Wednesday, January 31, 2018

A violent patient in ICU

Q: A violent patient in ICU with a psychiatric disorder or drug/alcohol withdrawal should be asked directly: "Do you feel like hurting yourself or others?"

A) True
B) False


Answer: True

It is both helpful and respectful to have an honest and non-threatening behavior towards a patient who tends toward violence. Addressing violence directly helps!

Also, many other non-pharmacological recommendations may help like friendly gestures,  avoiding direct eye contact, not to approach the patient from behind,  standing at least two arm's lengths away, avoiding argument or giving commands.


References: 

1. Hill S, Petit J. The violent patient. Emerg Med Clin North Am 2000; 18:301. 

2. Richmond JS, Berlin JS, Fishkind AB, et al. Verbal De-escalation of the Agitated Patient: Consensus Statement of the American Association for Emergency Psychiatry Project BETA De-escalation Workgroup. West J Emerg Med 2012; 13:17.

Tuesday, January 30, 2018

Use of fiber in patients on vasopressor

Q: Fiber should be added to the enteral formulae in critically ill patients who are on vasopressors.

A) True
B) False


Answer:  False

Evidence for the regular use of fiber in critically ill patients is very weak and should be avoided. It can be used on a trial basis in patients who develop persistent motility problem secondary to enteral nutrition. Patients on vasopressors may develop bezoars from fiber and should be added with caution.


References / further reading:

1. McIvor AC, Meguid MM, Curtas S, et al. Intestinal obstruction from cecal bezoar; a complication of fiber-containing tube feedings. Nutrition 1990; 6:115. 

2. Dobb GJ, Towler SC. Diarrhoea during enteral feeding in the critically ill: a comparison of feeds with and without fibre. Intensive Care Med 1990; 16:252.  

3. Taylor BE, McClave SA, Martindale RG, et al. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). Crit Care Med 2016; 44:390. 

Monday, January 29, 2018

PET scan and Takotsubo Cardiomyopathy

Q: "Inverse flow metabolism mismatch" on positron emission tomography (PET Scan) is the hallmark of which cardiac disease?

A) Marfan syndrome
B) Hypertrophic Cardiomyopathy
C) Pericarditis
D) Stress (takotsubo) cardiomyopathy
E) Dilated cardiomyopathy secondary to amyloidosis



Answer:  D

In recent literature PET scan has been advocated to confirm the diagnosis of stress cardiomyopathy. As expected, PET scan in stress cardiomyopathy shows a discrepancy between normal perfusion and reduced glucose utilization in dysfunction regions. This is referred as an "inverse flow metabolism mismatch".


Reference:


Testa M, Feola M. Usefulness of myocardial positron emission tomography/nuclear imaging in Takotsubo cardiomyopathy. World J Radiol 2014; 6:502.

Sunday, January 28, 2018

A Note on Abdomen-Brain Connection

A Note on Abdomen-Brain Connection 

Not embraced by everyone and one of the controversial indication to perform open abdomen is refractory intracranial hypertension. It is presumed that the decompression of abdomen by keeping abdomen open lowers the venous pressures and may augment venous outflow from the head and consequently decrease the intracranial pressure.



Reference:

Joseph DK, Dutton RP, Aarabi B, Scalea TM. Decompressive laparotomy to treat intractable intracranial hypertension after traumatic brain injury. J Trauma 2004; 57:687.

Saturday, January 27, 2018

Atropine test for Brain Death Determination

Q: The atropine test is considered positive for brain death determination if the heart rate response to intravenous injection of 2-3 mg atropine shows 

A) an increase in heart rate less than 3 percent
B) an increase in heart rate less than 10 percent
C) a decrease in heart rate more than 3 percent
D) a decrease in heart rate more than 10 percent
E) Patient develops ventricular tachycardia



Answer: A


The atropine test assesses bulbar parasympathetic activity on heart activity in brain-dead patients. 2-3 mg of atropine is injected under continuous monitoring of the EKG over 10 minutes. The test is considered negative if heart rate is not increased by more than 3%.


References:

1. Siemens P, Hilger HH, Frowein RA. Heart rate variability and the reaction of heart rate to atropine in brain dead patients. Neurosurg Rev 1989; 12 Suppl 1:282.

