Nimodipine and SAH

Q: 44 years old female is admitted to neuro critical care after the diagnosis of subarachnoid hemorrhage (SAH). Nimodipine 60 mg every four hours is initiated. Nimodipine may cause blood pressure (BP) fluctuations and hypotension?

A) True

B) False

Answer: A

Although the mechanism of benefit of nimodipine in SAH is unknown but it is considered to be a standard of care. Studies have shown that the Odd Ratio (OR) of good outcome after SAH is 1.86. Ideally, it should be started within 48 hours of symptom onset. Only oral Nimodipine is recommended as intravenous (IV) Nimodipine may become fatal. Nimodipine should be continue for consecutive three weeks, as it reduces the deficit, mortality, and delayed cerebral ischemia.

Nimodipine works via several mechanisms such as dilation of small arteries (may not be visible on angiogram), reduction of calcium-dependent excitotoxicity, diminished platelet aggregation, and inhibition of ischemia triggered by red blood cell products.

Said all of the above, Nimodipine tends to cause BP fluctuations and hypotension after administration and should be watched for and managed accordingly.

#neuro-critical-care

#pharmacology

References:

1. Treggiari MM, Rabinstein AA, Busl KM, et al. Guidelines for the Neurocritical Care Management of Aneurysmal Subarachnoid Hemorrhage. Neurocrit Care 2023.

2. Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ 1989; 298:636.

3. Dayyani M, Sadeghirad B, Grotta JC, et al. Prophylactic Therapies for Morbidity and Mortality After Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Network Meta-Analysis of Randomized Trials. Stroke 2022; 53:1993.

4. Dorhout Mees SM, Rinkel GJ, Feigin VL, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2007; :CD000277.

Abdominal pain in hyperglycemia

Q: Abdominal pain is more common in? (select one)

A) Diabetic ketoacidosis (DKA)

B) Hyperosmolar hyperglycemic state (HHS)

Answer: A

Abdominal pain in a hyperglycemic state is equivalent to DKA, proving otherwise. It's very rare in HHS. Although abdominal pain in DKA is more common in children simultaneously, it is not uncommon in adults. 

Abdominal pain in DKA has a prognostic value as it correlates with the severity of metabolic acidosis. In fact, it is universal when serum bicarbonate falls below ≤5 mEq/L. Said that abdominal pain has shown no correlation with the severity of hyperglycemia or dehydration.

The cause of abdominal pain in DKA is delayed gastric emptying and ileus due to metabolic acidosis and electrolyte abnormalities. Pancreatitis needs to be ruled out, particularly if pain persists after the resolution of ketoacidosis.

#endocrinology

References:

1. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009 Jul;32(7):1335-43. doi: 10.2337/dc09-9032. PMID: 19564476; PMCID: PMC2699725.

2. Malone ML, Gennis V, Goodwin JS. Characteristics of diabetic ketoacidosis in older versus younger adults. J Am Geriatr Soc 1992; 40:1100.

3. Umpierrez G, Freire AX. Abdominal pain in patients with hyperglycemic crises. J Crit Care. 2002 Mar;17(1):63-7. doi: 10.1053/jcrc.2002.33030. PMID: 12040551.

Surgery in UC

Q: Ulcerative Colitis (UC) patients who develop acute fulminant colitis may require? (select one)

A) emergent surgery

B) urgent surgery

Answer: B

There are two objectives of this question. First to emphasize the distinction between emergency and urgent surgeries. The second is to distinguish the indications of emergency and urgent indications in UC patients.

Emergency surgery implies immediate take to the operating room (OR). UC patients with life-threatening complication(s) such as colonic perforation, massive gastrointestinal(GI) hemorrhage, and/or toxic megacolon, should be taken to OR immediately. 

Urgent surgery means taking to the OR during the same hospitalization. UC patients with acute fulminant colitis should be first treated with medical therapy. In case of failed medical therapy, urgent surgery should be considered. Acute fulminant colitis is generally defined as more than 10 stools per day along with continuous bleeding, abdominal pain & distension, and acute severe toxic symptoms like fever and anorexia.

#GI

#surgical-critical-care

References:

1. Andersson P, Söderholm JD. Surgery in ulcerative colitis: indication and timing. Dig Dis 2009; 27:335.

2. Ordás I, Eckmann L, Talamini M, et al. Ulcerative colitis (seminar). The Lancet 2012; 380:1606. Available at: http://dx.doi.org/10.1016/S0140-6736(12)60150-0 (Accessed on August 28, 2023).

DASH diet

Q: 54 years old male is admitted to ICU with hypertensive crisis requiring two intravenous drips, and transition requires four oral meds. All workups for secondary hypertension remained negative. Dietician recommended DASH diet. What is the DASH diet?

Answer: Dietary Approaches to Stop Hypertension

As acronym says: the DASH diet can be effective in controlling hypertension, particularly in patients who require many meds to control it (In USA, the slang used for such patients is "professional hypertensives"). The major recommended components of DASH diet are:

• 4-5 servings of fruit per day
• 4-5 servings of vegetables per day, and 
• 2-3 servings of low-fat dairy per day, 
• <25 percent of daily caloric intake from fat

DASH diet helps in lowering both systolic and diastolic pressures. Surprisingly, it is found to be more effective than a diet only rich in fruits and vegetables alone. Moreover, when the DASH diet is combined with a low-sodium diet, it may work as equivalent to the antihypertensive agent(s).

