routes of succinylcholine

Q: 54-year-old male with severe vasculopathy started having seizures in the ICU and lost his IV access. After intramuscular benzodiazepine, the patient started losing his respiratory drive and started desaturating, though he continued to seize. Intubation is called, but due to seizure, may require Succinylcholine. Without IV access, it is OK to administer succinylcholine intramuscularly (IM).

A) True

B) False

Answer: A

Succinylcholine is a depolarizing neuromuscular blockade (NMB) with the fastest onset and shortest duration of all NMBs. Although Succinylcholine is designed and preferred to be given intravenously for Rapid Sequence Induction and Intubation (RSII), if the situation absolutely arises, it can be given IM at a higher dose of 3 to 4 mg/kg, though it may take up to 3-4 minutes for full effect, first reported almost 7 decades ago. 

It can be given intraosseously too and has been found to be comparable to the IV route (reference # 3)

Another less-known use of Succinylcholine is continuous infusion, mostly used in electroconvulsive therapy when a brief period of neuromuscular blockade is required, titrated to twitch depression.

#procedures

#pharmacology

References:

1. GLOWACKI ET, AUSTIN S, GREIFENSTEIN FE. Intramuscular doses of succinylcholine as an adjunct in anesthesia. Anesth Analg. 1958 Jul-Aug;37(4):211-6. PMID: 13583596.

2. VANDERVEEN JL, SNEDDON EA, SCHMIDT SJ. INTRAMUSCULAR SUCCINYLCHOLINE IN ADULTS. A CONTROLLED STUDY. Anesthesiology. 1963 Nov-Dec;24:765-9. doi: 10.1097/00000542-196311000-00003. PMID: 14071406.

2. Moore GP, Pace SA, Busby W. Comparison of intraosseous, intramuscular, and intravenous administration of succinylcholine. Pediatr Emerg Care. 1989 Dec;5(4):209-10. doi: 10.1097/00006565-198912000-00001. PMID: 2602189.

pericardiocentesis in PH patients

Q: Patients with which Pulmonary Hypertension Group (PH) have the highest chance of mortality from pericardial drainage? - select one

A) Group 1

B) Group 2

C) Group 3

D) Group 4

E) Group 5

Answer: A

One remarkable endeavor in pulmonary hypertension (PH) is its classification into five groups based on underlying pathology.

Group 1: Pulmonary Arterial Hypertension (PAH)

Group 2: PH Due to Left Heart Disease

Group 3: PH Due to Lung Diseases and/or Hypoxia

Group 4: Chronic Thromboembolic Pulmonary Hypertension (CTEPH)

Group 5: PH With Unclear or Multifactorial Mechanisms

Although it is known that any patient with PH has a higher chance of hemodynamic collapse during pericardiocentesis, knowing the patient's underlying pathology may help in clinical decision-making if the situation arises. Patients with Group 1 have higher mortality rates compared with other non-PAH groups during such a procedure, with an adjusted odds ratio (aOR) of 2.35 and a 95% confidence interval (CI) of 1.46-3.80.

Some reports suggest that performing this procedure gradually, under the guidance of a Pulmonary Artery Catheter (PAC/Swan-Ganz), may help.

#pulmonary

#procedures

References:

1. Vasquez MA, Iskander M, Mustafa M, et al. Pericardiocentesis Outcomes in Patients With Pulmonary Hypertension: A Nationwide Analysis from the United States. Am J Cardiol 2024; 210:232.

2. Singh A, Mosarla R, Carroll K, Sulica R, Pashun R, Bangalore S, Yuriditsky E. Pericardiocentesis in Severe Pulmonary Arterial Hypertension Guided by a Pulmonary Artery Catheter. JACC Case Rep. 2024 May 1;29(12):102339. doi: 10.1016/j.jaccas.2024.102339. PMID: 38984206; PMCID: PMC11232420.

3. Cabada-Garcia MJ et.al. Safety of pericardiocentesis in pulmonary arterial hypertension: a systematic review. Front Cardiovasc Med. 2025 Aug 18;12:1610419. doi: 10.3389/fcvm.2025.1610419. PMID: 40901363; PMCID: PMC12400511.

iNO weaning

Q: A 54-year-old female is in the ICU due to Pulmonary Arterial Hypertension (PAH) and has been dependent on inhaled Nitric Oxide (iNO) for the last few days. Every time there is an attempt to wean and discontinue iNO, the patient becomes hemodynamically unstable. Which one trick may help to wean and discontinue iNO relatively easily?

Answer: Addition of sildenafil 

It is well known that abrupt discontinuation of inhaled NO, particularly in patients who are dependent on it for many days, can precipitate rapid rebound of pulmonary hypertension and worsening of ventilation/perfusion (V/Q) mismatch, resulting in hypoxemia and/or hemodynamic instability. Risks continue to rise after the first 10-12 hours of dependence, particularly in older patients.

One marker for weaning-related hemodynamic instability is a patient whose blood pressure and hemodynamics respond well at initiation. Responders are at higher risk of instability on discontinuation!

Overlapping weaning with coadministration of sildenafil may transit weaning smoothly, along with slow weaning, may be over the days. Also, keeping FiO2 higher during weaning may help.

#pulmonary

#pharmacology

References:

1. Atz AM, Wessel DL. Sildenafil ameliorates effects of inhaled nitric oxide withdrawal. Anesthesiology 1999; 91:307.

2. Khawaja H, Sanders TA, Schreiber M, Bondi D, Shah P, Brennan G. Sildenafil as Bridge Therapy for Inhaled Nitric Oxide in Preterm Neonates. J Pediatr Pharmacol Ther. 2024 Oct;29(5):525-529. doi: 10.5863/1551-6776-29.5.525. Epub 2024 Oct 14. PMID: 39411417; PMCID: PMC11472410.

K_Kidney-Liver connection

Q: What is the K-Kidney-Liver connection in hepatic encephalopathy?

Answer: Exacerbation of hepatic encephalopathy in hypokalemia 

Although all electrolytes need to be managed in hepatic encephalopathy, potassium plays an integral role. Hypokalemia increases kidney ammonia production, which directly exacerbates hepatic encephalopathy.

