ICU room Pearls

2006-12-19T18:05:00.000-06:00

Tuesday December 19, 2006
Something to share !

Today we will take a little break to share this important statement:

"As you learn to become a doctor, there is a frequent sense of surprise, a feeling that you are not entitled to the kind of intrusion you are allowed into patients' lives. Without arguing, they permit you to examine them; it is impossible to imagine, when you do your very first physical exam, that someday you will walk in calmly and tell a man your grandfather's age to undress, and then examine him without thinking about it twice. You get used to it all, but every so often you find yourself marveling at the access you are allowed, at the way you are learning from their bodies, the stories, the lives and deaths of perfect strangers. They give up their privacy in exchange for some hope - sometimes strong, sometimes faint - of the alleviation of pain, the curing of disease. And gradually, with medical training, that feeling of amazement, that feeling that you are not entitled, scars over. You begin to identify more thoroughly with the medical profession - of course you are entitled to see everything and know everything; you're a doctor, aren't you? And as you accept this as your right, you move further from your patients, even as you penetrate more meticulously and more confidently into their lives."
- Perri Klass, M.D.

Read more about Dr. Klass here - source nih.gov

2006-08-21T08:48:00.000-06:00

Monday August 21, 2006
THAM

Introduction; In patients with acute respiratory distress syndrome (ARDS), permissive hypercapnia is a strategy to decrease airway pressures to prevent ventilator-induced lung damage by lowering tidal volumes and tolerating higher arterial carbon dioxide tension. A pure respiratory acidosis generally does not require alkali therapy. Alkali therapy is indicated for either a metabolic acidosis or a mixed acidosis. The choice of buffer is based on type of acidosis, cardiorespiratory status, and lung mechanics.

Problem with NaHCO3: Slow infusions of NaHCO3 can be used to treat non-anion gap metabolic acidosis and some forms of increased anion gap acidosis. But using NaHCO3 to treat type A (hypoxia-related) lactic acidosis can be hazardous, particularly under conditions of hypoxemia, inadequate circulation, and limited alveolar ventilation.

THAM: Under above circumstances, THAM is the preferable buffer because it does not increase PaCO2 and is excreted by the kidneys. Tromethamine (THAM) is a sodium-free alkalinizing agent that acts as a hydrogen ion (proton) acceptor. It is a weak base that combines with hydrogen ions from carbonic acid to form bicarbonate and cationic buffer. Administration of tromethamine decreases hydrogen ion concentration, which results in a decrease in carbon dioxide concentrations and an increase in bicarbonate concentrations. The administration of Tham also increases urine output through osmotic diuresis. Excretion of electrolytes and CO2 is also increased. Urine pH is raised along with the excretion of electrolytes.

Usual Dose:

Dose in ml's of 0.3M THAM = (1.1) (Wt. in Kg) (normal HCO3 – Pt’s HCO3)

OR

Dose in ml’s of 0.3M THAM = body wt in kg X base deficit in MEq/L x 1.1
Total dose should be administered over a period not less than 1 hour via central line.

.3M THAM solution is available as premix and is contra-indicated in renal failure, anuria and hyperkalemia. It may cause transient hypoglycemia and respiratory depression.

2006-08-10T06:42:00.000-06:00

Thursday August 10, 2006
Level of central line tip may predispose to thrombosis

Interesting retrospective review of 428 central lines (inserted into 334 patients) was done in UK to look into the level central line tip's relation to thrombosis 1. The median follow-up was 72 days.

* The chest radiograph obtained post-catheter insertion, as well as follow-up radiographs, linograms, venograms and Doppler ultrasounds (US), were reviewed.

They found that: "There was a significant difference in thrombosis rate between lines sited with the tip in a distal third of the superior vena cava (2.6%) compared with a proximal third of the superior vena cava (41.7%) - CVC with tips in a proximal position were 16 times more likely to thrombose than those in a distal position".

Related previous pearls:

CXR reading for optimum tip of central line
and
What if SC central line ends up in IJ vein?

Reference:

1. To clot or not to clot? That is the question in central venous catheters - Clinical Radiology, Volume 59, Issue 4, April 2004, Pages 349-355

tip of central line

2006-08-09T09:27:00.000-06:00

Saturday July 22, 2006
Do you need to pull back the central line?

Ideally, tip of central venous catheter should not lie in cardiac structures and the desirable position is mid superior vena cava.

