Severe hypermagnesemia

Q: 52 years old male with End Stage Renal Disease (ESRD) presented to Emergency Department (ED) with respiratory failure and hypotension. Patient was intubated in the field. In ED patient was found to have a complete heart block. ER physician emergently inserted an intravenous pacemaker which stabilizes the hemodynamics. On clinical exam, the patient is unresponsive and has lost reflexes. Labs showed abnormalities, but the most pronounced was a magnesium level of 17.0 mEq/L. Intravenous calcium is given. What should be the next step?



Answer: Emergent Dialysis

Magnesium has a fairly good therapeutic margin, but hypermagnesemia is a risk in some patients, particularly renal failure. Mild hypermagnesemia may cause weakness, nausea, vomiting, and hypotension, but it can become progressively life-threatening. Following are the ballpark clinical signs/symptoms depending on magnesium level.

• 4.0 mEq/L hyporeflexia
• 5.0 mEq/L Prolonged atrioventricular conduction
• 7.0-10.0 mEq/L - loss of patellar reflex
• 10.0-13.0 mEq/L - respiratory depression and various heart block
• Above 13.0 mEq/L - cardiac arrest/Asystole.

The mainstay of treatment is withdrawing magnesium supplementation, intravenous calcium, diuretics, and in severe cases, dialysis.

#electrolytes

Reference:

Bansal AD, Negoianu D, Warburton KM. An Unusual yet "Mg"nificent Indication for Hemodialysis. Semin Dial. 2016 May;29(3):247-50. doi: 10.1111/sdi.12479. Epub 2016 Feb 25. PMID: 26915350; PMCID: PMC5492508.

Plasmapheresis in severe refractory thyroid storm

Q: Periodic plasmapheresis every few months is a viable option instead of thyroidectomy in severe refractory thyroid storm?

A) True

B) False

Answer: B

Plasmapheresis can be used as a bridge in severe refractory thyroid storm while preparing for thyroidectomy. This is because plasmapheresis's effect is transient and lasts only for a day or two. Although there is weak evidence that plasmapheresis before urgent thyroidectomy may improve outcomes.

#endocrinology

References:

1. Vyas AA, Vyas P, Fillipon NL, et al. Successful treatment of thyroid storm with plasmapheresis in a patient with methimazole-induced agranulocytosis. Endocr Pract 2010; 16:673.

2. Tieken K, Paramasivan AM, Goldner W, et al. THERAPEUTIC PLASMA EXCHANGE AS A BRIDGE TO TOTAL THYROIDECTOMY IN PATIENTS WITH SEVERE THYROTOXICOSIS. AACE Clin Case Rep 2020; 6:e14.

CXR in AAT

Q: Emphysematous bullae are predominantly present in ___________ region in alpha-1 antitrypsin (AAT) deficiency? (select one)

A) apical

B) basilar

Answer: B

Although not a rule, classically, CXR in AAT shows basilar predominant emphysematous bullae. This leads to redistribution of vascular flow to less involved upper lobes. 

CXR shows markedly visible hyper-expansion with paucity of vascular structures at the bases.

#pulmonary

#radiology

Reference:

Huang YT, Wencker M, Driehuys B. Imaging in alpha-1 antitrypsin deficiency: a window into the disease. Ther Adv Chronic Dis. 2021 Jul 29;12_suppl:20406223211024523. doi: 10.1177/20406223211024523. PMID: 34408834; PMCID: PMC8367205.

Miller Fisher's syndrome

Q: Which lab is diagnostic of Miller-Fisher syndrome (MFS)?

Answer:  Anti-GQ1b antibodies

Miller-Fisher syndrome (MFS) is a variant of GBS (Guillain–Barré syndrome), accounting for approximately 5% of cases. Clinically it is diagnosed by a descending paralysis, proceeding in the reverse order of the more common form of GBS. It affects the eye muscles first and presents with the triad of

• ophthalmoplegia
• ataxia
• areflexia

Also, Ataxia predominantly affects the gait and trunk, with the limbs relatively spared. Anti-GQ1b antibodies are present in 90% of cases.

#neurology

References: 

1. Teener JW. Miller Fisher's syndrome. Semin Neurol. 2012 Nov;32(5):512-6. doi: 10.1055/s-0033-1334470. Epub 2013 May 15. PMID: 23677659. 

2. Rocha Cabrero F, Morrison EH. Miller Fisher Syndrome. 2022 Jun 27. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 29939539.

Anemia in CHF

Q: Which of the following contributes to anemia in congestive heart failure (CHF) patients?  - select one

A) Dilutional anemia 

B) Iron deficiency anemia

C) Use of angiotensin converting enzyme(ACE) inhibitors 

D) Anemia of chronic disease

E) All of the above

Answer: E

This question aims to address the multifactorial causes of anemia in CHF patients. It is important to pay attention to less known causes of anemia in these patients, such as dilutional anemia or direct anemic effect of ACE inhibitors. Level of anemia correlates directly with poor prognosis. Although some factors can be modified or treated, such as dilutional or Fe-deficiency anemia, some are essential and can't be modified, such as use of ACE inhibitors.