Other causes of acute exacerbation of hepatic encephalopathy are:

• Gastrointestinal bleeding
• Infection/sepsis 
• Metabolic alkalosis
• Renal insufficiency
• Hypovolemia
• Hypoxia
• Sedative
• Hypoglycemia
• Constipation
• Hepatocellular carcinoma 
• Hepatic vein or portal vein thrombosis

#hepatology

#neurology

#electrolyte

References:

1. Ullah H, Et.al.. Hypokalemia as a responsible factor related with the severity of hepatic encephalopathy: a wide multination cross-sectional study. Ann Med Surg (Lond). 2023 Jun 23;85(6):2427-2431. doi: 10.1097/MS9.0000000000000470. PMID: 37363515; PMCID: PMC10289733.

2. Javed MW, Ahmad E, Ahmad H, Nayyer ZA. IMPACT OF HYPOKALEMIA ON HEPATIC ENCEPHALOPATHY AND ITS EFFECT ON DURATION OF STAY IN HOSPITAL. J Ayub Med Coll Abbottabad. 2024 Jul-Sep;36(3):506-509. doi: 10.55519/JAMC-03-13014. PMID: 39623823.

3. Mikkelsen ACD, Thomsen KL, Vilstrup H, Aagaard NK. Hypokalaemia - an active contributor to hepatic encephalopathy? Metab Brain Dis. 2023 Jun;38(5):1765-1768. doi: 10.1007/s11011-022-01096-0. Epub 2022 Nov 3. PMID: 36326977.

VPA side effects

Q: Valproic Acid (VPA) overdose may cause? - select one

A) anion gap metabolic acidosis (AGA)

B) non-anion gap metabolic acidosis (NAGA)

Answer: A

VPA has seen renewed enthusiasm in US ICUs because of its efficacy in delirium. That also brings concern for VPA toxicity. Besides the dreaded complications of cerebral edema and subclinical hyperammonemia and Valproate-related hyperammonemic encephalopathy, popularly known as VHE, it can also cause significant electrolyte and metabolic abnormalities. The most common are

• hypernatremia
• hyperosmolality
• hypocalcemia, and 
• elevated anion gap metabolic acidosis

- Hypernatremia occurs because VPA is administered as a sodium salt.

- Hyperosmolality occurs because VPA and its metabolites are low-molecular-weight, osmotically active acids.

- AGA may occur from mitochondrial dysfunction, carnitine deficiency, and/or overproduction of toxic VPA metabolites, which are themselves anions.

- Hypocalcemia occurs as calcium binds to anionic VPA metabolites.

#toxicity

#electrolytes

References:

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

2. Sammar A, Tawfik M, Fatima F, Butler A, Aylor-Lee K. Valproate-Induced Hyperammonemic Encephalopathy Causing New-Onset Seizures. Cureus. 2023 Oct 18;15(10):e47288. doi: 10.7759/cureus.47288. PMID: 38021840; PMCID: PMC10656206.

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

CRRT and magnesium

Q: Use of Regional citrate anticoagulation in Continuous Renal Replacement Therapy (CRRT) will cause? - Select one

A) hypermagnesemia

B) hypomagnesemia

Answer: B

Regional citrate anticoagulation should be considered a major intervention in all patients requiring CRRT, as it may cause alkalosis due to citrate. The concentration of buffers, i.e.,  bicarbonate and lactate, should be reduced. Also, citrate can bind magnesium. Dialysate magnesium should be raised to 0.75 mmol/L from 0.5 mmol/L.

#procedures

#nephrology

References:

1. DePriest J, Dodson C, Phelps B. The Impact of Regional Citrate Anticoagulation on Magnesium Replacement During CRRT. Hosp Pharm 2023; 58:255.

2. Billiet N, Merckx L, van der Laenen M, Vanelderen P, Boer W. Magnesium profiles in renal replacement therapy (rrt) on icu: citrate CVVH (CICVVH) vs. intermittent haemodialysis (IHD). Intensive Care Med Exp. 2015 Oct 1;3(Suppl 1):A630. doi: 10.1186/2197-425X-3-S1-A630. PMCID: PMC4796953.

EKG and RVMI

Q: In acute Right Ventricular Myocardial Infarction (RVMI), which electrocardiogram (EKG) lead's ST-elevation has the highest sensitivity and specificity?

Answer: V4R

Patients with inferior-posterior ST-elevation MI mostly have RVMI, causing the classic triad of:

• hypotension
• elevated jugular venous pressure (JVP), and 
• clear lung fields

ST elevation >1 mm in lead V4R has> 90% sensitivity and specificity for scintigraphic evidence of RV infarction and 80% for echocardiographic evidence of RV dysfunction. A clinical pearl to remember is that the right-sided ST elevation is often transient, lasting less than 10 hours in 50% of patients with RV infarction.

#cardiology

References:

1. Watanabe S, Onuma J, Ishida R, Masuda R, Usui M. Clinical Significance of V4R ST-Segment Elevation on a Synthesized 18-Lead Electrocardiogram in Patients With Anterior ST-Segment Elevation Myocardial Infarction. Catheter Cardiovasc Interv. 2026 Jul;108(1):221-227. doi: 10.1002/ccd.70646. Epub 2026 Apr 26. PMID: 42036972.

2. Braat SH, Brugada P, de Zwaan C, et al. Value of electrocardiogram in diagnosing right ventricular involvement in patients with an acute inferior wall myocardial infarction. Br Heart J 1983; 49:368.

3. Candell-Riera J, Figueras J, Valle V, et al. Right ventricular infarction: relationships between ST segment elevation in V4R and hemodynamic, scintigraphic, and echocardiographic findings in patients with acute inferior myocardial infarction. Am Heart J 1981; 101:281.

SAH, SIADH and CSW

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Q: Hyponatremia in Subarachnoid hemorrhage (SAH) due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting can be distinguished by? 

A) level of hyponatremia 

B) serum osmolality

C) urine sodium

D) urine osmolality 

E) intravascular volume status

Answer: E

Hyponatremia in SAH may occur via two mechanisms, i.e., SIADH or cerebral salt wasting. Both are physiologically distinct entities, but hard to differentiate. Both entities have similar levels of hyponatremia, low serum osmolality (<274 mosmol/kg), high urine sodium (>40 mEq/L), and high urine osmolality (>100 mosmol/kg).

  

The major distinguishing feature is intravascular volume status. Patients with SIADH are euvolemic or maybe even hypervolemic. In contrast, patients with cerebral salt wasting tend to be hypovolemic.