Simple tip: If the tip of central venous catheter is above the superior margin of Right mainstem bronchus, it is unlikely to be in atrium.

2006-07-21T22:42:00.000-06:00

Friday July 21, 2006
Prohibiting cell phones in ICUs - Are we over-reacting !

Truely speaking, there have been no studies to determine the harm or benefit of mobile/cell phones in ICUs. Generally, cell phones are prohibited in hospitals, particularly in ICUs and telemetry floors due to concern of EMI* with pacemakers, ventilators, infusion pumps and other electronic units. It became pretty standard with a report published about 12 years ago 1.

* EMI = electromagnetic interference

At the 2003 meeting of the ASA (American Society of Anesthesiologists), 7878 five-questions survey, regarding modes of communication in the ORs/ICUs, were distributed. 4018 responses were received 2.

65% of surveyed reported using pagers as their primary mode of communications,
17.5% of surveyed reported using cell-phones as their primary mode of communications and
17.5% used overhead paging (or did not respond to this question)

And

Among the 2607 respondents using pagers, 1179 (45%) reported experiencing significant delays in communication and 407 indicated that these delays led to medical error or patient injury.
31% of cell-phone users reported delays in communications.
Only 2.4% of the respondents indicated that they had ever experienced interference between a cell phone and a medical device.

It has been suggested that through proper policy controls, hospitals can provide a more safe environment taking advantage of this 2-way communication technology, with a reduction in the risk of medical error or injury resulting from delay !!.

It has been recommended that as far as cell phones be kept at least 1 meter away from medical equipment, they seems safe 3.

Similar theme was echoed in an editorial in BMJ about 3 years ago: Mobile phones in hospitals (BMJ 2003;326:460-461 - 1 March)

Related previous pearl: Noise level in ICUs

References: click to get abstract/article
1. Mobile telephones interfere with medical electrical equipment - Australas Phys Eng Sci Med.1994 Mar;17(1):23-7.
2. Communication in Critical Care Environments: Mobile Telephones Improve Patient Care - Anesth Analg 2006;102:535-541
3. Modern Wireless Telecommunication Technologies and Their Electromagnetic Compatibility with Life-Supporting Equipment - Anesth Analg 2005;101:1393-1400

Thursday July 20, 2006

Q: what is "cryo reduced plasma"?

A; Yesterday we learned that: one unit of cryoprecipitate is derived from one unit of fresh frozen plasma (FFP). Left over FFP, after removal of cryoprecipitate is called supernatant plasma or CRYO-REDUCED PLASMA.

Clinical Significance: Cryo-reduced plasma is used as a treatment in plasmapheresis for TTP, not responding to regular plasma exchange with FFP. Some physicians even use it as first line for plasmapheresis/Therapeutic Plasma Exchange (TPE) for a patient with Thrombotic Thrombocytopenic Purpura (TTP).

2006-07-19T20:53:00.001-06:00

Wednesday July 19, 2006

Q: Why we call it cryoprecipitate?

A: The name explains everthing. cryoprecipitate means "cold precipitate". When FFP is thawed slowly at 4 degree C, a white precipitate forms at the bottom of the bag, which can then be separated from the supernatant plasma. This precipitate is rich in fibrinogen, factor VIII, von Willebrand factor, factor XIII, and fibronectin - and call crayoprecipitate. One unit of cryoprecipitate is derived from fresh frozen plasma (FFP) prepared from a unit of whole blood and as it is only a little precipitate at the bottom of the bag, 1 unit of cryoprecipitate comprised only a volume of 10-20 mL.

Contents:

80-100 units of factor VIII, which consists of both the procoagulant activity and the von Willebrand factor,
150-250 mg of fibrinogen,
50-100 units of factor XIII, and
50-60 mg of fibronectin.

Half life is about one year if stored at -18 degree C. When ordered (generally given as 6 units at a time), cryoprecipitate is thawed back to 37 degree C. Once thawed it must be kept at room temperature and has an expiration time of 4 to 6 hours.

Previous related pearls: How much FFP? and Some facts about FFP

2006-07-17T23:01:00.000-06:00

Tuesday July 18, 2006

Q: How IV (intravenous) DDAVP (desmopressin) should be given?

