Ceftaroline

Q: Ceftaroline has been called fifth generation cephalosporin because it has added activity against?

A) Methicillin-resistant Staphylococcus aureus (MRSA)
B) Pseudomonas aeruginosa
C) Neisseria gonorrhoeae
D) Klebsiella
E) Moraxella catarrhalis


Answer: A

Ceftaroline and ceftobiprole are the only two fifth generation cephalosporins known.

This took care of criticism on cephalosporins of being "LAME" - as they had  no activity  against Listeria, Atypicals (including Mycoplasma and Chlamydia), MRSA, and enterococci.

Further reading is at the link of the reference.



Reference:

1. Duplessis C, Crum-Cianflone NF. Ceftaroline: A New Cephalosporin with Activity against Methicillin-Resistant Staphylococcus aureus (MRSA). Clinical medicine reviews in therapeutics. 2011;3:a2466. doi:10.4137/CMRT.S1637.

Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3140339/

Rhabdomyolysis

Q: All of the following are indicated in rhabdomyolysis except?

A) 0.9 NS infusion
B) Alkalinization of urine
C) Mannitol 
D) Forced diuresis
E) Hemodialysis (HD)


Answer: E

All of the above are well known parts of management of rhabdomyolysis but HD failed to show any benefit in removing myoglobin or in prevention of kidney injury.



References: 

1. Mikkelsen TS, Toft P. Prognostic value, kinetics and effect of CVVHDF on serum of the myoglobin and creatine kinase in critically ill patients with rhabdomyolysis. Acta Anaesthesiol Scand 2005; 49:859.

FELi

Q: What is FELi?

 Answer: The fractional excretion of lithium (FELi)

Humans have endogenous lithium present in their circulation. Renally filtered lithium gets reabsorbed in the proximal tubule. So, proximal reabsorption of lithium is increased in prerenal disease, which will decrease the lithium excretion. In kidney disease, this excretion is increased as proximal tubule fails to reabsorb lithium. 

• Normal value of FELi is 20%
• FELi below 15 % is consistent with prerenal causes
• FEli above 25% signifies renal disease

The beauty of FELi is that it is not influenced by loop or thiazide (except chlorothiazide) diuretics. Unfortunately, not all labs have the capacity to perform FELi.



References:

1. Boer WH, Koomans HA, Dorhout Mees EJ. Acute effects of thiazides, with and without carbonic anhydrase inhibiting activity, on lithium and free water clearance in man. Clin Sci (Lond) 1989; 76:539. 

2. Steinhäuslin F, Burnier M, Magnin JL, et al. Fractional excretion of trace lithium and uric acid in acute renal failure. J Am Soc Nephrol 1994; 4:1429.

Amio-Warfarin interaction

Q: 64  year old male is admitted to ICU with atrial fibrillation and rapid ventricular rate (A.fib-RVR). Patient is chronically on warfarin at home for previous episodes of Deep Vein Thrombosis (DVTs) and pulmonary embolisms (PEs). Cardiology service decides to initiate Amiodarone bolus followed by drip. As interaction between amiodarone and warfarin is well known, how much should be the dose of warfarin cut done?

A) Completely stop
B) cut by 50%
C) cut by 25%
D) No adjustment needed
E) Tell cardiology they are wrong to start Amiodarone!



Answer; C

As Amiodarone may potentiates the effect of warfarin, it's dose should be cut back by about 25 percent. This inference is obtained from the cohort of 754 patients of a Swedish registry, who were on chronic warfarin treatment and in whom amiodarone was started. Though, close monitoring of INR is advised. Another caution  is to closely monitor the thyroid function. Amiodarone is prone to cause thyrotoxicosis which may potentiates the effect of warfarin.

E is not a good practice!


References: 

1. Holm J, Lindh JD, Andersson ML, Mannheimer B. The effect of amiodarone on warfarin anticoagulation: a register-based nationwide cohort study involving the Swedish population. J Thromb Haemost 2017; 15:446. 

2. Kurnik D, Loebstein R, Farfel Z, et al. Complex drug-drug-disease interactions between amiodarone, warfarin, and the thyroid gland. Medicine (Baltimore) 2004; 83:107.

PRES syndrome

Q: All of the following can be the symptoms of  reversible posterior leukoencephalopathy syndrome (RPLS) (PRES) except ?

A) Localized headache at the back of the head
B) Preceded by hypertensive crisis by 24 hours or longer
C) Anton's syndrome
D) Seizures
E) Altered consciousness


Answer: A

Headache in PRES syndrome is usually characterized as constantly moderate to severe, non-localized, and unresponsive to analgesia.