  

#electrolytes

#nephrology

#neurology

  

  

References:

  

1. Muehlschlegel S. Subarachnoid Hemorrhage. Continuum (Minneap Minn) 2018; 24:1623.

  

2. Sterns RH, Silver SM. Cerebral salt wasting versus SIADH: what difference? J Am Soc Nephrol. 2008 Feb;19(2):194-6. doi: 10.1681/ASN.2007101118. Epub 2008 Jan 23. PMID: 18216309.

DAPT score

Q: The DAPT (Dual antiplatelet therapy) score is created to decide whether DAPT should be started, continued, or stopped? - Select one

A) at the time of the insertion of coronary stents

B) in the event of major surgery while the patient is on DAPT

C) at 12 months after insertion of a coronary stent

D) in patients with major bleeding risk

Answer: C

The DAPT score was developed to determine whether extended DAPT (i.e., beyond 12 months) might be appropriate. The DAPT score is based on eleven variables:

• Age 
• Diabetes Mellitus
• Cigarette Smoking Within Last Two Years
• Prior Myocardial Infarction or Percutaneous Coronary Intervention
• History of Congestive Heart Failure or Left Ventricular Ejection Fraction lower than 30%
• Hypertension
• Renal Insufficiency
• Peripheral Arterial Disease
• Myocardial Infarction at Presentation
• Stenting of Vein Graft
• Stent Diameter less than 3mm

Entering the data into the calculator will show the change in Risk if DAPT is continued or discontinued.

*Calculator link in reference #3

#cardiology

References:

1. Tian J, Wang Z, Wang Y, et al. Extended Dual Antiplatelet Therapy for Multivessel Coronary Artery Disease. N Engl J Med 2026; 395:233.

2. Mihatov N, Secemsky EA, Kereiakes DJ, Steg G, Serruys PW, Chichareon P, Shen C, Yeh RW. Utility of the dual antiplatelet therapy score to guide antiplatelet therapy: A systematic review and meta-analysis. Catheter Cardiovasc Interv. 2021 Mar;97(4):569-578. doi: 10.1002/ccd.29352. Epub 2020 Oct 28. PMID: 33111495; PMCID: PMC8620187.

3. https://tools.acc.org/DAPTriskapp/#!/content/calculator/

Vanc in critically ill patients

Q: Critically ill patients may require ___________ vancomycin loading doses? - select one

A) higher

B) lower

Answer: A

Critically ill patients usually have a high volume of distribution, which may increase vancomycin clearance. These patients may require higher vancomycin loading doses up to 25 to 30 mg/kg to achieve optimal vancomycin levels, particularly in the initial phase of illness. 

In these patients, it should be kept in mind that concomitant renal insufficiency or the need for renal replacement therapy/dialysis may significantly alter the need. Close monitoring of peak and, particularly, trough levels should guide therapy.

#pharmacology

#ID

References:

1. Pongchaidecha M, Changpradub D, Bannalung K, et al. Vancomycin Area under the Curve and Pharmacokinetic Parameters during the First 24 Hours of Treatment in Critically Ill Patients using Bayesian Forecasting. Infect Chemother 2020; 52:573.

2. Ishigo T, Ibe Y, Fujii S, et al. Effect of renal clearance on vancomycin area under the concentration-time curve deviations in critically ill patients. J Infect Chemother 2023; 29:769.

3. Alsultan A, Dasuqi SA, Almohaizeie A, et al. External Validation of Obese/Critically Ill Vancomycin Population Pharmacokinetic Models in Critically Ill Patients Who Are Obese. J Clin Pharmacol 2024; 64:353.

Haloperidol vs Droperidol

Q: 52 years old male admitted to ICU for acute psychosis became violent towards medical staff. Pharmacy suggested Droperidol. How Droperidol is different from Haloperidol?

Answer: Droperidol has an advantage over haloperidol in that it has:

• more rapid onset of action 
• shorter duration of effect
• can be used as monotherapy
• IM works as well as IV 

Droperidol is an analog of haloperidol. It has an advantage over haloperidol, with a more rapid onset of action (3-10 minutes) and a shorter duration of action (2-4 hours). In contrast, the onset of action of haloperidol, whether given intravenously (IV) or intramuscularly (IM), occurs within 30 to 60 minutes, and the duration of action can last up to a full day. Droperidol can be given IV or IM; however, compared with haloperidol, IM droperidol is rapidly absorbed and is preferable if the patient is not cooperative enough to allow IV access. Administration of Haloperidol usually requires co-administration of other drugs such as benzodiazepines, whereas droperidol works well as a monotherapy. 

#psychiatry

#pharmacology

References:

1. Battaglia J. Pharmacological management of acute agitation. Drugs 2005; 65:1207.

2. Thomas H Jr, Schwartz E, Petrilli R. Droperidol versus haloperidol for chemical restraint of agitated and combative patients. Ann Emerg Med 1992; 21:407.

3. Knott JC, Taylor DM, Castle DJ. Randomized clinical trial comparing intravenous midazolam and droperidol for sedation of the acutely agitated patient in the emergency department. Ann Emerg Med 2006; 47:61.

4. Page CB, Parker LE, Rashford SJ, et al. A Prospective Before and After Study of Droperidol for Prehospital Acute Behavioral Disturbance. Prehosp Emerg Care 2018; 22:713.

Acute HIV lasting longer than 2 weeks

Q: A 24-year-old male who just returned from vacation presented to the ED with a mononucleosis-like illness. Given a history of unprotected sex while on vacation, an HIV test was sent, which unfortunately came back positive. Patient reports his symptoms have been lasting for the last three weeks. What's the importance of his acute HIV infection lasting longer than usual?

Answer: Correlate with more rapid progression to AIDS 

Symptoms of acute HIV infection are usually most like a mononucleosis-like illness with fever, lymphadenopathy, sore throat, rash, myalgia/arthralgia, diarrhea, and headache. 

It is rarely realized that up to 60 percent of patients who acquire HIV may never experience these symptoms, which is both good and bad! Good - because those patients whose symptoms are severe and last longer than the usual 2-week period are found to correlate with more rapid progression to AIDS. Bad - because they may not get diagnosed for a long time!

During the acute HIV phase, there is rapid viral replication and infection of CD4 cells, and the plasma viral RNA level is usually very high. There may also be a transient drop in CD4 cell count.