2. Huttemann E, Schelenz C, Sakka SG, et al. Atropine test and circulatory arrest in the fossa posterior assessed by transcranial Doppler. Intensive Care Med. 2000;26:422–5.

3. Cardan C, Roth A, Biro J. The atropine test in the assessment of brain death. Rev Chir Oncol Radiol O R L Oftalmol Stomatol Chir. 1983;32:393–7

Friday, January 26, 2018

Armored Endotracheal Tube

Q: Give at least three characteristics of an Armored endotracheal tube (A-ETT) popularly known as a 'reinforced endotracheal tube'?


Answer: A reinforced ETT is advocated when there is a concern for tracheal compression. It has a metal wire coil embedded in the wall of the tube.

1. It has more flexibility but less collapsibility.

2. The tube connector of armored tubes is not detachable (unlike standard ETT).
3. As they are relatively more flexible, it is very hard to intubate without a stylet. 

It is an excellent replacement for ETT when more flexibility but less collapsibility (i.e resistance to occlusion) is desired such as in;


  • fiberoptic intubation
  •  intubation through a tracheotomy 
  • upper body surgeries
  • when a patient requires prone position

Thursday, January 25, 2018

non-long-bone-trauma causes of fat embolism

Q: Give ten examples of conditions causing 'fat embolism' other than long bone trauma? 

Answer: Though 'fat embolism' is mostly due to long bone traumas but many non-traumatic conditions (though uncommon) can be the cause of fat embolism. List is long but few ICU related causes may be (also see references):
  1. Chest compressions with or without rib fractures 
  2. Burns 
  3. Pancreatitis 
  4. Osteomyelitis 
  5. Prolonged steroid therapy 
  6. Sickle cell hemoglobinopathies 
  7. Lipid infusion 
  8. Cyclosporin A solvent 
  9. Intraoperative cell salvage 
  10. Cardiopulmonary bypass


References / further reading:

1. de Lima E Souza R, Apgaua BT, Milhomens JD, et al. Severe fat embolism in perioperative abdominal liposuction and fat grafting. Braz J Anesthesiol 2016; 66:324. 

2. Jacob S, Courtwright A, El-Chemaly S, et al. Donor-acquired fat embolism syndrome after lung transplantation. Eur J Cardiothorac Surg 2016; 49:1344. 

3. Schrufer-Poland T, Singh P, Jodicke C, et al. Nontraumatic Fat Embolism Found Following Maternal Death after Cesarean Delivery. AJP Rep 2015; 5:e1. 

4. Schonfeld SA, Ploysongsang Y, DiLisio R, et al. Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients. Ann Intern Med 1983; 99:438. 

5. Garza JA. Massive fat and necrotic bone marrow embolization in a previously undiagnosed patient with sickle cell disease. Am J Forensic Med Pathol 1990; 11:83. 

6. Levine M, Skolnik AB, Ruha AM, et al. Complications following antidotal use of intravenous lipid emulsion therapy. J Med Toxicol 2014; 10:10. 


Wednesday, January 24, 2018

Local anesthesia in CVC

Q: During inserting non-tunneled Central Venous Catheter (CVC) in ICU, it is recommended to infiltrate a large amount of local anesthesia into subcutaneous (SC) tissues. 

A) True
B) False


Answer: B

Infiltrating skin and SC tissues with local anesthesia is needed prior to inserting CVC in ICU but large infiltration can cause two problems.

1.  a large infiltration of local anesthesia in the SC tissue will distort anatomical landmarks (particularly making it difficult if no bedside ultrasound is available).

2. A  large infiltration of local anesthesia in the SC tissue may compress vein making access more difficult, particularly in dehydrated patients.

Tuesday, January 23, 2018

Use of cryoprecipitate in uremic bleeding

Q: Which of the following can be used in bleeding suspected secondary to uremia?

A) Dialysis 
 B) Desmopressin (DDAVP) 
 C) Estrogen 
D) Cryoprecipitate 
 E) All of the above 


 Answer: E

Objective of above question is to highlight the role of Cryoprecipitate in uremic bleeding. Dialysis, Estrogen, DDAVP and correction of anemia are known to help in uremic bleeding. Use of cryoprecipitate in this regard is less well known. It may be a very useful information in post surgical patients with baseline renal insufficiency, who remain unresponsive to DDAVP. It can start it's effect within one hour of infusion to shorten the bleeding time. Exact mechanism of action is not known but it is suspected that cryoprecipitate carries substances that enhance platelet aggregation, such as factor VIII:von Willebrand factor multimers or fibrinogen. 