    

DASH diet may also be associated with a lower risk of colorectal cancer, other cardiovascular diseases, and gout. It may also decrease premature mortality.

    

    

#cardiology

#nutrition

    

References:

    

1. Schwingshackl L, Bogensberger B, Hoffmann G. Diet Quality as Assessed by the Healthy Eating Index, Alternate Healthy Eating Index, Dietary Approaches to Stop Hypertension Score, and Health Outcomes: An Updated Systematic Review and Meta-Analysis of Cohort Studies. J Acad Nutr Diet 2018; 118:74.

    

2. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med 1997; 336:1117.

    

3. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med 2001; 344:3.

    

4. Rai SK, Fung TT, Lu N, et al. The Dietary Approaches to Stop Hypertension (DASH) diet, Western diet, and risk of gout in men: prospective cohort study. BMJ 2017; 357:j1794

    

5.Fung TT, Hu FB, Wu K, et al. The Mediterranean and Dietary Approaches to Stop Hypertension (DASH) diets and colorectal cancer. Am J Clin Nutr 2010; 92:1429.

6. Salehi-Abargouei A, Maghsoudi Z, Shirani F, Azadbakht L. Effects of Dietary Approaches to Stop Hypertension (DASH)-style diet on fatal or nonfatal cardiovascular diseases--incidence: a systematic review and meta-analysis on observational prospective studies. Nutrition 2013; 29:611.

Success rate of RSI

Q: With proper planning and preparation, the success rate of rapid sequence intubation is almost 99%.

A) True

B) False

Answer: A

The major reason for failed intubation, defined as "can't intubate, can't oxygenate," is mostly due to poor pre-procedure preparation under stressful conditions outside the OR, where unfortunately highly trained anesthesia staff is not always present. 

Said that when proper planning is done, full backup support is obtained, maximum pre-oxygenation is done, and the Neuro-Muscular Blockade (NMB) is properly administrated - the success rate is 99.6 percent with succinylcholine and 99.9 percent with rocuronium. 

This conclusion came from the famous National Emergency Airway Registry (NEAR) and two large multi-center data comprising almost 15,000 intubations.

#procedures

References:

1.April MD, Arana A, Pallin DJ, et al. Emergency Department Intubation Success With Succinylcholine Versus Rocuronium: A National Emergency Airway Registry Study. Ann Emerg Med 2018; 72:645.

2. Sagarin MJ, Barton ED, Chng YM, et al. Airway management by US and Canadian emergency medicine residents: a multicenter analysis of more than 6,000 endotracheal intubation attempts. Ann Emerg Med 2005; 46:328.

3. Walls RM, Brown CA 3rd, Bair AE, et al. Emergency airway management: a multi-center report of 8937 emergency department intubations. J Emerg Med 2011; 41:347.

caloric test in brain death exam

Q: During 'caloric testing' for brain death examination, water should be used at? (select one)

A) Iced (zero) degree

B) Room temperature

Answer: A

During caloric testing for brain death examination, water should be chilled/iced. That's why it is also called the 'cold caloric test.' This is probably the strongest stimulus to determine brain death from all clinical exams. Few important points to remember besides using iced water:

• The external ear should be examined before confirming the patency of ear canal. Tympanic membrane should be visible.
• Each ear should be tested separately, 5 minutes apart. 
• At least 50 mL of ice water should be instilled into each ear canal 
• Head should be elevated to 30 degrees

If the eyes conjugately move toward the irrigated side, the brain death exam is negative (which means the patient can't be declared dead).

#procedures

#neurology

References:

1. Hicks RG, Torda TA. The vestibulo-ocular (caloric) reflex in the diagnosis of cerebral death. Anaesth Intensive Care. 1979 May;7(2):169-73. doi: 10.1177/0310057X7900700210. PMID: 507352.

2. Machado C. Diagnosis of brain death. Neurol Int. 2010 Jun 21;2(1):e2. doi: 10.4081/ni.2010.e2. PMID: 21577338; PMCID: PMC3093212.

3. Munakomi S, Lui F. Caloric Reflex Test. [Updated 2023 Apr 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557481/

First degree AV block nomenclature

Q: First-degree AV block is a misnomer?

A) True

B) False

Answer: A

First-degree Atrioventricular block is defined as a prolonged PR interval of >200 ms at resting heart rates. In a true sense, it is just delayed or slowed AV conduction. It is not a true block. Instead of first-degree AV block, it should be called "prolonged AV conduction." It mostly occurs in the AV node but may also occur in the His-Purkinje system.

Previously, it was thought to be completely a benign condition, but new research argues to investigate it thoroughly as it may signify a serious underlying cardiac disease.

