June 2007 Archive for icuroom.net

2007-06-30T11:17:00.000-04:00

Saturday June 30, 2007
Regarding Tracheostomy tube change

Tracheostomy tubes, frequently placed in critically ill patients who require prolonged airway access. It usually requires 7 days for maturation of the tracheal cutaneous tract. Changing tracheostomy tube prior to this may result in dissection between tissue planes, creating a false passage or lumen and loss of the airway. If situation arise to change tracheostomy tube before seven days (like due to cuff leak etc), it is always appropriate to keep backup measures with oxygen mask and endotracheal intubation in case tract get lost, desaturation or hemodynamic instability. Ideally, Bronchoscope should be kept handy too.

One trick in premature tracheostomy tube change is to do it over airway exchange catheter to avoid false lumen passage. You may use suction catheter, nasogastric tube or any tube to pass over.

Reference:

The tracheostomy tube change: a review of techniques - British Journal of Hospital Medicine, Vol. 62, Iss. 3, 14 Mar 2001, pp 158 - 163

2007-06-29T11:24:00.000-04:00

Friday June 29, 2007
Difference between Lactate Ringer's and Normal Saline solutions

Lactated Ringer's Solution was invented about 125 years ago by a British physiologist Sydney Ringer and never lost a day in its popularity. Let see its difference from normal saline.

Normal Saline is the solution of 0.9% NaCl. It has a slightly higher degree of osmolality compared to blood. One litre of Normal Saline contains

154 mEq/L of Na+ and
154 mEq/L of Cl−

Lactated Ringer's (per litre) Solution contains:

130 mEq/L of Na+ but total cations of 137 mEq/L , so still is isotonic.
109 mEq/L of Cl−
28 mEq/L of lactate
4 mEq/L of potassium
3 mEq/L of calcium.

Lactate converts to bicarbonate in liver.

Bonus Pearl: Patients with lactic acidosis usually have inadequate liver metabolism of lactate so conversion to HCO3- from the infused lactate of LR is impaired and may give false readings of serial lactate measurements but may be a better choice in regular situations where hyperchloremia restricts use of normal saline.

2007-06-28T21:07:00.000-04:00

Thursday June 28, 2007
Nasogastric tube syndrome

Q; 65 year old female admitted to ICU 9 days ago with small bowel obstruction. Pt. is now stable and actually is about to get transferred out of unit. Patient suddenly start complaining of choking sensation with two hands on neck. Monitor shows oxygen desaturation. Patient intubated emergently. No laryngeal or vocal edema seen on laryngoscope but vocal cord paralysis noted.

A; Nasogastric tube syndrome : Nasogastric tube syndrome was described about 25 years ago by Sofferman and coll. It is a life-threatening complication of an indwelling (more than a week) nasogastric tube. The syndrome may present as complete vocal cord abductor paralysis. The syndrome is thought to result from perforation of the NG tube-induced esophageal ulcer and infection of the posterior cricoid region (postcricoid chondritis) with subsequent dysfunction of vocal cord abduction. Unilateral paralysis of cord is also described. Treatment is protection of airway, removal of NG tube and antibiotics. Some advocates antireflux therapy too. Another variant is described with no esophageal ulcer but possibly because of ischemia of the laryngeal abductor muscle secondary to physical compression of the postcricoid blood vessels by NG tube.

References: Please click to get abstract

1. The nasogastric tube syndrome: two case reports and review of the literature. Head Neck. 2001 Jan;23(1):59-63.
2. A variant form of nasogastric tube syndrome. Intern Med. 2005 Dec;44(12):1286-90.
3. Case Report - Nasogastric Tube Syndrome: The Unilateral Variant - Medical Principles and Practice Vol. 12, No. 1, 2003
4. Sofferman, R.A. and Hubbell, R.N., "Laryngeal Complications of Nasogastric Tubes," ANNALS OTOLOGY, RHINOLOGY, AND LARYNGOLOGY, 90:465-468, 1981.

2007-06-27T19:20:00.000-04:00

Wednesday June 27, 2007
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

2007-06-26T18:14:00.000-04:00

Tuesday June 26, 2007
Soda-bicarb to prevent contrast induced nephropathy

Q: How you write the order for soda bicarbonate infusion in preventing contrast induced nephropathy ?

A: Use 154meq/L of sodium bicarbonate (3 amps) in 1 litre of D5W.