#ID

References:

1. Pedersen C, Lindhardt BO, Jensen BL, et al. Clinical course of primary HIV infection: consequences for subsequent course of infection. BMJ 1989; 299:154.

2. Chéret A. Acute HIV-1 Infection: Paradigm and Singularity. Viruses. 2025 Mar 3;17(3):366. doi: 10.3390/v17030366. PMID: 40143294; PMCID: PMC11945883.

3. Cowan E, Vail RM, Shah SS, et al. Diagnosis and Management of Acute HIV Infection [Internet]. Baltimore (MD): Johns Hopkins University; 2024 Dec. Available from: https://www.ncbi.nlm.nih.gov/books/NBK563020/

Colchicine and pericarditis

Q: Colchicine is found to be effective in pericarditis caused by? - select one

A) systemic inflammatory diseases

B) bacterial pericarditis

C) malignancy-related pericarditis

Answer: A

Colchicine is widely used for pericarditis, but it should be reserved for specific situations. Its use may be particularly harmful in bacterial pericarditis, where it may impair the clearance of the infectious organism. Similarly, it has no role in malignancy-related pericarditis and/or pericardial effusion. Also, it is not recommended in patients with recurrent pericarditis.

Said above, colchicine is an effective treatment in acute idiopathic, viral, and pericarditis caused by systemic inflammatory diseases and post-cardiac injury & surgery patients. If used, it is recommended to continue for 12 weeks after an initial episode, though many patients may develop diarrhea, nausea, and vomiting. In such cases, the dose can be decreased. Rare side effects are bone marrow suppression and liver and muscle injuries. The dose should be adjusted for lower renal GFR.

#cardiology

#pharmacology

References:

1. Schulz-Menger J, Collini V, Gröschel J, et al. 2025 ESC Guidelines for the management of myocarditis and pericarditis. Eur Heart J 2025; 46:3952.

2. Alabed S, Cabello JB, Irving GJ, et al. Colchicine for pericarditis. Cochrane Database Syst Rev 2014; :CD010652.

3. Imazio M, Brucato A, Belli R, et al. Colchicine for the prevention of pericarditis: what we know and what we do not know in 2014 - systematic review and meta-analysis. J Cardiovasc Med (Hagerstown) 2014; 15:840.

Transmission of human babesiosis

Q: Babesiosis is mostly transmitted by? - select one

A) blood transfusion

B) solid organ transplantation

C) transplacental

D) tick vectors

Answer: D

The objective of this question is to emphasize that babesiosis has increased considerably in the Northeast of the USA and is an emerging infectious disease of concern. 

The major cause is the rising deer population with concomitant increased tick density, due to lack of predators and insufficient culling of the herd. Another major reason is the expanding real estate in wooded areas.

Rash is the crucial differential diagnosis from Lyme disease, as rash rarely occurs in babesiosis. Both diseases may co-exist, though.

In its severe form, it can cause renal and liver insufficiency, ARDS, CHF, severe anemia, DIC, and shock. Spontaneous splenic rupture may occur from excessive erythrophagocytosis, a marker of high mortality.

#ID

References:

1. Krause PJ, Auwaerter PG, Bannuru RR, et al. Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA): 2020 Guideline on Diagnosis and Management of Babesiosis. Clin Infect Dis 2021; 72:185.

2.  Dumic I, Patel J, Hart M, et al. Splenic Rupture as the First Manifestation of Babesia Microti Infection: Report of a Case and Review of Literature. Am J Case Rep 2018; 19:335.

3. Krause PJ. Human babesiosis. Int J Parasitol. 2019 Feb;49(2):165-174. doi: 10.1016/j.ijpara.2018.11.007. Epub 2019 Jan 26. PMID: 30690090.

Angioedema Following Discontinuation of ACE Inhibitor Therapy

Q: Angioedema may occur even after Angiotensin Converting Enzyme inhibitor (ACE-I) is discontinued?

A) True

B) False

Answer: A

Although it is true that the only reliable treatment of ACE-I-induced angioedema is to discontinue it, it may take many months before it takes effect, and almost half of the patients may have a recurrent episode, particularly in the first month. Risk may get higher if the patient has any other reason to have angioedema.

#pharmacology

References:

1. Beltrami L, Zanichelli A, Zingale L, et al. Long-term follow-up of 111 patients with angiotensin-converting enzyme inhibitor-related angioedema. J Hypertens 2011; 29:2273.

2. Perman B, Narechania S, Malesker M. Geriatric Pharmacotherapy Case Series: Recurrent Angioedema Following Discontinuation of ACE Inhibitor Therapy. Sr Care Pharm. 2023 Jan 1;38(1):16-20. doi: 10.4140/TCP.n.2023.16. PMID: 36751921.

DDAVP and Hemophilia

Q: Desmopressin (DDAVP) can be given in bleeding patients with? - select one

A) hemophilia A

B) hemophilia B 

Answer: A

Hemophilia is simply divided into two types of factor deficiency

• Hemophilia A - deficiency of Factor VIII
• Hemophilia B - deficiency of Factor IX

DDAVP is a synthetic analog of vasopressin that also releases factor VIII and its carrier protein, von Willebrand factor (VWF), from storage pools in platelet granules and endothelial cells.

Factor IX is not present in storage pools; therefore, DDAVP has no role in Hemophilia B.

#hematology

References:

1. Reardon B, Pasalic L, Favaloro EJ. A Review of Desmopressin Use in Bleeding Disorders: An Unsung Hero? Biomolecules. 2025 Jul 5;15(7):967. doi: 10.3390/biom15070967. PMID: 40723839; PMCID: PMC12292229.

2. Kavakli K, Aydinok Y, Karapinar D, Balkan C. DDAVP treatment in children with haemophilia B. Br J Haematol. 2001 Sep;114(3):733-4. doi: 10.1046/j.1365-2141.2001.02924-2.x. PMID: 11553008.

3. Leissinger C, Carcao M, Gill JC, Journeycake J, Singleton T, Valentino L. Desmopressin (DDAVP) in the management of patients with congenital bleeding disorders. Haemophilia. 2014 Mar;20(2):158-67. doi: 10.1111/hae.12254. Epub 2013 Aug 12. PMID: 23937614.