Anton's syndrome, also known as Anton–Babinski syndrome, is an interesting phenomenon in which despite presenting clear evidences to patients of their blindness, they remain adamant that "they can see". This is due to confabulation supported by fill in the missing sensory input.

Not necessarily but if present, the hypertensive crisis may precede other symptoms by 24 hours or longer.



References:

1. Stott VL, Hurrell MA, Anderson TJ. Reversible posterior leukoencephalopathy syndrome: a misnomer reviewed. Intern Med J 2005; 35:83. 

2. Fugate JE, Claassen DO, Cloft HJ, et al. Posterior reversible encephalopathy syndrome: associated clinical and radiologic findings. Mayo Clin Proc 2010; 85:427. 

3. Lysandropoulos AP, Rossetti AO. Postictal cortical visual impairment: a symptom of posterior reversible encephalopathy. Epilepsy Behav 2010; 17:276.

Mitral annular calcification

Q: Your cardiac valvular diagnosis?

Answer: Mitral annular calcification 

 It is an aging (atherosclerotic) process and a major cause of mitral incompetence. ​

Urea - an ineffective osmole

Q: Urea is called an "ineffective osmole". What does it mean?


Answer: Urea equilibrates freely across the cell membranes, means when the plasma concentration of  urea changes, the intracellular concentration of the solute changes in parallel, and there is little or no water shift across the cells.

In contrast, glucose alters the balance and distribution of water across the cell membranes, and is called an "effective osmole".

pyroglutamic acidosis

Q; 52 year old chronically ill female is admitted to ICU with hypotension, tachycardia and elevated anion gap metabolic acidosis. Patient is ruled out for lactic acidosis as well as ketoacidosis. Toxicology screen is negative. Osmolar gap is normal. Patient does not take any prescription medicine. Due to severe acidosis renal service is consulted for continuous renal replacement therapy (CRRT). Renal fellow in his note wrote "suspected pyroglutamic acidosis". Out of the following which over the counter drug can cause pyroglutamic acidosis in therapeutic dose?

A) Aspirin (ASA)
B) Acetaminophen (Tylenol)
C) NSAIDs
D) Ranitidine (H2 Blocker)
E) Calcium Carbonate (TUMS)


Answer: B

Acetaminophen if taken on regular basis, despite at therapeutic doses may cause anion gap metabolic acidosis. This is distinct from any other form of acidosis, and occurs due to the accumulation of  pyroglutamic acid. For unknown reason chronically ill and malnourished females are more susceptible to it. Proposed mechanism is due to either congenital or acquired  glutathione deficiency secondary to malnourishment. Two other drugs found to be associated with it are flucloxacillin and vigabatrin. It is also described with pregnancy. Other name for this acidosis is 5-oxoprolinemia. Diagnosis is via presence of high pyroglutamic acid, either in urine or blood. Treatment is correction of acidosis, avoidance of risk factors and replenishment of glutathione stores.



References:

1. Humphreys BD, Forman JP, Zandi-Nejad K, et al. Acetaminophen-induced anion gap metabolic acidosis and 5-oxoprolinuria (pyroglutamic aciduria) acquired in hospital. Am J Kidney Dis 2005; 46:143.

2.  Duewall JL, Fenves AZ, Richey DS, et al. 5-Oxoproline (pyroglutamic) acidosis associated with chronic acetaminophen use. Proc (Bayl Univ Med Cent) 2010; 23:19.

Acute Pericarditis

Q: 54 year old male is back in Emergency Department(ED) with chest pain ten days after his discharge from hospital. He was previously admitted for Acute Myocardial Infarction (AMI). Due to EKG changes in ED, patient is admitted to ICU. Further workup confirmed acute pericarditis. Which of the following is NOT a good choice to use during management of acute pericarditis  following AMI?

A) aspirin 
B) colchicine 
C) Nonsteroidal anti-inflammatory drugs (NSAIDs)
D) Acetaminophen 
E) Proton-Pump-Inhibitors (PPI)


Answer: C

In symptomatic pericarditis after an AMI, NSAIDs should be avoided as it may impair scar formation. Recommended treatment is aspirin (ASA) with colchicine. Acetaminophen can also be used as symptomatic treatment. PPIs help to relief GI symptoms secondary to ASA and colchicine. 


Reference:

Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute pericarditis. Circulation 2007; 115:2739.

Colistin and CRRT

Q: Which one drug need adjustment on Continuous Renal Replacement Therapy (CRRT), because it get adsorption to the membrane?


Answer: Colistin

Many drugs get adsorption to CRRT membrane but does not require adjustment of dose solely for adsorption. Colistin is the only drug which requires adjustment of dose as 40 to 60 percent of it get adsorption to membrane, and very little get recovered in the effluent.


