PAC complications reduction

Q: Most of the trauma while inserting a Pulmonary Artery Catheter (PAC) is due to inflation of the balloon during the catheter advancement?

A) True

B) False

Answer: B

Keeping the balloon at the tip of PAC (Swan-Ganz catheter) inflated while advancing the catheter minimizes the complications. Most of the complications during PAC insertion occur due to the direct exposure of the tip to the cardiac tissues. These include arrhythmias, catheter misplacement, perforation, rupture of the heart valve, and/or rupture of the pulmonary artery.  Once inflated, the balloon covers most of the tip and protects it from causing trauma. 

Similarly, keeping the balloon deflated during retrieval (backing off) is advisable.

#procedures

Reference:

1. Narumiya C, Isobe F. [Insertion procedure of the Swan-Ganz catheter]. Kyobu Geka. 2010 Jul;63(8 Suppl):607-11. Japanese. PMID: 20715426. 

2. Bossert T, Gummert JF, Bittner HB, Barten M, Walther T, Falk V, Mohr FW. Swan-Ganz catheter-induced severe complications in cardiac surgery: right ventricular perforation, knotting, and rupture of a pulmonary artery. J Card Surg. 2006 May-Jun;21(3):292-5. doi: 10.1111/j.1540-8191.2006.00235.x. PMID: 16684066.

feeding (gastric vs intestinal)

A note on Pros and Cons of gastric feeding in ICU

It should be understood that gastric feeding is more physiologic. It buffers gastric acid better. The gastropancreatic reflexes and gastrin release are more balanced. It enhances the pancreatic responses prior to food reaching the upper small bowel. In long term, it is easier to place and convenient to use. Moreover, the stomach can relatively tolerate a larger volume and higher osmotic load. 

Post-pyloric feeding should be utilized in situations where there is a chance of delayed gastric emptying, severe gastroesophageal reflux disease (GERD) and/or esophagitis causing nausea, vomiting, or aspiration pneumonia. Paralytic agents affect gastric motility more and post-pyloric feeding may be required if gastric intolerance may become an issue. 

#GI

References:

1. Tamion F, Hamelin K, Duflo A, Girault C, Richard JC, Bonmarchand G. Gastric emptying in mechanically ventilated critically ill patients: effect of neuromuscular blocking agent. Intensive Care Med. 2003 Oct;29(10):1717-22. doi: 10.1007/s00134-003-1898-5. Epub 2003 Jul 30. PMID: 12897996. 

2. Weledji EP. Perspectives on paralytic ileus. Acute Med Surg. 2020;7(1):e573. Published 2020 Oct 4. doi:10.1002/ams2.573 

3. Murray MJ, DeBlock H, Erstad B, Gray A, Jacobi J, Jordan C, McGee W, McManus C, Meade M, Nix S, Patterson A, Sands MK, Pino R, Tescher A, Arbour R, Rochwerg B, Murray CF, Mehta S. Clinical Practice Guidelines for Sustained Neuromuscular Blockade in the Adult Critically Ill Patient. Crit Care Med. 2016 Nov;44(11):2079-2103. doi: 10.1097/CCM.0000000000002027. PMID: 27755068.

Danger Space

 Q: What is "Danger Space" in the anatomy of the head and neck? 

Answer: Going from vertebra to pharyngeal area (posterior to anterior), there are three spaces:

1. Prevertebral space

2. Danger space

3. Retropharnygeal space

Danger Space extends from the base of the skull downwards freely through the entire posterior mediastinum to the level of the diaphragm. Vertebrally it corresponds with T11-T12. 

Clinical significance: Potentially, it provides a very functional route for the contiguous spread between the neck and the chest.

#ID

#anatomy

References: 

1. Reynolds SC, Chow AW (2009). "Severe soft tissue infections of the head and neck: a primer for critical care physicians". Lung. 187 (5): 271–9. doi:10.1007/s00408-009-9153-7. PMID 19653038. 

2. Mark, R., Song, S., & Mark, P. (2018). Taking heed of the 'danger space': acute descending necrotising mediastinitis secondary to primary odontogenic infection. BMJ case reports, 2018, bcr2018225019. https://doi.org/10.1136/bcr-2018-225019 

3. Grodinsky M, Holyoke EA. The fasciae and fascial spaces of the head, neck and adjacent regions. Am J Anat 1938;63:367-408.

CDS

 Q: 64 years old male is admitted to ICU with sudden onset of severe neck pain, stiffness, and fever. CT scan of the neck reads possible "Crowned Dens Syndrome." What is Crowned Dens Syndrome? 

Answer: Crowned dens syndrome is a rheumatological disorder that mimics an acute infectious process. It is due to the deposition of hydroxyapatite crystals, or calcium pyrophosphate in the periodontoid tissues, and gives an appearance of the dens on imagings. CT scan of the neck usually shows periodontoid calcification of C1-C2, with an appearance of a crown or halo surrounding the odontoid process. 

Symptoms of CDS are fever associated with acute severe shoulder girdle and neck stiffness. Diagnosis is via elevation of acute phase reactants. Treatment is nonsteroidal anti-inflammatory drugs (NSAIDs). Colchicine works well too.

#rheumatology

References:

1. Aouba A, Vuillemin-Bodaghi V, Mutschler C, De Bandt M. Crowned dens syndrome misdiagnosed as polymyalgia rheumatica, giant cell arteritis, meningitis or spondylitis: an analysis of eight cases. Rheumatology (Oxford) 2004; 43:1508. 

 2.Uh M, Dewar C, Spouge D, Blocka K. Crowned dens syndrome: a rare cause of acute neck pain. Clin Rheumatol 2013; 32:711.

AP-CML

 Q: Accelerated phase (AP) of Chronic Myeloid Leukemia (CML) should be considered a part of the blast phase (BP) CML? 