RBC Ghosts

Q: Red Blood Cell (RBC) ghosts can be seen mostly with which bacterial infection?

Answer: Clostridium perfringens

RBC ghosts are RBC membranes devoid of hemoglobin. This occurs when intravascular lysis causes hemoglobin to leak into the plasma. RBC ghosts are usually seen in fulminant bacteremia, and most commonly with Clostridium perfringens. Other major infections that may create RBC ghosts are:

• Malaria
• Babesia
• Leishmania
• Bartonella
• Protozoa

C. perfringens can cause massive, life-threatening hemolysis via its alpha toxin, a pore-forming toxin that binds glycosylphosphatidylinositol (GPI) anchored proteins and inserts into cell membranes. Interestingly, this massive hemolysis may give rise to laboratory errors, such as faulty sample collection.

#hematology

#ID

#laboratory-science

References:

1. Hübl W, Mostbeck B, Hartleb H, et al. Investigation of the pathogenesis of massive hemolysis in a case of Clostridium perfringens septicemia. Ann Hematol 1993; 67:145.

2. Kennedy CL, Lyras D, Cordner LM, et al. Pore-forming activity of alpha-toxin is essential for clostridium septicum-mediated myonecrosis. Infect Immun 2009; 77:943.

3. Rodriguez FJ, Ritter MJ, Tauscher CD, Moore SB. Transfusion medicine illustrated. Massive hemolysis secondary to alpha-toxin release. Transfusion 2005; 45:127.

hMPV and Lung transplant

Q: A 63-year-old male with a recent double lung transplant is transferred back from the ward to the ICU due to respiratory distress and requires intubation. On bronchoscopy, Human metapneumovirus (hMPV) was found. What's the importance of finding hMPV infection in lung transplant patients?

Answer: Predictive of chronic lung allograft dysfunction (CLAD) 

Although hMPV is considered mild in the general population, in lung transplant patients, it may cause severe disease. About one third of hMPV-infected lung transplant recipients developed chronic lung allograft dysfunction (CLAD) progression within the next twelve months, with lack of early lung function recovery predicting long-term CLAD progression.

#transplantation

#ID

References:

1. Permpalung N, Sait AS, Bazemore K, et al. Human Metapneumovirus and Parainfluenza Virus Infections in Lung Transplant Recipients: The Effects on Lung Allograft and Clinical Outcomes. Transplantation 2021; 105:2625.

2. Hulot S, Prunet V, Coiffard B, Zandotti C, Boschi C, D'Journo XB, Hraiech S, Reynaud-Gaubert M, Colson P, Cassir N. Fatal acute respiratory distress syndrome caused by donor-derived human metapneumovirus after lung transplantation. Am J Transplant. 2025 Oct;25(10):2239-2243. doi: 10.1016/j.ajt.2025.05.020. Epub 2025 May 17. PMID: 40389161.

3. de Zwart A, Riezebos-Brilman A, Lunter G, Vonk J, Glanville AR, Gottlieb J, Permpalung N, Kerstjens H, Alffenaar JW, Verschuuren E. Respiratory Syncytial Virus, Human Metapneumovirus, and Parainfluenza Virus Infections in Lung Transplant Recipients: A Systematic Review of Outcomes and Treatment Strategies. Clin Infect Dis. 2022 Jul 6;74(12):2252-2260. doi: 10.1093/cid/ciab969. PMID: 35022697; PMCID: PMC9258934.

Propofol use in colonoscopy

Case: A 57-year-old male is admitted to the ICU with severe lower gastrointestinal bleed (LGIB). Patient is not intubated. GI service requested assistance in procedural anesthesia and preferred to use propofol because they wanted better sedation to evaluate as many serrated lesions during colonoscopy. The intensivist is worried about apnea and decided to use the lowest possible dose. The patient was thought to be awake but started having a fit of coughing and wheezing.

Discussion: It has become almost standard practice to use propofol for colonoscopy sedation, particularly when the colonoscopist wants to improve surveillance of serrated lesions (reference # 4). Also, it improves patient satisfaction and reduces nausea and vomiting, as propofol has anti-emetic properties. 

The intensivist's dilemma is finding the right balance during administration, as apnea can be unpredictable with any dosing. Unfortunately, suboptimal propofol dosing can cause coughing and/or laryngospasm. The best strategy is to stay prepared before the procedure for intubation and for hemodynamic instability, with constant close monitoring.

#procedures

#pharmacology

#GI

References:

1. Johnson G, Okoli GN, Askin N, et al. Propofol for sedation during colonoscopy. Cochrane Database Syst Rev 2025; 10:CD006268.

2. Padmanabhan A, Frangopoulos C, Shaffer LET. Patient Satisfaction With Propofol for Outpatient Colonoscopy: A Prospective, Randomized, Double-Blind Study. Dis Colon Rectum 2017; 60:1102.

3. Gan TJ, Jin Z, Ayad S, et al. Fifth Consensus Guidelines for the Management of Postoperative Nausea and Vomiting: Executive Summary. Anesth Analg 2025.

4. Quaye AN, Hisey WM, Mackenzie TA, et al. Association of Sedation Depth With Detection of Small Serrated Polyps and Serrated Polyp Counts During Colonoscopy: A Registry-Based Cohort Study. Anesth Analg 2026; 142:617.

CPM and ODS

Q: Why "central pontine myelinolysis (CPM)" is not a correct term for a neurological complication in the overly rapid correction of hyponatremia?

Answer: Previously, CPM was used for decades to describe the neurological complication of overly rapid correction of hyponatremia. But the term was discarded for two reasons, and a new term, "osmotic demyelination syndrome (ODS)," was coined.

First, it's not an anatomic restriction process. Demyelination can be more diffuse and does not even necessarily involve the pons.

Second, and less well-known, not all patients with central pontine myelinolysis (CPM) have experienced a rapid increase in serum sodium!

The word 'syndrome' is added as it is an amalgam of many clinical signs and symptoms, though mostly neurological, such as

• Quadriparesis
• Dysarthria 
• Dysphagia
• Pseudobulbar Palsy*
• Gait instability
• Locked-in syndrome
• Delirium
• Coma

*marked by emotional lability, facial weakness, and uncontrolled crying or laughing

#electrolytes

#neurology

References:

1. Ayus JC, Wheeler JM, Arieff AI. Postoperative hyponatremic encephalopathy in menstruant women. Ann Intern Med 1992; 117:891.