Reference:

Markou N, Fousteri M, Markantonis SL, et al. Colistin pharmacokinetics in intensive care unit patients on continuous venovenous haemodiafiltration: an observational study. J Antimicrob Chemother 2012; 67:2459.

Cataminal pneumothoraces and thoracic endometriosis

Q: 34 year old female with 2 episodes of right sided spontaneous pneumothoraces in last 2 years presented again with right sided chest pain. This time a component of hemothorax is also noted on radiological workup. Diagnosis of cataminal pneumothoraces and thoracic endometriosis is made.  All of the following are parts of management of recurrent cataminal  pneumothoraces except?

A) chest tube insertion
B)  blebectomy 
C)  pleurodesis
D) hormonal suppression
E) pneumonectomy


Answer:  E

Thorax is the most frequent site of extra-pelvic endometriosis. Gold standard diagnosis is histological confirmation. Without histological diagnosis, it should be referred as 'probable thoracic endometriosis'. Patients with frequent symptomatic presentation requires further surgical intervention with blebectomy, pleurodesis and hormonal suppression. Pneumonectomy is not required but in resistant and in debilitating cases pleurectomy or hysterectomy with bilateral salpingo-oophorectomy (BSO) may be needed.

Cataminal pneumothorces refers to episodes of pneumothorax corresponding to menses of the patient, otherwise should be called noncataminal pneumothraces.


References: 

1. Alifano M, Jablonski C, Kadiri H, et al. Catamenial and noncatamenial, endometriosis-related or nonendometriosis-related pneumothorax referred for surgery. Am J Respir Crit Care Med 2007; 176:1048.

2. Legras A, Mansuet-Lupo A, Rousset-Jablonski C, et al. Pneumothorax in women of child-bearing age: an update classification based on clinical and pathologic findings. Chest 2014; 145:354.

3. Bagan P, Le Pimpec Barthes F, Assouad J, et al. Catamenial pneumothorax: retrospective study of surgical treatment. Ann Thorac Surg 2003; 75:378.

Physical exam and free intra-abdominal air

Q: 68 year old male was admitted to ICU for pneumonia six days ago. Patient is  intubated, and on combo of sedation/analgesia. Patient has previous history of various abdominal surgeries and visible scars on abdomen. Patient continue to have high naso-gastric (NG) output. This morning patient abdominal exam shows distention as per previous days but with new finding of tympany with percussion over the upper right upper quadrant (RUQ) in liver territory. What is the biggest worry?


Answer: Free intra-abdominal air.

Ileus is common in ICU, particularly in patients with previous abdominal surgeries. But percussion over upper RUQ should stay dull as liver lies there. If percussion over the liver (precisely over anterior lower right rib cage and just below right rib cage) is tympanitic, it may indicate serious complication of intestinal perforation causing intra-abdominal air. Also, sign of tenderness with percussion may call for further evaluation for peritonitis. 

Early mobilization in ICU

TIPS FOR CHOOSING A FUNCTIONAL OUTCOME TOOLS FOR PATIENTS IN ICU 

The use of outcome measures by physical therapists to assess mobility status and functional performance of patients is a vital element of clinical and research practice in ICU.

Parry et al. (Intensive Care Med (2015) 41:744–762) addressed the assessment of impairment and activity limitations in the critically ill. This manuscript is a systematic review and identified 26 measurement instruments and their clinometric properties. Interestingly, only six were ICU-specific instruments. On that same year, McWilliams et al. (2015) published the “Manchester Mobility Score”, which is also considered an ICU-specific tool.

Each one of the available ICU-specific tools have their strengths and also their weaknesses. When deciding which tool to use for patients in ICU, it is important to consider the clinometric analysis to determine the best tool for an institution or individual clinician.

Here is a list of the available ICU-specific tools and some references:

1.     Perme ICU Mobility Score ( Perme Score)

a.     Nydahl P et al. The German translation of the Perme ICU Mobility Score and inter-rater reliability between physiotherapists and nurses. European Journal of Physiotherapy. Pages1-7. Published online: 24 Nov 2017. DOI: 10.1080/21679169.2017.1401660

b.    Kawaguchi YMF et al. Perme Intensive Care Unit Mobility Score and ICU Mobility Scale: translation into Portuguese and cross-cultural adaptation for use in Brazil. J Bras Pneumol. 2016;42(6):429-431. PMID: 28117473

c.     Perme C et al. A tool to assess mobility status in critically ill patients: the Perme Intensive Care Unit Mobility Score. Methodist Debakey Cardiovasc J. 2014 Jan-Mar; 10(1):41-9. PMID: 24932363

d.    Nawa RK et al. Initial interrater reliability for a novel measure of patient mobility in a cardiovascular intensive care unit. J Crit Care. 2014 Jun;29(3):475. PMID: 24630690