A) Yes 

B) No 

Answer: B 

Chronic myeloid leukemia (CML) is a myeloproliferative disorder associated with Philadelphia chromosome. The objective of this question is to highlight the fact that chronic phase (CP) CML, accelerated phase (AP) CML, and blast phase (BP) CML are three distinct scenarios.

All three entities are differentiated on the basis of myeloblast count, percentage of basophils, additional chromosomal abnormalities, and clinical features. Further, AP-CML can be a de novo or a transformation of CP CML - where prognosis and treatments may be different.  Like, CP-CML responds well to treatment with a BCR-ABL1 tyrosine kinase inhibitor (TKI). 

There are three usually followed criteria for AP-CML: 1) World Health Organization (WHO), 2) European LeukemiaNet (ELN) and 3) MD Anderson Cancer Center (MDACC). 

#oncology

References:

1. Mukherjee S, Kalaycio M. Accelerated Phase CML: Outcomes in Newly Diagnosed vs. Progression From Chronic Phase. Curr Hematol Malig Rep. 2016 Apr;11(2):86-93. doi: 10.1007/s11899-016-0304-7. PMID: 26932346. 

2. Aladağ E, Haznedaroğlu İC. Current perspectives for the treatment of chronic myeloid leukemia. Turk J Med Sci. 2019 Feb 11;49(1):1-10. doi: 10.3906/sag-1810-81. PMID: 30761815; PMCID: PMC7350850.

HD in Carbamazepine overdose

Q:  What is the best way to assess the effectiveness of hemodialysis in carbamazepine toxicity? 

 Answer:  Unfortunately, hemodialysis (HD) is not very effective in carbamazepine toxicity as it is highly protein-bound. Although, as a last resort it can be employed but only high-flux hemodialysis may work or the use of albumin-containing dialysate. Continuous venovenous hemodialysis (CVVHD) can be employed in hemodynamically unstable patients but results may not be as desirable. 

Another option is to use charcoal hemoperfusion but it is not easily available at most institutions and is not as safe as regular HD. It may cause thrombocytopenia, coagulopathy, hypothermia, hypocalcemia, hypophosphatemia, and hypoglycemia. The data on plasmapheresis/plasma exchange is also very limited. 

If HD is employed to remove carbamazepine, the best way to know if it's working is to measure the concentration of carbamazepine in the dialysate.

Administration of soda bicarbonate with QRS measurement continues to be the mainstay of treatment in carbamazepine overdose (reference #2).

#toxicology

References:

1. Schuerer DJ, Brophy PD, Maxvold NJ, et al. High-efficiency dialysis for carbamazepine overdose. J Toxicol Clin Toxicol 2000; 38:321. 

2. Bradberry SM, Thanacoody HK, Watt BE, et al. Management of the cardiovascular complications of tricyclic antidepressant poisoning : role of sodium bicarbonate. Toxicol Rev 2005; 24:195.

3. Bek K, Koçak S, Ozkaya O, et al. Carbamazepine poisoning managed with haemodialysis and haemoperfusion in three adolescents. Nephrology (Carlton) 2007; 12:33.

Hyperfiltration

 Q: Glomerular hyperfiltration is a protective sign in diabetic patients? 

A) Yes 

B) No 

 Answer: B

Early in the course in some diabetic patients the Glomerular Filtration Rate (GFR) becomes higher than normal. This is called glomerular hyperfiltration, and is defined as "GFR 20 percent or more above that in age-matched, healthy controls without diabetes." Unfortunately, it is not a good sign. Hyperfiltration predicts a higher risk of greater albuminuria and so the progression of Diabetic Kidney Disease (DKD). 

These patients benefit from the nephroprotective effect of the renin-angiotensin system (RAS) and sodium-glucose co-transporter 2 (SGLT2) inhibitors.

#nephrology

References:

1. Vora JP, Dolben J, Dean JD, et al. Renal hemodynamics in newly presenting non-insulin dependent diabetes mellitus. Kidney Int 1992; 41:829. 

2. Tonneijck L, Muskiet MH, Smits MM, et al. Glomerular Hyperfiltration in Diabetes: Mechanisms, Clinical Significance, and Treatment. J Am Soc Nephrol 2017; 28:1023. 

3. Magee GM, Bilous RW, Cardwell CR, et al. Is hyperfiltration associated with the future risk of developing diabetic nephropathy? A meta-analysis. Diabetologia 2009; 52:691. 

4. Ruggenenti P, Porrini EL, Gaspari F, et al. Glomerular hyperfiltration and renal disease progression in type 2 diabetes. Diabetes Care 2012; 35:2061.

SSRIs and QTc

 Q: 68 years old male collapsed at home, where EMS found him in polymorphic ventricular tachycardia (torsade de pointes). He was revived and is now in ICU. His wife informed that recently the dose of one of his anti-depressants (SSRI) was increased. Which of the following Selective Serotonin Reuptake Inhibitors (SSRIs) is most prone to cause prolong QTc interval?

A) Citalopram 

B) Escitalopram 

C) Fluoxetine 

D) Paroxetine 

E) Sertraline

Answer: A

All of the SSRIs can cause prolonged QTc. It is a dose-dependent effect. Usually, most patients have no clinical impact, but Citalopram (Celexa) may cause a life-threatening arrhythmia, usually torsade de pointes. This effect is likely at the dose of 60 mg per day. It is recommended not to exceed the dose above 40 mg per day. If required serum concentrations of citalopram can be followed. 

Moreover, when a higher dose is needed, close monitoring of electrolytes particularly potassium and magnesium should be done. Also, care should be taken to avoid drug-drug interactions with polypharmacy.

Celexa is one of the most common SSRIs prescribed in the USA.

#psychiatry

#pharmacology

References:

1. FDA Drug Safety Communication: Revised recommendations for Celexa (citalopram hydrobromide) related to a potential risk of abnormal heart rhythms with high doses http://www.fda.gov/Drugs/DrugSafety/ucm297391.htm (Accessed on August 11, 2021).