Reference:

Janson PA, Jubelirer SJ, Weinstein MJ, Deykin D. Treatment of the bleeding tendency in uremia with cryoprecipitate. N Engl J Med 1980; 303:1318.

Monday, January 22, 2018

Spironolactone in CHF

Q: Which of the following is the proposed mechanism of action causing beneficial effects of the aldosterone-receptor blocker (Spironolactone) in congestive heart failure?

A) Averting sodium retention
B) Averting myocardial fibrosis
C) Averting potassium loss
D) increasing the myocardial uptake of norepinephrine
E) All of the above


Answer: E

Mechanism of action of an aldosterone-receptor blocker is complex. Some effects are well known Like Choices A and C. Objective of the above question is to highlight their role by averting myocardial fibrosis (Choice B). It reduces the risk of sudden death from arrhythmias. Also, myocardial uptake of norepinephrine (choice D) has been demonstrated in the animal models.


References:

1. Pitt B et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999 Sep 2;341(10):709-17.

2. Buss SJ et. al. Spironolactone preserves cardiac norepinephrine reuptake in salt-sensitive Dahl rats. Endocrinology. 2006 May;147(5):2526-34.

Sunday, January 21, 2018

Intubation in Trauma

Q: 22 years old male is admitted to ICU with abdominal Gunshot Wound (GSW). Surgical service is planning to take patient to the OR. Patient Blood Pressure is 110/60 mm Hg and heart rate is 120 bpm. Patient is protecting his airway. Volume resuscitation is underway. Patient should be preemtively intubated

A) True
B) False


Answer: False

Risk of hypotension following intubation should always be a major concern in each and every intubation, and should be weighed against the benefits of intubation. Above case is used as a classical example where delaying intubation may allow more time for hemodynamic resuscitation. Hypotension following intubation can be detrimental and fatal.


Reference:


Heffner AC, Swords DS, Nussbaum ML, et al. Predictors of the complication of postintubation hypotension during emergency airway management. J Crit Care 2012; 27:587.

Saturday, January 20, 2018

Propofol and rebound seizure

Q: Abrupt withdrawal of which of the following intravenous (IV) infusion drug may cause rebound seizures and should be "weaned off" with coverage of other anti-epileptic drugs during management of status epileptics?

A) Lorazepam
B) Propofol
C) Phenobabital
D) Phenytoin
E) Levetiracetam


Answer: B

Propofol should be weaned off as abrupt withdrawal of propofol may cause rebound seizures due to its very short half life. Coverage should be established with other longer-acting anti-epileptic drug. Lorazepam and Phenobarbital have relative longer half lives and provide good umbrella when short acting propofol is taken off.

Phenytoin and Levetiracetam are not given as IV infusion.


Reference: 

Stecker MM1, Kramer TH, Raps EC, O'Meeghan R, Dulaney E, Skaar DJ. Treatment of refractory status epilepticus with propofol: clinical and pharmacokinetic findings. Epilepsia. 1998 Jan;39(1):18-26.

Friday, January 19, 2018

scoring systems to assess the risk of bleeding secondary to warfarin

Q: All of the following are the scoring systems to assess the risk of bleeding secondary to warfarin intake in atrial fibrillation patients except

 A) ATRIA 
 B) HAS-BLED 
 C) OBRI 
 D)HEMORR2HAGES 
E) CURB 65


Answer: E

Except for CURB 65 all other (choices A, B, C, D) are the scoring systems to assess the bleeding risk in patients receiving warfarin for atrial fibrillation.

CURB 65 is a severity score to estimate the mortality risk from community-acquired pneumonia and is utilized as a determination tool to decide between inpatient vs outpatient treatment.



References:


1. Donzé J, Rodondi N, Waeber G, et al. Scores to predict major bleeding risk during oral anticoagulation therapy: a prospective validation study. Am J Med 2012; 125:1095.