Give 3ml/kg/hr one hr prior to the exam.Give 1ml/kg/hr during the exam and for 6 hours after the exam.

2007-06-25T11:33:00.000-04:00

Monday June 25, 2007
Regarding disposable plastic laryngoscope blade

Is disposable plastic laryngoscope blade acceptable ?

Answer is "No".
To save money and in some cases to decrease infection rate, there has been temptation in many institutions to use disposable plastic laryngoscope blade.

One study recently published from france 1 in which 284 adult patients requiring rapid sequence induction (for intubation) were randomly assigned to either plastic single-use or reusable metal blades.

In the case of failed intubation, a second attempt was performed using metal blade.

The primary endpoint of the study was the rate of failed intubations.
The secondary endpoint was the incidence of complications (oxygen desaturation, lung aspiration, and oropharynx trauma).

Results:
On the first attempt, the rate of failed intubation was significantly increased in plastic blade group (17 vs. 3%).
In plastic blade group, all initial failed intubations were successfully intubated using metal blade, but in metal blade group, 50% of failed intubations were still difficult after the second attempt.
There was a significant increase in the complication rate in plastic group (15 vs. 6%).

Study concluded that in rapid sequence induction of anesthesia, the plastic laryngoscope blade should not be recommended for use.

Editors' note: Possible reasons of poor outcome from plastic blades include uneven curvatures, poor allignment or fitting with laryngoscope and chances of breaking down durin procedure.

References: click to get article

Comparison of Plastic Single-use and Metal Reusable Laryngoscope Blades for Orotracheal Intubation during Rapid Sequence Induction of Anesthesia. - Anesthesiology. 104(1):60-64, January 2006.

2007-06-24T16:38:00.000-04:00

Sunday June 24, 2007
Supraclavicular approach of subclavian central line (video)

Watch this very nicely done video of supraclavicular approach of subclavian central line (from EMPAR.TV)

supraclavicular approach of subclavian central line

(Total time 10:34 minutes)

Previous related pearl: Where is Subclavian vein ?

2007-06-23T16:22:00.000-04:00

Saturday June 23, 2007
Borderline extubation and difficult Airway !

Scenario: You decide to extubate morbidly obese patient but parameters are borderline. There is a good air cuff leak. Earlier notes indicate 'difficut intubation' with non-visualization of vocal cords. What could be your option ?

Answers: To extubate over exchange catheter and leave catheter inside respiratory tract till success of extubation is assured. One study showed maintenance of airway upto 72 hours.

Make patient sits 45 to 60 degrees in bed. Explain the discomfort. Preoxygenate with 100% oxygen for about 10 minutes. Check for cuff leak. Pass exchange catheter in ETT as much tolerated gently and extubate. Leave exchange catheter taped to forehead. Another advantage is ventilation with catheter till ETT can be reinserted if required.

References: Click to get articles/abstract

1. The use of an endotracheal ventilation catheter in the management of difficult extubations - Canadian Journal of Anesthesia, Vol 43, 90-93,

2. Airway Management in Critical Illness - Chest. 2007; 131:608-620

3. Extubation of the Patient After a Difficult Intubation - Ann Thorac Surg 1998;65:1778-1780

2007-06-22T09:44:00.000-04:00

Friday June 22, 2007
"Locked-in" Syndrome (coma vigilante)

"patient is a silent and unresponsive witness to everything that is happening" - from story of Nick Chisholm 1

Patient with Locked-in syndrome is a fully conscious person, but all the voluntary muscles of the body are completely paralyzed, other than those that control eye movement. Term was first introduced about 25 years ago by Plum and Posner with complete occlusion of the basilar artery. 3

Any catastrophy involving ventral pons can cause this syndrome like massive stroke, traumatic head injury, ruptured aneurysm, pontine infarction after prolonged vertebrobasilar ischaemia, haemorrhage, tumor, central pontine myelinolysis, pontine abscess or postinfective polyneuropathy. As all of the nerve tracts responsible for voluntary movement pass through the ventral pons but fortunately or unfortunately, consciousness are above the level of the ventral pons. 2

Only supportive rehabilitation is the answer.Being an intensivist, it is extremely important to educate staff and to protect patient from any physical or psychological harm (like procedure without adequate analgesia), with upmost understanding that it is an "imprisoned mind buried alive in a dead body’’ (as said for character with paralysis like locked-in syndrome in Thérèse Raquin by Emile Zola - 1868).