2. Girardin FR, Gex-Fabry M, Berney P, et al. Drug-induced long QT in adult psychiatric inpatients: the 5-year cross-sectional ECG Screening Outcome in Psychiatry study. Am J Psychiatry 2013; 170:1468. 

3. Castro VM, Clements CC, Murphy SN, et al. QT interval and antidepressant use: a cross sectional study of electronic health records. BMJ 2013; 346:f288. 

4. Bird ST, Crentsil V, Temple R, et al. Cardiac safety concerns remain for citalopram at dosages above 40 mg/day. Am J Psychiatry 2014; 171:17.

IBD-PSC

 Q: Primary Sclerosing Cholangitis (PSC) is usually associated with? (select one)

A) Crohn's disease 

B) Ulcerative colitis

Answer: B

Almost 90 percent of patients with PSC have ulcerative colitis (UC), though vice versa is not necessary. This is due to the fact that patients who have both PSC and inflammatory bowel disease (IBD) carry a different phenotype than patients who have only IBD. All patients with IBD who have abnormal liver enzymes particularly serum alkaline phosphatase should undergo workup for PSC. 

Clinically distinct features of patients who have both UC and PSC is pancolitis with active histologic activity despite the minimal endoscopic activity.

#GI

References:

1. Tung BY, Brentnall T, Kowdley KV, et al. Diagnosis and prevalence of ulcerative colitis in patients with sclerosing cholangitis (abstract). Hepatology 1996; 24:169A. 

2. Loftus EV Jr, Harewood GC, Loftus CG, et al. PSC-IBD: a unique form of inflammatory bowel disease associated with primary sclerosing cholangitis. Gut 2005; 54:91. 

3. Boonstra K, van Erpecum KJ, van Nieuwkerk KM, et al. Primary sclerosing cholangitis is associated with a distinct phenotype of inflammatory bowel disease. Inflamm Bowel Dis 2012; 18:2270. 

4. Jørgensen KK, Grzyb K, Lundin KE, et al. Inflammatory bowel disease in patients with primary sclerosing cholangitis: clinical characterization in liver transplanted and nontransplanted patients. Inflamm Bowel Dis 2012; 18:536.

Anbx in Nontyphoidal Salmonella gastroenteritis

 Q: All of the following are the indications for antimicrobial therapy in nontyphoidal Salmonella gastroenteritis EXCEPT? 

A) Severe diarrhea 

B) High or persistent fever 

C) Need for hospitalization 

D) Blood-stained diarrhea 

Answer: D

Antimicrobial therapy is usually not recommended for nontyphoidal salmonella gastroenteritis. This increases the risk for asymptomatic Salmonella carriage without any benefit. Antimicrobials should be used only if diarrhea is severe (> 10 stools per day), fever is either high or persistent, or there is a need for hospitalization. 

The blood in the stool is not an indication for antimicrobial in nontyphoidal salmonella gastroenteritis. Moreover, salmonella gastroenteritis is rarely marked by overt blood in the stool. It should raise the suspicion of Shigella or enterohemorrhagic E. coli.

#ID

#GI

References:

1. Onwuezobe IA, Oshun PO, Odigwe CC. Antimicrobials for treating symptomatic non-typhoidal Salmonella infection. Cochrane Database Syst Rev 2012; 11:CD001167. 

2. Hung YT, Lay CJ, Wang CL, Koo M. Characteristics of nontyphoidal Salmonella gastroenteritis in Taiwanese children: A 9-year period retrospective medical record review. J Infect Public Health. 2017 Sep-Oct;10(5):518-521. doi: 10.1016/j.jiph.2016.09.018. Epub 2017 Feb 13. PMID: 28209468.

Digi-bind

 Q: Digoxin-specific antibody (Fab) fragments can be given as an IV push in a 'code' situation?

A) Yes

B) No

Answer: A

Ideally, Fab fragments should be given as an intravenous (IV) piggy bag over a half-hour period, but during cardiac arrest (code) or impending cardiac arrest, it can be given as a slow IV push. 

Another objective of this question is to emphasize the need for caution in giving Fab fragments to patients who are chronically on digoxin. In such patients, digoxin induced arrhythmia - such as AV nodal block - without hemodynamic compromise (means only EKG changes), should be treated with half of the calculated dose. Full dose Fab fragments in these patients may unmask the heart failure and may put the patient in cardiogenic shock or atrial fibrillation with the rapid ventricular response (A.fib. with RVR).

#cardiology

#pharmacology

References:

1. Bateman DN. Digoxin-specific antibody fragments: how much and when? Toxicol Rev. 2004;23(3):135-43. doi: 10.2165/00139709-200423030-00001. PMID: 15862081.

2. Chan BS, Buckley NA. Digoxin-specific antibody fragments in the treatment of digoxin toxicity. Clin Toxicol (Phila). 2014 Sep-Oct;52(8):824-36. doi: 10.3109/15563650.2014.943907. Epub 2014 Aug 4. PMID: 25089630.

ESR and APR

 Q: 'Erythrocyte sedimentation rate' (ESR) is a/an ____________ acute phase reactant? (select one)

A) direct

B) indirect

Answer: B

Acute phase reactants (APR) are the proteins whose serum concentrations increase (positive) or decrease (negative) by at least 25 percent during inflammatory states such as infection, trauma, tumor, infarction, or autoimmune diseases. 

'Erythrocyte sedimentation rate' (ESR) is actually not a protein, rather it represents the increased viscosity of the serum due to these acute-phase proteins, mostly fibrinogen. That's why it is called indirect APR.

#inflammation

Reference:

Bedell SE, Bush BT. Erythrocyte sedimentation rate. From folklore to facts. Am J Med 1985; 78:1001.

Quinsy

 Q: 26 years old male is admitted to ICU for airway vigilance and signs of sepsis due to peritonsillar abscess. On physical exam, the uvula is expected to deviate towards? (select one) 

A) the affected side 

B) the unaffected side

Answer: B

Peritonsillar abscess is popularly known as quinsy. This is a suppurative extension of acute tonsillitis into the peritonsillar space. It is common in young adults. It is usually an abscess formation near the superior pole of the tonsil. Signs and symptoms consist of fever, odynophagia, sore throat which tends to be unilateral, otalgia, muffled voice (hot potato voice), trismus, unilateral deviation of the uvula towards the unaffected side, and soft palate edema.  