A: DDAVP, short name of 1-deamino-8-D-arginine vasopressin and also known as desmopressin is use for varity of reasons in ICUs including uremic bleeding diasthesis, some platelet disorders, to boost the plasma level of factor VIII and von Willebrand factor (VWF) and in diabetes insipidus. It may be given as nasal spray or subcutaneous injection but in ICUs mostly get administrated via IV route.

DDAVP should be diluted in 100 ml of normal saline and given by slow intravenous infusion over 30 minutes. The usual dose is 0.3 mcg/kg. Rapid infusion may result in tachycardia, flushing, tremor and abdominal discomfort. Also thrombosis and even myocardial infarction after an infusion of DDAVP has been reported and should be used with caution in patients with signs of arterial disease.

2006-07-17T01:16:00.000-06:00

Monday July 17, 2006
Intensivists' compensation

We looked into recent surveys' from different sources and found the following:

* All compensations in US dollar annually
* K = 1000

Average base salary compensation for intensivist has been ranged from annual 195K (new graduate) to 240K (3/5 years experienced). Highly experienced intensivist (15-20 years) should have compensation around 255K - 263K annual.

Latest market: all these surveys were published atleast a year ago and in last 12 months advertisements for intensivists' opportunities continue to show rising trend of salaries even upto 225-250K for new graduates.

Academic factor: Intensivist at a university setting make less but have better life style due to house staff availability and protected time for research (average 168 K), while critical care staff physicians employed by a non-university-affiliated hospital gets higher compensation (avaerage 240K) but more burn out.

Total clinical time in university setting is around 26-34 weeks per year but in private groups it all depends on local needs with 40-47 weeks (with 4 weeks vacation and one week for CME). Many groups prefer to work in block scheduling (like '7 days on 7 days off' to wear off burn out).

VA factor: VA system intensivits have good benefits and life style (like their university based colleagues) but salary remained low around 130-140K 3. Recently, there are strong indications that salaries would go up.

eICU factor: Recently eICU physicians have been offered higher than average compensation with heavy investments in this sector from major health systems but still very few intensivists have been found to take it as a full time employment.

Subspeciality factor: Overall critical care anesthesiologists and critical care non-trauma surgeons were under-compensated per one survey 1. Out of all PEDIATRIC intensivists found to be in highest demand due to lowest supply.

Geographical: Region wise east coast (particularly north east) has about 5-10% less compensation in all fields as compared to other regions.

Benefits: Benefits and bonuses upto 15% on top of base salary is a norm. In benfits - continuing medical education (CME) allowance range from 1000 - 5000 per year with average of 3000 US annual. 401 K (retirement), ADD, life insurance are usually part of the package but 3 essential benefits should include
Malpractice with tail coverage
Health/dental benefits for self and family
CME

Mal-practice coverage: As a standard, malpractice with tail should be covered. New graduates often fail to ask for tail coverage and later found themselves in hot water with a condition call 'locked by the tail'. If candidate fail to negotiate but in later years want to relocate or leave the group, tail buying costs around 30K to 80K, depending on region. Tail buying is 200% of annual malpractice premiums.

Non-compete clause: Ideally, there should not be any non-compete or restrictive covenant clause as intensivists are unlikely to carry their own patient base but when private group is contracted or busy in one ICU its natural to have restrictive covenant and should be accepted as standard business practice.

References:

1. Compensation for Physicians in Critical Care - Compensation of Critical Care Professionals 2005 - Society of Critical Care Medicine
2. The 2005 AMGA (American Medical Group Association) Medical Group Compensation and Financial Survey - cejkasearch.com
3. Testimony of Dr. Stephen P. Rosenthal President National Association of VA Physicians and Dentists
4. Intensive care unit physician staffing: Financial modeling of the Leapfrog standard - Critical Care Medicine. Interface of Public Policy and Critical Care Medicine. 34(3) Suppl:S18-S24, March 2006.

2006-07-16T04:50:00.000-06:00

Sunday July 16, 2006
Optimum patients' load for intensivist

ICUs in united stated range anywhere from 6 to 24 beds or may be more. At this point, it is not clear at what point intensivist's efficiency plateau out and effects the overall outcome.

