

D) aVR

Answer: D

It is very important to distinguish sinus tachycardia from other forms of tachycardia at the bedside. Sinus tachycardia may be merely a physiologic response to a wide variety of clinical conditions including fever, volume depletion, sepsis, anemia, hypoxia, PE, coronary ischemia, pain, anxiety, hyperthyroidism, drugs, and others. 

By definition, sinus tachycardia is determined by three basic criteria 

  • Heart Rate above 100, 
  • Rhythm regular
  • Normal P vector 

The best way to establish a normal P vector is by confirming positive (upright) P waves in leads I, II, and aVL, and a negative (inverted) P wave in lead aVR.



1. Becker DE. Fundamentals of electrocardiography interpretation. Anesth Prog. 2006;53(2):53-64. doi:10.2344/0003-3006(2006)53[53:FOEI]2.0.CO;2 

2. Noble RJ, Hillis JS, Rothbaum DA. Electrocardiography. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 33. Available from: https://www.ncbi.nlm.nih.gov/books/NBK354/