It requires quick recognization and treatment with drainage and/or antibiotics to avoid airway compromise. In severe edema, steroids can be considered.

#ID

#ENT

#surgical-critical-care

References:

1. Galioto NJ. Peritonsillar Abscess. Am Fam Physician. 2017 Apr 15;95(8):501-506. PMID: 28409615.

2. Steyer TE. Peritonsillar abscess: diagnosis and treatment. Am Fam Physician. 2002 Jan 1;65(1):93-6. Erratum in: Am Fam Physician 2002 Jul 1;66(1):30. PMID: 11804446.

shocks

 Q; Patients with severe acute myocardial infarction (MI) can have? (select one)

A) cardiogenic shock 

B) obstructive shock 

C) hemorrhagic shock 

D) all of the above

Answer: D

The objective of the above question is to highlight the fact that most shock situations are rarely a pure single entity. They may start as a single form of shock such as distributive, hypovolemic, hemorrhagic, or mechanical but soon culminate into a combined form of shock. 

One of the examples is severe acute MI which may start as a pure cardiogenic shock but with a ruptured left ventricular wall, may become an obstructive shock because of cardiac tamponade - or hemorrhagic shock with blood loss. Similarly, septic shock may start as a pure distributive shock bur after massive volume resuscitation, may culminate into mechanical shock due to abdominal compartment syndrome, and/or cardiogenic shock due to acute right heart failure.

#hemodynamics

References:

1. Standl T, Annecke T, Cascorbi I, Heller AR, Sabashnikov A, Teske W. The Nomenclature, Definition and Distinction of Types of Shock. Dtsch Arztebl Int. 2018;115(45):757-768. doi:10.3238/arztebl.2018.0757

2. Kislitsina ON, Rich JD, Wilcox JE, et al. Shock - Classification and Pathophysiological Principles of Therapeutics. Curr Cardiol Rev. 2019;15(2):102-113. doi:10.2174/1573403X15666181212125024

Applying lidocaine while inserting chest-tube

 Q: While anesthetizing the chest area to insert thoracostomy tube (chest tube) - think of a step missing from below as the anesthesia needle moves forward. 

1. Apply lidocaine to skin and subcutaneous (SC) tissues 

 2. Apply lidocaine to the periosteum of the rib above and the rib below 

3. Avoid the lower rib margin 

4. Apply lidocaine into the muscles of the intercostal space where the chest tube is planned 

5. Apply lidocaine to the area of the parietal pleura where the tube will enter the pleural space.

Answer: The objective of this question is to highlight an important step frequently missed by the operators while anesthetizing the area for the chest tube insertion.

After applying lidocaine to the skin and the SC tissues, and going forward, the anesthesia needle should be aspirated back to make sure that the needle is not in the intercoastal artery or vein. The damage to an intercoastal vessels can be fatal. In lean and thin patients this may need to be done as a first step.

#procedure

References:

1. Kwiatt M, Tarbox A, Seamon MJ, et al. Thoracostomy tubes: A comprehensive review of complications and related topics. Int J Crit Illn Inj Sci. 2014;4(2):143-155. doi:10.4103/2229-5151.134182

2. Durai R, Ng PC. How to insert a perfect chest drain. Acta Chir Belg. 2009 Oct;109(5):652-4. doi: 10.1080/00015458.2009.11680510. PMID: 19994817.

Florinef

 A note on Fludrocortisone 

Fludrocortisone is actually 9-alpha-fluorohydrocortisone. It is a synthetic mineralocorticoid. It increases renal sodium and water reabsorption leading to intravascular volume expansion. Fludrocortisone is frequently used in outpatient settings, particularly in End-Stage Renal Disease (ESRD) patients. If possible, it should be continued in ESRD patients in ICU if there is no major contraindication. Independently, it has low efficacy in acute situations. It takes about five to seven days to show clinical effect. The dose is anywhere from 0.05 mg to 0.2 mg per day. 

Said that Dr. Annane showed that the addition of Fludrocortisone with stress dose steroid may reduce 90-days mortality in septic shock (see reference #2) - though the level of evidence is weak. This may be due to the fact that Fludrocortisone by itself provides synergism to the pressor effect of sympathomimetic drugs/drips.  

Fludrocortisone has an interesting side effect of supine hypertension. It may also worsen edema and CHF. It has a tendency to cause hypokalemia, which may be beneficial in renal patients but should be a lookout in other patients.

#hemodynamics

References:

1. Chobanian AV, Volicer L, Tifft CP, et al. Mineralocorticoid-induced hypertension in patients with orthostatic hypotension. N Engl J Med 1979; 301:68. 

2. Annane D, et al. CRICS-TRIGGERSEP Network. Hydrocortisone plus Fludrocortisone for Adults with Septic Shock. N Engl J Med. 2018 Mar 1;378(9):809-818. doi: 10.1056/NEJMoa1705716. PMID: 29490185. 

3. Veazie S, Peterson K, Ansari Y, et al. Fludrocortisone for orthostatic hypotension. Cochrane Database Syst Rev 2021; 5:CD012868.

Lasix-albumin drip

 Q: Albumin-furosemide infusion is usually more efficacious than furosemide (Lasix) infusion alone? 

A) True

B) False

Answer: B

Although this is a very common practice in ICUs to add albumin with furosemide, popularly known as Lasix-albumin drip, to increase the diuresis. This is done with the hope that as these patients usually have low albumin, and the addition of albumin will bring the extracellular fluid within the vascular space and keep furosemide within the vascular space, and so will increase efficacy of the diuresis and natriuresis. 

Unfortunately, this practice lacks any evidence. There is no extra net sodium loss. This has been demonstrated in both nephrotic syndrome and cirrhotic patients.