2. Karp BI, Laureno R. Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore) 1993; 72:359.

3. Treves B, Consalvo F, Delogu G, Morena D, Padovano M, Santurro A, Scopetti M, Fineschi V. Osmotic demyelination syndrome: revisiting the diagnostic criteria through two fatal cases. BMC Neurol. 2024 Nov 5;24(1):428. doi: 10.1186/s12883-024-03934-3. PMID: 39497060; PMCID: PMC11536822.

Transfusion in burn patients

Q: Blood transfusion to keep hemoglobin threshold above 10 g/dL in burn patients may improve mortality.

A) True

B) False

Answer: B

Overneeded blood transfusion in burn patients may actually contribute to increased morbidity and mortality, as burn patients hemoconcentrate during the first few hours after a severe burn. Anemia may occur as bone marrow function stays depressed in these patients. Despite this, erythropoietin has no role in burn-related anemia. 

As with any general subset of patients, except for patients with coronary syndrome (ACS) who may require a threshold of 10 g/dL, burn patients should not be treated any differently in terms of blood transfusion. Rather, restrictive blood transfusion may be preferred again to prevent hemoconcentration and avoid undue Acute Lung Injury (ALI).

#burn

#hematology

References:

1. Kwan P, Gomez M, Cartotto R. Safe and successful restriction of transfusion in burn patients. J Burn Care Res 2006; 27:826.

2. Palmieri TL, Caruso DM, Foster KN, et al. Effect of blood transfusion on outcome after major burn injury: a multicenter study. Crit Care Med 2006; 34:1602.

3. Higgins S, Fowler R, Callum J, Cartotto R. Transfusion-related acute lung injury in patients with burns. J Burn Care Res 2007; 28:56.

Definition of Dyspnea

Q: As per American Thoracic Society (ATS), which of the following factor is NOT a part of definition of dyspnea? - select one

A) Anatomical

B) Environmental

C) Physiological

D) Psychological

E) Social

Answer: A

A consensus statement of the American Thoracic Society defines dyspnea as:

"Dyspnea is a term used to characterize a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses."

It's an important definition to understand the wide spectrum of dyspnea, describing cause and effect. The keywords are: - a "subjective experience", "qualitatively distinct sensations", "vary in intensity", various factors inducing "secondary physiological and behavioral responses."

#pulmonary

#psychology

# environmental-sciences

#social-sciences

Reference:

Parshall MB, Schwartzstein RM, Adams L, et al. An official American Thoracic Society statement: update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med 2012; 185:435.

A succussion splash, Virchow's node and Sister Mary Joseph's node

Q: With the following three physical findings, what's the diagnosis, if proven otherwise?

• A succussion splash 
• A left Virchow's node
• Sister Mary Joseph's node

Answer: Metastatic gastric cancer

The objective of this question is to emphasize again the most vital art of the medicine - the physical exam.

A succussion splash is elicited by placing the stethoscope over the upper abdomen and rocking the patient back and forth at the hips. There may be a "splash" sound. It signifies Gastric Outlet Obstruction if positive after three hours of the meal. 

Virchow's node is a palpable supraclavicular lymph node, and Sister Mary Joseph's node is a palpable periumbilical lymph node.

* The author of this question highly recommends reading the case report in reference #4.

#oncology

#physical-exam

References:

1. Ferguson CM. Inspection, Auscultation, Palpation, and Percussion of the Abdomen. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 93. Available from: https://www.ncbi.nlm.nih.gov/books/NBK420/

2. Kobayashi T, Sato R, Kaneko N, Sato J, Kakugawa Y, Funayama Y. [Advanced Gastric Cancer with Virchow's Lymph Node Metastasis-A Long-Term Survival Case]. Gan To Kagaku Ryoho. 2024 Aug;51(8):821-823. Japanese. PMID: 39191712.

3. Whang TB, Wang L, Peng DH. Gastric carcinoma of the umbilicus: case report of Sister Mary Joseph nodule. Cutis. 2010 Feb;85(2):90-2. PMID: 20349683.

4. Fill S, Taran A, Schulz HU, Kahl S, Kalinski T, Smith B, Costa SD. Sister Mary Joseph's nodule as the first sign of pregnancy-associated gastric cancer: a case report. World J Gastroenterol. 2008 Feb 14;14(6):951-3. doi: 10.3748/wjg.14.951. PMID: 18240358; PMCID: PMC2687068.

Premedication in IV Fe infusion

Q: Premedication with diphenhydramine should be given before intravenous (IV) Iron (Fe) transfusion due to the risk of allergic reaction.

A) True

B) False

Answer: B

Surprisingly, and contrary to popular practice, Diphenhydramine before IV Fe infusion is strongly associated with an increased likelihood of an infusion reaction!

In regular IV Fe infusion, no premedication is required. The rules of thumb for premedication prior to IV Fe infusion are:

• history of asthma, 
• inflammatory arthritis,
• more than one drug allergy, or
• Clinician's suspicion of any other underlying disease which may trigger the reaction

Usually, premedication with IV 125 mg of methylprednisolone and an H2 blocker is recommended.

To note, patients with a history of inflammatory arthritis, a dose of IV methylprednisolone, 125 mg followed by 1 mg/kg prednisone per day orally for four days is recommended.

The best prevention against an IV Fe reaction is to infuse slowly and consult with pharmacy to find the formulation with the least risk of reaction. If a reaction occurs, only methylprednisolone is required without any H2 blocker.

#allergy

#elements

References:

1. Barton JC, Barton EH, Bertoli LF, et al. Intravenous iron dextran therapy in patients with iron deficiency and normal renal function who failed to respond to or did not tolerate oral iron supplementation. Am J Med 2000; 109:27.

2. Auerbach M, Chaudhry M, Goldman H, Ballard H. Value of methylprednisolone in prevention of the arthralgia-myalgia syndrome associated with the total dose infusion of iron dextran: a double blind randomized trial. J Lab Clin Med 1998; 131:257.

3. Gómez-Ramírez S, Shander A, Spahn DR, Auerbach M, Liumbruno GM, Vaglio S, Muñoz M. Prevention and management of acute reactions to intravenous iron in surgical patients. Blood Transfus. 2019 Mar;17(2):137-145. doi: 10.2450/2018.0156-18. Epub 2018 Oct 16. PMID: 30418128; PMCID: PMC6476739.