2. Apostolakis S, Lane DA, Guo Y, et al. Performance of the HEMORR(2)HAGES, ATRIA, and HAS-BLED bleeding risk-prediction scores in patients with atrial fibrillation undergoing anticoagulation: the AMADEUS (evaluating the use of SR34006 compared to warfarin or acenocoumarol in patients with atrial fibrillation) study. J Am Coll Cardiol 2012; 60:861. 

 3. Lim WS, van der Eerden MM, Laing R, et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax 2003; 58:377.

Thursday, January 18, 2018

Padua Prediction Score

Q: Padua Prediction Score is designed to assess the risk of?

A) Venous ThromboEmbolism in hospitalized patients with liver disease
B) Pulmonary Embolism in hospitalized patients with liver disease
C) Venous ThromboEmbolism in hospitalized patients with renal disease
D) Pulmonary Embolism in hospitalized patients with renal disease


Answer: A

Padua Prediction score assesses the risk of Venous thromboembolism (VTE) in hospitalized patients with liver disease. Prophylaxis against VTE is highly under-utilized in patients with liver disease due to the misconception that they are "auto-anticoagulated" because their INR is high. INR is not a true indicator of auto-anticoagulation in patients with liver disease. Unfortunately, due to this misconception among medical staff, the adjusted hazard ratio (HR) of VTE in patients with the significant liver disease is 1.71, at lease shown in one study. 

One online calculator can be found here 


References: 

1. Ng KJ, Lee YK, Huang MY, et al. Risks of venous thromboembolism in patients with liver cirrhosis: a nationwide cohort study in Taiwan. J Thromb Haemost 2015; 13:206. Bogari H, Patanwala AE, Cosgrove R, Katz M. 

2. Risk-assessment and pharmacological prophylaxis of venous thromboembolism in hospitalized patients with chronic liver disease. Thromb Res 2014; 134:1220.

Wednesday, January 17, 2018

ARDS

Q: Acute Respiratory Distress Syndrome (ARDS) is a diagnosis of exclusion?

A) True
B) False


Answer: True

This is an essential and an important concept to be abreast of. Establising a diagnosis of ARDS requires many other related conditions to be ruled out such as pleural effusions, atelectasis, lung mass, diffuse alveolar hemorrhage, congestive heart failure, fluid overload, idiopathic acute exacerbation of pre-existing interstitial lung disease, malignancy and others. It also requires certain criteria to be fulfilled as established in Berlin criteria of ARDS.



Reference:

The ARDS Definition Task Force -Acute Respiratory Distress Syndrome The Berlin Definition - JAMA. 2012;307(23):2526-2533

Tuesday, January 16, 2018

Seven "NOs"

Q: Which seven "NOs" are required to safely forego CT imaging of the chest in adults with blunt thoracic trauma '?


Answer:  The NEXUS research group has validated 'decision instrument' (DI) to help determine which adults (more than 15 years old) with blunt thoracic trauma, within the last 24 hours, can safely forego CT imaging of the chest, with the major objective to reduce indiscriminate use of CT scans in ED. The first iteration of the NEXUS decision instrument included the following seven criteria
  1. Age  more than 60 years
  2. Chest pain 
  3. Intoxication 
  4. Abnormal mental status 
  5. Chest wall tenderness 
  6. Distracting painful injury 
  7. Rapid deceleration mechanism (ie, fall of more than 20 feet, or Motor Vehicle Collision at more than 40 m/65 km/hour
There was also a subsequent iteration of the NEXUS decision instrument known as Chest CT-All, where criteria were updated with four replacements
  1. Abnormal plain chest radiograph
  2. Sternal tenderness
  3. Thoracic spine tenderness 
  4. Scapular tenderness
  5. Chest wall tenderness 
  6. Distracting painful injury 
  7. Rapid deceleration mechanism (ie, fall of more than 20 feet, or Motor Vehicle Collision at more than 40 m/65 km/hour
Chest CT-All criteria have a variant known as "CT-Major", where even the 7th point was taken out!


References: 

1. Rodriguez RM, Anglin D, Langdorf MI, et al. NEXUS chest: validation of a decision instrument for selective chest imaging in blunt trauma. JAMA Surg 2013; 148:940. 

2. Rodriguez RM, Langdorf MI, Nishijima D, et al. Derivation and validation of two decision instruments for selective chest CT in blunt trauma: a multicenter prospective observational study (NEXUS Chest CT). PLoS Med 2015; 12:e1001883.