#nephrology

References:

1. Fliser D, Zurbrüggen I, Mutschler E, et al. Coadministration of albumin and furosemide in patients with the nephrotic syndrome. Kidney Int 1999; 55:629. 

2. Chalasani N, Gorski JC, Horlander JC Sr, et al. Effects of albumin/furosemide mixtures on responses to furosemide in hypoalbuminemic patients. J Am Soc Nephrol 2001; 12:1010.

Whirl sign

 Q: What is 'CT whirl sign' in 'closed-loop bowel obstruction'? 

Answer: As the name implies closed-loop bowel obstruction is a segment of the bowel with no proximal or distal outlet due to obstruction at two places. Although sounds simple, it is a surgical emergency, which requires early intervention, as necrosis due to ischemia and perforation can occur very quickly. Restoration of perfusion is urgently needed. Sometimes it needs full abdominal exploration. Another caveat is its difficult diagnosis via imaging. 

CT whirl sign: A closed-loop obstruction should be suspected if a C or U-shaped distended, fluid-filled bowel segment with prominent mesenteric vessels converging on a point of torsion or incarceration is seen. 

Other clues in imaging are the presence of a triangular bowel loop, the beak sign (gradual narrowing of the bowel), and the two collapsed bowel loops adjacent to the obstruction site.

#surgical-critical-care

References:

1. Mbengue, A., Ndiaye, A., Soko, T. O., Sahnoun, M., Fall, A., Diouf, C. T., Régent, D., & Diakhaté, I. C. (2015). Closed loop obstruction: pictorial essay. Diagnostic and interventional imaging, 96(2), 213–220. https://doi.org/10.1016/j.diii.2013.10.011 

2. Ho YC. "Venous cut-off sign" as an adjunct to the "whirl sign" in recognizing acute small bowel volvulus via CT scan. J Gastrointest Surg 2012; 16:2005. 

3. Elsayes, K. M., Menias, C. O., Smullen, T. L., & Platt, J. F. (2007). Closed-loop small-bowel obstruction: diagnostic patterns by multidetector computed tomography. Journal of computer assisted tomography, 31(5), 697–701. https://doi.org/10.1097/RCT.0b013e318031f516. 

4. Edwards, M. K., Kuppler, C. S., Croft, C. A., & Eason-Bates, H. M. (2018). Adhesive Closed-loop Small Bowel Obstruction. Clinical practice and cases in emergency medicine, 2(1), 31–34. https://doi.org/10.5811/cpcem.2017.10.35927

Vitamin K

 Q: Vitamin K can be administrated after diluting with orange juice?

A) Yes

B) No

Answer: A

Administration of Vitamin K (phytonadione) in ICU via intravenous (IV) infusion is common, but this should always be remembered that despite all precautions such as enough dilution and slow infusion fatal reaction may occur with IV infusion. Extra precaution should be taken if a patient is receiving vitamin K for the first time. Moreover, this can occur via the intramuscular (IM) route too where there is an extra risk of hematoma formation. The subcutaneous route is safe but carries the risk of erratic and unpredictable absorption. 

The objective of this question is to emphasize that the oral route is the best route for vitamin K unless an urgent reversal of coagulopathy is needed. It can also be administrated by diluting in beverages if a pill cannot be swallowed. 

Another mistake many clinicians do is by ordering an ala-carte dose of 10 mg even in non-urgent cases. A lower dose of 1 to 2.5 mg is usually sufficient. 10 mg should be given in extremely urgent cases of bleeding.

#pharmacology

#hematology

References:

1. Vanier MC and Ngo TT. Reversal of overanticoagulation with vitamin K1: A plea for oral administration. Can J Hosp Pharm. 2006;59:125-135. 

2. Ageno W, Gallus AS, Wittkowsky A, Crowther M, Hylek EM, Palareti G. Oral anticoagulant therapy: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(2)(suppl):e44s-e88s. doi:10.1378/chest.11-2292

Scleroderma Renal Crisis

 Q: Which of the following is NOT a part of the classic scleroderma renal crisis (SRC)? (select one)? 

A) Abrupt malignant hypertension 

B) Acute oliguric renal failure 

C) Severe proteinuria 

D) Microangiopathic hemolysis anemia 

E) Thrombocytopenia 

 Answer: C 

SRC is one of the most dreaded complications of scleroderma Although some level of kidney involvement is a norm in scleroderma, it rarely progresses to chronic renal failure. SRC may occur in 10-15 percent of cases. What makes it scarier is that it usually occurs early in the course and can catch physicians as well as patients off guard. One clinical predictor is the patient with diffuse cutaneous Systemic Sclerosis (dcSSc). Patients with limited cutaneous systemic sclerosis (lcSSc) are less inclined to develop this. It has the following classic clinical characteristics:

• Abrupt onset of high/malignant hypertension. (some reports of normal blood pressure)
• Acute oliguric renal failure 
• Urinalysis with only mild proteinuria with few cells or casts 
• Microangiopathic hemolytic anemia 
• Thrombocytopenia 

The above pathologies lead to the possible symptoms of shortness of breath from pulmonary edema, headache, blurred vision, retinal microhemorrhages, hypertensive encephalopathy, and seizures. 

Please see reference #3 for recent updates on SRC's management.

#rheumatology

#nephrology

References:

1. Traub YM, Shapiro AP, Rodnan GP, et al. Hypertension and renal failure (scleroderma renal crisis) in progressive systemic sclerosis. Review of a 25-year experience with 68 cases. Medicine (Baltimore) 1983; 62:335. 

2. Shanmugam VK, Steen VD. Renal disease in scleroderma: an update on evaluation, risk stratification, pathogenesis and management. Curr Opin Rheumatol 2012; 24:669.