#cardiology

#hematology

References:

1. Androne AS, Katz SD, Lund L, et al. Hemodilution is common in patients with advanced heart failure. Circulation 2003; 107:226.

2. Ishani A, Weinhandl E, Zhao Z, et al. Angiotensin-converting enzyme inhibitor as a risk factor for the development of anemia, and the impact of incident anemia on mortality in patients with left ventricular dysfunction. J Am Coll Cardiol 2005; 45:391.

3. Tanner H, Moschovitis G, Kuster GM, Hullin R, Pfiiffner D, Hess OM, Mohacsi P. The prevalence of anemia in chronic heart failure. Int J Cardiol. 2002 Nov;86(1):115-21. doi: 10.1016/s0167-5273(02)00273-5. PMID: 12400591.

4. Crosato M, Steinborn W, Anker SD. Anemia in chronic congestive heart failure: frequency, prognosis, and treatment. Heart Fail Monit. 2003;4(1):2-6. PMID: 12808478.

oxygen sensors

Q: What is the body's major stimulus for Erythropoietin (EPO) production?

Answer: decreased oxygen delivery 

Though simple, an essential concept is to understand that the human body is designed to respond against reduced oxygen delivery, either caused by anemia or hypoxemia. The human body contains factors called hypoxia-inducible factor (HIF), comprised of alpha and beta subunits (HIF-1-alpha and HIF-1-beta). HIF regulates EPO transcription and is popularly known as "oxygen sensors." 

It can be said that the 'oxygen sensor' regulates life. Low oxygen delivery stimulates the O2 sensor. These sensors are designed to perform many other associated mechanisms to regain and maintain normoxia. In normal humans, oxygen quickly destroys these sensors (negative feedback) to protect against polycythemia.

#hematology

References:

1. Semenza GL. Oxygen sensing, homeostasis, and disease. N Engl J Med 2011; 365:537.

2. Franke K, Gassmann M, Wielockx B. Erythrocytosis: the HIF pathway in control. Blood 2013; 122:1122.

3. Semenza GL. Involvement of oxygen-sensing pathways in physiologic and pathologic erythropoiesis. Blood 2009; 114:2015.

4. Yoon D, Ponka P, Prchal JT. Hypoxia. 5. Hypoxia and hematopoiesis. Am J Physiol Cell Physiol 2011; 300:C1215.

CSF to serum glucose ratio in acute bacterial meningitis

Q: What is the usual CSF to serum glucose ratio in acute bacterial meningitis (ABM)?

Answer: ≤0.4

Although conventionally, it is taught that the cerebrospinal fluid (CSF) glucose in ABM should be below 40 mg/dL, a reasonable approach would be to look for CSF to serum glucose ratio, which should be ≤0.4. Other usual findings in ABM are protein >200 mg/dL and Leucocytosis with predominant neutrophils. 

Said that it is not necessary for all findings need to be present in ABM. A clinician's judgment, combined with history and prevalent community epidemiology, plays an essential role.

#ID

#neurology

References:

1. Tamune H, Takeya H, Suzuki W, Tagashira Y, Kuki T, Honda H, Nakamura M. Cerebrospinal fluid/blood glucose ratio as an indicator for bacterial meningitis. Am J Emerg Med. 2014 Mar;32(3):263-6. doi: 10.1016/j.ajem.2013.11.030. Epub 2013 Nov 26. PMID: 24361137.

2. Powers WJ. Cerebrospinal fluid to serum glucose ratios in diabetes mellitus and bacterial meningitis. Am J Med. 1981 Aug;71(2):217-20. doi: 10.1016/0002-9343(81)90108-x. PMID: 7258216.

most common extrapulmonary site of infection for blastomycosis

Q: Which is the most common extrapulmonary site of infection for blastomycosis? - select one

A) Skin

B) Bone and joint

C) Genitourinary system 

D) Central nervous system

E) Adrenal gland

Answer: A

Pneumonia is the most common presentation in blastomycosis. The acute phase of pneumonia is usually missed as symptoms are almost impossible to distinguish from other common causes of pneumonia/pneumonitis. Patients are usually in a chronic pneumonia phase at the presentation time and carry other extrapulmonary symptoms. The findings on the skin are the most helpful clues after history and epidemiological distribution. A patient may present with a verrucous lesion with irregular borders of gray to violet colors. 

Their appearance is very close to squamous cell carcinoma and may prompt biopsy, which reveals the diagnosis with the presence of microabscesses at the periphery of the lesions and broad-based budding organisms. Lesions are usually ulcerative lesions and may bleed easily.

#ID

#dermatology

References:

1. G Caldito E, Ajiboye O, Flores E, Antia C, Demarais P. The importance of skin exam in chronic pulmonary blastomycosis. IDCases. 2020 May 13;20:e00812. doi: 10.1016/j.idcr.2020.e00812. PMID: 32455114; PMCID: PMC7235621.