Monday, January 15, 2018

PPV and fluid responsiveness

Q: Recent literature has shown that pulse pressure variation (PPV) is a better indicator of fluid responsiveness than central venous pressure (CVP). But applicability of PPV  is limited. Which conditions should be met to obtain reliable PPV?


Answer:

1. Patient should be mechanically ventilated
2. Patient should not be spontaneously triggering the ventilator
3. Tidal Volume (TV) on ventilator should be  ≥8 mL/kg of ideal body weight
4. Patient should be in normal sinus rhythm
5. Patient has no major alternations to chest wall compliance (making open chest patients ineligible) 

PPV of 12 -15 percent is usually associated with volume responsiveness.


References/further reading:

1. Pinsky MR. Functional haemodynamic monitoring. Curr Opin Crit Care 2014; 20:288.


2. Marik PE, Cavallazzi R, Vasu T, et al. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med. 2009;37(9):2642-7


3. Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a critical analysis of the evidence. Chest 2002; 121:2000.


4. Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med 2000; 162:134.

Sunday, January 14, 2018

Markers of successful reperfusion from fibrinolysis in acute STEMI

Q: Out of the following which markers are preferable in to predict successful reperfusion from fibrinolysis in acute ST elevation myocardial infarction (STEMI)?

A) CK-MB
B) Myoglobin
C) Troponin
D) A and B
E) Reperfusion arrhythmias


Answer: 

Troponin is now treated like a holy grail in STEMI but rapidly rising and falling CK-MB or/and myoglobin are more reliable indicator of successful reperfusion after fibrinolysis in STEMI. Although reperfusion arrhythmia is common after successful fibrinolysis in acute STEMI, it is neither a sensitive nor a specific sign.


References:

1. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. www.acc.org/qualityandscience/clinical/statements.htm 

2. Christenson RH, Ohman EM, Topol EJ, et al. Assessment of coronary reperfusion after thrombolysis with a model combining myoglobin, creatine kinase-MB, and clinical variables. TAMI-7 Study Group. Thrombolysis and Angioplasty in Myocardial Infarction-7. Circulation 1997; 96:1776. 

3. Tanasijevic MJ, Cannon CP, Antman EM, et al. Myoglobin, creatine-kinase-MB and cardiac troponin-I 60-minute ratios predict infarct-related artery patency after thrombolysis for acute myocardial infarction: results from the Thrombolysis in Myocardial Infarction study (TIMI) 10B. J Am Coll Cardiol 1999; 34:739. 

4. Berger PB, Ruocco NA, Ryan TJ, et al. Incidence and significance of ventricular tachycardia and fibrillation in the absence of hypotension or heart failure in acute myocardial infarction treated with recombinant tissue-type plasminogen activator: results from the Thrombolysis in Myocardial Infarction (TIMI) Phase II trial. J Am Coll Cardiol 1993; 22:1773.

Saturday, January 13, 2018

2 vs 3 lumens dialysis catheter

Q: Three-lumen dialysis catheter, popularly known as trialysis, is more popular than two-lumen dialysis catheter for practical purposes with advantage of one extra port. But it is not an ideal catheter for continuous renal replacement therapy (CRRT). Give at least three reasons why three-lumen dialysis catheter is inferior to two-lumen dialysis catheter (trialysis catheter).


Answer: 

1. Presence of extra port/lumen in catheter take toll on diameters of other two lumens and decreases the internal diameter of the two dialysis lumens. Consequently it may hamper the blood flows.

2. Infusion of critical medications like antibiotics, inotrope or pressors may  get more rapidly cleared by dialysis.

3. Calcium infused via third lumen of dialysis catheter may get recirculated and cause unreliable effect and measurement of ionized calcium.

Although, infusion via third lumen of intravenous fluids, heparin or blood products seems safe so far.

Friday, January 12, 2018

ATHOS-3 Trial

Q: In the recently published ATHOS-3 trial, which of the following drug has shown a promising value in the treatment of 'high output vasodilatory shock'?