3. Nagaraja V. (2019). Management of scleroderma renal crisis. Current opinion in rheumatology, 31(3), 223–230. https://doi.org/10.1097/BOR.0000000000000604

Poxes

 Q: 42 years old male recently with a history of HIV is admitted to ICU with COVID-19. On examination, noticed to have large firm, dome-shaped papules on the genitals. ID service made the diagnosis of Molluscum contagiosum virus (MCV) (Poxvirus). Which areas of the body are typically spared providing clues to the diagnosis? (select one) 

 A) palms and soles 

B) axillae and popliteal fossae

Answer: A

Few risk factors for the Molluscum contagiosum virus in adults are sexual transmission, contact sports, inherited immunodeficiencies, and treatment with immunosuppressive drugs. It occurs as firm, dome-shaped papules. Pruritus may not be present. Characteristically, palms and soles are spared. 

In non-sexual transmissions usual areas of involvement are trunk, axillae, antecubital popliteal fossae, and crural folds. It may cause conjunctivitis by touching. Lesions in sexually transmitted MCV are present in the groin, genitals, proximal thighs, and lower abdomen. In HIV and immunocompromised patients, lesions are usually large and called giant molluscum and are widespread in the body due to underlying systemic disease. 

There are four genera of poxviruses 

• Orthopox causes smallpox (variola), vaccinia (Indian-subcontinent), cowpox, monkeypox (west and central africa), and rabbitpox viruses 
• Parapox causes orf, pseudocowpox, bovine papular stomatitis viruses 
• Yatapox causes tanapox and yaba monkey tumor viruses 
• Molluscipox causes molluscum contagiosum virus (MCV) 

Chickenpox is not a true pox virus and is caused by the herpes virus varicella-zoster.

#ID

References:

1. Zorec TM, Kutnjak D, Hošnjak L, et al. New Insights into the Evolutionary and Genomic Landscape of Molluscum Contagiosum Virus (MCV) based on Nine MCV1 and Six MCV2 Complete Genome Sequences. Viruses 2018; 10. 

2. Vora RV, Pilani AP, Kota RK. Extensive Giant Molluscum Contagiosum in a HIV Positive Patient. J Clin Diagn Res. 2015;9(11):WD01-WD2. doi:10.7860/JCDR/2015/15107.6797

DAPT and Diabetes

 Q: The effect of clopidogrel may be ___________ in diabetic patients?

A) decreased

B) increased

Answer: A

Physiologically, diabetic patients tend to have high platelet activation. This leads to relatively higher circulating immature platelets in their blood, and so the decreased function of anti-platelet drugs. The diabetic patients who present with coronary symptoms though should not be treated differently but their potential lack of response to Dual Anti-Platelet Therapy (DAPT) should be kept in mind. 

Diabetic patients who are compliant but less responsive to DAPT, may require a higher dose of Aspirin (ASA) and/or stronger platelet inhibitors like prasugrel or ticagrelor instead of clopidogrel.

#cardiology

#pharmacology

References:

1. Bouman HJ, van Werkum JW, Hackeng CM, et al. The importance of anticoagulant agents in measuring platelet aggregation in patients treated with clopidogrel and aspirin. J Thromb Haemost 2008; 6:1040. 

2. Duzenli MA, Ozdemir K, Aygul N, et al. Comparison of increased aspirin dose versus combined aspirin plus clopidogrel therapy in patients with diabetes mellitus and coronary heart disease and impaired antiplatelet response to low-dose aspirin. Am J Cardiol 2008; 102:396. 

3. Angiolillo DJ, Bernardo E, Zanoni M, et al. Impact of insulin receptor substrate-1 genotypes on platelet reactivity and cardiovascular outcomes in patients with type 2 diabetes mellitus and coronary artery disease. J Am Coll Cardiol 2011; 58:30. 

4. Grove EL, Hvas AM, Kristensen SD. Immature platelets in patients with acute coronary syndromes. Thromb Haemost 2009; 101:151. 

5. Michos ED, Ardehali R, Blumenthal RS, et al. Aspirin and clopidogrel resistance. Mayo Clin Proc 2006; 81:518. 

6. Gurbel PA, Bliden KP, Butler K, et al. Response to ticagrelor in clopidogrel nonresponders and responders and effect of switching therapies: the RESPOND study. Circulation 2010; 121:1188.

Therapeutic hyperventilation

 Q: In "therapeutic hyperventilation", what is the rate of decrease in cerebral blood flow (CBF) per 1 mm Hg decrease in PCO2?

Answer: 1 mmHg decrease in PaCO2 avails about 3 percent drop in cerebral blood flow (CBF). 

 Hyperventilation has been utilized in acute situations to lower the Intra-Cranial Pressure (ICP). In acute situations, hyperventilation can be instituted to bring PaCO2 down to 26-30 mmHg. This results in vasoconstriction, and so decreases the intracranial blood volume. An additional benefit of this therapeutic alkalosis is to achieve some shield against post-injury acidosis. 

Said that this effect last somewhere from 1 to 24 hours. More importantly, is to be careful in reversing therapeutic hyperventilation. The normal ventilatory rate should be brought back over hours to avoid the rebound effect. 

Therapeutic hyperventilation should be used as an acute rather desperate intervention when elevated ICP threatens life or organ with cerebral edema, bleed, or mass. It should never be employed as a prophylactic measure. It should be used by an experienced person and should be used judiciously particularly in patients with traumatic brain injury (TBI) or acute stroke. Vasoconstriction due to respiratory alkalosis may cause a critical decrease in local cerebral perfusion and may worsen the injury.

#neurology

#neuruosurgery

#trauma

#surgical-critical-care

References:

1. Marik PE, Varon J, Trask T. Management of head trauma. Chest 2002; 122:699. 

2. Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med 2002; 347:43. 

3. Yundt KD, Diringer MN. The use of hyperventilation and its impact on cerebral ischemia in the treatment of traumatic brain injury. Crit Care Clin 1997; 13:163. 

4. Stocchetti N, Maas AI, Chieregato A, van der Plas AA. Hyperventilation in head injury: a review. Chest 2005; 127:1812. . 