2.     Chelsea Critical Care Physical Assessment Tool (CPAx)

a.     Corner EJ, et al. The Chelsea critical care physical assessment tool (cpax): validation of an innovative new tool to measure physical morbidity in the general adult critical care population; an observational proof-of-concept pilot study. Physiotherapy 99 (2013) 33–41. PMID: 23219649

b.    Corner EJ et al. Construct validity of the Chelsea critical care physical assessment tool: an observational study of recovery from critical illness. Crit Care. 2014 Mar 27; 18(2):R55. PMID: 24669784

c.     Corner EJ et al. The responsiveness of the Chelsea Critical Care Physical Assessment tool in measuring functional recovery in the burns critical care population: an observational study. Burns. 2015 Mar; 41(2):241-7 PMID: 25554262.

3.     Functional Status Score for ICU (FSS-ICU)

a.      Huang M et al. Functional Status Score for the ICU: An International Clinimetric Analysis of Validity, Responsiveness, and Minimal Important Difference. Crit Care Med. 2016 Aug 3. PubMed PMID: 27488220.

b.    Thrush et al. The clinical utility of the Functional Status Score for the Intensive Care Unit (FSS-ICU) at a longterm acute care hospital: a prospective cohort study. Phys Ther. 2012;92. PMID: 22956427

c.     Zanni et al. Rehabilitation therapy and outcomes in acute respiratory failure: an observational pilot project. J Crit Care2010 Jun;25(2):254-6

4.     ICU Mobility Scale (IMS)

a.     Hodgson C et al. Feasibility and inter-rater reliability of the ICU mobility scale. Heart lung. 2014 jan-feb; 43(1):19-24. PMID: 24373338

5.     Manchester Mobility Score ( MMS)

a.     McWilliams D et al. Enhancing rehabilitation of mechanically ventilated patients in the intensive care unit: a quality improvement project. J Crit Care. 2015 Feb; 30(1):13-8.

PMID: 25316527.

6.     Physical function outcome measure (PFIT)

a.     Skinner EH et al. Development of a physical function outcome measure (PFIT) and a pilot exercise training protocol for use in intensive care. Crit Care Resusc. 2009 Jun;11(2):110-5. PMID: 19485874

b.    Denehy L et al .A physical function test for use in the intensive care unit: validity, responsiveness, and predictive utility of the physical function ICU test (scored). Phys ther. 2013 dec;93(12):1636-45. PMID: 23886842

7.     Surgical Optimal Mobilisation Score (SOMS)

a.   Kasotakis G et al. The surgical intensive care unit optimal mobility score predicts mortality and length of stay. Crit Care Med. 2012 Apr; 40(4):1122-8. PMID: 22067629.

b.    Meyer MJ et al. Surgical Intensive Care Unit Optimal Mobilisation Score (SOMS) trial: a protocol for an international, multicentre, randomised controlled trial focused on goal-directed early mobilisation of surgical ICU patients. BMJ Open. 2013 Aug 19; 3(8):e003262. PMID: 23959756

c.     Piva S et al. The Surgical Optimal Mobility Score predicts mortality and length of stay in an Italian population of medical, surgical, and neurologic intensive care unit patients. J Crit Care. 2015 Dec;30(6):1251-7.PMID: 26315654 

Q: What could be the consequence of injecting air with the local anesthesia in the skin and subcutaneous tissue while inserting Central Venous Catheter (CVC) in ICU?


Answer: Presence of significant amount of air in skin and subcutaneous tissue may interfere with the transmission of ultrasound waves later while putting CVC.

Carotenemia

Q: 62 year old male with metastatic renal cell carcinoma is transferred from the oncology floor to ICU with sepsis. Physical exam showed marked yellowish discoloration of the skin. Which of the following diseases can cause carotenemia (xanthoderma = yellow discoloration of skin) which may be confused with jaundice

A) nephrosis
B) diabetes mellitus
C) liver insufficiency
D) hypothyroidism
E) all of the above


Answer: E 

Objective of above question is to signify the importance of  good physical examination in various conditions. Skin discoloration can be of many types and can be confusing. All of the above diseases can cause carotenemia by decreasing conversion of beta carotene into retinol. Many diseases require treatment with retinol and may present with this clinical finding (case in the question) 5 . Another important cause of carotenemia is anorexia nervosa, which may present with many nutritional, electrolyte and vitamin deficiencies simultaneously. Also, it is more common in population with predominantly vegetarian diet. 