2. McBride JA, Gauthier GM, Klein BS. Clinical Manifestations and Treatment of Blastomycosis. Clin Chest Med. 2017 Sep;38(3):435-449. doi: 10.1016/j.ccm.2017.04.006. Epub 2017 Jun 12. PMID: 28797487; PMCID: PMC5657236.

IV Ketorolac and IV Morphine interaction

Q: Which precaution should be taken while giving IV Ketorolac in post-operative patients who are also getting IV Morphine?

Answer: Use different ports to avoid precipitation

When giving Ketorolac intravenously through the same IV catheter as morphine, the two drugs have been known to combine and form a precipitate. Line flushing can push the blockage through and may cause embolism. Different ports should be used for each drug.

Another less well-known fact is that ketorolac potentiates the effect of morphine which may cause respiratory depression in postop patients.

#pharmacology

#surgical-critical-care

References:

1. Feng-Sheng Lin,Tzu-Fu Lin,Yu-Chang Yeh,Chih-Peng Lin &Wei-Zen Sun Compatibility and stability of ketorolac tromethamine and morphine hydrochloride in 0.9% sodium chloride injection - Pages 99-103 | Published online: 19 Jul 2013 The Pain Clinic - Volume 19, 2007 - Issue 3 https://doi.org/10.1179/016911107X268701 

2. Picard P, Bazin JE, Conio N, Ruiz F, Schoeffler P. Ketorolac potentiates morphine in postoperative patient-controlled analgesia. Pain. 1997 Dec;73(3):401-406. doi: 10.1016/S0304-3959(97)00128-0. PMID: 9469531.

RCVS

Q: Seizure is more common with? (select one)

A) Reversible cerebral vasoconstriction syndrome (RCVS) 

B) Reversible posterior leukoencephalopathy syndrome (RPLS)

Answer: A

RCVS, like RPLS is also due to dysregulation of cerebral arterial tone. A major differentiating feature is the quality of headaches. In RCVS, headaches are classically sudden in contrast to insidious in RPLS. Visual symptoms, seizures, and MRI abnormalities are less common with RCVS. To make things confusing, both can occur together.

RCVS is actually an umbrella term for various etiologies. It is usually due to reversible multifocal narrowing of the cerebral arteries and presents as thunderclap-like headache. It may also manifest as a focal neurologic. It is mostly benign. 

The other names are migrainous vasospasm, migraine angiitis, Call-Fleming syndrome, Call syndrome, thunderclap headache-associated vasospasm, drug-induced cerebral arteritis, postpartum cerebral angiopathy, benign angiopathy of the central nervous system, and central nervous system pseudovasculitis.

#neurology

References:

1. Jun-O'Connell AH, Sundar B, Morris M. The Spectrum of Cerebral Vasoconstriction: A Diagnostic Conundrum. J Neurol Stroke 2016; 4:00119.

2. Singhal AB, Hajj-Ali RA, Topcuoglu MA, et al. Reversible cerebral vasoconstriction syndromes: analysis of 139 cases. Arch Neurol 2011; 68:1005.

Side effect of Rasburicase

Q; 58 years old male with previous history of tumor lysis syndrome, which was successfully treated with Rasburicase a few months ago, is in relapse. Re-dose with Rasburicase is prescribed again. Which one precaution should be exercised?

Answer: Treatment for anaphylaxis at the bedside.

One of the rare but dreaded side effects of Rasburicase is anaphylaxis. The risk goes substantially high with repeated dose(s). This risk stays high even if the dose is repeated months after the first dose.

#pharmacology

#oncology

Reference: 

Allen KC, Champlain AH, Cotliar JA, et al. Risk of anaphylaxis with repeated courses of rasburicase: a Research on Adverse Drug Events and Reports (RADAR) project. Drug Saf 2015; 38:183.

Sight threatening in Graves' orbitopathy

Q; 32 year old female with Grave's disease and with a known orbitopathy (exophthalmos) is in ICU for the management of thyroid storm. Patient complains of  loss of color vision. You next step of management?

A) Continue to observe

B) Warm compression

C) Intravenous (IV) thyroxine bolus

D) IV dexamethasone 4 mg

E) Orbital decompression surgery

Answer: D

Visual impairment in Graves' orbitopathy is a medical as well as a surgical emergency. The most common initial complaint is loss of color vision. Ophthalmology should be called immediately for urgent orbital decompression. Meanwhile 4 mg IV dexamethasone should be given immediately as a first step.

#endocrinology

#opthalomplogy

References:

1. Tramunt B, Imbert P, Grunenwald S, Boutault F, Caron P. Sight-threatening Graves' orbitopathy: Twenty years' experience of a multidisciplinary thyroid-eye outpatient clinic. Clin Endocrinol (Oxf). 2019 Jan;90(1):208-213. doi: 10.1111/cen.13880. Epub 2018 Nov 19. PMID: 30339291.

2. Bartalena L. Sight-Threatening Graves’ Ophthalmopathy. [Updated 2019 Jan 3]. In: Feingold KR, Anawalt B, Boyce A, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK279098/

Sodium and CHF

Q: Hyponatremia in congestive heart failure (CHF) parallel the severity of the heart failure?