A) Vitamin C
B) Hydrocortisone
C) pRBC (blood)
D) Angiotensin II
E) Phenylephrine


Answer: D

Angiotensin II is the new sensation! In the recently published trial - ATHOS-3 (Angiotensin II for the Treatment of High-Output Shock), which randomized 321 patients (163 received angiotensin II, and 158 received placebo), the primary endpoint was reached by more patients in the angiotensin II group (114 of 163 patients, 69.9%) than in the placebo group (37 of 158 patients, 23.4%) (odds ratio, 7.95; 95% confidence interval [CI], 4.76 to 13.3; P < 0.001).

The primary endpoint was a response with respect to mean arterial pressure (MAP) at hour 3 after the start of infusion, with response defined as an increase from baseline of at least 10 mm Hg or an increase to at least 75 mm Hg, without an increase in the dose of background vasopressors.


Read abstract at link with reference

Reference:

Khanna A et al. "Angiotensin II for the Treatment of Vasodilatory Shock". New Engl J Med. 2017. 377:419-30. :: http://www.nejm.org/doi/full/10.1056/NEJMoa1704154

Thursday, January 11, 2018

DIC and Organs

Q: Out of the following major organs, which organ is more prone to insult in acute disseminated intravascular coagulation (DIC)

A) Renal 
B) Liver 
C) Lung
D) Central nervous system (CNS)
E) Adrenal


Answer: 

Vascular micro-thrombosis, hemorrhage, leading to tissue hypoxia is a well known mechanism for organ dysfunctions in acute DIC. Kidney is the most vulnerable organ in acute DIC. In ICU, it requires high vigilance as need for CRRT may arise very quickly.



Reference:

Siegal T, Seligsohn U, Aghai E, Modan M. Clinical and laboratory aspects of disseminated intravascular coagulation (DIC): a study of 118 cases. Thromb Haemost 1978; 39:122.

Wednesday, January 10, 2018

Bonferroni Correction

Q: What Is the Bonferroni Correction? 


Answer: In statistical analysis, if  multiple comparisons are done (or hypotheses tested) e.g. various subgroups analysis performed in a clinical trial, the chance of a false positive result increases (Type I error) as the number of subgroup increases. The Bonferroni correction is a mathematical way to compensate for that error.

So if n is the number of hypotheses/subgroups/comparisons to obtain a desired p value of 0.05

for n=20 :: the Bonferroni correction for each individual hypothesis would be 0.05/20=0.0025

In other words, The Bonferroni correction is an adjustment made to P values when a large (dependent or independent) statistical tests are being performed simultaneously on a single data set.


Reference:

Mittelhammer, Ron C.; Judge, George G.; Miller, Douglas J. (2000). Econometric Foundations. Cambridge University Press. pp. 73–74

Tuesday, January 9, 2018

Ketamine in Status Epilepticus

Q: Ketamine works better in which phase of status epilepticus? (select one)

A) Early
B) Later


Answer:  Later

Ketamine is a good choice if there is no response to benzodiazepines or barbiturates in status epilepticus. Ketamine is more effective in later phase of status epilepticus. 

Ketamine is an N-methyl-D-aspartase (NMDA) antagonist. It works better when gamma-aminobutyric (GABA) agonists or promoters (eg, benzodiazepines and barbiturates) have lost some effectiveness.


References:

1. Sheth RD, Gidal BE. Refractory status epilepticus: response to ketamine. Neurology 1998; 51:1765. 

2. Gaspard N, Foreman B, Judd LM, et al. Intravenous ketamine for the treatment of refractory status epilepticus: a retrospective multicenter study. Epilepsia 2013; 54:1498. 

3. Basha MM, Alqallaf A, Shah AK. Drug-induced EEG pattern predicts effectiveness of ketamine in treating refractory status epilepticus. Epilepsia 2015; 56:e44. 

 4. Mazarati AM, Wasterlain CG. N-methyl-D-asparate receptor antagonists abolish the maintenance phase of self-sustaining status epilepticus in rat. Neurosci Lett 1999; 265:187.

Monday, January 8, 2018

Candidemia - risk factors

Q: All of the following are the risk factors for candidemia in ICU except?