#cardiology

References/further reading:

1. Holmqvist F, Daubert JP. First-degree AV block-an entirely benign finding or a potentially curable cause of cardiac disease? Ann Noninvasive Electrocardiol. 2013 May;18(3):215-24. doi: 10.1111/anec.12062. PMID: 23714079; PMCID: PMC6932444.

2. Liu M, Du Z, Sun Y. Prognostic significance of first-degree atrioventricular block in a large Asian population: a prospective cohort study. BMJ Open. 2022 Apr 4;12(4):e062005. doi: 10.1136/bmjopen-2022-062005. PMID: 35379649; PMCID: PMC8981319.

Methotrexate and Anbx

Q: 58 years old female with rheumatoid arthritis is admitted to ICU with community-acquired pneumonia. Home medications include Methotrexate. Which group of antibiotics should be preferably avoided?

A) Fluoroquinolone

B) Penicillin

Answer: B

Penicillin has been shown to compete with the renal tubular secretion of methotrexate and hence its clearance when co-prescribed. Concurrent use of methotrexate and penicillin may increase the toxicity of methotrexate, particularly neutropenia.

Similar effects are reported from Bactrim.

#pharmacology

References: 

1. Methotrexate induced neutropenia associated with coprescription of penicillins: serious and under-reported? - Rheumatology 2006 45(3):361-362

2. Pharmacokinetic interaction between methotrexate and piperacillin/tazobactam resulting in prolonged toxic concentrations of methotrexate - Journal of Antimicrobial Chemotherapy 2006 58(1):228-230

3. Methotrexate-induced pancytopenia associated with co-prescription of penicillin and trimethoprim Clinical Rheumatology, Volume 26, Number 1, January 2007 , pp. 134-135(2)

PAC balloon inflation timing

Q: Why is it important to inflate the balloon of Pulmonary Artery Catheter (Swan-Ganz Catheter) as soon as it enters Right Atrium?

Answer: During Pulmonary Artery Catheter insertion, care must be taken so as to inflate the balloon as soon as the atrial wave is noticed in the monitor. 

This helps to avoid endocardial lesion in the tricuspid valve. Also, it prevents right atrium and right ventricle wall perforation.

#procedures

Reference: 

Auxiliadora-Martins M, Apinagés Dos Santos E, Adans Wenzinger D, Alkmim-Teixeira GC, de M Neto GC, Sankarankutty AK, de Castro E Silva O, Martins-Filho OA, Basile-Filho A. Perforation of the right ventricle induced by pulmonary artery catheter at induction of anesthesia for the surgery for liver transplantation: a case report and reviewed of literature. Case Rep Med. 2009;2009:650982. doi: 10.1155/2009/650982. Epub 2009 Dec 31. PMID: 20066172; PMCID: PMC2804058.

BPD and BD

Case: 36 years old physician is admitted to ICU with a suicide attempt after failing "maintenance of certification' (MOC) exam. If diagnosed with a mental health disorder, which diagnosis is most likely? (select one)

A) Borderline Personality Disorder (BPD) 

B) Bipolar disorder (BD)

Answer: A

It is hard to distinguish between BPD and bipolar disorders. The two major diagnostic features which contrast each other are:

1. Mood syndromes in BPD are usually triggered by environmental stress, mostly perceived as rejection or failure. In contrast, mood syndromes in bipolar disorder are less connected to events.

2. The depressive part of bipolar disorder lasts way longer than BPD.

#psychiatry

Reference:

Paris J, Black DW. Borderline personality disorder and bipolar disorder: what is the difference and why does it matter? J Nerv Ment Dis. 2015 Jan;203(1):3-7. doi: 10.1097/NMD.0000000000000225. PMID: 25536097.

CAC in CAD

Q:  In coronary artery disease (CAD), Coronary Artery Calcium (CAC) deposition occurs mostly in which layer of the vessel? (select one)

A) intimal layer 

B) medial layer 

Answer: A

This question highlights the distinction between etiologies of calcium deposition in coronary and noncoronary diseases.

CAC deposition occurs due to smooth muscle cell apoptosis. It begins as microscopic calcifications from 0.5 to 15 micrometers, and as the disease progresses can grow up to  >3 mm. 

Most CAC occurs in the intimal layer of the coronary arteries. But, in patients with non-coronary diseases such as kidney insufficiency and hyperparathyroidism, it is usually seen in the medial layer of the vessel.  Said that patients with noncoronary diseases may have high risk of cardiac events.

#cardiology

References:

1. Mori H, Torii S, Kutyna M, et al. Coronary Artery Calcification and its Progression: What Does it Really Mean? JACC Cardiovasc Imaging 2018; 11:127.

2. Burke AP, Weber DK, Kolodgie FD, Farb A, Taylor AJ, Virmani R. Pathophysiology of calcium deposition in coronary arteries. Herz. 2001 Jun;26(4):239-44. doi: 10.1007/pl00002026. PMID: 11479935.

local lido with and without epi

Q: Local lidocaine administration with epinephrine requires? (select one)

A) higher than usual dose

B) lower than usual dose

Answer: A

1% lidocaine is usually used for procedures under local anesthesia. It can be administrated either with or without epinephrine. The maximum allowable dose is 4 to 5 mg/kg without epinephrine. If epinephrine is added, the maximum allowable dose can be increased to 5 to 7 mg/kg. This is due to the fact local epi. can induce some vasoconstriction which requires a higher than usual dose of lidocaine.