References: 

1.  Aktuna D, Buchinger W, Langsteger W, Meister E, Sternad H, Lorenz O, et al. [Beta-carotene, vitamin A and carrier proteins in thyroid diseases]. Acta Med Austriaca. 1993. 20(1-2):17-20.

2. Stawiski MA, Voorhees JJ. Cutaneous signs of diabetes mellitus. Cutis. 1976 Sep. 18(3):415-21.

3. Sale TA, Stratman E. Carotenemia associated with green bean ingestion. Pediatr Dermatol. 2004 Nov-Dec. 21(6):657-9

4. Takita Y, Ichimiya M, Hamamoto Y, Muto M. A case of carotenemia associated with ingestion of nutrient supplements. J Dermatol. 2006 Feb. 33(2):132-4.

5. Dasanu CA, Dutcher J, Alexandrescu DT. Yellow skin discoloration associated with sorafenib use for treatment of metastatic renal cell carcinoma. South Med J. 2007 Mar. 100(3):328-30.

Thiazide diuretic and Diabetes

Q: 54 year old male is admitted to ICU with Diabetes Ketoacidosis (DKA). Review of his home medications list showed antihypertensives which includes diuretic therapy. Which of the following diuretic (select one) is found to be associated with the Type 2 Diabetes?

A) Thiazide
B) Furosemide
C) Amiloride 
D) Spironolactone
E) Triamterene


Answer: A 

It is said the with each 0.5 mEq/L decrease in serum potassium there is a association of  about a 45 percent higher risk of new diabetes. Thiazide diuretics causes a resultant decrease in insulin secretion. Possible mechanism is a failure of potassium channels to close in response to rising plasma glucose concentrations, causing decrease in insulin secretion. On the positive note, this risk can be mitigated by proper potassium supplement or choosing low dose of thiazide diuretics.


References:

1.  Kostis JB, Wilson AC, Freudenberger RS, et al. Long-term effect of diuretic-based therapy on fatal outcomes in subjects with isolated systolic hypertension with and without diabetes. Am J Cardiol 2005; 95:29. 

2. Harper R, Ennis CN, Heaney AP, et al. A comparison of the effects of low- and conventional-dose thiazide diuretic on insulin action in hypertensive patients with NIDDM. Diabetologia 1995; 38:853.

3. Helderman JH, Elahi D, Andersen DK, et al. Prevention of the glucose intolerance of thiazide diuretics by maintenance of body potassium. Diabetes 1983; 32:106. 

4. Shafi T, Appel LJ, Miller ER 3rd, et al. Changes in serum potassium mediate thiazide-induced diabetes. Hypertension 2008; 52:1022. 

5. Zillich AJ, Garg J, Basu S, et al. Thiazide diuretics, potassium, and the development of diabetes: a quantitative review. Hypertension 2006; 48:219.

Dig. toxicity

Q: One vial of digoxin antibody (Fab) fragments binds how much of digoxin?


Answer:   About 0.5 mg of digoxin 

If there is no time to calculate the dose of antibody (Fab) fragments or can't be calculated, 'rule of thumb' is to use 10 vials for adults or 5 vials for children, in acute ingestion of digoxin toxicity.


Reference:

DigiFab package insert. Savage Laboratories. Melville, NY 2004.

Jelly Fish Sting (Toxicology)

Q: 24 year old scuba diver is admitted to ICU after jellyfish sting as previously he had a delayed anaphylactic reaction. Patient is complaining of massive burning at the site of sting. Nurse on duty is a wave-surfer. He advised to try topical lidocaine. Besides numbing the effected area, what added advantage lidocaine has in jelly fish sting?


Answer: Lidocaine, also prevents the further nematocyst discharge! And helps to squelch the stinging cells of jellyfish still stuck to the skin. 

Beside lidocaine, other treatments which can be considered for symptomatic relief are ethanol and ammonia. Acetic acid has been used widely but lately fell out of favor.



References:

1.  Morabito R, Marino A, Dossena S, La Spada G,  "Nematocyst discharge in Pelagia noctiluca (Cnidaria, Scyphozoa) oral arms can be affected by lidocaine, ethanol, ammonia and acetic acid". Toxicon. June 2014:: 83: 52–8.

Suppurative thrombophlebitis

Q: Fungi are more common in peripheral vein suppurative thrombophlebitis than in superior/inferior vena cava suppurative thrombophlebitis?

A) True
B) False


Answer: B

Though common sense may say that fungi should be more common in peripheral vein suppurative thrombophlebitis, but Fungi are more common in superior/inferior vena cava suppurative thrombophlebitis. This is particularly related to total parenteral nutrition (TPN) infusion.

