Friday August 21, 2009 (pediatric pearl day)
Uniqueness of Neonatal/ Infantile Myocardium compared to adult myocardium


Neonatal myocardium has a large supply of mitochondria, nuclei and endoplasmic reticulum to support cell growth and protein synthesis but these are non-contractile tissues which render the myocardium stiff and non-compliant. This may impair filling of the left ventricle and limit the ability to increase the cardiac output by increasing stroke volume (Frank Starling mechanism). Stroke volume is therefore relatively fixed and the only way of increasing cardiac output is by increasing heart rate. The cardiac index (defined as the cardiac output related to the body surface area to allow a comparison between different sizes of patients) is increased by 30-60 percent in neonates and infants to help meet the increased oxygen consumption.

The sympathetic nervous system is not well developed predisposing the neonatal heart to bradycardia. Anatomical closure of the foramen ovale occurs between 3 months and one year of age.

Neonatal myocardium is distinctly more sensitive to extracellular calcium levels than is mature myocardium. This has been ascribed to the poorly developed sarcoplasmic reticulum of neonatal myocardium and is dependent on serum calcium to maintain optimal contractility. Calcium is an important inotrope in newborns and its optimization is critical in low cardiac output syndrome.

Thursday August 20, 2009
Armour Thyroid

Armour Thyroid is a "natural" thyroid replacement medication that is available by prescription. It is made from thyroid glands of pigs and contains two different thyroid hormones. It provide 38 mcg levothyroxine (T4) and 9 mcg liothyronine (T3) per grain of thyroid.

Wednesday August 19, 2009

Q; 52 year old female presented with headache and vision change. You did retinal exam. Your Diagnosis?

Hypertensive retinopathy (Malignant phase)


The detection of hypertensive retinopathy with the use of an ophthalmoscope has long been regarded as part of the standard evaluation of persons with hypertension. This clinical practice is supported by both previous and current reports of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC), which list retinopathy as one of several markers of target-organ damage in hypertension.

Tuesday August 18, 2009


Q; Succinylcholine is contraindicated (relatively) for intubation in which poisoining?


Answer: Organophosphate poisoining.

Organophosphate may potentiate effects of succinylcholine. Succinylcholine is relatively contraindicated in Organophosphate poisoining.

Monday August 17, 2009

Q; Is menstrual bleeding a contraindication to thrombolytic therapy in Acute MI or Stroke?



Answer: No

There may be a clinically significant increase in the risk of moderate bleeding during menstruation. But lifesaving benefit of thrombolytic therapy for acute myocardial infarction should generally not be withheld because of active menstruation. Potential patients should be advised that they might require transfusion for increased menstrual flow.

Sunday August 16, 2009
Causes of False-Positive Troponin Results (Lab interference / errors)

• Heterophile antibodies
• Human anti-mouse antibodies
• Autoantibodies
• Fibrin clots
• Rheumatoid factor
• Microparticles in specimen
• Interference by endogenous components in blood (bilirubin, hemoglobin, lipemia)
• High concentration of alkaline phosphatase
• Immunocomplex formation
• Analyzer malfunction
  

Saturday August 15, 2009
Ramsay Sedation Scale

Clinical Score depending on Level of Sedation Achieved

6 - Asleep, no response
5 - Asleep, sluggish response to light glabellar tap or loud auditory stimulus
4 - Asleep, but with brisk response to light glabellar tap or loud auditory stimulus
3 - Patient responds to commands
2 - Patient cooperative, oriented, and tranquil
1 - Patient anxious, agitated, or restless

Friday August 14, 2009 (pediatric pearl)
Uniqueness of Pediatric Upper Airway

Previous related pearls:
Uniqueness of Pediatric Lower Airway - Part 1
Uniqueness of Pediatric Lower Airway - Part 2

The frequency of acute respiratory failure is higher in infants and young children than in adults for several reasons. This difference can be explained by defining anatomic compartments and their developmental differences in pediatric patients that influence susceptibility to acute respiratory failure.