#procedures

#pharmacology

References:

1. McCreight A, Stephan M. Local and regional anesthesia. In: Textbook of Pediatric Emergency Procedures, 2nd edition, King C, Henretig FM (Eds), Lippincott Williams & Wilkins, Philadelphia 2008.

2. McGee DL. Anesthetic and analgesic technique. In: Roberts and Hedges Clinical Procedures in Emergency Medicine, 5th edition, Roberts JR, Hedges JR (Eds), Saunders Elsevier, Philadelphia 2010.

Acute CHF in schizophrenia treatment

Q: 32 years old male was discharged four weeks ago from the hospital when he was admitted due to severe schizophrenia. He now presented to the emergency department with shortness of breath and was found to be in acute congestive heart failure. Which of the following drug is the probable culprit? (select one)

A) Risperidone 

B) Quetiapine 

C) Olanzapine 

D) Ripiprazole 

E) Clozapine 

Answer: E

Although rare, clozapine-induced myocarditis can cause cardiomyopathy, and all patients should be watched closely in the first month of prescription for congestive heart failure (CHF) symptoms. Ideally, all patients should be ruled out for any underlying cardiac pathology before starting clozapine.

As expected, treatment is the discontinuation of medicine and supportive treatment. Fortunately, with discontinuation of clozapine, cardiomyopathy usually resolves.

#cardiology

#pharmacology

#psychiatry

References:

1. Haas SJ, Hill R, Krum H, et al. Clozapine-associated myocarditis: a review of 116 cases of suspected myocarditis associated with the use of clozapine in Australia during 1993-2003. Drug Saf 2007; 30:47.

2. http://www.accessdata.fda.gov/drugsatfda_docs/label/2016/019758s080lbl.pdf (Accessed on August 17, 2023).

DD in elderly patient

Case: 82 years old female who, earlier in the day, went through Endoscopic retrograde cholangiopancreatography (ERCP) is transferred from the floor (ward) with hypotension. Patient has chronic steroid-dependent Chronic obstructive pulmonary disease (COPD). Labs are pending, but as the other four components of 'Reynolds pentad' are absent on clinical exam, suppurative cholangitis can be safely ruled out by differential diagnosis? 

A) True

B) False

Answer; B

This question aims to highlight that clinical exams can be highly deceiving in elderly patients and those patients who are on steroid treatment. 

In view of this patient's early history of undergoing ERCP, severe (suppurative) cholangitis cannot be ruled out just by the absence of Reynolds pentad, i.e., fever, abdominal pain, jaundice, and hypotension. Patterns of obstructive enzymes on the Liver Function Test (LFT) and imagings are required to establish the diagnosis.

Proper diagnosis is imperative as  AOSC (acute obstructive suppurative cholangitis) in the elderly can quickly become fatal.

#hepatology

References:

1. Arima N, Uchiya T, Hishikawa R, Saito M, Matsuo T, Kurisu S, Umeki M, Kita Y, Koyama T, Hatta T, et al. [Clinical characteristics of impacted bile duct stone in the elderly]. Nihon Ronen Igakkai Zasshi. 1993 Nov;30(11):964-8. Japanese. doi: 10.3143/geriatrics.30.964. PMID: 8295355.

2. Skinner TR, Scott IA, Martin JH. Diagnostic errors in older patients: a systematic review of incidence and potential causes in seven prevalent diseases. Int J Gen Med. 2016 May 20;9:137-46. doi: 10.2147/IJGM.S96741. PMID: 27284262; PMCID: PMC4881921.

OMG and AchR-Ab

Q: Patients with Ocular Myasthenia Gravis (OMG) are more likely to be seronegative for acetylcholine receptor antibodies (AChR-Ab) than patients with Generalized Myasthenia Gravis (GMG).

A) True

B) False

Answer: A

Reasons are not fully understood why ocular muscles are distinctly involved in MG? And why do about 15 percent of patients only develop OMG and never progress to GMG? 

There are four proposed mechanisms for this:

1. The most likely reason is the fact that levator palpebrae superioris is under constant activation (eye-opening) and is susceptible to fatigue. 

2. The junctional folds of muscle endplates are sparse in the extraocular and levator muscles. This leads to a lower safety factor for neuromuscular transmission.

3. The complement regulatory genes are expressed differently in extraocular muscles. This reduces the protective mechanisms to complement-mediated tissue injury.

4. Patients with OMG are more likely to be seronegative for acetylcholine receptor antibodies (AChR-Ab) than patients with GMG. This may be the reason for the development of only OMG, but not GMG.

#neurology

References:

1. Kaminski HJ, Maas E, Spiegel P, Ruff RL. Why are eye muscles frequently involved in myasthenia gravis? Neurology 1990; 40:1663.

2. Kaminski HJ, Li Z, Richmonds C, et al. Susceptibility of ocular tissues to autoimmune diseases. Ann N Y Acad Sci 2003; 998:362.