Drs. Saqib Dara, MD and Bekele Afessa, MD from Division of Pulmonary and Critical Care Medicine, Mayo Clinic College of Medicine, Rochester, MN looked into the issue with regression analyses of about 25,00 patients. They divided intensivits' patients load into 4 groups:

1:7.5,
1:9.5,
1:12, and
1:15

They found that the ICU period with one intensivist for 15 beds had a longer adjusted ICU LOS (length of stay). Although the ICU period with an intensivist-to-bed ratio of 1:7.5 had the shortest ICU LOS ratio, the difference was not statistically significant compared to the periods with intensivist-to-ICU bed ratios of 1:9.5 or 1:12.

This is the only study of its kind from single institution but it appears that optimum number of patients, intensivist should carry to produce maximum outcome is around 12 or less.

It is all good work of intensivists' that observed ICU mortality did not differ significantly in any group despite progressive increase of load of work.

Reference: click to get article/abstract
Intensivist-to-Bed Ratio - Association With Outcomes in the Medical ICU - chest. 2005;128:567-572.

2006-07-15T05:56:00.000-06:00

Saturday July 15, 2006

Case: 32 year old male with history of HIV presented to ED with complaint of upper quadrant pain. Initial lab shows elevated LFT and severe acidosis with bicarb of 8 in initial chemistry. You quickly start working through your mnemonic of increased anion gap acidosis - "CAT MUD PILES" !! *. Lactic acid level reported 9.4 mg/dl. CT scan of abdomen done to rule out ischemic colitis but showed only hepatic steatosis. Patient clinically does not appears toxic or septic though you started him on IV fluid and prophylactic antibiotics. Pt. is ruled out for DKA and other causes of acidosis also. What is the probable source of his severe lactic acidosis ?

Answer: Cause is patient's HIV medicines (HAART - Highly Active Anti-Retroviral Therapy), mostly likely the nucleoside reverse-transcriptase inhibitors (NRTIs), - stavudine. NRTIs can cause hyperlactatemia by disrupting the function of the mitochondria. This is known as mitochondrial toxicity. NRTIs also cause fatty liver (hepatic steatosis), may be acute liver failure, and inefficient liver cannot metabolize lactic acid quickly resulting in severe hyperlactatemia.

This week The New England Journal of Medicine has posted a free article Intensive Care of Patients with HIV Infection (N Engl J Med 2006; 355:173-181, Jul 13, 2006).

* The mnemonic "CAT MUD PILES" is a easy way to remember the differential for an increased anion gap acidosis

Carbon monoxide, Cyanide,
Alcoholic ketoacidosis,
Toluene,

Methanol,
Uremia,
Diabetic ketoacidosis,

Paraldehyde, Phenformin,
Iron, Isoniazid,
Lactic acidosis,
Ethylene glycol,
Salicylates.

SC CVC in IJ

2006-07-14T07:49:00.000-06:00

Friday July 14, 2006
If SC central line ends up in IJ vein ?

It is always a possibility that central venous catheter placed in subclavian (SC) vein may take path upward and travel in internal jugular (IJ) vein. Incidence is about 5.4% and does not vary with side of insertion or with the head position during the procedure 1.

First 2 preventive measures,

1) One study clearly showed that if you direct 'tip of J-wire' caudally, the relative risk for cannulating the ipsilateral internal jugular vein is low 2.

OR

2) After cannulating subclavian vein, apply little pressure at ipsilateral IJ vein while passing wire. If wire stop threading or resistance felt, it means you need to pull back wire for few centimeters (making sure you don't loose vein cannulation) and thread again.

Alternatively, after you place subclavian catheter, before applying sutures there are 2 ways to make sure you are not in IJ vein.

1) Hook central line to central venous pressure (CVP) measurement. Apply firm pressure over the ipsilateral IJ vein in the supraclavicular region for approximately 10 seconds. Quick change in transducer pressure and waveform, like CVP increased by 5 mm Hg (fictitious rise in CVP) or flattening of waveforms indicates jugular misplacement of the catheter tip. Its called Internal Jugular Vein Occlusion Test 3.

OR

2) Flush about 3 -5 cc of saline and put your sthethoscope or even finger on ipsilateral IJ vein to hear or feel the bruit/flow.

In case, you don't do above maneuvers while inserting SC central line and CXR shows IJ placement, pull central venous cather back upto 4-5 cm from punture point and try above maneuvers. Another trick you can apply in case you have to pull back catheter and pass over J-wire again - thread J-wire only partially till you are sure you are in vein, pull back catheter completely (preferably use new catheter to avoid risk of infection) , slightly curve the tip of catheter downwards (like S tip PA-catheters) and pass with little twist.