A) True

B) False

Answer: If hyponatremia occurs solely due to CHF, studies have shown that the patient survival is significantly decreased below serum sodium of 137 mEq/L. Moreover, it is almost considered end-stage once it crosses below 125 mEq/L. 

Unfortunately, hyponatremia is not only a poor prognostic in long-term CHF but also in patients who get admitted to the hospital with an exacerbation of CHF. It correlates with mortality in-hospital and 30-days.

#cardiology

References: 

1. Goldberg A, Hammerman H, Petcherski S, et al. Hyponatremia and long-term mortality in survivors of acute ST-elevation myocardial infarction. Arch Intern Med 2006; 166:781.

2. Klein L, O'Connor CM, Leimberger JD, et al. Lower serum sodium is associated with increased short-term mortality in hospitalized patients with worsening heart failure: results from the Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) study. Circulation 2005; 111:2454.

3. Gheorghiade M, Abraham WT, Albert NM, et al. Relationship between admission serum sodium concentration and clinical outcomes in patients hospitalized for heart failure: an analysis from the OPTIMIZE-HF registry. Eur Heart J 2007; 28:980.

4. Sato N, Gheorghiade M, Kajimoto K, et al. Hyponatremia and in-hospital mortality in patients admitted for heart failure (from the ATTEND registry). Am J Cardiol 2013; 111:1019.

Paraneoplastic syndromes associated with gastric cancer

Case: 42 years old male is admitted to ICU with severe uncontrolled hypertension (HTN). Subsequent workup led to the diagnosis of polyarteritis nodosa (PAN) due to gastric cancer. This tends to be a good sign.

A) True

B) False

Answer: A

Although paraneoplastic manifestations of gastric tumor are usually late in the disease, polyarteritis nodosa is unique in a sense that it appears early as a single manifestation and a sign of a surgically curable gastric cancer.

Other paraneoplastic manifestations are "sign of Leser-Trélat", acanthosis nigricans, microangiopathic hemolytic anemia, membranous nephropathy, and hypercoagulable states popularly known as Trousseau's syndrome.

#oncology

#rheumatology

References:

1. Poveda F, González-García J, Picazo ML, et al. Systemic polyarteritis nodosa as the initial manifestation of a gastric adenocarcinoma. J Intern Med 1994; 236:679.

2. Taketa T, Ohigashi S, Suzuki K, Sudo K, Shiozaki H, Suzuki A, Blum MA, Ajani JA, Onodera H. Paraneoplastic neurological syndromes associated with gastric cancer: a case report and review of the literature. Clin J Gastroenterol. 2012 Oct;5(5):355-60. doi: 10.1007/s12328-012-0328-z. Epub 2012 Aug 28. PMID: 26181075.

Thyrotoxic Periodic Paralysis (TPP)

Q: Out of the following, which one can be used as an adjuvant treatment in Thyrotoxic Periodic Paralysis (TPP)?

A) Calcium Channel Blockers

B) Nonselective Beta Blockers 

C) Corticosteroids

D) Intravenous magnesium

E) Intravenous Dextrose

Answer: B (Nonselective Beta Blockers -propranolol)

In Thyrotoxic Periodic Paralysis (TPP), propranolol, a nonselective beta-blocker, has been shown to prevent the intracellular shift of potassium and phosphate by blunting the hyperadrenergic stimulation of Na+/ K+–ATPase. 

Studies have shown, propranolol given alone (orally or iv) normalizes serum potassium levels for an average of 2 hours. Nonselective Beta Blocker can be a good adjuvant treatment in TPP permissive blood pressure.

#endo

References:

1. Shayne P, Hart A. Thyrotoxic periodic paralysis terminated with intravenous propranolol. Ann Emerg Med. 1994;24(4):736–740.

2. Birkhahn RH, Gaeta TJ, Melniker L. Thyrotoxic periodic paralysis and intravenous propranolol in the emergency setting. J Emerg Med. 2000;18(2):199–202.

3. Lin SH, Lin YF. Propanolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis. Am J Kidney Dis. 2001;37(3):620–623.

4. Huang TY, Lin SH. Thyrotoxic hypokalemic periodic paralysis reversed by propranolol without rebound hyperkalemia. Ann Emerg Med. 2001;37(4):415–416.

5. Yeung RT, Tse TF. Thyrotoxic periodic paralysis: effect of propranolol. Am J Med. 1974;57(4):584–590.

wake-up stroke

Q: What is a "wake-up" stroke?

Answer: "Wake up" label is applied to patients who notice stroke symptoms on waking up from sleep. In such situations, stroke timing criteria should be established from the last time known to be normal; usually the time they went to bed. Family members can also be inquired about when they observed the patient in a normal functional status last time. 

If this time period is more than 4.5 hours, patients are usually not eligible for thrombolytic therapy. An alternative is to perform an MRI, which may show an acute ischemic stroke that is diffusion-positive and FLAIR-negative.