3. Sommer N, Melms A, Weller M, Dichgans J. Ocular myasthenia gravis. A critical review of clinical and pathophysiological aspects. Doc Ophthalmol 1993; 84:309.

Leg ulcer in SCD patients

Case: 32 years old African-American female with a known history of Sickle Cell Disease (SCD) getting recovered in ICU from a Sickle cell crisis and complained of severe leg pain; on examination found to have a painful ulcer site. Venous duplex is negative. Your next step?

A) Prophylactic antibiotic

B) IVC filter

C) Workup for pulmonary hypertension (P-HTN)

D) Lower Extremity angiogram

Answer: C

This question aims to highlight that leg ulcers in SCD patients are highly associated with morbidities like Deep Venous Thrombosis (DVT) and P-HTN.

Leg ulcer in SCD patients is usually not an infectious process. It requires good wound care. There is no need for prophylactic antibiotics (choice A).

IVC filter is not the first line of management in DVT, so inserting a prophylactic IVC filter (choice B) is unnecessary.

A lower extremity angiogram can be pursued if there is a threat to limb viability. This should not be the 'next best action of management' (choice D).

Leg ulcers in SCD patients are way more painful than in other patients. This is one of the characteristics of leg ulcers in this patient population.

If the venous duplex is negative, wound care, pain management, topical opioids, lower extremity elevation, and compression bandages usually suffice. In unresolved cases, surgical debridement may be needed.

#hematology

#pulmonary

#dermatology

References:

1. Gladwin MT, Sachdev V, Jison ML, Shizukuda Y, Plehn JF, Minter K, Brown B, Coles WA, Nichols JS, Ernst I, Hunter LA, Blackwelder WC, Schechter AN, Rodgers GP, Castro O, Ognibene FP. Pulmonary hypertension as a risk factor for death in patients with sickle cell disease. N Engl J Med. 2004 Feb 26;350(9):886-95. doi: 10.1056/NEJMoa035477. PMID: 14985486.

2. Gordeuk VR, Castro OL, Machado RF. Pathophysiology and treatment of pulmonary hypertension in sickle cell disease. Blood. 2016 Feb 18;127(7):820-8. doi: 10.1182/blood-2015-08-618561. Epub 2016 Jan 12. PMID: 26758918; PMCID: PMC4760088.

HRQOL after lung transplant

Q: All of the following have been shown to improve Health-Related Quality of Life (HRQOL) after lung transplantation EXCEPT? (select one)

A) Male gender

B) Pulmonary rehabilitation

C) Psychosocial intervention

D) Pet ownership 

Answer: A

HRQOL after lung transplantation depends on various factors such as preoperative severity of illness, frailty prior to transplant, renal dysfunction, nutritional factors, and primary graft dysfunction. Many interventions can improve HRQOL such as good pulmonary rehabilitation, apps to record self-care, and psychosocial intervention.

Contrary to popular belief, pet ownership is found to be associated with higher life satisfaction, optimism, and perceived social support without any untoward medical consequences or high risks of infection.

Female gender has some favorable greater improvement in HRQOL than male gender.

#transplantation

#pulmonary

References: 

1. Irani S, Mahler C, Goetzmann L, et al. Lung transplant recipients holding companion animals: impact on physical health and quality of life. Am J Transplant 2006; 6:404.

2. Vasiliadis HM, Collet JP, Poirier C. Health-related quality-of-life determinants in lung transplantation. J Heart Lung Transplant 2006; 25:226.

3. Finlen Copeland CA, Vock DM, Pieper K, et al. Impact of lung transplantation on recipient quality of life: a serial, prospective, multicenter analysis through the first posttransplant year. Chest 2013; 143:744.

mechanism by which lactulose improve hepatic encephalopathy

Q; Lactulose improves hepatic encephalopathy by? (select one)

A) Acidification of the gut lumen

B) Alkalization of the gut lumen

Answer: A

• The conversion of Lactulose to lactic acid results in acidification of the gut lumen. This favors the conversion of NH4 + to NH3 and the passage of NH3 from tissues into the lumen.
• Gut acidification inhibits ammoniagenic coliform bacteria, leading to increased levels of nonammoniagenic lactobacilli.
• Lactulose also works as a cathartic, reducing colonic bacterial load.

#GI

#hepatology

References:

1. Shuliat'ev IS, Il'chenko LIu, Vinnitskaia EV, Petrakov AV, Sil'verstrova SIu. Laktuloza v lechenii pechenochnoĭ éntsefalopatii u bol'nykh tsirrozom pecheni [Lactulose in treatment of hepatic encephalopathy in patient with liver cirrhosis]. Eksp Klin Gastroenterol. 2002;(5):38-41, 127. Russian. PMID: 12619575.

2. Luo M, Li L, Lu CZ, Cao WK. Clinical efficacy and safety of lactulose for minimal hepatic encephalopathy: a meta-analysis. Eur J Gastroenterol Hepatol. 2011 Nov;23(12):1250-7. doi: 10.1097/MEG.0b013e32834d1938. PMID: 21971378.