References: Click to get abstract/article

1. Misplacement of subclavian venous Catheters: Importance of head position and choice of puncture site. BJA1990; 64: 632-33
2. Direction of the J-tip of the guidewire, in Seldinger technique, is a significant factor in misplacement of Subclavian vein catheter: A randomized, controlled study - Anesth Analg 2005;100:21-24
3. Internal Jugular Vein Occlusion Test For Rapid Detection Of Misplaced Subclavian Vein Catheter - The Internet Journal of Anesthesiology. 2005. Volume 9 Number 1

2006-07-13T06:53:00.000-06:00

Thursday July 13, 2006

Case: 54 year old male with history of alcoholic cirrhosis, brought to ED after fall and found to have intracranial bleed. INR noted to be 1.5. Neurology service wrote for FFP (fresh frozen plasma) and IV Vitamin K. Patient admitted to ICU after neurosurgery decided to go conservative route. At admission patient mental status seems appropriate but 2 hours after admission you have been called as patient noted to have seizures by bedside staff. On arrival you noticed patient having generalized muscular contractions but he respond appropriately to your questions.

Probable etiology is: Hypocalcemia induced by citrate present in FFP.

Citrate is usually used in blood products as anticoagulant. It binds to free calcium to form soluble calcium citrate, thereby lowering the free (ionized) but not the total serum calcium concentration. It is important to check the ionized calcium instead of total serum calcium. The slower infusion rate has shown significantly less reduction in ionized calcium than did the higher infusion rates.

Prophylactic calcium infusion is not recommended with each blood product transfusion unless clinically indicated. Citrate is normally rapidly excreted by the liver and transient hypocalcemia is not necessary to treat. However, when a patient receives more than 1 unit of erythrocytes/blood product every 5 minutes or the capacity of the liver to metabolize citrate effectively is exceeded (like in our patient above with cirrhosis), the associated hypocalcemia can cause depressed ventricular contractility and decreased peripheral vascular resistance, causing arrhythmias, hypotension and neurologic symptoms of tetany.

Remember: In addition to calcium, citrate binds to magnesium, which can result in clinically important hypomagnesemia too.

2006-07-12T06:49:00.000-06:00

Wednesday July 12, 2006

Case: 47 year old morbidly obese female with baseline history of COPD, successfully extubated post-op and admitted to ICU for overnight observation after gastric bypass surgery. Patient appears more lethargic in late evening and ABG was drawn which showed PH of 7.20, PO2 of 59 and PCO2 of 98 (pt's baseline PCO2 is around 55). You ordered nebulizer treatments and applied full face mask's noninvasive positive pressure ventilation (BiPAP) with setting of 10/5 (IPAP of 10 cm H2O and EPAP of 5 cm H20) and ordered ABG after one hour. Followup ABG is PH of 7.24, PO2 of 72 and PCO2 of 86. Patient is still lethargic.Your next step would be:

A) Increase IPAP with followup ABG in 1-2 hours

B) Change to nasal mask with followup ABG in 1-2 hours

C) Intubate patient

D) Continue present settings with followup ABGin 1-2 hours

Answer: C

Noninvasive positive pressure ventilation (BiPAP) should be use with caution in fresh gastric bypass patients and there should be a low threshold to intubate if situation arise. BiPAP pumps air into the small gastric pouch and can lead to complications like breakdown of suture lines, bowel perforation and gastric distension. Though one small study of 27 patients didn't show either any complication or advantage of BiPAP in the first 24 postoperative hours of severely obese patients with comorbid illnesses who have undergone elective gastric bypass 1 but there are case reports in literature showing potential complication and geniune concern for use of of bi-level positive airway pressure after gastric bypass surgery 2.

Reference: click to get abstract/article
1.The effect of bi-level positive airway pressure on postoperative pulmonary function following gastric surgery for obesity - Respiratory Medicine Volume 96, Issue 9, September 2002, Pages 672-676
2. A potential complication of bi-level positive airway pressure after gastric bypass surgery - Obes Surg. 2004 Feb;14(2):282-4.