#neurology

References:

1. Peter-Derex L, Derex L. Wake-up stroke: From pathophysiology to management. Sleep Med Rev. 2019 Dec;48:101212. doi: 10.1016/j.smrv.2019.101212. Epub 2019 Sep 23. PMID: 31600679.

2. Tsai JP, Albers GW. Wake-Up Stroke: Current Understanding. Top Magn Reson Imaging. 2017 Jun;26(3):97-102. doi: 10.1097/RMR.0000000000000126. PMID: 28277462.

3. Rimmele DL, Thomalla G. Wake-up stroke: clinical characteristics, imaging findings, and treatment option - an update. Front Neurol. 2014 Mar 26;5:35. doi: 10.3389/fneur.2014.00035. PMID: 24723908; PMCID: PMC3972483.

4. Rubin MN, Barrett KM. What to do With Wake-Up Stroke. Neurohospitalist. 2015 Jul;5(3):161-72. doi: 10.1177/1941874415576204. PMID: 26288674; PMCID: PMC4530419.

imputability in blood transfusion

Q: What is imputability in blood transfusion?

Answer: Imputability is a term used in Transfusion-transmitted infection (TTI) and refers to the confidence that the infection came from the transfusion. It is considered a serious matter and so comes with various conditions/criteria:

• evidence of the pathogen in the transfused component
• in the donor at the time of donation
• in another component from the same donor
• in another recipient of a component from the same donor
• there must not be any other exposure of the recipient to the pathogen
• the recipient must not have been infected with the pathogen before receiving the transfusion
• there must be evidence that the specific bacterial organism in the component is the same as the organism in the recipient (by deoxyribonucleic acid [DNA] testing or extended phenotypic comparison)

#hematology

#transfusion

#ID

References:

1. Evan M Bloch, MD - Transfusion-transmitted bacterial infection :: © 2022 UpToDate, Inc.

2. Politis C, Wiersum-Osselton J, Richardson C, Grouzi E, Sandid I, Marano G, Goto N, Condeço J, Boudjedir K, Asariotou M, Politi L, Land K. Adverse reactions following transfusion of blood components, with a focus on some rare reactions: Reports to the International Haemovigilance Network Database (ISTARE) in 2012-2016. Transfus Clin Biol. 2022 Aug;29(3):243-249. doi: 10.1016/j.tracli.2022.03.005. Epub 2022 Apr 26. PMID: 35476961.

3. Jain A, Kaur R. Hemovigilance and blood safety. Asian J Transfus Sci. 2012 Jul;6(2):137-8. doi: 10.4103/0973-6247.98911. PMID: 22988376; PMCID: PMC3439750.

Cell-Saver storage and use

Q: Blood salvaged intraoperatively from one patient can be stored and later used for other patients of the same blood type.

A) True

B) False

Answer: B

Although it is true that blood salvaged intraoperatively, popularly known as "Cell-Saver," can be stored for future use but it should only be used for the same patient and NEVER BE FOR ANY OTHER PATIENT. Salvaged blood can be used for up to 6 hours on the same patient or 24 hours if stored properly at 1-6°C. 

It is presumed that blood is collected under standard aseptic conditions and labeled properly for the same patient and expiration time with a sticker: "For Autologous Use Only."

#hematology

Reference:

1. Boulos L, Kuebler JD, Angona R, Sweeney D, Wang H, Nocera E, Cholette JM. Cell Saver Blood Reinfusion Up to 24 Hours Post Collection in Pediatric Cardiac Surgical Patients Does Not Increase Incidence of Hospital-Acquired Infections or Mortality. J Extra Corpor Technol. 2021 Sep;53(3):161-169. doi: 10.1182/ject-2100015. PMID: 34658406; PMCID: PMC8499635.

2. Almeida RM, Leitão L. The use of cell saver system in cardiac surgery with cardiopulmonary bypass. Rev Bras Cir Cardiovasc. 2013 Mar;28(1):76-82. English, Portuguese. doi: 10.5935/1678-9741.20130012. PMID: 23739936.

3. Michele Heath, Aryeh Shander ::Surgical blood conservation: Blood salvage : © 2022 UpToDate, Inc.

Plankton sign on chest ultrasound?

Q: What is the plankton sign on chest and abdominal ultrasound?

Answer: The plankton sign, while performing ultrasound, refers to swirling, punctiform internal echoes within an otherwise anechoic pleural effusion. It appears slow and whirling, which may be buffered by cardiac and respiratory movements. It is highly suggestive of debris within effusion or even hemothorax, hemoperitoneum, or hemorrhagic ascites. 

You may watch the video here: https://www.youtube.com/watch?v=WDxxJVqWrQE

#ultrasound

Reference:

Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. (2008) Chest. 134 (1): 117-25. doi:10.1378/chest.07-2800

liver induced thrombocytopenia

Q: What is the etiology behind liver induced thrombocytopenia?

Answer: Although it is a well known fact that liver impairment leads to thrombocytopenia but rarely its mechanism of action is elucidated. It is due to two major reasons. 