3. Hudson M, Schuchmann M. Long-term management of hepatic encephalopathy with lactulose and/or rifaximin: a review of the evidence. Eur J Gastroenterol Hepatol. 2019 Apr;31(4):434-450. doi: 10.1097/MEG.0000000000001311. PMID: 30444745; PMCID: PMC6416096.

Vocal cord pearl? - Diagnosis?

Scenario: As you are intubating a patient you visualize the following picture.

Answer: Vocal Fold Polyp

A vocal fold polyp is a fluid-filled lesion that may occur unilaterally or bilaterally. They may vary in size and may be either "sessile" or pedunculated". They are most commonly thought to be caused by vocal abuse or trauma, cigarette smoking, or vocal fold hemorrhage. Vocal characteristics often include hoarseness, diplophonia (audible perception of two distinct pitches), and stridor (noisy breathing). A vocal fold polyp though usually require surgical removal but conservative and speech therapy can be tried.

#procedure

#ENT

References:

1. Vasconcelos D, Gomes AOC, Araújo CMT. Vocal Fold Polyps: Literature Review. Int Arch Otorhinolaryngol. 2019 Jan;23(1):116-124. doi: 10.1055/s-0038-1675391. Epub 2019 Jan 14. PMID: 30647795; PMCID: PMC6331298.

2. Jeong WJ, Lee SJ, Lee WY, Chang H, Ahn SH. Conservative management for vocal fold polyps. JAMA Otolaryngol Head Neck Surg. 2014 May;140(5):448-52. doi: 10.1001/jamaoto.2014.243. PMID: 24676626.

Renal protection in severe malaria

Q: Which of the following antipyretic is found to be renal protective in severe malaria? (select one)

A) Acetaminophen 

B) Prednisone

C) Ibuprofen 

Answer: A

Interestingly, acetaminophen is not only the choice to control fever in severe malaria, it also provides protection against renal dysfunction. High fever is common in severe malaria corresponding with endogenous pyrogens release at the time of schizont rupture. Very high fever in such settings may also lead to seizures.

Kidney insufficiency is common in severe malaria due to high extracellular hemoglobin in the setting of intravascular hemolysis which leads to oxidative renal tubular damage. This gets further complicated by fever, dehydration and schizont rupture.

Oral acetaminophen, 1 gram every 6 hours for 72 hour till malaria can be controlled found to provide independent renal protection in severe malaria.

#ID

#renal

References:

1. Conroy AL, Hawkes MT, Leligdowicz A, et al. Blackwater fever and acute kidney injury in children hospitalized with an acute febrile illness: pathophysiology and prognostic significance. BMC Med 2022; 20:221.

2. Plewes K, Kingston HWF, Ghose A, et al. Acetaminophen as a Renoprotective Adjunctive Treatment in Patients With Severe and Moderately Severe Falciparum Malaria: A Randomized, Controlled, Open-Label Trial. Clin Infect Dis 2018; 67:991.

Glucocorticoid-induced myopathy

Q: 52 years old female with severe history of steroid-dependent asthma is admitted to ICU with impending respiratory failure, requiring intubation. Glucocorticoid-induced myopathy is suspected. Glucocorticoid-induced myopathy is irreversible?

A) True

B) False

Answer: B

Although fluorinated glucocorticoid preparation like dexamethasone is less likely to cause myopathy than nonfluorinated preparation such as prednisone, weaning and discontinuation is the best treatment to resolve myopathy. Fortunately, this weakness is reversible. Although resistance exercises and using the lowest possible dose may help, prolonged intake of steroids eventually takes its toll on the muscle.

Less appreciated is the fact that glucocorticoid myopathy may affect the respiratory muscles like our patient in the above question. In this population of patients, lower inspiratory muscle strength and endurance are reported, though there is no evidence of decreased maximal expiratory pressures.

#pulmonary

#pharmacology

#musculoskeletal

References:

1. Bowyer SL, LaMothe MP, Hollister JR. Steroid myopathy: incidence and detection in a population with asthma. J Allergy Clin Immunol 1985; 76:234.

2. Akkoca O, Mungan D, Karabiyikoglu G, Misirligil Z. Inhaled and systemic corticosteroid therapies: Do they contribute to inspiratory muscle weakness in asthma? Respiration 1999; 66:332.

3. Wu K, Michalski A, Cortes D, et al. Glucocorticoid-induced myopathy in people with asthma: a systematic review. J Asthma 2022; 59:1396.

Acidosis and NMBs

Q: Acidosis may _______________ the effects of Neuromuscular blockades (NMBs)? - select one

A) prolongs

B) shortens

Answer: A

Metabolic and respiratory acidosis may prolong the effects of NMBs. This occurs via two mechanisms. First, the affinity of NMBs increases for postjunctional neuronal nicotinic acetylcholine receptors (nAChRs). Second, acidosis causes hypocalcemia which results in prolonging the effect of NMB. This effect becomes more pronounced as PH drops below 7.3. Conversely, with PH above 7.51, the effect of NMBs gets shortened mostly of nondepolarizing NMBs.