5. Coles JP, Minhas PS, Fryer TD, et al. Effect of hyperventilation on cerebral blood flow in traumatic head injury: clinical relevance and monitoring correlates. Crit Care Med 2002; 30:1950. 

6. Imberti R, Bellinzona G, Langer M. Cerebral tissue PO2 and SjvO2 changes during moderate hyperventilation in patients with severe traumatic brain injury. J Neurosurg 2002; 96:97.

Vertigo

 Q: 62 years old male is admitted to ICU with hypovolemic shock and electrolyte imbalance. Patient is experiencing symptoms of vertigo associated with severe nausea and vomiting (NV). Severe NV is more likely with? (select one)

A) central vertigo 

B) peripheral vertigo

Answer: A

Vertigo is broadly divided into two types:

• Central vertigo as the name implied is due to lesions in the central nervous system (CNS)
• Peripheral vertigo is likely due to origin from the inner ear

The objective of the question is to emphasize the role of history taking in the complex phenomenon of vertigo. Like, central vertigo with vertebrobasilar insufficiency usually lasts only for few minutes but peripheral vertigo is likely to be occurring for hours. This assessment is vital as patients with central lesions i.e., stroke, hemorrhage, or multiple sclerosis (MS) may require quick imaging and neuro team involvement. 

About 20 percent of ischemic strokes affect the posterior circulation due to ischemia of the posterior inferior cerebellar or the vertebral artery. In suck strokes, central vertigo may be the only presenting symptom. 

#Neurology

#ENT

 References:

1. Baloh RW. Differentiating between peripheral and central causes of vertigo. Otolaryngol Head Neck Surg. 1998 Jul;119(1):55-9. doi: 10.1016/S0194-5998(98)70173-1. PMID: 9674515.

2. Huon LK, Wang TC, Fang TY, Chuang LJ, Wang PC. Vertigo and stroke: a national database survey. Otol Neurotol. 2012 Sep;33(7):1131-5. 

3. Lee H, Sohn SI, Cho YW, Lee SR, Ahn BH, Park BR, Baloh RW. Cerebellar infarction presenting isolated vertigo: frequency and vascular topographical patterns. Neurology. 2006 Oct 10;67(7):1178-83. 

4. Hacke W, Zeumer H, Ferbert A, Brückmann H, del Zoppo GJ. Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar occlusive disease. Stroke. 1988 Oct;19(10):1216-22.

Killian's triangle

 Q: 55 years old male is admitted to ICU with aspiration pneumonia. The patient reports issue with swallowing - associated with gurgling sounds and mass in the neck.  CT scan of the neck reads weakness in the Killian's triangle. What is Killian's triangle? 

 Answer: Killian's triangle, also known as Killian dehiscence, is a triangular-shaped area of muscular weakness in the wall of the pharynx, between the transverse fibers of the cricopharyngeus muscle and the oblique fibers of the lower inferior constrictor (thyropharyngeus) muscle. 

Clinical significance: It is the site of Zenker's diverticulum (ZD). ZD is an upper esophageal sac-like outpouching of the mucosa and submucosa.

#surgical-critical-care

#GI

References:

1. Tabola R, Lewandowski A, Cirocchi R, et al. Zenker diverticulum: Experience in surgical treatment of large diverticula. Medicine (Baltimore). 2018;97(19):e0557. doi:10.1097/MD.0000000000010557 

2.  Kensing KP, White JG, Korompai F, Dyck WP. Massive bleeding from a Zenker's diverticulum: case report and review of the literature. South Med J 1994; 87:1003. 

3. Herbella FA, Dubecz A, Patti MG. Esophageal diverticula and cancer. Dis Esophagus 2012; 25:153. 

4. Bowdler DA, Stell PM. Carcinoma arising in posterior pharyngeal pulsion diverticulum (Zenker's diverticulum). Br J Surg 1987; 74:561.

EVALI

 Q: EVALI can occur without respiratory symptoms?

A) True

B) False

Answer: A

EVALI stands for E-cigarette/Vaping product use Associated Lung Injury. In the last 3 years, a significant rise has been amongst young individuals for its abuse. Interestingly, despite EVALI signs apparent on chest-x-ray, there may not be any respiratory symptoms. In some cases, in the initial phase gastrointestinal (GI) symptoms may be pre-dominant with nausea, vomiting, diarrhea, and abdominal pain. 

In typical cases, respiratory symptoms include shortness of breath (SOB), cough, generalized chest or pleuritic chest pain, and rarely hemoptysis. Fever, chills, tachycardia, tachypnea, and hypoxemia are common. 

There is no specific guideline available for treatment but most physicians prefer empiric antibiotics and a short course of steroids.

#pulmonology

#toxicology

References:

1. Matta P, Hamati JN, Unno HL, Fox MD. E-cigarette or Vaping Product Use-Associated Lung Injury (EVALI) Without Respiratory Symptoms. Pediatrics 2020; 145. 

2. Layden JE, Ghinai I, Pray I, et al. Pulmonary Illness Related to E-Cigarette Use in Illinois and Wisconsin - Final Report. N Engl J Med 2020; 382:903. 

3. Rao DR, Maple KL, Dettori A, et al. Clinical Features of E-cigarette, or Vaping, Product Use-Associated Lung Injury in Teenagers. Pediatrics 2020; 146.

DPP-4 side effects

 Q: 54 years old obese male with a long-standing type 2 Diabetes Mellitus (DM-2) is admitted to ICU with acute abdominal pain as well as shortness of breath associated with pedal edema. A few weeks ago, Sitagliptin was added to the drug regimen of his diabetic management. What are the few differential diagnoses? 

Answer: Dipeptidyl peptidase 4 (DPP-4) is getting popular in outpatient clinics for the management of DM-2. DPP-4 is a Glucagon-like peptide 1 (GLP-1)-based therapy. It is an effective medicine as it works through various mechanisms which are attractive to clinicians including an increase glucose-dependent insulin secretion, decrease gastric emptying (decrease food intake - weight loss), and reduce postprandial glucagon. Another attractive feature is the rare occurrence of hypoglycemia with its use. 