Fosphenytoin and phenytoin

Q: Which statement is true? - Select one

A) Fosphenytoin is the water-soluble prodrug of phenytoin

B) Fosphenytoin is the lipid-soluble prodrug of phenytoin

Answer: A

Fosphenytoin is a water-soluble prodrug that converts into phenytoin. It was created in the hope that it would act faster. It can also be given intramuscularly, which is an advantage when an IV line is not available. It can also be given three times faster, an advantage in status epilepticus scenarios.

Phenytoin carries various risks such as local irritation, tissue necrosis, and "purple glove syndrome", and if given faster, can cause cardiac arrhythmias. Fosphenytoin may negate those risks due to its water solubility.

#pharmacology

#neurology

References:

1. Madhiyazhagan M, Roshan R, Dhanapal SG, Joseph JV, Ganesan P, Mathew V, A Kundavaram PP. Comparison of Phenytoin and Fosphenytoin in Treatment of Active Seizures in the Emergency Department. Neurol India. 2023 May-Jun;71(3):447-452. doi: 10.4103/0028-3886.378665. PMID: 37322738.

2. Aaronson PM, Belgado BS, Spillane JP, Kunisaki TA. Evaluation of intramuscular fosphenytoin vs intravenous phenytoin loading in the ED. Am J Emerg Med. 2011 Nov;29(9):983-8. doi: 10.1016/j.ajem.2010.05.005. Epub 2010 Aug 3. PMID: 20685063.

3. DeToledo JC, Ramsay RE. Fosphenytoin and phenytoin in patients with status epilepticus: improved tolerability versus increased costs. Drug Saf. 2000 Jun;22(6):459-66. doi: 10.2165/00002018-200022060-00004. PMID: 10877039.

Clopidogrel & PPIs

Q: Which of the following Proton Pump Inhibitors (PPIs) is most likely to decrease the effect of clopidogrel? - select one

A) Lansoprazole

B) Omeprazole

C) Pantoprazole

D) Rabeprazole 

Answer: B

The interaction between clopidogrel and PPIs is overrated. Two ways to minimize this interaction are:

1. Avoid omeprazole, as clopidogrel and omeprazole share hepatic CYP2C19 metabolism. Other PPIs like pantoprazole, lansoprazole, and rabeprazole are less likely to interact. 

2. Taking clopidogrel and PPIs four or more hours apart.

#GI

#pharmacology

References:

1. Axelsson MAB, Parodi López N, Wikström Jonsson E, Wallerstedt SM. Efficacy and Safety of Clopidogrel With and Without a Proton Pump Inhibitor: A Systematic Review and Meta-Analysis. Basic Clin Pharmacol Toxicol. 2025 Aug;137(2):e70087. doi: 10.1111/bcpt.70087. PMID: 40685887; PMCID: PMC12277936.

2. Juurlink DN. Proton pump inhibitors and clopidogrel: putting the interaction in perspective. Circulation 2009; 120:2310.

HIV and OB transmission

Q: Antiretroviral use during pregnancy, at the time of delivery, and breastfeeding can eliminate the chances of HIV transmission by? - select one

A) about 50%

B) almost 100%

Answer: A

Over the years, antiretroviral therapy (ART) has become more of a preventive drug than a treatment. Interestingly and fortunately, use of ART during pregnancy, at the time of delivery, and breastfeeding can eliminate transmission almost 100%. 

The sad part is that the data up to 2024 showed that 1.4 million children under 15 years of age were living with HIV globally. And in resource-limited but high-burden countries, like Angola, Chad, and Nigeria, less than 50 percent of the pregnant or breastfeeding women living with HIV are receiving antiretroviral medicines.

#epidemiology

#ID

#Ob-gyn

References: 

1. Eke AC, Lockman S, Mofenson LM. Antiretroviral Treatment of HIV/AIDS During Pregnancy. JAMA. 2023 Apr 18;329(15):1308-1309. doi: 10.1001/jama.2023.5076. PMID: 37010862; PMCID: PMC10390091.

2. Short WR, Lowenthal ED, Momplaisir F, Powis KM, Scott RK, Yee LM, Miller ES, Mofenson LM. HIV and Pregnancy: Navigating Complex Decision Making and Preventing Perinatal Transmission. Curr HIV/AIDS Rep. 2025 Jun 7;22(1):36. doi: 10.1007/s11904-025-00745-0. PMID: 40481940; PMCID: PMC12145298.

3. Fleșeriu T, Meliț LE, Mărginean CO, Pop AV, Văsieșiu AM. Maternal HIV Infection and Antiretroviral Therapy in Pregnancy: Implications for Vertical Transmission, Fetal Safety, and Long-Term Infant Outcomes. Pathogens. 2025 Aug 19;14(8):818. doi: 10.3390/pathogens14080818. PMID: 40872328; PMCID: PMC12389244.

Sarcoid and IBD

Q: Sarcoidosis seems to have a greater tendency to exist with which of the following gastrointestinal immune/inflammatory disorders? - select one

A) Crohn disease

B) Ulcerative colitis

Answer: A

Bronchoalveolar lavage fluid lymphocytosis, elevated CD4/CD8 lymphocyte ratios, and nonnecrotizing granulomas in the lungs can be seen in both disorders, suggesting a possible common pathogenic mechanism between the two diseases. 

It is important to differentiate between coexistence of both disorders from pure intestinal sarcoidosis. Other manifestations of Crohn disease include pyoderma gangrenosum, rectal and perianal lesions, and enterocutaneous fistulas. Also, intestinal sarcoidosis usually involves only the mucosa, whereas Crohn disease can be transmural, with crypt inflammation, aphthae, and ulcers.

The concurrence of sarcoidosis and ulcerative colitis is rare.

#GI

References:

1. Mitchell DN, Rees RJ. Sarcoidosis and Crohn's disease. Proc R Soc Med 1971; 64:944.

2. D'Ercole C, Zullo A, Bragazzi MC, Campo SM. Sarcoidosis and coeliac disease: do not forget the association! Intern Emerg Med 2012; 7 Suppl 1:S25.