#pharmacology

#acidosis

References:

1. Waud BE, Waud DR. Interaction of calcium and potassium with neuromuscular blocking agents. Br J Anaesth 1980; 52:863.

2. Yamauchi M, Takahashi H, Iwasaki H, Namiki A. Respiratory acidosis prolongs, while alkalosis shortens, the duration and recovery time of vecuronium in humans. J Clin Anesth 2002; 14:98.

SGLT2 and blood count

Q: sodium-glucose co-transporter 2 (SGLT2) inhibitors may induce? (select one)

A) Anemia

B) Polycythemia

Answer: B

Conventionally, it is believed that all drugs tend to cause anemia, but this is not true. Some drugs can cause polycythemia as well. Some well-known drugs are erythropoietin (EPO), testosterone/anabolic steroids, and performance-enhancement drugs. SGLT2 is a new addition to the list. 

Diuretics do not cause pure polycythemia, but by decreasing serum/cell ratio, it causes pseudo-polycythemia.

#pharmacology

#hematology

References:

1. Sano M, Goto S. Possible Mechanism of Hematocrit Elevation by Sodium Glucose Cotransporter 2 Inhibitors and Associated Beneficial Renal and Cardiovascular Effects. Circulation 2019; 139:1985.

2. Chin-Yee B, Solh Z, Hsia C. Erythrocytosis induced by sodium-glucose cotransporter-2 inhibitors. CMAJ 2020; 192:E1271.

VPA toxicity

Q: Patients with Valproic acid (VPA) toxicity develop all of the following EXCEPT? (select one)

A) hyponatremia

B) hyperosmolality

C) hypocalcemia

D) anion gap acidosis

E) elevated osmolal gap

Answer: A

Knowing how to treat drug overdose is essential in ICU. This question aims to identify the lab evidence of valproic acid overdose. The use of valproic acid is on the rise as an anti-delirium agent in ICU. 

VPA is a high-sodium salt compound. It contains 13.8 mg sodium per 100 mg of VPA. Toxicity results in significant hypernatremia. It contains osmotically-active acids, resulting in osmolal and anion gaps. Hypocalcemia develops when calcium binds anionic VPA metabolites.

Treatment is usually supportive. Hemodialysis can be carried out in extreme cases.

#toxicity

References:

1. Anderson, GO, Ritland, S. Life threatening intoxication with sodium valproate. Clin Toxicol 1995; 33:279.

2. Khoo SH, Leyland MJ. Cerebral edema following acute sodium valproate overdose. J Toxicol Clin Toxicol 1992; 30:209.

3. Mortensen PB, Hansen HE, Pedersen B, et al. Acute valproate intoxication: biochemical investigations and hemodialysis treatment. Int J Clin Pharmacol Ther Toxicol 1983; 21:64.

tPA in HD catheter

Q: Once-weekly instillation of tissue plasminogen activator (tPA, alteplase) in hemodialysis catheter? (select one)

A) lowers catheter malfunction 

B) lowers catheter-related bacteremia 

C) Both A and B

Answer: C

At least one small trial of 225 hemodialysis-dependent patients from Calgary, Canada, showed that once-weekly instillation of tissue plasminogen activator (tPA or alteplase) - 1 mg in each lumen - not only lowers the catheter malfunction (20 vs. 35 percent) but also catheter-related bacteremia (4.5 vs. 13 percent). The reduction in bacteremia is probably due to less thrombosis-led infection. Said that practice is not widely used.

#nephrology

#procedures

Reference:

Hemmelgarn BR, Moist LM, Lok CE, et al. Prevention of dialysis catheter malfunction with recombinant tissue plasminogen activator. N Engl J Med 2011; 364:303.

Signs of MH

Q: What usually precedes first in Malignant Hyperthermia (MH)? (select one)

A) hypercarbia

B) tachycardia

C) muscle rigidity

D) peaked T waves

Answer: A

While in OR or ICU, if a patient is intubated, an unexplained increase in end-tidal carbon dioxide (ETCO2) associated tachypnea (breathing over the ventilator) is the first sign, followed by tachycardia. Core body hyperthermia follows. These are considered hallmarks or 'first three signs' of MH.

Masseter or generalized muscle rigidity may occur or persist despite paralysis with a neuromuscular blocker, and EKG changes of hyperkalemia usually occur last. Isolated rhabdomyolysis may also occur.

#pharmacology

#muscles

References:

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

2. Larach MG, Localio AR, Allen GC, et al. A clinical grading scale to predict malignant hyperthermia susceptibility. Anesthesiology 1994; 80:771.

alcohol-related seizures

Q: Status epilepticus is the hallmark of alcohol withdrawal seizures?

A) True

B) False

Answer: B

Status epilepticus in an alcoholic patient should lead a clinician to consider other etiologies. It is very unlikely to withdraw from alcohol with status epilepticus. Structural or infectious etiology should be ruled out.

The classic ETOH-associated withdrawal seizures occur within 12 to 48 hours as generalized tonic-clonic convulsions, but progress to status is unlikely.

Patient usually has a prolonged history of ETOH. It rarely occurs in young people. A typical patient is usually in their 40s or 50s. It usually occurs as a single event or a cluster of a few events within a short period - but rarely culminates into a status. 