References: Click to get articles/abstract

1. The patient's journey: Living with locked-in syndrome - BMJ 2005;331:94-97 (9 July)
2. Locked-in Syndrome - enotes.com
3. Plum F, Posner JB. The diagnosis of stupor and coma. Philadelphia: FA Davis, 1982; 377
4. Locked-in syndrome: a catastrophic complication after surgery - British Journal of Anaesthesia, 2004, Vol. 92, No. 2 286-288

2007-06-21T11:22:00.001-04:00

Thursday June 21, 2007
Calcium infusion and thrombophlebitis

One important factor while writing order for IV calcium is of central line availability. If central line is not available, it is better to write order for calcium gluconate instead of calcium chloride. Calcium infusion tends to cause thrombophlebitis and chances are higher with calcium chloride as it contains 3 times more elemental calcium in camparison to same dose of calcium gluconate.

1 gram of Calcium gluconate contains 4.65 mEq of elemental Calcium, and
1 gram of Calcium chloride contains 13.6 mEq of elemental Calcium.

2007-06-20T15:10:00.000-04:00

Wednesday June 20, 2007
Resistant (uncontrolled bleeding) / Life-threatening diffuse alveolar

hemorrhageDiffuse alveolar hemorrhage remained a condition with high mortality. Usual treatment is high dose IV metilprednisolone (1g/day) for three to five days and in more severe cases to add IV cyclophosphamide (cyclophosphamide has a delayed effect, but may provide synergistic action with steroid). Plasmapheresis has been described to be effective particularly in diffuse alveolar hemorrhage associated with Goodpasture syndrome.But what if bleeding is non-stop and life-threatening ?Answer is off label use of activated Factor VII. In 3 cases reported from University of North Carolina at Chapel Hill - bleeding stops and oxygenation improved within minutes 1.

Reference: click to get abstract

Successful Treatment of Diffuse Alveolar Hemorrhage with Activated Factor VII - 16 March 2004 Volume 140 Issue 6 Pages 493-494

2007-06-19T13:15:00.000-04:00

Tuesday June 19, 2007
Hypothermia

Q: What temperature defines clinical hypothermia ?

A: 95 F (35 C)

References:

1. Thermal disorders - Critical Care Medicine: The Essentials [Third Edition] by John J Marini, Arthur P Wheeler - page 467

2007-06-18T14:11:00.001-04:00

Monday June 18, 2007
Scleroderma Renal Crisis (SRC)

Scleroderma Renal Crisis is one of the few rheumatological emergency where early diagnosis and treatment can make big difference in outcome. Wrong diagnosis may lead to wrong management pathway and eventually to very high mortality. SRC is heralded with hypertensive crisis associated with acute renal failure but the pearl is to avoid IV Labetolol or nitroprusside and gradually decrease blood pressure with PO angiotensin-converting enzyme (ACE) inhibitors. calcium channel blockers may help. Renal dialysis is a last resort. Another important differential diagnosis is from SLE (renal). It has been suggested that use of steroids is associated with onset of scleroderma renal crisis.

See this precise review article on SRC here from Department of Rheumatology and Internal Diseases, Medical University in Białystok, Poland. (2005)

References: Click to get articles/abstract

1. What Is Scleroderma Renal Crisis and How Is it Managed? via medscape.com with free registration2. Long-Term Outcomes of Scleroderma Renal Crisis - 17 October 2000 Volume 133 Issue 8 Pages 600-603 - annals3. Scleroderma Renal Crisis: The Sword of Damocles. - JCR: J. of Clinical Rheum. 10(5):234-235, October 2004.
4. Rheumatologic Renal Disease: SLE vs. Scleroderma - ucsf.edu.
5. Corticosteroid-induced scleroderma renal crisis, MJA 2002 177 (8): 459-459

2007-06-17T13:34:00.000-04:00

Sunday June 17, 2007
Critical Care Nephrology

"If you ask me to put all Critical Care Medicine together in 2 words, I will say it is 'urine output'. Where there is a 'pee', there is a 'hope' in ICU !"

A Nephrologist.

icuroom.net recommends to have CRITICAL CARE NEPHROLOGY, AN ISSUE OF CRITICAL CARE CLINICS, 21-2 as a good handy reference for Critical Care Nephrology.