2006-07-11T18:24:00.000-06:00

Tuesday July 11, 2006
Paracentesis with seldinger technique / with central venous catheter kit

During paracentesis regular single, double or triple lumen central venous catheter may provide some benefits over angiocath (catheter over needle). Using regular central venous catheter kit's needle, advance till you get ascitic fluid. Now pass J-wire through needle upto appropriate length ------->remove the needle ----> advance your catheter over wire -----> remove the wire ----> if you don't see fluid, slowly pull back the catheter till you get flow. Advantages of this technique:

1) This is relatively safe as paracentesis needle in available kits are usually long and may carry risk of trauma if you keep advancing at non-ascitic area. (In commercial kits, usual length of catheter and needle is about 19 cm/ 7.5 inches).

2) While advancing catheter away from needle, it may get kinked. Catheter getting advanced over wire is unlikely to get kinked.

3) Use catheter from original kit as it may provide advantage of bigger diameter but in large fluid removal you may use tripple lumen catheter and leave it lock like regular central line for 4/5 days to drain required fluid everyday.

4) Multiple ports may allow you to drain in 2/3 bags/bottles simultaneously.

Editors' note: Contributor of this peal is a practicing intensivist but request to hold his and institution's name. We often post bedside tips which are fully anecdotal and individual's idea and may not be evidence based. Use it per your discretion.

2006-07-10T20:49:00.000-06:00

Monday July 10, 2006

Q; How much intavenous albumin should be given to patient while removing ascitic fluid via paracentesis?

A; Per 2004 guidelines published in Hepatology 2004 Mar;39(3):841-56, for management of adult patients with ascites due to cirrhosis by Practice Guidelines Committee, American Association for the Study of Liver Diseases (AASLD),

"Post-paracentesis albumin infusion may not be necessary for a single paracentesis of less than 4 to 5 L. For large-volume paracenteses, an albumin infusion of 8 to 10 g per liter of fluid removed can be considered". (Grade II-2 evidence - Cohort or case-control analytic studies).

Read full guidelines here

2006-07-09T09:24:00.000-06:00

Sunday July 9, 2006
NAVEL

“NAVEL" is a mnemonic for position of the structures at the inguinal ligament, from lateral to medial. It is always helpful to stand beside patient before attempting femoral central line and say NAVEL and try to feel femoral artery and visualize femoral vein before putting needle. Again!, at the inguinal ligament, from lateral to medial

Femoral Nerve
Femoral Artery
Femoral Vein
Empty space
Lymphatics

2006-07-08T20:27:00.000-06:00

Saturday July 8, 2006

Q: 21 year old male presented to ER with chest pain. CXR showed small spontaneous pneumothorax with less than 3 cm from apex to cupola. Saturation is 99% on room-air. Management is ?

A) Observation

B) Observation with oxygen

C) Aspiration of the pneumothorax

D) Aspiration of the pneumothorax with application of Heimlich valve or a water seal device

E) Chest tube to suction

Ans. is B (or A)

Clinically stable patient with small primary pneumothorax with less than 3 cm from apex to cupola, should be observed. There is some evidence available that administration of oxygen may speed up resolution of the pneumothorax (exercise caution in patients with COPD).

Read 2 guidelines for management of spontaneous pneumothorax:

1) An American College of Chest Physicians Delphi Consensus Statement Chest. 2001;119:590-602
2) BTS guidelines for the management of spontaneous pneumothorax Thorax 2003;58:ii39

2006-07-07T19:50:00.000-06:00

Friday July 7, 2006

Q: Which antibiotic interferes with the measurement of serum creatinine and cause "pseudo-acute renal failure" ?

Ans: Cefoxitin: Cefoxitin effects routine measurement of serum creatinine, resulting in falsely elevated levels of renal function. Cefoxitin is a second generation wide spectrum cephalosporin. Other medications which can interfere includes methyldopa and levodopa.

2006-07-06T20:55:00.000-06:00

Thursday, July 6, 2006

Case: 54 year old essentially healthy female admitted to floor with abdominal pain, and found to have only constipation as all major workup reported negative. Primary care physician wrote for fleet enemas till constipation get resolved. You have been called as patient was found in bed having "seizure like symptoms"(which you later diagnosed as tetany). On arrival, you found monitor showing arrhythmias and systolic BP in 70s. You asked for STAT labs, started IVF bolus and pressor. Lab shows phophate level of 12 mg/dl (3.87 mmol/L), magnesium of 0.8 meq/L (0.4 mmol/L) and calcium of 4.5 meq/L (2.25 mmol/L)and Cr of 2.4 mg/dl (pt. had normal kidney function on admission). Patient recovered as electrolytes were replaced and kidney function recovered with hemodynamic support.