The extrathoracic airway (extending from the nose to the subglottic region of the trachea) has significant differences in pediatric versus adult patients include the following:

• Neonates and infants are obligate nasal breathers until the age of 2-6 months because of the proximity of the epiglottis to the nasopharynx. Nasal congestion can lead to clinically significant distress in this age group.
• The small size of the airway is one of the primary differences in infants and children younger than 8 years compared with older patients.
• Infants and young children have a large tongue that fills a small oropharynx.
• Infants and young children have a cephalic larynx. The larynx is opposite vertebrae C3-4 in children versus C6-7 in adults. Larynx cone-shaped: narrowest at subglottic cricoid ring - Softer, more pliable: may be gently flexed or rotated anteriorly
• The epiglottis is larger and more horizontal to the pharyngeal wall in children than in adults. The cephalic larynx and large epiglottis can make laryngoscopy challenging.
• Vocal cords slanted: anterior commissure more inferior
• Infants and young children have a narrow subglottic area. In children, the subglottic area is cone shaped, with the narrowest area at the cricoid ring. A small amount of subglottic edema can lead to clinically significant narrowing, increased airway resistance, and increased work of breathing. Older patients and adults have a cylindrical airway that is narrowest at the glottic opening.
• In slightly older children, adenoidal and tonsillar lymphoid tissue is prominent and can contribute to airway obstruction.
• Upper airway contributes 50% to total airway resistance compared to about 20% in adults.
• Infant head is relatively larger: naturally flexed in supine position. Extension of head may result in tracheal extubation; while flexion may lead to main stem intubation.

Thursday August 13, 2009
KING LT (laryngeal tube) intubation

The king airway is a blind insertion, just like combi tube. It's a double lumen airway. It occludes the esophagous and ventilates through the opening on the side of the tube. King LT is an advanced airway where ventilations through it go into the trachea, and the esophagus is occluded.

Wednesday August 12, 2009
Fluid Resuscitation and Intra-Abdominal Hypertension

Tuesday, August 11, 2009
Intracerebroventricular Administration of Drugs

Reference: Cook AM, et al. Pharmacotherapy 2009;29(7):832

Guidelines do not currently exist for drug administration via the intracerebroventricular route, however, a good review was just published in Pharmacotherapy.

Methods of administration include:

· Directly into the lumbar cistern (thecal sac), Intrathecally

o Low risk and easily performed at bedside, however, requires separate puncture for subsequent doses which increases risk of infection

· Directly into the lateral ventricle

o Repeated taps not routinely performed due to risk of neurovascular injury or intracranial hemorrhage

· Permanent access through implanted catheter connected to reservoir

o e.g. Ommaya reservoir

· Ventriculostomy

o Ideal for situations requiring limited time for CSF drainage or intraventricular drug administration. Should use caution and close monitoring of intracranial pressure


Considerations for drug administration:

· Volume of solution

o Affects the distribution or clearance of drug. Increasing volume would result in an alteration in the normal intracranial components to maintain normal intracranial pressure.

· Rate of instillation

o Slow instillation recommended to allow for extracellular fluid displacement to prevent tissue damage. Recommend small volumes <3ml>

Monday August 10, 2009
Quick and Dirty on Vasopressors and Inotropes



Vasopressor activity on the following receptors are agonistic:

• a1 receptors-- peripheral arteries-- peripheral vasoconstriction
• b1 receptors-- coronary smooth muscle-- increased heart rate and contractility
• b2 receptors—smooth muscle—increases force of contractility in the heart
• DA1 receptors-- renal, mesenteric, and coronary beds-- vasodilation and increase urine output.
• V1, receptors-- vascular smooth muscle--vasopressor;
• V2 receptors-- renal collecting duct system--natural diurectic
  

Vasopressors:

• Dopamine: receptor action is dependent on dose… DA1 1-5 microgram/kg/min + HR; b1 5-10 microgram/kg/min, ++ HR, + MAP, + CO; a1 > 10 microgram/kg/min + SVR, + MAP, + HR, +CO
• Epinephrine: b1 >> a1 1-20 microgram/min ++ SVR, +MAP, +HR, +CO
• Norepinephrine: a1 > b1 1-80 microgram/min, ++ SVR, ++MAP , ?+HR, ?+CO
• Phenylephrine: a1 2-200 micrograms/min; ++SVR, +MAP, ?+HR, ?+ CO
• Vasopressin: V1 V2 0.04 units/min ++SVR, +MAP, ?+HR, ? +CO
  
  

Inotropes:

• Dobutamine: b1, b2 2-20 microgram/kg/min ááCO áHR âSVR ?âMAP
• Milrinone: PDE inhibitor in vascular and cardiac smooth muscle which improves calcium handling causing dilation. In cardiac muscle, the inhibition of phosphodiesterase results in increased levels of cAMP, resulting in increased chronotropic and inotropic effects.
  