2007-06-16T14:01:00.000-04:00

Saturday June 16, 2007
Changing double lumen endotracheal tube (ETT) to single lumen

Q; You have been asked to change double lumen endotracheal tube (DLT) on a patient after thoracic surgery. Due to excessive tapping, you cannot read anything but see 2 lumens - white and blue. Which lumen you will use to pass change over catheter ?

A; White color (Tracheal)

Double lumen endobronchial tubes are usually used in thoracic surgery. Double lumen tubes have 2 cuffed lumens

1. Endobronchial (usually blue) and
2. Tracheal (usually white)

DLT is less stable than single lumen ETT. DLT is of wide diameter and meant to be changed immediately post-operatively unless severe laryngeal edema prevents it. Tracheal port should be used to change the DLT to single lumen ETT over wire/catheter.

2007-06-15T15:51:00.000-04:00

Friday June 15, 2007
ETT size for Bronchoscope !

It is no brainer to have reasonably wide diameter of endotracheal tube (ETT) to accomodate bronchoscope. Size 8 (mm in internal diameter) is said to be a good and acceptable ETT for adult bronchoscopy. But to be precise:

the internal diameter of ETT should be aleast more than (or =) 2 mm of external diameter of bronchoscope.

Reference: clickable

British Thoracic Society guidelines on diagnostic flexible bronchoscopy - British Thoracic Society Bronchoscopy Guidelines Committee, a Subcommittee of the Standards of Care Committee of the British Thoracic Society Thorax 2001;56(Suppl 1):i1-i21 ( February )

2007-06-14T09:41:00.000-04:00

Thursday June 14, 2007
Intravenous Magnesium in Subarachnoid Hemorrhage (vs Nimodipine)

The prophylactic use of nimodipine, a calcium channel blocker, in aneurysmal subarachnoid hemorrhage is a standard of practice to reduce the risk of ischemic brain injury. Recently one study published in 'Neurosurgery' 1 to see if magnesium being a calcium antagonist, can have same effect as it also promotes dilatation of cerebral arteries, and relatively has a high safety margin.

104 patients with aneurysmal subarachnoid hemorrhage were randomized to receive either magnesium sulfate (n=53) (loading 10 mg/kg followed by 30 mg/kg daily) or nimodipine (n=51) (48 mg/d) intravenously until at least postoperative Day 7.

Primary outcome parameters set were

incidence of clinical vasospasm and
cerebral infarction

Secondary outcome measures targeted were

incidence of transcranial Doppler/angiographic vasospasm,
the neuronal markers (neuron-specific enolase, S-100), and
the patients' Glasgow Outcome Scale scores at discharge and after 1 year.

In the magnesium group , 15% patients experienced clinical vasospasm and 38% experienced transcranial Doppler/angiographic vasospasm compared with 27% and 33% patients in the nimodipine group.

Overall, the rate of infarction attributable to vasospasm was virtually the same (19 versus 22%). There was no difference in outcome between groups.

Study concluded that the efficacy of magnesium in preventing delayed ischemic neurological deficits in patients with aneurysmal subarachnoid hemorrhage seems to be comparable with that of nimodipine.

Reference: clickable
Intravenous Magnesium versus Nimodipine in the Treatment of Patients with Aneurysmal Subarachnoid Hemorrhage: A Randomized Study - Neurosurgery. 58(6):1054-1065, June 2006.

2007-06-13T10:31:00.000-04:00

Wednesday June 13, 2007
Hypotension from intravenous Amiodarone

Continuing our theme from yesterday on Amiodarone, it would be of interest to know that hypotension from IV amiodarone bolus is mostly not due to amiodarone itself but due to its solubilized vehicle called polysorbate 80.

Polysorbate 80 itself can decreases heart rate by depressing AV nodal conduction and has property of increasing atrial and ventricular myocardial refractory period but can cause hypotension due to histamine releasing effect.

Polysorbate 80 is also blamed for Acute amiodarone-induced hepatitis but literature is scant on it.

References: click to get abstract/article

1. Pharmacology and Toxicology of a New Aqueous Formulation of Intravenous Amiodarone (Amio-Aqueous) Compared with Cordarone IV. - American Journal of Therapeutics. 12(1):9-16, January/February 2005.

2. Effects of amiodarone with and without polysorbate 80 on myocardial oxygen consumption and coronary blood flow during treadmill exercise in the dog - J Cardiovasc Pharmacol. 1991 Jul;18(1):11-6.