Ans: Enema induced hyperphosphatemia

The Fleet enema contains 19 g of monobasic sodium phosphate and 7 g of dibasic sodium phosphate per 118 mL of fluid. If series of enemas given, inorganic phosphate salts can readily get absorbed from the gastrointestinal tract and can cause hyperphosphatemia even in patients with normal kidneys. Severe hyperphosphatemia results in acute hypocalcemia and hypomagnesemia. Tetany, seizures, bradycardia prolonged QT interval, dysrhythmias, coma, and cardiac arrest are the possible consequences. Treatment is supportive and replacement of electrolytes. Dialysis may be needed if other measures fail.

2006-07-05T20:11:00.001-06:00

Wednesday, July 5, 2006
SPECT as a 'gold standard' to determine Brain Death ?

Angiography has been considered the gold standard for diagnosis of Brain Death for decades. With arrival of new technologies, we try to move more and more towards non-invasive procedures.

Dr. Munari from Italy looked into 20 clinically brain dead patients. ( 99mTc-HMPAO) SPECT and four-vessel angiography were performed in the same session, with no time delay in between. Then, the results of SPECT and angiography were interpreted separately by a specialist in nuclear medicine and a neuroradiologist, respectively; both of them were blind to the results of the other investigation. Both angiography and SPECT confirmed BD in 19 of 20 patients: angiography showed the absence of filling of intracranial arteries, while SPECT showed a picture of empty skull. For one patient, angiography showed slight and late filling of vessels while SPECT showed faint traces of uptake.For this patient, the tests were repeated 48 hrs later, and both showed the arrest of intracranial circulation, thus confirming brain death.

SPECT = Single Photon Emission Computed Tomography

It was concluded by the authors that: SPECT is a good candidate for the gold standard of diagnosis as:
It is noninvasive and, therefore, free from complications and can be repeated for patients who are not brain dead with no harm;
It shows a clear-cut picture of empty skull, an image that can be easily understood by physicians and even by patient's relatives;
It fully fits the definition of whole Brain death, showing the absence of whole brain perfusion, down to the foramen magnum.

See interesting Power point presentation on

Brain Death: The Neurologist's Perspective from Stephen T. Mernoff, MD, Clinical Assistant Professor of Neurology, Brown Medical School. Also see our neurology section for various related topics as
Brain death determination (Source MGH stroke service)
Pre-Apnea test checklist (sample from virginia.edu)
Post-Apnea test checklist (sample from virginia.edu)

References: click to get abstract/article

1. Confirmatory tests in the diagnosis of brain death: Comparison between SPECT and contrast angiography - Critical Care Medicine. 33(9):2068-2073, September 2005

2006-07-04T09:28:00.000-06:00

Happy Birthday America
How many attempts to intubate?

Its hard to give up procedure if you are failing it !!. For intubation, ASA (American Society of Anesthesiologists) recommends to limit laryngoscopic attempts to three. Dr. Thomas C. Mort from Hartford Hospital, CT entered 2833 Critically-ill patients, suffering from cardiovascular, pulmonary, metabolic, neurologic, or trauma-related deterioration into an emergency intubation quality improvement database. Data confirmed that the number of laryngoscopic attempts were directly proportional with the incidence of airway and hemodynamic adverse events (more than 2 attempts).
incidence of hypoxemia went from 11.8% to 70%,
incidence of regurgitation of gastric contents went from 1.9% to 22%,
incidence of aspiration of gastric contents went from 0.8% to 13%,
incidence of bradycardia went from 1.6% to 21%, and
incidence of cardiac arrest went from 0.7% to 11%

Call for help !! and remember, to limit intubation attempts to 3, unless untill you are trained to deal with 'difficult intubations'.

References: click to get abstract/article

1. Emergency tracheal intubation: complications associated with repeated laryngoscopic attempts - Anesth Analg 2004;99:607-613

2006-07-03T15:00:00.000-06:00

Monday July 3, 2006
Simplify D-dimer

D-dimer has great negative predictive value in excluding pulmonary embolism (PE) or deep vein thrombosis (DVT). So far we had to send blood for laboratory-based quantitative D-dimer.

