Thursday, October 31, 2013

Q: When IV calcium is contraindicated in symptomatic hypocalcaemia?
Answer: Hypocalcaemia induced by severe life threatening hypophosphatemia

Essential to the treatment of phosphate toxicity is increasing urinary excretion. In patients with normal renal function, expansion of the extracellular space with saline have shown to increase renal phosphate excretion. Therefore, aggressive hydration is the mainstay of treatment, guided by urine output. Dialysis is usually not required, but should be considered given clinical situation as Hemodialysis can clear phosphate at a significantly higher rate than that achieved by normal kidneys.
IV calcium infusion in hypocalcaemia from severe hypophosphatemia can be dangerous because of the possibility of metastatic calcifications when the calcium-phosphate concentration product is >70 mg2/dL2.


References:
1. Orias M, Mahnensmith RL, Perazella M. Extreme hyperphosphatemia and acute renal failure after a phosphorus-containing bowel regimen. Am J Nephrol.1999;19 :60– 63

2. Sutters M, Gaboury CL, Bennett WM. Severe hyperphosphatemia and hypocalcemia: a dilemma in patient management. J Am Soc Nephrol.1996;7 :2056– 2061

3. Knobel B, Petchenko P. Hyperphosphatemic hypocalcemic coma caused by hypertonic sodium phosphate (Fleet) enema intoxication. J Clin Gastroenterol.1996;23 :217– 219

4. Feig PU, Hirszel P, Galen MA, Rosenworcel E, Raisz LG. Hemodialysis in the treatment of life-threatening hyperphosphatemia. Clin Exp Dial Apheresis.1982;6 :105– 111

Tuesday, October 29, 2013

The ACCP (American College of Chest Physicians) Mnemonic for intubation

APPROACH

A = Assess
P = Pre-Oxygenate
P = Prepare
R = Review  (backup plan)
O = Oxygen cut off determination - to re-bag at what sat% level
A = Administer (drugs)
C = Confirm tube placement
H = Hold tube till secure

Monday, October 28, 2013

Q: Which one disease process is found to be protective in ARDS?
Answer: Sounds weird! but its Diabetes
Click on following reference!
Singla A, Modrykamien AM (2012) Diabetes Mellitus: Protective in Development of ARDS. J Pulmon Resp Med 2:e119

Sunday, October 27, 2013

On Daily weight and fluid balance in ICU

PURPOSE:

Monitoring of fluid balance (FB) can be achieved by subtracting recorded fluid output from input or by measuring changes in body weight (BW). The latter approach is difficult in the critically ill. Recently, hospital beds have become available with the ability to directly weigh patients in the intensive care unit (ICU) patients directly. We sought to compare FB estimates obtained by these 2 methods in a cohort of critically ill patients.

MATERIALS AND METHODS:

Between November 2010 and May 2011, all patients admitted in our ICU for more than 2 consecutive days and nursed on a Hill-Rom (Batesville, Ind) Total Care bed were weighed daily at midnight hours. Fluids charting was done by electronic spreadsheet with automated 24 hours calculation. Differences in BW and FB between 2 consecutive days were compared using correlation and Bland-Altman analysis. Corrections for unmeasured fluids losses were performed using a predetermined formula based on peak temperature and intubation status.

RESULTS:

We obtained complete data in 160 (31%) of 504 admissions exceeding 2 days (153 patients) resulting in 435 data points. The change in BW over 24 hours and FB for the same period was only weakly correlated before (r = 0.34; P < .001; Fig. 1) or after correction for insensible fluid losses (r = 0.34; P < .001). On Bland-Altman plot, the mean bias was small (0.07 kg), but the 95% limits of agreement, very large (-5.8 and 6.0 kg). The lack of agreement increased with the magnitude of the changes.

CONCLUSION:


  • Obtaining daily weights in ICU patients proved difficult.
  • Compliance was poor.
  • The correlation between changes in BWs and FB was weak.

Further studies are required to establish if accurate and reproducible daily weighing of ICU patients is feasible.


Reference:

Schneider AG, Baldwin I, Freitag E, Glassford N, Bellomo R., Estimation of fluid status changes in critically ill patients: fluid balance chart or electronic bed weight? - J Crit Care. 2012 Dec;27(6):745.e7-12


Friday, October 25, 2013

Q: For average patient, Gentamicin should be given per (choose one)?