3. Histamine-releasing properties of Polysorbate 80 in vitro and in vivo: correlation with its hypotensive action in the dog - Agents Actions, 1985 Sep;16(6):470-7.

4. I.V. Amiodarone: What Do We Really Know About It? Cardiac Electrophysiology Review, Volume 2, Number 1 / March, 1998

5. Early acute hepatitis with parenteral amiodarone: a toxic effect of the vehicle? - Gut, Vol 34, 565-566, 1993

2007-06-12T13:15:00.000-04:00

Tuesday June 12, 2007
Bedside tip !

If you opt to use intravenous Amiodarone, try to give it via central line as phlebitis is a common side effect, if given peripherally. It is reported in upto 16% 1 of cases particularly if given beyond 24 hours.

Related previous pearls:

Why we call it Am-iod-arone !
Amiodarone Neurotoxicity !
Amiodarone pulmonary toxicity

References: click to get abstract/article

1. Amiodarone as a First-Choice Drug for Restoring Sinus Rhythm in Patients With Atrial Fibrillation - Chest. 2000;117:1538-1545

2007-06-11T13:03:00.000-04:00

Monday June 11, 2007
Clinical Diagnosis ?

Janeway lesions

Janeway lesions are non-tender, erythematous (or haemorrhagic) macules in the palms or soles, and are pathognomonic of infective endocarditis. They appear as flat, painless, red to bluish-red spots on the palms and soles. On pathology, it may show evidence of suppuration and microabscesses without treatment. On appropriate therapy, it may show only inflammatory reaction.

Keep as reference an excellent article published in chest 30 years ago: Janeway's lesion and an Osler's node in - A consideration of the differences between a infectious endocarditis, Chest 1976;70;239-243 - pdf document

2007-06-10T00:46:00.000-04:00

Sunday June 10, 2007
Frist EKG (ECG) Machine

In this first EKG Machine, Right and Left hands and Left legs were immersed in jars of salt solution as electrodes !

Willem Einthoven (The Netherlands), used the string galvanometer to describe various deflections as features of a number of cardiovascular disorders. He was awarded the 1924 Nobel Prize for Physiology or Medicine for his discovery.

Note: This image is in the public domain because its copyright has expired in the United States and those countries with a copyright term of life of the author plus 100 years or less.

2007-06-09T19:40:00.000-04:00

Saturday June 9, 2007
The calcium phosphate precipitation and microemboli via TPN

If a patient is receiving total parental nutrition (TPN) and develops respiratory compromise, TPN should be immediately stopped and inspected for any precipitation. The calcium phosphate precipitates, although rare can form and when infused acts like microemboli. A filter can be utilized to overcome the problem when infusing TPN. Other ways to avoid the problem

Infuse TPN within 24 hours of preparation.
Use Ca-gluconate instead of CaCl.
Keep the Ca:PO4 ratio greater than 1:2.
Keep the total amount of Ca and PO4 less than 45 mEq/L.

Read case report and very extensive discussion on this topic: Microvascular Pulmonary Emboli Secondary to Precipitated Crystals in a Patient Receiving Total Parenteral Nutrition - Chest. 1999;115:892-895

References (Clickable):

1. Calcium and phosphates compatibilities in parenteral nutrition admixtures Tunis Med. 2006 Nov;84(11):677-82

2. Intravenous in-line filters: filtering the evidence. Curr Opin Clin Nutr Metab Care. 2003 May;6(3):319-25

3. Total parenteral nutrition associated crystalline precipitates resulting in pulmonary artery occlusions and alveolar granulomas. Dig Dis Sci. 2003 Jul;48(7):1352-4.

4. Pulmonary deposition of calcium phosphate crystals as a complication of home total parenteral nutrition, Journal of Parenteral and Enteral Nutrition, Vol 13, Issue 2, 209-213

2007-06-08T13:18:00.000-04:00

Friday June 8, 2007
What Dig. level makes you happy ?

Digoxin is known to provid reduction in hospitalizations among patients with heart failure and depressed left ventricular systolic function without improving mortality (DIG trial -The Digitalis Investigation Group trial) 1. Very interesting work published in JAMA about 3 years ago (about 3800 patients) as a followup of above trial - looking into mortality association with different Digoxin level 2 . What they found:

* SDC = serum digoxin concentration
* Patients were divided into 3 groups based on SDC at 1 month

Patients with SDCs of 0.5 to 0.8 ng/mL had a 6.3% lower mortality rate compared with patients receiving placebo.
No reduction in mortality among patients with SDCs of 0.9 to 1.1 ng/mL,

And
Patients with SDCs of 1.2 ng/mL and higher had an 11.8% higher absolute mortality rate than patients receiving placebo.