A) Central venous catheters (CVC)
B) Total parenteral nutrition (TPN)
C) Hemodialysis
D) Broad-spectrum antibiotics
E) Daily bathing with chlorhexidine


Answer: 

Candidemia in ICU is a huge burden and carries a high mortality. All of the above except choice E are the risk factors for candidemia in ICU. Even a mere suspicion of it should call for a consideration to removal of CVC. Quick de-escalation of broad-spectrum antibiotics should be a standard of care. Also, trauma and surgical units may be prone to higher incidence of candidemia. As per recent updated clinical practice guideline for the management of candidiasis (2016) from the Infectious Diseases Society of America (IDSA), daily bathing of ICU patients with chlorhexidine has shown to decrease the incidence of bloodstream infections in general, and candidemia in particular.



Reference:

Pappas PG, Kauffman CA, Andes DR, et al. Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America. Clin Infect Dis 2016; 62:e1.

Sunday, January 7, 2018

On the Nomenclature of Vasculitides

Q: 2012 International Chapel Hill Consensus Conference (CHCC2012) is about Nomenclature of? (Select one)

A) Inflammatory Bowel Diseases

B) Vasculitides
C) Viral encephalitis
D) Obstetric emergencies 
E) Acute Lymphocytic Lymphoma


Answer: B

 International Chapel Hill Consensus Conference on the Nomenclature of Vasculitides, popularly known as CHCC2012 divide and define various vasculitis on the basis of 

  • Large-vessel vasculitis
  • Medium-vessel vasculitis
  • Small-vessel vasculitis
  • Variable-vessel vasculitis
  • Single-organ vasculitis
  • Vasculitis associated with systemic disease
  • Vasculitis associated with probable etiology



Reference:

Jennette JC, Falk RJ, Bacon PA, et al. 2012 revised International Chapel Hill Consensus Conference Nomenclature of Vasculitides. Arthritis Rheum 2013; 65:1.

Saturday, January 6, 2018

Hb level and refeeding syndrome

Q: Hypophosphatemia is the hallmark of the refeeding syndrome in malnourished patients. Patients with higher hemoglobin (Hb) levels are at higher risk of refeeding hypophosphatemia

A) True
B) False


Answer: True

Chronic dehydration in severely malnourished patients causes hemo-concentration and manifests as higher hemoglobin level in lab workup! And is considered as one of the predictors in refeeding hypophosphatemia. 


Reference:

Brown CA, Sabel AL, Gaudiani JL, Mehler PS. Predictors of hypophosphatemia during refeeding of patients with severe anorexia nervosa. Int J Eat Disord 2015; 48:898.

Friday, January 5, 2018

Young age and CVA

Q: Young age is an independent risk factor for malignant middle cerebral artery (MCA) territory infarction (select one)

A) True
B) False 



Answer: True

After ischemic infarct, the development of space-occupying cerebral edema which is severe enough to cause elevated intracranial pressure (ICP) and brain herniation is regarded as malignant infarction. It may sound surprising but old age provides a protective effect due to cerebral atrophy. It is more  accommodative of cerebral edema after infarct! 

It carries extremely high mortality.



References:


1. Krieger DW, Demchuk AM, Kasner SE, et al. Early clinical and radiological predictors of fatal brain swelling in ischemic stroke. Stroke 1999; 30:287. 

2. Hacke W, Schwab S, Horn M, et al. 'Malignant' middle cerebral artery territory infarction: clinical course and prognostic signs. Arch Neurol 1996; 53:309.

Thursday, January 4, 2018

NSAIDs and CIN

Q: Out of the following which one drug should be hold to prevent contrast induced nephropathy (CIN)?

A) Angiotensin-converting enzyme (ACE-I)

B) Angiotensin II receptor blockers (ARBs)
C) Nonsteroidal anti-inflammatory agents (NSAIDs)
D) Vitamin C
E) Hydralazine


Answer: C

Reflexively, ACE-I comes to the mind as an answer, but there is no evidence that ACE-Is or ARBs (or Hydralazine) increase the risk of CIN.

Actually NSAIDs increased the risk of CIN more than any other drugs, and should be stopped 24 to 48 hours prior to the study/procedure. 

Vitamin C has shown some benefit in CIN.


References: 

1. Rosenstock JL, Bruno R, Kim JK, et al. The effect of withdrawal of ACE inhibitors or angiotensin receptor blockers prior to coronary angiography on the incidence of contrast-induced nephropathy. Int Urol Nephrol 2008; 40:749.

2. Weisbord SD, Bruns FJ, Saul MI, Palevsky PM. Provider use of preventive strategies for radiocontrast nephropathy in high-risk patients. Nephron Clin Pract 2004; 96:c56. 