Said that it is still not considered the first line of therapy in DM-2.

The drugs included in this class are Sitagliptin, Saxagliptin, Linagliptin, and Alogliptin. There are few side effects which in-patients physicians need to be aware of: 

• Exacerbation of congestive heart failure (CHF) 
• Nasopharyngitis 
• Acute pancreatitis 
• Hepatitis 
• Inflammatory bowel disease 
• Severe skin reactions 
• Severe joint pain 
• Myalgias and muscle spasms

#endocrinology

#pharmacology

References:

1. Filippatos TD, Athyros VG, Elisaf MS. The pharmacokinetic considerations and adverse effects of DPP-4 inhibitors [corrected]. Expert Opin Drug Metab Toxicol. 2014 Jun;10(6):787-812. doi: 10.1517/17425255.2014.907274. Epub 2014 Apr 19. Erratum in: Expert Opin Drug Metab Toxicol. 2014 Oct;10(10):1455. PMID: 24746233. 

2. Wu S, Chai S, Yang J, Cai T, Xu Y, Yang Z, Zhang Y, Ji L, Sun F, Zhan S. Gastrointestinal Adverse Events of Dipeptidyl Peptidase 4 Inhibitors in Type 2 Diabetes: A Systematic Review and Network Meta-analysis. Clin Ther. 2017 Sep;39(9):1780-1789.e33. doi: 10.1016/j.clinthera.2017.07.036. Epub 2017 Aug 18. PMID: 28827024.

3. Kasina SVSK, Baradhi KM. Dipeptidyl Peptidase IV (DPP IV) Inhibitors. [Updated 2021 Jun 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542331/

TD

 Q: 72 years old female is recovering in ICU from urosepsis. Patient continues to have periods of delirium with unusual body movements. The psychiatry service diagnosed patient with Tardive Dyskinesis (TD) and advised to discontinue a few home drugs. What does "Tardive" mean in Tardive Dyskinesia? 

 

Answer: Tardive means late 

TD is a medication-induced hyperkinetic movement disorder. The most well-known culprits are dopamine receptor-blocking agents i.e., antipsychotic drugs. The two antiemetics which are found to cause TD are metoclopramide and prochlorperazine. As the name applied - Tardive - the onset can be from 4 weeks to six months after the start of a culprit agent. Symptoms are usually subtle and fluctuating. Unfortunately, the cumulative accumulation of drugs makes it worse. 

TD involves various kinds of hyperkinetic movements including orofacial dyskinesia, athetosis, dystonia, chorea, and tics. 

This nomenclature has a clinical implication. The best management is the early recognition of symptoms and discontinuation of the offending drug. By definition, a diagnosis of TD requires symptoms that must persist for at least four weeks after the removal of the offending drug.  

#neurology

#psychiatry

#pharmacology

References: 

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), American Psychiatric Association, Arlington, VA 2013.

2. Vasan S, Padhy RK. Tardive Dyskinesia. 2021 May 3. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 28846278. 

3. Cornett EM, Novitch M, Kaye AD, Kata V, Kaye AM. Medication-Induced Tardive Dyskinesia: A Review and Update. Ochsner J. 2017 Summer;17(2):162-174. PMID: 28638290; PMCID: PMC5472076.

Glucose and CRRT

 Q: Glucose free solution should be used in diabetic patients who require continuous renal replacement therapy (CRRT)?

A) True

B) False

Answer: B

Although the standard glucose-free solution is available for use in CRRT, it is preferable to continue to use a solution with a concentration of 100 mg/dL of glucose even in diabetic patients. It may be attractive to use glucose-free solution to have better control of hyperglycemia but the risk of possible hypoglycemia with a glucose-free solution in CRRT can be immediately life-threatening. Also, there are case reports of ketoacidosis in patients who underwent CRRT with glucose-free solutions.  

#nephrology

#endocrinology

References:

1. Ting S, Chua HR, Cove ME. Euglycemic Ketosis During Continuous Kidney Replacement Therapy With Glucose-Free Solution: A Report of 8 Cases. Am J Kidney Dis. 2020 Dec 3:S0272-6386(20)31140-9. doi: 10.1053/j.ajkd.2020.10.014. Epub ahead of print. PMID: 33278477.

2. Parikh R, Khanin Y, Wanchoo R, Barnett R, Sharma P. CRRT-associated ketoacidosis: A series of 5 cases. Clin Nephrol. 2021 Jun 18. doi: 10.5414/CN110460. Epub ahead of print. PMID: 34142948.

Angiotensin-2

Q: Angiotensin-2 works by increasing which of the electrolyte in the cytoplasm? (select one)

A) Sodium

B) Potassium

C) Calcium

D) Magnesium

E) Phosphorus

Answer: C

The mechanism of action of Angiotensin II is known for more than four decades. Angiotensin II is part of the renin-aldosterone-angiotensin (RAAS) system. Angiotensin receptors i.e., AT1 & AT2 are G-coupled protein receptors and angiotensin-II as their ligand. Stimulation of AT1 & AT2 increases cytosolic calcium causing vasoconstriction. Moreover, it also increases aldosterone and vasopressin secretion.

#hemodynamics

References:

1. Catt KJ, Mendelsohn FA, Millan MA, Aguilera G. The role of angiotensin II receptors in vascular regulation. J Cardiovasc Pharmacol 1984; 6 Suppl 4:S575. 

2. Fyhrquist F, Metsärinne K, Tikkanen I. Role of angiotensin II in blood pressure regulation and in the pathophysiology of cardiovascular disorders. J Hum Hypertens. 1995 Nov;9 Suppl 5:S19-24. PMID: 8583476. 

3. Benigni A, Cassis P, Remuzzi G. Angiotensin II revisited: new roles in inflammation, immunology and aging. EMBO Mol Med. 2010;2(7):247-257. doi:10.1002/emmm.201000080