Study suggested that the effectiveness of digoxin therapy in men with heart failure and a left ventricular ejection fraction of 45% or less may be optimized in the SDC range of 0.5 to 0.8 ng/mL.

Read interesting article: DIGOXIN DELUSIONS (from ucsf.edu)

References: Click to get abstract

1. The Effect of Digoxin on Mortality and Morbidity in Patients with Heart Failure, The Digitalis Investigation Group - NEJM, Vol 336, Feb 20, 1997, number 8

2. Association of Serum Digoxin Concentration and Outcomes in Patients With Heart Failure -JAMA. 2003;289:871-878.

2007-06-07T13:57:00.000-04:00

Thursday June 7, 2007
Tachyphylaxis Associated With Continous Cisatracurium (Nimbex)

Tachyphylaxis is common among patients treated with neuromuscular blockers and varies with clinical situation like burn patients are more prone to have resistance with pancuronium. Cisatracurium is a very common neuromuscular blocker prescribed in ICUs, particularly it is a prefered agent in patients with major organ failures as it has a clearance mechanism independent of organ function. Other advantges of cisatracurium is no vagolytic effects ( minor histamine-releasing properties) and less association with prolonged muscle weakness. One disadvantage of continuous cisatracurium therapy is possible tachyphylaxis after 48-72 hours and may require escalating dose of the drug.

Reference:

Tachyphlaxis Associated With Continous Cisatracurium Versus Pancuronium Therapy - Pharmacotherapy, Pharmacotherapy 22(7):823-830, 2002

2007-06-06T10:44:00.000-04:00

Wednesday June 6, 2007

Q: Which cardiac medicine may lead to mesenteric ischemia?

A: Digitalis 1.

Digitalis has been found to cause vasoconstriction of both arterial and venous smooth muscle cells in the mesenteric vasculature. Acute intestinal ischemia could be the most deceiving clinical condition and requires very high index of suspicion. Acute mesenteric ischemia is a deadly disease, difficult to diagnose in timely fashion and delayed intervention resulting mostly in fatal outcome.

Clinical Findings: There generally are minimal clinical, laboratory and radiologic findings. Fever, abdominal pain which may be severe, nausea, vomiting. Although non specific, marked increase in serum lactate is common.

Causes: Acute Occlusion of Superior mesenteric artery, atherosclerosis, thrombosis, venous thrombosis.

Treatment: Early diagnosis and resection of dead bowel. Generally diagnosed at Laparotomy.

Prognosis: Rapidly leads to Multi Organ Dysfunction Syndrome with very high mortality rate.

Reference: click to get abstract

1. Nonocclusive mesenteric ischemia induced by digitalis - International Journal of Colorectal Disease, Volume 19, Number 3, May 2004, pp. 277-280(4)

2007-06-05T10:37:00.000-04:00

Tuesday June 5, 2007
Prescribing vitamin B6 with linezolid

Linezolid is found to be associated with 2 major side effects: cytopenias and peripheral neuropathy 1. When Vitimain B6 (PYRIDOXINE) was prescribed for peripheral neuropathy, interestingly it was found to help in reversing cytopenias more than peripheral neuropathy 2 . Dose of vitamin B6 used was 50 mg PO once a day.So far we have only few case reports but Vitamin B6 is safe and inexpensive and most experts don't see any harm in prescribing it along with linezolid.

References: click to get article

1. Severe sensory neuropathy associated with long-term linezolid use - Neurology.2005; 64: 926-927
2. Reversal of linezolid-associated cytopenias, but not peripheral neuropathy, by administration of vitamin B6 - Journal of Antimicrobial Chemotherapy 2004 54(4):832-835

2007-06-04T11:06:00.000-04:00

Monday June 4, 2007
Triad of Hepato-Pulmonary Syndrome

Q: What is the triad of hepatopulmonary syndrome ?