#toxicology

#neurology

References:

1. Victor M, Brausch C. The role of abstinence in the genesis of alcoholic epilepsy. Epilepsia 1967; 8:1.

2. Rathlev NK, D'Onofrio G, Fish SS, et al. The lack of efficacy of phenytoin in the prevention of recurrent alcohol-related seizures. Ann Emerg Med 1994; 23:513.

DF

Q:  Maddrey discriminant function is a formula to determine the disease severity and mortality risk in patients with alcoholic hepatitis. The calculation of Maddrey 'discriminant' function (DF) includes all EXCEPT? (select one)

A) prothrombin time (sec) 

B) control prothrombin time (sec)

C) serum bilirubin

D) AST/ALT ratio

Answer: D

Maddrey discriminant function is a formula to determine the disease severity and mortality risk in patients with alcoholic hepatitis. 

Discriminant Function = 4.6 * (Pt's PT - Control PT) + TBili

There are two objectives of this question. 

First, to emphasize that the extent of hepatic function is best presented by prothrombin time. That's why AST/ALT ratio is NOT included in this formula (choice D). 

Second, to highlight that why it is called Maddrey 'discriminant' function. Because it helps to discriminate between patients who may benefit from treatment with or without glucocorticoids. Patients with a DF value ≥32 may benefit from glucocorticoid treatment; as such alcoholic patients may have high short-term mortality.

#hepatology

References: 

1. Imperiale TF, McCullough AJ. Do corticosteroids reduce mortality from alcoholic hepatitis? A meta-analysis of the randomized trials. Ann Intern Med 1990; 113:299.

2. Maddrey WC, Boitnott JK, Bedine MS, et al. Corticosteroid therapy of alcoholic hepatitis. Gastroenterology 1978; 75:193.

EGPA and lungs

Q: The involvement of lungs and no other organs is a good prognostic sign in Eosinophilic granulomatosis with polyangiitis (EGPA; Churg-Strauss)?

A) True

B) False

Answer: A

EGPA is an antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis of the small and medium-sized arteries.

Although lung is the most commonly involved organ in EGPA, also known as Churg-Strauss disease, vasculitis of extrapulmonary organs is mostly responsible for morbidity and mortality. In fact, the most commonly used score, the Five-factor score (FFS), to determine disease activity does not even involve lungs. It counts older age, heart, GI, and kidney involvement but absence of ENT symptoms. The presence of ENT symptoms and involvement of only the lungs are considered good prognostic signs. 

Said that recently (2021) American College of Rheumatology/Vasculitis Foundation (ACR/VF) guidelines recommends approaching the initial treatment of EGPA by differentiating patients into severe and non-severe disease. If pulmonary hemorrhage is present, it predispose patients to severe disease.

The absence of ANCA and minimal symptoms are also good prognostic signs.

#vasculitis

#rheumatology

References:

Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation Guideline for the Management of Antineutrophil Cytoplasmic Antibody-Associated Vasculitis. Arthritis Care Res (Hoboken) 2021; 73:1088.

Guillevin L, Pagnoux C, Seror R, et al. The Five-Factor Score revisited: assessment of prognoses of systemic necrotizing vasculitides based on the French Vasculitis Study Group (FVSG) cohort. Medicine (Baltimore) 2011; 90:19.

Ca in hyperkalemia

Q; Which of the following increases the cardiotoxicity of hyperkalemia? (select one)

A) Hypercalcemia

B) Hypocalcemia

Answer: B

Hypocalcemia increases the cardiotoxicity of hyperkalemia; that's why calcium is usually the first line of action in an unstable patient with EKG changes and 'near code.' Ca directly antagonizes membrane actions of hyperkalemia. Hyperkalemia induces depolarization of cardiac muscles' resting membrane potential and leads to sodium channel inactivation. This decreases membrane excitability. Ca prevents this effect of hyperkalemia.

Calcium works within 5 minutes and can be repeated in 5 minutes if EKG changes persist in such patients. The effect lasts for 30 to 60 minutes. Usually, this management is combined with other modalities such as 'Insulin with glucose' and bicarbonate infusion. Many clinicians may forget the caveat that bicarbonate should be administrated after calcium infusion, as post-bicarb calcium may combine with already administrated bicarbonate and form calcium-carbonate in the body. Calcium should be given first and bicarbonate afterwards. It is important to understand that all these measures are temporary and meant to buy time till definite treatment can be employed to resolve hyperkalemia.

#electrolytes

#cardiology

References:

1. Long B, Warix JR, Koyfman A. Controversies in Management of Hyperkalemia. J Emerg Med 2018; 55:192.

2. Winkler AW, Hoff HE, Smith PK. Factors affecting the toxicity of potassium. Am J Physiol 1939; 127:430.

3. Lindner G, Burdmann EA, Clase CM, Hemmelgarn BR, Herzog CA, Małyszko J, Nagahama M, Pecoits-Filho R, Rafique Z, Rossignol P, Singer AJ. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med. 2020 Oct;27(5):329-337. doi: 10.1097/MEJ.0000000000000691. PMID: 32852924; PMCID: PMC7448835.