This is again a good reminder of discontinuation of "lines" if they are not needed.


References:

1. Khan EA, Correa AG, Baker CJ. Suppurative thrombophlebitis in children: a ten-year experience. Pediatr Infect Dis J 1997; 16:63.

2. Strinden WD, Helgerson RB, Maki DG. Candida septic thrombosis of the great central veins associated with central catheters. Clinical features and management. Ann Surg 1985; 202:653.

HIV, TB and ART Treatment

Q: 44 year old male with history of HIV and drug noncompliance presented to ED with mental status change and seizure. CT scan and MRI were promptly done, and patient is transferred to ICU. Astute radiologist called you to say that there appears to be a huge suspicion of tuberculoma in brain. Infectious disease service is consulted. You noticed that though treatment for tuberculous meningitis is written but no orders are written for HIV antiretroviral therapy (ART). Your thoughts?


Answer:  There should be a gap of few weeks between the treatment of tuberculous meningitis and ART. Initiation of ART may be complicated by the immune reconstitution inflammatory syndrome (IRIS), which can manifest as reactivation of latent TB, progression of active TB, or clinical deterioration in patients previously improving on anti-tuberculous therapy. 



References:

1. Nahid P, Dorman SE, Alipanah N, et al. Official American Thoracic Society/Centers for Disease Control and Prevention/Infectious Diseases Society of America Clinical Practice Guidelines: Treatment of Drug-Susceptible Tuberculosis. Clin Infect Dis 2016; 63:e147.

2. Pepper DJ, Marais S, Maartens G, et al. Neurologic manifestations of paradoxical tuberculosis-associated immune reconstitution inflammatory syndrome: a case series. Clin Infect Dis 2009; 48:e96.

3.  Tuon FF, Mulatti GC, Pinto WP, et al. Immune reconstitution inflammatory syndrome associated with disseminated mycobacterial infection in patients with AIDS. AIDS Patient Care STDS 2007; 21:527. 

4. Frequency, severity, and prediction of tuberculous meningitis immune reconstitution inflammatory syndrome. Clin Infect Dis 2013; 56:450.

"Utley Maneuver"

Q: What is "The little dutch boy maneuver" or the "Utley Maneuver"?



Answer: 

Tracheo-innominate artery fistula is the most dreaded complication of tracheostomy, as tracheal tube tip (or cuff) erodes into the anterior wall of the trachea resulting in a fistula communication with the innominate artery.

Innominate artery passes anteriorly across the trachea.

This is considered to be a clinical diagnosis, as bleeding can be so abrupt and massive that there may not be anytime for diagnostic workup. 

"The little dutch boy maneuver" is a bedside maneuver when a finger can be placed through the tracheostomy stoma, positioned distally into the trachea, and the finger is then pulled anteriorly to compress the artery against the sternum. Substantial pressure should be applied to tamponade the artery (sufficient to lift the torso anteriorly) - till patient can be rushed to OR for emergent repair.

Other less aggressive bedside maneuvers include 

• overinflation of tracheostomy cuff
• Oral re-intubation and pass Endotracheal tube (ETT) distal to the tracheostomy site and overinflate the cuff.

During all these high drama scenarios, focus should be maintained on patient's oxygenation either via tube or bag mask ventilation.


Reference:

1. Ridley, R. W.; Zwischenberger, J. B. (2006-08-01). "Tracheoinnominate fistula: surgical management of an iatrogenic disaster". The Journal of Laryngology & Otology. 120 (8): 676–680.

Q; 42 year old female is admitted to ICU due to Mobitz type II second degree AV block. Patient initially presented to ED with cough and fever, but admitted to ICU after astute nurse in ED noted possible AV block on monitor, later confirmed by EKG. You were unable to identify any cause of AV block from her present or family history, list of medications or physical examination. Name few disease processes which should be of your concern?


Answer:

• Amyloidosis 
• Sarcoidosis
• Lyme disease 
• Endocarditis with abscess formation
• Hyperkalemia 
• Hypervagotonia

It may be of interest to know that, in patients under 60 years of age who present with otherwise unexplained or previously undetected heart block, cardiac sarcoidosis has been identified in up to 35 percent of patients.


References:

1. Nery PB, Beanlands RS, Nair GM, et al. Atrioventricular block as the initial manifestation of cardiac sarcoidosis in middle-aged adults. J Cardiovasc Electrophysiol 2014; 25:875. 

2. Takaya Y, Kusano KF, Nakamura K, Ito H. Outcomes in patients with high-degree atrioventricular block as the initial manifestation of cardiac sarcoidosis. Am J Cardiol 2015; 115:505. 