A) Ideal or adjusted body weight

or

B) Actual body weight?


Answer:  A - Ideal body weight

To administer Aminoglycoside antibiotics, for total dosing 
  •  For patients whose weight is 1-1.2 times their ideal body weight, use ideal body weight.
  • For patients weighing more than 1.2 times ideal body weight, use adjusted body weight.  
Serum level monitoring are needed to ensure safety and efficacy.  Also, patients anticipated to receive aminoglycosides for more than 2 weeks should be considered for audiometry.

Thursday, October 24, 2013



Q: What is the optimum way of drawing Vancomycin trough level?


Answer: 

Usually Vancomycin peak is not required, and Vancomycin trough is recommended.

Vancomycin trough should be drawn when steady state is achieved, ideally less than 30 minutes before fourth dose.

1 ml of blood is sufficient for draw in vacutainer red top.

Wednesday, October 23, 2013

Q: What care should be taken on giving Linezolid (Zyvox) to patients who are on HD (hemodialysis)?


Answer: Administer after HD session as about 40% of drug is removed via HD. This point is usually get missed as in normal circumstances, Linezolid does not require any adjustment in renal insufficiency.

Linezolid get metabolized via liver but does require any adjustment in mild to moderate liver insufficiency, either.

Patients on CRRT does not require any adjustments but may require higher/more frequent administration.

Tuesday, October 22, 2013

Q: Why Glycopyrrolate is always used with Neostigmine for 'reversal' of neuromuscular blockade after surgery?


Answer:  Glycopyrrolate is used in conjunction with neostigmine, a neuromuscular blocking reversal agent, to prevent neostigmine's muscarinic effects particularly bradycardia. In case if not available (as recently, the shortage status in USA), atropine can be used.

Monday, October 21, 2013

Q: What is the target PETCO2 (Capnography) value during CPR?


Answer: Between 10 and 20 mm Hg.

If PETCO2 values less than 10 mm Hg or less measured after initiation of ACLS, it is associated with poor outcome. And, if value start rising abruptly, it indicates ROSC (Return Of Spontaneous Circulation).

PETCO2 is the maximum partial pressure of CO2 at the end a breath. It is about 36- 40 mm Hg in healthy adults.

Saturday, October 19, 2013

Passive Leg raising (PLR) and EtCO2 connection

A PLR-induced increase in EtCO2 >5 % predicted a fluid induced increase in CI >15 % with sensitivity of 71 % (95 % confidence interval: 48–89 %) and specificity of 100 (82–100) %.
Reference:
End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test - Intensive Care Med (2013) 39:93–100

Friday, October 18, 2013

Recommended Cuff Sizes for Accurate Measurement of Blood Pressure

PATIENT RECOMMENDED CUFF SIZE
Adults (by arm circumference)
22 to 26 cm
12 × 22 cm (small adult)
27 to 34 cm
16 × 30 cm (adult)
35 to 44 cm
16 × 36 cm (large adult)
45 to 52 cm
16 × 42 cm (adult thigh)
(For ease of use, adult cuffs for BP monitoring can be divided into 4 sizes - Small, Medium, Large and Thigh cuffs)

Objective of above pearl is to emphasis that ideally arm cuff can't be applied to thigh, often a common practice.

Reference:
Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN, et al.; Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research. Recommendations for blood pressure measurement in humans and experimental animals. Part 1: blood pressure measurement in humans. Hypertension 2005;45:142–61

Thursday, October 17, 2013

Q: To obtain venous blood gas (VBG), what is the minimum time for the tourniquet to be off? 



Answer:  At least a minute

 If a tourniquet is used to facilitate venipuncture, it should be released about one minute before the sample for venous blood gas is drawn to avoid false values in VBG induced by local ischemia.



Reference:


Wednesday, October 16, 2013

Q: How much is the average fluid deficit in Hyperosmolar hyperglycemic state (HHS), previously known as hyperosmolar hyperglycemic nonketotic coma (HHNK)?


Answer:  About 9 liters

According to the consensus statement published by the American Diabetes Association, diagnostic features of HHS may include
  • Plasma glucose level of 600 mg/dL or greater
  • Effective serum osmolality of 320 mOsm/kg or greater
  • Profound dehydration, up to an average of 9L
  • Serum pH greater than 7.30
  • Bicarbonate concentration greater than 15 mEq/L
  • Small ketonuria and absent-to-low ketonemia
  • Some alteration in consciousness


Reference:

Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. Dec 2006;29(12):2739-48

Tuesday, October 15, 2013

Q: What is hemiballismus?