Reference:

Dellinger RP. Crit Care Med 2008;36(1):296

Sunday August 9, 2009
Picture Diagnosis

What is your diagnosis?

Hint is Arrow

.



Answer: Pneumothorax after central line placement.

Note the abnormally placed central line extending upwards from subclavian vein into internal jugular vein along with pneumothorax.

Saturday August 8, 2009


Q; Troponins, once secreted, remains elevated for how many days?

Answer: Troponin, once secreted, remains elevated for 7-10 days.

Friday August 7, 2009 (pediatric pearl)
Uniqueness of Pediatric Lower Airway - Part 2

(see Uniqueness of Pediatric Lower Airway - Part 1 here)

The frequency of acute respiratory failure is higher in infants and young children than in adults for several reasons. This difference can be explained by defining anatomic compartments and their developmental differences in pediatric patients that influence susceptibility to acute respiratory failure.

The intrathoracic airways and lung include the conducting airways and alveoli, the interstitia, the pleura, the lung lymphatics, and the pulmonary circulation. Noteworthy differences among pediatric children include the following:

• Infants and young children have fewer alveoli than do adults. The number dramatically increases during childhood, from approximately 20 million after birth to 300 million by 8 years of age. Therefore, infants and young children have a relatively small area for gas exchange.
• The alveolus is small. Alveolar size increases from 150-180 to 250-300 µm during childhood.
• Collateral ventilation is not fully developed; therefore, atelectasis is more common in children than in adults. During childhood, anatomic channels form to provide collateral ventilation to alveoli. These pathways are between adjacent alveoli (pores of Kohn), bronchiole and alveoli (Lambert channel), and adjacent bronchioles. This important feature allows alveoli to participate in gas exchange even in the presence of an obstructed distal airway.
• Smaller intrathoracic airways are more easily obstructed than larger ones. With age, the airways enlarge in diameter and length.
• Infants and young children have relatively little cartilaginous support of the airways. As cartilaginous support increases, dynamic compression during high expiratory flow rates is prevented.

Thursday August 6, 2009
Heparin Induced HyperKalemia

Hyperkalemia from Heparin is a well know phenomenon and has been detected particularly on geriatric, renal insufficient and diabetic patients. Hyperkalemia can be anywhere from .3 to 1.7 mEq/Litre. It usually occurs around on day 3 with SQ heparin (as for DVT prophylaxis) but can occur early with IV heparin 1,2,3,4.

Hyperkalemia has been reported with low- molecular weight heparins too but risk is low 5, 6, 7.

Mechanism of action: Heparin induce hypoaldosteronism and can subsequently lead to hyperkalemia 6.

Treatment: Best thing is to discontinue the culprit but if heparin is absolutely required, fludrocortisone (.1 mg/day) has been reported to be effective in heparin-induced hyperkalemia 8.



References: Click to get abstracts/articles

1. Case report - Heparin-induced hyperkalemia after cardiac surgery - Ann Thorac Surg 2002;74:1698-1700

2. Heparin-induced hyperkalemia -The Annals of Pharmacotherapy: Vol. 24, No. 3, pp. 244-246.

3. Heparin Induced HyperKalemia - Endocrine Abstracts (2002) 4 P26

4. Heparin-Induced Hyperkalemia Confirmed by Drug Rechallenge. American Journal of Physical Medicine & Rehabilitation. 79(1):93-96, January/February 2000.

5. Early onset of hyperkalemia in patients treated with low molecular weight heparin: a prospective study - Pharmacoepidemiol Drug Saf.2004 May;13(5):299-302.

6. Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis - Pathophysiology of Haemostasis and Thrombosis 2002;32:107-110

7. Low Molecular Weight Heparins Can Lead To Hyperkalaemia The Internet Journal of Geriatrics and Gerontology . 2005. Volume 2 Number 2.

8. Fludrocortisone for the treatment of heparin-induced hyperkalemia - The Annals of Pharmacotherapy: Vol. 34, No. 5, pp. 606-610

Wednesday August 5, 2009


Scenario: 25 year old patient presented to the emergency room with complaint of 2 days history of muscular weakness which is symmetric and descending and diplopia. He denies any fever or chills. He does give the history of having injury to the face. He works as marine driller. His symptoms are progressively getting worse. His vitals signs reveal no fever, and bradycardia with the heart rate of 48 and blood pressure of 120/80 mm hg. His Slow vital capacity was 1 liter (33% of predicted). He was admitted in intensive care unit.