Birnie DH, Sauer WH, Bogun F, et al. HRS expert consensus statement on the diagnosis and management of arrhythmias associated with cardiac sarcoidosis. Heart Rhythm 2014; 11:1305.

Q: 54 year old male with long standing diabetes travelling from Thailand is admitted to ICU with sepsis, osteomylitis (diabetic foot) and Diabetic-Keto-Acidosis (DKA). Review of his home medications include fusidic acid. 'Charge nurse' ask your advice on possible contact isolation.  Fusidic acid is a  (select one)

A) Steroid antibiotic
B) Adjuvant treatment in Urinary Tract Infections (UTIs)
C) Treatment for gastroesophageal reflux (GERD) disease
D) First line of local cream in burn  patients
E) Decreases pulmonary pressure


Answer: A

 Fusidic acid is a steroid antibiotic which is not approved in USA for use. It is developed sometimes in 1960s and is available worldwide. It is available in injections, topical (cream), eye-drops and oral forms. As resistance to various antibiotics are on rise, there is a renewed interest in its use recently. It is effective primarily on gram-positive bacteria such as Staphylococcus, Streptococcus, and Corynebacterium species. It is bacteriostatic, and so mostly used as an adjunctive treatment. It is effective for use with other antibiotics in chronic osteomyelitis secondary to MRSA; like rifampin and flucloxacillin.



References:

1. Falagas ME, Grammatikos AP, Michalopoulos A. Potential of old-generation antibiotics to address current need for new antibiotics. Expert Rev Anti Infect Ther. 2008; 6(5):593-600 

2. "Fusidic acid in skin and soft tissue infections". International Journal of Antimicrobial Agents. 12 Suppl 2: S59–66. 

3. Howden BP, Grayson ML (2006). "Dumb and dumber—the potential waste of a useful antistaphylococcal agent: emerging fusidic acid resistance in Staphylococcus aureus". Clin Infect Dis. 42 (3): 394–400

Q: All of the following are clinical criteria to liberate patient from mechanical ventilation except?

A) Pulseox saturation more than or equal to 90 percent
B) Arterial pH more than 7.30
C) Core temperature 38 to 38.5ºC
D) Hemodynamic stability, without myocardial ischemia
E) Hemoglobin level more than or equal to 7 mg/dL


Answer: B

Collective task force facilitated by the American College of Chest Physicians, the American Association for Respiratory Care, and the American College of Critical Care Medicine, has divided requirements to initiate patient to liberate from ventilators into basic and optional (clinical) criterias.

Basic criteria includes five major components

• The cause of the respiratory failure has improved
• Adequate oxygenation
• Arterial pH more than 7.25
• Hemodynamic stability
• Patient is able to initiate an inspiratory effort

Optional criteria includes

• Hemoglobin level 7
• No marked fever
• Adequate mental status

Reference:

MacIntyre NR, Cook DJ, Ely EW Jr, et al. Evidence-based guidelines for weaning and discontinuing ventilatory support: a collective task force facilitated by the American College of Chest Physicians; the American Association for Respiratory Care; and the American College of Critical Care Medicine. Chest 2001; 120:375S.

Q: 34 year old female is admitted to ICU after video-assisted thoracoscopic surgery(VATS) due to persistent severe nausea and an episode of vomiting in recovery area. All of the following are predictor of Postoperative Nausea and Vomiting  (PONV) except?

A) complain of nausea and vomiting prior to the surgery 
B) Female gender 
C) Smoking status 
D) Young age
E) History of motion sickness


Answer: C

It may be of interest to know that non-smoking status is an independent risk factor for PONV. As expected, all other choices in the question are good predictors of PONV. 

Female gender is considered to be the strongest overall predictor for PONV.



References:

1. Cohen MM, Duncan PG, DeBoer DP, Tweed WA. The postoperative interview: assessing risk factors for nausea and vomiting. Anesth Analg 1994; 78:7.

2. Stadler M, Bardiau F, Seidel L, et al. Difference in risk factors for postoperative nausea and vomiting. Anesthesiology 2003; 98:46.

3.  Apfel CC, Heidrich FM, Jukar-Rao S, et al. Evidence-based analysis of risk factors for postoperative nausea and vomiting. Br J Anaesth 2012; 109:742.

4. Sinclair DR, Chung F, Mezei G. Can postoperative nausea and vomiting be predicted? Anesthesiology 1999; 91:109.

5. Palazzo M, Evans R. Logistic regression analysis of fixed patient factors for postoperative sickness: a model for risk assessment. Br J Anaesth 1993; 70:135.