3. Dvoršak B, Kanič V, Ekart R, Bevc S, Hojs R. Ascorbic Acid for the prevention of contrast-induced nephropathy after coronary angiography in patients with chronic renal impairment: a randomized controlled trial. Ther Apher Dial. 2013 Aug;17(4):384-90. 

Wednesday, January 3, 2018

Nimodipine and SAH

Q: "Nimodipine" is the standard of care in patients after Sub-Arachnoid-Hemorrhage (SAH) to prevent vasospasm as it showed to decrease the incidence of either angiographic or symptomatic vasospasm. (Select one)

A) True
B) False


Answer: False

Enteral Nimodipine is the standard of care in patients with SAH. Due to its calcium-channel-blocker activity, it is assumed to prevent vasospasm and to have a vasodilatory effects on cerebral vessels. But, six major studies 1-6 over the span of 15 years failed to provide a convincing evidence that nimodipine decreases the incidence of either angiographic or symptomatic vasospasm. Despite that, Nimodipine has shown to improve outcomes in SAH in multiple studies 5-7. Various alternative explanations have been put forward for its mechanism of action including
  • reduction of calcium-dependent excitotoxicity
  • decrease platelet aggregation
  • dilation of small arteries not visible on angiograms
  • inhibition of ischemia triggered by red blood cell products



References:


1. Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 1983; 308:619. 


2. Philippon J, Grob R, Dagreou F, et al. Prevention of vasospasm in subarachnoid haemorrhage. A controlled study with nimodipine. Acta Neurochir (Wien) 1986; 82:110. 


3. Petruk KC, West M, Mohr G, et al. Nimodipine treatment in poor-grade aneurysm patients. Results of a multicenter double-blind placebo-controlled trial. J Neurosurg 1988; 68:505. 


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


5. Barker FG 2nd, Ogilvy CS. Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis. J Neurosurg 1996; 84:405. 


6. Feigin VL, Rinkel GJ, Algra A, et al. Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage: a systematic review. Neurology 1998; 50:876.


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

Tuesday, January 2, 2018

Angioedema after thrombolytics in CVA

Q: 54 year old male is started on thrombolytics therapy after he presented with stroke like symptoms within three hours. Patient developed swelling of the tongue after few minutes of infusion of thrombolytics. There is a concern for orolingual angioedema. All of the following are the proper actions to follow except?

A) Check home med-list to see if he is on angiotensin converting enzyme inhibitors (ACE-I)
B) Revisit CT scan to see if there is a sign of ischemia in the frontal lobe
C) Perform CT of the tongue to rule out hematoma of the tongue
D) administer corticosteroids and antihistamines 
E) No matter what - continue the thrombolytics 
F) Intubate the patient if there is a sign of stridor



Answer:  E

Orolingual angioedema after the initiation of thrombolytics is not an uncommon scenario. Revisiting history, physical exam and radiological data may help to establish proper diagnosis within minutes. Patients on ACE-I  are on increased risk to develop orolingual angioedema (choice A). Patients who have evidence of ischemia in the frontal lobe on CT scan are more prone to it (Choice B). On physical exam, angioedema is usually present on the contralateral side of the ischemic hemisphere. It may be of importance to rule out hematoma of the tongue secondary to thrombolytics (Choice C). Strong consideration should be given to discontinue the thrombolytics in such circumstances (Choice E is wrong). Airway management in such scenarios are the first priority (Choices D and F).




References:

1. Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013; 44:870. 

2. Hurford R, Rezvani S, Kreimei M, et al. Incidence, predictors and clinical characteristics of orolingual angio-oedema complicating thrombolysis with tissue plasminogen activator for ischaemic stroke. J Neurol Neurosurg Psychiatry 2015; 86:520. 

3. Myslimi F, Caparros F, Dequatre-Ponchelle N, et al. Orolingual Angioedema During or After Thrombolysis for Cerebral Ischemia. Stroke 2016; 47:1825. 

4. Hill MD, Lye T, Moss H, et al. Hemi-orolingual angioedema and ACE inhibition after alteplase treatment of stroke. Neurology 2003; 60:1525. 

5.  Chodirker WB. Reactions to alteplase in patients with acute thrombotic stroke. CMAJ 2000; 163:387.