Diagnosis: Botulism (110 cases in US per year with 3 percent being wound Botulism)

Differential diagnosis: Mysthenia Gravis, Lambert-Eaton syndrome, Guillain-Barre’s syndrome, poliolmyelitis, Ticks paralysis, heavy metal intoxication.


Botulism has an acute onset with bilateral cranial neuropathies and symmetric descending weakness. Key feature include:

• Patient is afebrile
• Symmetric neurological deficit
• Patient is responsive
• Normal or slow heart rate and normal blood pressure
• No sensory deficit
• Blurred vision
  

Treatment:

• Equine serum botulism antitoxin
• Penicillin G intravenously 3 grams every 4 hours

Tuesday August 4, 2009
Heparin rebound phenomenon

Heparin rebound phenomenon, is considered to be a contributive factor in excessive postoperative bleeding after cardiac surgery. It is due to the reappearance of anticoagulant activity despite adequate neutralization with protamine.This phenomenon is well known since atleast last 45 years 1.

The underlying etiology is due to the fact that a significant amount of heparin remains bound to plasma proteins and escape neutralization by protamine. Later this heparin get released and may contribute to excessive postoperative bleeding after cardiac surgery. Though logically, the treatment is more administration of prtoamine but caution should be taken as high and inappropriate protamine dose may lead to 'acute' pulmonary hypertension 2 and interestingly failed to show decrease in blood product adminstration 3 or any difference in the thrombelastographic profiles or coagulation screen (PT, PTT, ACT and platelets) 2. Also life threatening protamine reactions is another risk need to be considered 5.




Note: This Heparin rebound phenomenon is different from Rebound increase in Thrombin Generation and Activity after cessation of intravenous heparin in patients with acute coronary syndromes which is also often referred as heparin rebound phenomenon 4.





References: click to get abstract/article

1. Heparin rebound phenomenon in extracorporeal circulation - Surg Gynecol Obstet.1962 Aug;115:191-8.

2. Heparin rebound phenomenon--much ado about nothing? - Blood Coagul Fibrinolysis. 1992 Apr;3(2):187-91.

3. Can extra protamine eliminate heparin rebound following cardiopulmonary bypass surgery? - J Thorac Cardiovasc Surg 2004;128:211-219

4. Rebound Increase in Thrombin Generation and Activity After Cessation of Intravenous Heparin in Patients With Acute Coronary Syndromes - Circulation. 1995;91:1929-1935.

5. Life Threatening Protamine Reactions In Cardiac Surgery: Literature Review With A Case Report - The Internet Journal of Thoracic and Cardiovascular Surgery. 2005. Volume 7 Number 1.

Monday August 3, 2009
Atenolol in renal failure

One must use caution while prescribing atenolol to patients with renal insufficiency. The elimination half-life of atenolol is extensively prolonged in patient with renal failure. The normal half life of atenolol is 6 to 7 hours; however, in renal failure patients the half-life may be extended to more than 100 hours 2.

The recommended dosage are following:

• CrCl 35 mL/min or greater - normal dosing
• CrCl 15 - 35 mL/min - MAX. dose 50 mg orally QD
• CrCl less than 15 mL/min - MAX. dose 25 mg orally QD
• Hemodialysis: 25-50 mg orally after each dialysis session.

Treatment of atenolol overdose in a patient with renal failure is recommended with serial hemodialysis and charcoal hemoperfusion 3. On the contrary, metoprolol is extensively metabolized via the hepatic system.



References:

1.Atenolol-DOSAGE AND ADMINISTRATION - rxlist.com

2.Atenolol kinetics in renal failure - Clin Pharmacol Ther. 1980 Sep;28(3):302-9

3. Treatment of atenolol overdose in a patient with renal failure using serial hemodialysis and hemoperfusion and associated echocardiographic findings Vet Hum Toxicol. 2000 Aug;42(4):224-5.

Sunday August 2, 2009
Why Arixtra doesn't cause HIT (Heparin induced thrombocytopenia)






ARIXTRA (Fondaparinux) is not a heparin. ARIXTRA is the first and only pentasaccharide antithrombotic agent inhibiting only factor Xa

Saturday August 1, 2009

Procedure tip - Straight to Cuff Stylet Shaping