First, adequate liver production not only depends on bone marrow's hematopoietic stem cell function but also on thrombopoietin (TPO) production in the liver. In liver insufficiency TPO production goes down and so the number of platelets in the blood. 

 Second, hepatic insufficiency leads to compensatory splenomegaly. This hypersplenism causes sequestration of platelets further augmenting the thrombocytopenia.. 

#hepatology

#hematology

References:

1. Rios R, Sangro B, Herrero I, Quiroga J, Prieto J. The role of thrombopoietin in the thrombocytopenia of patients with liver cirrhosis. Am J Gastroenterol. 2005 Jun;100(6):1311-6. doi: 10.1111/j.1572-0241.2005.41543.x. PMID: 15929762.

2. Hanafiah M, Shahizon AM, Low SF, Shahrina MH. Severe thrombocytopenia due to hypersplenism treated with partial splenic embolisation. BMJ Case Rep. 2013 Jul 5;2013:bcr2013010163. doi: 10.1136/bcr-2013-010163. PMID: 23833091; PMCID: PMC3736271.

Stigmata of IE

Q: In comparison to subacute infective endocarditis (IE), which of the following is more common in acute IE? - select one

A) Janeway lesions

B) Osler nodes 

C) Roth spots

Answer: A

Three major stigmata of Infective Endocarditis (IE) are 

1. Janeway lesions are microabscesses with neutrophil infiltration of capillaries and have the following three characteristics

• Nontender
• appears as erythematous macules 
• usually found on the palms and soles 

2. Osler nodes are the sequelae of vascular occlusion by microthrombi leading to localized immune-mediated vasculitis and have the following three characteristics

• tender
• occurs subcutaneous and appears as violaceous nodules 
• found mostly on the pads of the fingers and toes (may also occur on the thenar and hypothenar eminences)

3. Roth spots are very rare  to find in IE and are also the sequelae of vascular occlusion by microthrombi leading to localized immune-mediated vasculitis, and have the following three characteristics 

• exudative
• edematous hemorrhagic lesions
• found on the retina with pale centers

#ID

References:

1. Gunson TH, Oliver GF. Osler's nodes and Janeway lesions. Australas J Dermatol. 2007 Nov;48(4):251-5. doi: 10.1111/j.1440-0960.2007.00397.x. PMID: 17956487.

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

Hypercalcemia treatment

Q: Bisphosphonates should be used very early in the treatment of symptomatic patients with hypercalcemia?

A) True

B) False

Answer: B

Although bisphosphonates are more effective than calcitonin and saline for symptomatic patients with hypercalcemia, it takes 2-4 days to have a clinical effect. This requires them to be given in the early phase of hypercalcemia in combination with saline and/or calcitonin.

On the contrary, due to receptor downregulation, calcitonin loses its efficacy after 48 hours. 

#electrolytes

#endocrinology

References:

1. Turner JJO. Hypercalcaemia - presentation and management . Clin Med (Lond). 2017 Jun;17(3):270-273. doi: 10.7861/clinmedicine.17-3-270. PMID: 28572230; PMCID: PMC6297576.

2. Basso SM, Lumachi F, Nascimben F, Luisetto G, Camozzi V. Treatment of acute hypercalcemia. Med Chem. 2012 Jul;8(4):564-8. doi: 10.2174/157340612801216382. PMID: 22571195.

stool sample

Q: 34 years old male with known history of HIV is admitted to ICU with severe diarrhea. Ideally, stool sample should be sent to laboratory within? (select one)

A) 30 minutes

B) 60 minutes

C) 6 hours

D) 24 hours

Answer: A

To have the best yield from a stool sample, two basic principles should be followed:

• not be refrigerated
• ideally must be received by the lab within 30 minutes

A warm and fresh stool maximizes the chances of detecting trophozoites. Trophozoites are considered the active, infective form of protozoa. The stool should be preserved in Cary-Blair media in small community hospitals where 24/7 lab services are unavailable.

#GI

References:

1. Jones J, Reinke SN, Ali A, Palmer DJ, Christophersen CT. Fecal sample collection methods and time of day impact microbiome composition and short chain fatty acid concentrations. Sci Rep. 2021 Jul 7;11(1):13964. doi: 10.1038/s41598-021-93031-z. PMID: 34234185; PMCID: PMC8263620.

2. Abrahamson M, Hooker E, Ajami NJ, Petrosino JF, Orwoll ES. Successful collection of stool samples for microbiome analyses from a large community-based population of elderly men. Contemp Clin Trials Commun. 2017 Sep;7:158-162. doi: 10.1016/j.conctc.2017.07.002. Epub 2017 Jul 6. PMID: 29250605; PMCID: PMC5726580.

3. Wasfy M, Oyofo B, Elgindy A, Churilla A. Comparison of preservation media for storage of stool samples. J Clin Microbiol 1995; 33:2176.

Triad of HPS

Q: Describe the triad of Hepatopulmonary syndrome (HPS)?

Answer: HPS is a triad created by the interlink pathophysiology of abnormal arterial oxygenation caused by intrapulmonary vascular dilatations (IPVD) in the setting of liver disease portal hypertension, or congenital portosystemic shunts.