Q: All of the following are parts of skin care to avoid pressure ulcer in long term ICU patients except?

A) Keep the skin clean and dry (but avoid excess dryness)
B) Clean the skin cleansing with a pH-balanced cleansing agent 
C) Use the hot water to clean skin
D) Avoid vigorous massage over bony prominences
E)  Keep skin clean from incontinence or wound drainage


Answer: C

Pressure ulcers in long term ICU patients is a major issue. It is extremely underscored. Education of ICU staff including intensivists is lacking in this area.

All of the choices above are true except "C" as hot water will increase damage to the skin.



Related article: 

Pressure Ulcers in the Intensive Care Unit: An Analysis of Skin Barrier Risk Factors - He, Minjuan BS; & et al  Advances in Skin & Wound Care: November 2016 - Volume 29 - Issue 11 - p 493–498

Link: http://journals.lww.com/aswcjournal/Fulltext/2016/11000/Pressure_Ulcers_in_the_Intensive_Care_Unit___An.6.aspx

Q: 52 year old male with End Stage Renal Disease is admitted to ICU with fever, hypotension and probable AV graft infection. Infectious Disease (ID) service strongly suspect Infective Endocarditis (IE) but Transesophageal Echocardiography (TEE) failed to provide and definite answer of vegetation. What should be the next step to confirm or rule out Infective Endocarditis(IE)?


Answer: Cardiac CT

If TEE fails to provide definite evidence of IE, the next step is to perform cardiac CT. It is very sensitive, similar in accuracy to detect abscess and pseudoaneurysm, and probably superior to TEE for evaluation of paravalvular extension of infection. It also has an advantage of evaluating the coronary arteries at the same time. From logistic perspective, CT of other parts of the body can be performed at the same time if infective emboli is suspected like to brain or torso.


References:

1. Bruun NE, Habib G, Thuny F, Sogaard P. Cardiac imaging in infectious endocarditis. Eur Heart J 2014; 35:624.

2. Feuchtner GM, Stolzmann P, Dichtl W, et al. Multislice computed tomography in infective endocarditis: comparison with transesophageal echocardiography and intraoperative findings. J Am Coll Cardiol 2009; 53:436. 

Q: 34 year old female who is on long term peritoneal dialysis for End Stage Renal Disease is admitted to ICU for community acquired pneumonia. Nephrology service decided to continue peritoneal dialysis while patient is in ICU. On third day of admission in ICU peritoneal fluid appeared to be blood stained. Labs including hemoglobin remains stable. Clinically patient continue to show signs of improvement. Your next step?

A) Order serial H/H (Hb and Hematocrit)
B) Obtain CT of abdomen to rule out retroperitoneal hematoma
C) Obtain menstrual history from patient
D) Make her NPO 
E) Order CPK to rule out rhabdomyolysis 


Answer: C

Though there could be other causes of blood stained peritoneal dialysate but in a young female patient who has no other clinical signs of deterioration, the most common cause is menstruation unless proved otherwise! It is either due to ovulation which occurs in mid-cycle or due to endometriosis , where retrograde menstruation could be the reason of blood stained peritoneal dialysate. Alike hematuria, even one cc of blood is enough to give the whole peritoneal dialysate an appearance of blood stained. It requires rapid flushes and instillation of heparin in the dialysate to prevent catheter clotting. Usually, it clears on its own.


References:

1. Tse KC, Yip PS, Lam MF, et al. Recurrent hemoperitoneum complicating continuous ambulatory peritoneal dialysis. Perit Dial Int 2002; 22:488.

2. Dimitriadis CA, Bargman JM. Gynecologic issues in peritoneal dialysis. Adv Perit Dial 2011; 27:101. 

Q: All of the following are the risk factors for refractory vasoplegia after coronary artery bypass grafting (CABG) except?

A) decreased left ejection fraction
B) prolonged aortic cross-clamp times
C) female gender
D) preoperative use of ACE-inhibitors
E) all of the above


Answer: C

Objective of above question is to highlight the dreaded situation of refractory vasoplegia after coronary bypass. Refractory vasoplegia with its domino effect can lead to more complications like postoperative bleeding, acute renal injury (AKI), liver dysfunction, neurologic dysfunction, and prolonged ventilator time.

Males are more prone to vasodilatory shock than females.


References:

1. Kristof AS, Magder S. Low systemic vascular resistance state in patients undergoing cardiopulmonary bypass. Crit Care Med 1999; 27:1121. 

2. Cremer J, Martin M, Redl H, et al. Systemic inflammatory response syndrome after cardiac operations. Ann Thorac Surg 1996; 61:1714.