Answer: Ballism was defined as " Repetitive, but constantly varying, large amplitude involuntary movements of the proximal parts of the limbs. This activity is almost ceaseless and movements are often complex and combined"  Hemiballismus means 'half ballistic', refers to the violent, flailing movements observed on one side of the body.

Clinical significance:  It could be one clinical signs of Stroke, Traumatic Brain Injury, ALS, Nonketotic Hyperglycemia, Tumor, Hypoglycemia due to pentamidine, cerebral toxoplasmosis etc.

http://youtu.be/t9jcccWzVPs

Monday, October 14, 2013

Q: What is the major clinical difference between Parkinson's disease and tardive dyskinesia patients on examination?


Answer: Parkinson's patients have difficulty moving, whereas tardive dyskinesia patients have difficulty not moving!

Tardive dyskinesia, usually a side effect of anti psychotics is characterized by repetitive, involuntary, purposeless movements like grimacing, tongue protrusion, lip smacking, puckering, pursing of the lips,  rapid eye blinking etc.

Sunday, October 13, 2013

Q: Hypermagnesemia causes (choose one)
A) Increase anion gap
 or
B) Decrease Anion Gap?
Answer:
Few common etiologies of decrease An-ion gap in ICU are
  • hypoalbuminemia,
  • hypercalcemia,
  • hyperkalemia,
  • hypermagnesemia,
  • lithium toxicity, and
  • multiple myeloma.

Saturday, October 12, 2013

A note on role of magnesium in Digoxin toxicity induced tachyarrhythmia


Digi-Bind, a direct antidote in digoxin toxicity,  is not always readily available from hospital pharmacy. Moreover, it takes time to kick its effect in.

Magnesium is an excellent choice as a temporizing anti-arrhythmic agent, particularly in ventricular tachycardia or fibrillation. 2 grams of IV magnesium sulfate can be given over 5 minutes. It is very effective in terminating digoxin induced arrhythmia. Treatment can be continued as an IV drip with 1-2 gram/hour with close monitoring to keep therapeutic level between 4 and 5 mEq/L.

Beside its role at intracellular level, magnesium has also been described as an indirect antagonist of digoxin.

As a side note, 2 other important aspects, which should not be ignored is
  • treatment of hypo or hyper kalemia.
  • Avoidance of calcium specially in the presence of hyperkalemia as it can sets in fatal ventricular tachycardia or fibrillation. This is due to the fact that intracellular calcium levels are already high in digoxin toxicity.

Friday, October 11, 2013

Q: Define Endarterectomy procedure?

Answer: Endarterectomy is a surgery to clean out an artery and restore normal blood flow. It clears unwanted material from the inside of an artery mostly occluding atheromatous deposits. Ideally, it leaves a smooth lining within the vessel.

2 mostly performed endarterectomies are coronary endarterectomy and carotid endarterectomy.

Wednesday, October 9, 2013

Q: What is Mackler's triad?


Answer:

It is not always presents but may be diagnostic of Boerhaave's syndrome (esophageal rupture)
  • chest pain,
  • vomiting and
  • subcutaneous emphysema

Source:

Woo KM, Schneider JI (November 2009). "High-risk chief complaints I: chest pain--the big three". Emerg. Med. Clin. North Am. 27 (4): 685–712

Sunday, October 6, 2013

Q: Fomepizole can be use in methanol or ethylene glycol poisoning, but not in Ethanol poisoning. Why?


Answer:  Fomepizole not only prolongs the half-life of ethanol but allows for greater level of intoxication at lower doses.

Fomepizole slows the production of acetaldehyde by alcohol dehydrogenase and allows more time for acetaldehyde dehydrogenase to detoxify it. Consequently, a patient will have a prolonged and deeper level of intoxication for even at small dosage of ethanol.

Saturday, October 5, 2013

Q: Which one electrolyte could be a marker of morbidity and mortality in Organophosphate (OP) poisoning?