3. Mills K, Fatima S, Fas N. Crohn's Disease Diagnosed in a Man with Sarcoidosis: Coincidence or Correspondence? Case Rep Gastrointest Med. 2022 May 27;2022:5943468. doi: 10.1155/2022/5943468. PMID: 35669381; PMCID: PMC9166977.

Risk factors for CAPS

Q: In patients with antiphospholipid antibodies (aPL), which of the following carries the highest risk for Catastrophic antiphospholipid syndrome (CAPS)? - select one

A) Active systemic lupus erythematosus (SLE)

B) Cancer 

C) Infection

D) Pregnancy (or postpartum)

E) Surgery 

Answer: C

Contrary to conventional belief that estrogen use, pregnancy, postpartum, or active systemic lupus erythematosus (SLE) are the highest risk factors for CAPS, infection carries about 10 times more chances of bringing CAPS in patients with aPL or antiphospholipid syndrome (APS).

Above all, in its acute phase, infection (choice C) is the highest thrombotic risk. Another well-known reason for CAPS still stays valid, i.e., inadequate anticoagulation in a patient with known APS.

#rheumatology

References:

1. Cervera R, Rodríguez-Pintó I, Legault K, Erkan D. 16th International Congress on Antiphospholipid Antibodies Task Force Report on Catastrophic Antiphospholipid Syndrome. Lupus 2020; 29:1594.

2. Stammler R, Nguyen Y, Yelnik C, et al. Precipitating factors of catastrophic antiphospholipid syndrome: the role of anticoagulant treatment in a series of 112 patients. J Thromb Haemost 2023; 21:1258.

ECMO and HCPS

Q: Extracorporeal membrane oxygenation (ECMO) has shown no survival benefit in Hantavirus Cardiopulmonary Syndrome (HCPS) and should be considered only when death seems to be the probable outcome.

A) True

B) False

Answer: B

Early insertion of vascular sheaths and preemptive cannulation are associated with a higher survival rate, up to 65-80%, in HCPS. Mortality seems to increase once hemodynamic instability occurs later in the course.

Evidence showed that if a cardiac index remained below 2.5 L/minute/m2 despite volume, pressor, and inotropic support, ECMO should be pursued early in the course. 

Interestingly, ECMO in HCPS has been known to be beneficial for the last three decades (reference #1).

#hemodynamics

#ID

References:

1. Crowley MR, Katz RW, Kessler R, et al. Successful treatment of adults with severe Hantavirus pulmonary syndrome with extracorporeal membrane oxygenation. Crit Care Med 1998; 26:409.

2. Wernly JA, Dietl CA, Tabe CE, et al. Extracorporeal membrane oxygenation support improves survival of patients with Hantavirus cardiopulmonary syndrome refractory to medical treatment. Eur J Cardiothorac Surg 2011; 40:1334.

3. Yao H, McDonald EG. Extracorporeal membrane oxygenation for the treatment of severe refractory hantavirus cardiopulmonary syndrome. CMAJ 2016; 188:E528.

Hyperparathyroid crisis

Q: What are the three major causes of parathyroid crisis, also known as hypercalcemic crisis?

Answer: Parathyroid or hyperparathyroid crisis is clinically marked by severe abdominal pain, nausea, vomiting, peptic ulcer, pancreatitis, and, in particular, central nervous system dysfunction. 

The diagnosis relies on serum calcium concentration usually above 15 mg/dL and serum PTH 20 times the upper limit of normal. Concomitant bone disease and nephrolithiasis are usually present.

The three major causes are:

1. severe illness

2. volume depletion

3. infarction of a parathyroid adenoma

#endocrinology

References:

1. Ahmad S, Kuraganti G, Steenkamp D. Hypercalcemic crisis: a clinical review. Am J Med 2015; 128:239.

2. Muntaser A, Thelen A, Sehgal AR, McHenry CR. Hyperparathyroid crisis: Characteristics and outcomes. Am J Surg. 2023 Mar;225(3):477-480. doi: 10.1016/j.amjsurg.2022.10.028. Epub 2022 Oct 18. PMID: 36307336.

3. Bondeson AG, Bondeson L, Thompson NW. Clinicopathological peculiarities in parathyroid disease with hypercalcaemic crisis. Eur J Surg 1993; 159:613.

yellow fever vaccine and immunocompromised hosts

Q: A 52-year-old male recovering in the ICU after a heart-kidney transplant announces he will travel to South Africa to celebrate his successful outcome and freedom from dialysis. He asks the intensivist for advice, who advises against such travel as he may need to take the yellow fever vaccine. Why should the yellow fever vaccine ideally be avoided in immunocompromised hosts?

Answer: It contains a live attenuated viral strain 

Ideally, immunocompromised travelers due to any underlying disease process (such as asplenia or thymic dysfunction) or drugs (such as steroids) should avoid the yellow fever vaccine, or wait 4-12 weeks after stopping such drugs. It contains a live attenuated viral strain. Experts even advise omitting such travel to endemic areas and even accepting deportation instead of accepting the yellow fever vaccine if forced on arrival. If absolutely required, peak season should be avoided.

Some patients who are on TNF-alpha inhibitors, interleukin-1– and interleukin-6–blocking agents, immunosuppressive monoclonal antibodies targeting immune cells, alkylating drugs, and antimetabolites may not be aware of underlying risk. Similarly, patients with asplenia, renal failure, chronic liver disease, advanced HIV, diabetes, myasthenia gravis, thymoma, or prior thymectomy are at particular risk.

Fatal myeloencephalitis or yellow fever vaccine–associated viscerotropic disease may occur.

#ID

References:

1. Rubin LG, Levin MJ, Ljungman P, et al. 2013 IDSA clinical practice guideline for vaccination of the immunocompromised host. Clin Infect Dis 2014; 58:e44.

2. Cetron MS, Marfin AA, Julian KG, et al. Yellow fever vaccine. Recommendations of the Advisory Committee on Immunization Practices (ACIP), 2002. MMWR Recomm Rep 2002; 51:1.

3. Mileno M. Preparation of Immunocompromised Travelers. In: Travel Medicine, 1st ed, Keystone JS, Freedman DP, Nothdurft HD, Connor BA (Eds), Mosby, Edinburgh 2004. p.249.

4. Kengsakul K, Sathirapongsasuti K, Punyagupta S. Fatal myeloencephalitis following yellow fever vaccination in a case with HIV infection. J Med Assoc Thai 2002; 85:131.