A: The triad of hepatopulmonary syndrome

liver disease,
increased A-a gradient, and
evidence of intrapulmonary vascular dilitations
(providing intrinsic cardiopulmonary disease is excluded)

About 8-10% of cirrhotics manifest clinical features of the hepatopulmonary syndrome. 2 major clinical signs are

Platypnea: Dyspnea improves when lying flat (opposite of orthopnea) and
Orthodeoxia: hypoxemia worsens upon sitting up and improves when lying flat.

Platypnea and orthodeoxia occur because the pulmonary AVMs (arterio-venous malformations) occur in the bases of the lung. Therefore, when sitting up or standing, blood pools at the bases of the lung and increase AV shunting and V/Q mismatch. Increasing the oxygen level can overcome this problem.

Note: Hepatopulmonary syndrome and Portopulmonary hypertension are 2 different conditions. Portopulmonary hypertension also occurs in end stage liver disease but pathphysiology is more similar to primary pulmonary hypertension with intense vasoconstriction of pulmonary capillaries and thickened pulmonary vasculature.

Refer to nice review article Portopulmonary hypertension and hepatopulmonary syndrome, Marius M Hoeper, Michael J Krowka, Christian P Strassburg, THE LANCET • Vol 363 • May 1, 2004

2007-06-03T17:35:00.000-04:00

Sunday June 3, 2007
Purple Urine Bag Syndrome

The purple urine bag syndrome is characterized by the purple discoloration of the urine, of collecting bag, and of draining tube. It is a rare condition associated with chronic catheterization of urinary tract. It is also called The King's Royal Urine as England's "Mad" King George III in early 19th century reported to have bouts of bluish/purplish color urine. Exact etiology is unknown and many explanations have been described. It is said to be a triad of

constipation,
alkaline urine and
bacteria in the urinary tract that produce the enzyme sulphatase/phosphatase like Pseudomonas aeruginosa, Proteus mirabilis, Morganella morganii and E. coli.

It has been said that constipation lead to bacterial overgrowth in colon and in combination with UTI produce this syndrome.Purple color is produced by combination of red and blue color. indirubin (red) is produced in this process and get dissolved in the plastic of the drainage bag, ostomy pouch, or urinary catheter, and indigo crystals (blue) in the urine coat the bag or tube, combining to form the purple color.The longer the drainage system is used, the deeper the purple color becomes. A strong odor often is associated with PUBS which gets stronger as temperature in the room rises ! Due to unknown reason, it is more common in female patients.Overall it is a benign condition. Treatment includes good hygiene, changing catheters as needed, avoiding constipation and if needed antibiotics.

2007-06-02T19:16:00.000-04:00

Saturday June 2, 2007
Linezolid infusion and exposure to light

Case: You have a patient diagnosed with vancomycin-resistant enterococci (VRE) and has been started on linezolid (Zyvox). While evaluating patient at bedside you saw a bag labelled with linezolid, due to infuse in 30 minutes. What would be your instruction to pharmacy ?

Answer: To protect the infusion bag of linezolid from light. Linezolid infusion bag need to be protected from light while awaiting infusion to avoid degradation. Once infusion is started, bag can be unwrap.Note: IV Zyvox may exhibit a yellow color that can intensify over time, but it is a benign effect and does not affect potency.

Reference: click to get abstract

1. Zyvox - rxlist.com

2007-06-01T13:38:00.000-04:00

Friday June 1, 2007
Phosphate level in acetaminophen-induced acute liver failure

Case: You transferred a patient from nearby community hospital with acetaminophen-induced acute liver failure. ALT / AST reported in thousands and last PT-INR of 2.7. On clinical exam patient is alert and oriented. Hemodynamics are stable. You alerted the hepatology team and send STAT labs. After 45 minutes you received a call from lab with 'critical value' of phosphate with 0.9 mg/dl. Is it a good sign or a bad sign?

Answer: Good SignHypophosphatemia in the setting of acetaminophen-induced acute liver failure is a good sign. It indicates regeneration of hepatocytes and reversal of acute liver failure. You may have to replace it aggressively.Conversely, hyperphosphatemia suggest impaired regeneration and is a poor prognostic sign and actually also said to be a sign of impending hepato-renal failure due to kidney's lost ability of lowering of serum phosphate 1.

Related previous pearl: Is serum phosphate level better than King’s College Hospital criteria in Tylonol Toxicity ?

Reference: click to get abstract

1. Serum Phosphate Is an Early Predictor of Outcome in severe Acetaminophen-Induced Hepatotoxicity , Hepatology, Volume 36, Issue 3 , Pages 659 - 665