Answer:  Potassium (Hypokalemia)

Potassium homeostasis appears to be altered in acute OP poisoning, though actual process in not understood completely. . As the potassium concentration decreases gradually patients start having signs like muscle twitching, respiratory distress etc. Studies have shown alteration in serum potassium concentration is directly proportional to the onset of life threatening signs and symptoms. In fact, Hypokalemia is a powerful marker of morbidity and mortality in OP poisoning. Also, class II anti-arrhythmic agents have been described as a candidate to become a therapeutic agent in OP poisoning.




References:

1. Zoltani C, Baskin S (2002). "Organophosphate Caused Cardia Toxicity: Action Potential Dynamics in Atrial Tissue". Army Research Laboratory: 1–15.

2. SIGNIFICANCE OF HYPOKALEMIA IN ACUTE ORGANOPHOSPHOROUS POISONING, Abstract,  D.R.Mahadeshwara Prasad, Department of Forensic Medicine and Toxicology,  Jawaharlal Nehru Medical College, Nehru Nagar, BELGAUM, Karnataka, India, Link: here

Friday, October 4, 2013

Q: What is the hazard of using sub-optimal dose of Atropine in Bradycardia?


Answer: 

Minimum dose of Atropine in Bradycardia is 0.5 mg (0.4mg to be precise). Doses less than 0.5 mg (0.2 mg in peds) may further decrease the rate. Though this pradoxical bradycardia has been questioned in some literature papers.


Various explanations have been proposed for that including stimulation of the vagus nerve causing bradycardia at low doses, as Atropine may crosses blood brain barrier. Another explanation given is at low doses, atropine may have affinity for presynaptic autoreceptors thus blocking the negative feedback loop of acetycholine and increasing presynaptic output of acetylcholine into the synaptic junction. This will activate m2 receptors on the heart and lead to bradycardia.  At higher doses the muscarinic blocking effects of Atropine causes tachycardia.


Thursday, October 3, 2013

Q: Why Esmolol is called Esmolol?


Answer:     The answer lies in the name Es-Molol

Esmolol has ester-methyl side chain.

Clinical significance: Ester-methyl side chain allows for quick hydrolysis by plasma esterases, giving short half life of 9 minutes. 


Wednesday, October 2, 2013

Q: How long does it take to see the maximum effect after IV administration of Labetalol?


Answer: 5 minutes



Labetalol bolus dose is about 0.25 mg/kg. It should be given by slow IV injection over a 2-minute period.



Additional doses in increment can be given with a total of 300 mg. The maximum effect usually occurs within 5 minutes of each injection.




Tuesday, October 1, 2013

Cardene vs Labetol

Introduction: Our purpose was to compare the safety and efficacy of food and drug administration (FDA) recommended dosing of IV nicardipine versus IV labetalol for the management of acute hypertension.

Methods: Multicenter randomized clinical trial. Eligible patients had 2 systolic blood pressure (SBP) measures ≥180 mmHg and no contraindications to nicardipine or labetalol. Before randomization, the physician specified a target SBP ± 20 mmHg (the target range: TR). The primary endpoint was the percent of subjects meeting TR during the initial 30 minutes of treatment.

 Results: Of 226 randomized patients, 110 received nicardipine and 116 labetalol. End organ damage preceded treatment in 143 (63.3%); 71 nicardipine and 72 labetalol patients. Median initial SBP was 212.5 (IQR 197, 230) and 212 mmHg (IQR 200,225) for nicardipine and labetalol patients (P = 0.68), respectively. Within 30 minutes, nicardipine patients more often reached TR than labetalol (91.7 vs. 82.5%, P = 0.039). Of 6 BP measures (taken every 5 minutes) during the study period, nicardipine patients had higher rates of five and six instances within TR than labetalol (47.3% vs. 32.8%, P = 0.026). Rescue medication need did not differ between nicardipine and labetalol (15.5 vs. 22.4%, P = 0.183). Labetalol patients had slower heart rates at all time points (P < 0.01). Multivariable modeling showed nicardipine patients were more likely in TR than labetalol patients at 30 minutes (OR 2.73, P = 0.028; C stat for model = 0.72)

 Conclusions: Patients treated with nicardipine are more likely to reach the physician-specified SBP target range within 30 minutes than those treated with labetalol.


 Reference:

a randomized comparative effectiveness trial of IV nicardipine versus labetalol use in the emergency department - Critical Care 2011, 15:R157