Unfortunately, the only curative treatment is liver transplant. And while waiting for transplant, support with oxygen to keep saturation > 88%. There is a rare form of HPS called granulomatous hepatitis, which is responsive to steroids and can be cured.

#hepatology

References:

1. Rodríguez-Roisin R, Krowka MJ. Hepatopulmonary syndrome--a liver-induced lung vascular disorder. N Engl J Med 2008; 358:2378.

2. Krowka MJ, Fallon MB, Kawut SM, et al. International Liver Transplant Society Practice Guidelines: Diagnosis and Management of Hepatopulmonary Syndrome and Portopulmonary Hypertension. Transplantation 2016; 100:1440.

3. Tzovaras N, Stefos A, Georgiadou SP, et al. Reversion of severe hepatopulmonary syndrome in a non cirrhotic patient after corticosteroid treatment for granulomatous hepatitis: a case report and review of the literature. World J Gastroenterol 2006; 12:336.

Treament neutropenic fever

Q: Broad spectrum monotherapy is adequate enough for early neutropenic fever after transplantation?

A) True

B) False

Answer: A

Studies have shown that broad-spectrum monotherapy is as good as dual or multi-regimen antibiotics in the early phase of neutropenic fever. In fact, it may be preferred to avoid the side effects of dual/multiple antibiotics. The underlying principle is to cover a broader spectrum of bacteria, including pseudomonas aeruginosa (gram-negative bacilli).

Preferred antibiotics in monotherapy are cefepime, meropenem, imipenem, piperacillin-tazobactam, or ceftazidime. It is prudent to check the resistance level from a local antibiogram.

#ID

References:

1. Freifeld AG, Bow EJ, Sepkowitz KA, et al. Clinical practice guideline for the use of antimicrobial agents in neutropenic patients with cancer: 2010 update by the infectious diseases society of america. Clin Infect Dis 2011; 52:e56.

2. Cometta A, Calandra T, Gaya H, et al. Monotherapy with meropenem versus combination therapy with ceftazidime plus amikacin as empiric therapy for fever in granulocytopenic patients with cancer. The International Antimicrobial Therapy Cooperative Group of the European Organization for Research and Treatment of Cancer and the Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto Infection Program. Antimicrob Agents Chemother 1996; 40:1108.

3. Paul M, Dickstein Y, Schlesinger A, et al. Beta-lactam versus beta-lactam-aminoglycoside combination therapy in cancer patients with neutropenia. Cochrane Database Syst Rev 2013; :CD003038.

4. Bow EJ, Rotstein C, Noskin GA, et al. A randomized, open-label, multicenter comparative study of the efficacy and safety of piperacillin-tazobactam and cefepime for the empirical treatment of febrile neutropenic episodes in patients with hematologic malignancies. Clin Infect Dis 2006; 43:447.

hearing loss in RV failure management

Q: 44 years old female is in cardiac ICU due to shortness of breath secondary to her underlying pulmonary hypertension and right ventricular (RV) dysfunction. She complains of sudden hearing loss. Which of the following drug can be a probable cause?

A) milrinone

B) inhaled Nitric Oxide (iNO)

C) sildenafil

D) hydralazine

E) lisinopril

Answer: C

A less known side effect of Phosphodiesterase-5 inhibitors (PD-5 I) such as sildenafil, vardenafil, and tadalafil is sudden hearing loss. This hearing loss is usually one-sided and occurs within the first 24 hours of initiation. In about two-thirds of patients, it can be permanent.

All other choices in the above question have no profile of this side effect so far.

#pharmacology

#pulmonary

#hemodynamics

References:

1. Thakur JS, Thakur S, Sharma DR, et al. Hearing loss with phosphodiesterase-5 inhibitors: a prospective and objective analysis with tadalafil. Laryngoscope 2013; 123:1527.

2. Khan AS, Sheikh Z, Khan S, et al. Viagra deafness--sensorineural hearing loss and phosphodiesterase-5 inhibitors. Laryngoscope 2011; 121:1049.

3. Maddox PT, Saunders J, Chandrasekhar SS. Sudden hearing loss from PDE-5 inhibitors: A possible cellular stress etiology. Laryngoscope 2009; 119:1586.

knotting of swan-ganz catheter

Q: While reviewing chest X-ray after floating Pulmonary Artery Catheter (PAC), you suspect possible knotting of catheter in right ventricle. Which one bedside trick may help in resolving knot before embarking on more invasive resolutions?


Answer: Inject about 20 mL of iced solution through the distal lumen 

If knotting of swan-ganz catheter(PAC) is suspected, many times injecting about 20 mL of cold sterile saline or iced solution through the distal lumen stiffens the catheter and help in resolving the knot. Interestingly, this trick was described almost 40 years ago, even before swan-ganz catheters later became popular in 1980s and 1990s. If this trick does not work, patient needs to go to cardiac catheter laboratory for placement of a wire under fluoroscopy. Alternatively, Interventional Radiology (IR) or vascular surgical service need to be consulted. In all ultimate failed cases, cardiothoracic surgery may require to perform open extraction of PAC.



 Reference: 

 Mond HG, Clark DW, Nesbitt SJ, Schlant RC. A technique for unknotting an intracardiac flow-directed balloon catheter. Chest 1975; 67:731.

increase the risk of Yersinia enterocolitica

Q: Name at least 3 conditions that may increase the risk of yersinia enterocolitica via blood transfusion?

Answer: Yersinia enterocolitica is an iron-avid organism. The following conditions may increase the risk of it via blood transfusion

• iron overload
• chelation therapy as it mobilizes iron 
• immunosuppression 
• asplenia 
• glucocorticoids

#transfusion

#ID

References:

1. Huovinen E, Sihvonen LM, Virtanen MJ, Haukka K, Siitonen A, Kuusi M. Symptoms and sources of Yersinia enterocolitica-infection: a case-control study. BMC Infect Dis. 2010 May 20;10:122. doi: 10.1186/1471-2334-10-122. PMID: 20487529; PMCID: PMC2883546.

2. Fàbrega A, Vila J. Yersinia enterocolitica: pathogenesis, virulence and antimicrobial resistance. Enferm Infecc Microbiol Clin. 2012 Jan;30(1):24-32. doi: 10.1016/j.eimc.2011.07.017. Epub 2011 Oct 22. PMID: 22019131.

3. Le Monnier O, Joseph L, Bodard S, Boudhabhay I. Hepato-splenic abscesses in a sickle cell disease patient. Am J Hematol 2022; 97:1118.

NSTI Anbx coverage

Q: Which of the following is appropriate for the initial antibiotic treatment of necrotizing soft tissue infections (NSTI) - select one

A) Vancomycin

B) Clindamycin

C) Piperacillin-tazobactam

D) Vancomycin, Piperacillin-tazobactam and Clindamycin

E) Vancomycin, Clindamycin and Metronidazole

Answer: D

The most important intervention besides calling surgical service in NSTI is the initiation of antibiotics at the earliest. It is important to broadly cover gram-negative and gram-positive organisms with piperacillin-tazobactam or carbapenem. Vancomycin or daptomycin should be added to cover methicillin-resistant Staphylococcus aureus (MRSA).

Clindamycin should be added to the regimen as an anti-ribosomal agent to inhibit exotoxin production. 

Choices A, B, and E have no gram-negative coverage and are incorrect.

Choice C has no anti-ribosomal activity and is incorrect.

#ID

#surgical-critical-care

References:

1. Louis A, Savage S, Utter GH, et al. NSTI Organisms and Regions: A Multicenter Study From the American Association for the Surgery of Trauma. J Surg Res 2019; 243:108.

2. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clin Infect Dis 2014; 59:147.

3. Zimbelman J, Palmer A, Todd J. Improved outcome of clindamycin compared with beta-lactam antibiotic treatment for invasive Streptococcus pyogenes infection. Pediatr Infect Dis J 1999; 18:1096.

Jellyfish sign on chest ultrasound

Q: What is Jellyfish sign on a chest ultrasound?

Answer: Jellyfish signs refer to an atelectatic lung that appears to be swimming within pleural effusion. This implies that the lung is neither consolidated nor adhered to pleura. It also implies that pleural effusion is probably a transudative as low viscosity of the fluid allows 'swimming' of the lung. 

You may see a video here: https://www.youtube.com/shorts/fx6rBMv6Gfc 

#pulmonary 

#ultrasound 

References: 

1. Han J, Xiang H, Ridley WE, Ridley LJ. Jellyfish sign: Pleural effusion. (2018) Journal of medical imaging and radiation oncology. 62 Suppl 1: 33. doi:10.1111/1754-9485.20_12785 

2. Francisco MJ, Rahal A, Vieira FA, Silva PS, Funari MB. Advances in lung ultrasound. (2016) Einstein (Sao Paulo, Brazil). 14 (3): 443-448. doi:10.1590/S1679-45082016MD3557

C Auris

Q: The drug of choice for Candida Auris is fluconazole.

A) True

B) False

Answer: B

C. Auris has become a subject of high concern due to its resistance and recent high transmission in health care facilities across the United States. Centers for Disease Control and Prevention (CDC) is still accumulating data and trying to figure out the sudden rise of this candida.

C. Auris has been found highly resistant to fluconazole. MIC resistance breakpoints 

• ≥32 mcg/mL for fluconazole
• ≥2 mcg/mL for amphotericin B
• ≥2 mcg/mL for caspofungin
• ≥4 mcg/mL for anidulafungin and micafungin

#ID

References:

1. Tsay S, Kallen A, Jackson BR, et al. Approach to the Investigation and Management of Patients With Candida auris, an Emerging Multidrug-Resistant Yeast. Clin Infect Dis 2018; 66:306.

2. Centers for Disease Control and Prevention. Candida auris. Antifungal Susceptibility Testing and Interpretation. https://www.cdc.gov/fungal/candida-auris/c-auris-antifungal.html (Accessed on September 25, 2022).