Simplify D-dimer is a new version of test which can be performed at bedside quickly and can provide instant clue 1. Check here to see details on test, that can be performed with a drop of blood at bedside.

Recently in chest, Dr. Kline and coll. from Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC reported that the posttest prevalence of PE among low-risk patients with negative d-dimer results by simplify D-dimer Assay was only 0.7% 2, supplementing the previous famous study on d-dimer by Dr. Wells 3.

Related previous pearls:
Wells Score of DVT ,
What if even thrombolysis fails in massive PE ?

References: click to get abstract/article

1. A new rapid bedside assay for D-dimer measurement (Simplify D-dimer) in the diagnostic work-up for deep vein thrombosis - J Thromb Haemost. 2003 Dec;1(12):2681-3.

2. Prospective Study of the Diagnostic Accuracy of the Simplify D-dimer Assay for Pulmonary Embolism in Emergency Department Patients Chest. 2006;129:1417-1423.)

3. Excluding Pulmonary Embolism at the Bedside without Diagnostic Imaging: Management of Patients with Suspected Pulmonary Embolism Presenting to the Emergency Department by Using a Simple Clinical Model and D-dimer - 17 July 2001 Volume 135 Issue 2 Pages 98-107, Annals

BNP

2006-07-02T18:50:00.000-06:00

Sunday July 2, 2006
So what is the cut off of BNP ?

When the landmark article on BNP published in The New England Journal of Medicine in July 2002 1, the cutoff point in establishing or excluding the diagnosis of congestive heart failure in patients with acute dyspnea was given at 100 pg per milliliter. But over time we learned that this level probably carries more negative predictive value and there may be a huge gray zone before a definite high BNP value, atleast in critical care setting. This month in Critical Care Medicine 2, Dr. Rana and coll. from Mayo Clinic College of Medicine, Rochester, MN looked into this gray zone. Their conclusion:

"When measured early after the onset of acute pulmonary edema, a BNP level of less than 250 pg/mL supports the diagnosis of acute lung injury. The high rate of cardiac and renal dysfunction in critically ill patients limits the discriminative role of BNP. No level of BNP could completely exclude cardiac dysfunction".

The median time from the onset of pulmonary edema to BNP testing was 3 hrs.

Other interesting findings in the study:

* The predictive value of BNP in the differentiation between ALI and cardiogenic pulmonary edema was comparable with PAOP (when measured) and superior to troponin and echocardiographic determination of ejection fraction. (Not supported by other studies - see related peal below).

*The accuracy of BNP improved if pts with renal failure were excluded.

* BNP levels of more than 950 pg/dL suggest congestive heart failure and BNP levels of less than 250 suggest ALI, the values in between have no diagnostic value.

Related previous pearls:

References: click to get abstract/article
1. Rapid Measurement of B-Type Natriuretic Peptide in the Emergency Diagnosis of Heart Failure - July 18, 2002,N Engl J Med 2002; 347:161-167, Jul 18, 2002
2. B-type natriuretic peptide in the assessment of acute lung injury and cardiogenic pulmonary edema - Critical Care Medicine. 34(7):1941-1946, July 2006.

2006-07-01T08:44:00.000-06:00

Elevation of the head of the bed- 30 or 45 degrees ?

Answer is probably 45 degrees.Elevation of the head of the bed is a must thing in ICU, unless some contra-indication. It is an essential part of VAP (ventilator associated pneumonia) bundle. But there is some debate about the extent of elevation need to be done. Accepted level is atleast 30 degrees but many guidelines wrote for 45 degrees. IHI recommends elevation anywhere from 30 to 45 degrees 3.

Study from The Netherlands 1 compared 109 patients in the supine group to 112 in the semirecumbent group. Target for semirecumbent group was 45 degrees but the targeted backrest elevation of 45° for semirecumbent positioning was not reached, so supine position (10°) was compared with achieved semirecumbent positioning (28°). Elevation of head of bed to 28° did not prevent the development of VAP.

7 years back Drakulovic and coll. published their landmark study in lancet showing 83% decrease of bacteriologically confirmed VAP in a group of patients treated in a semirecumbent position of 45° 2.

So the answer is probably 45 degrees or to be diplomatically right - atleast more than 30 degrees.

But is it easy to do and keep head of bed elevated to 45 degrees in practical world ?. The study group found that despite the presence of dedicated research nurses to control and maintain patient positioning, the semirecumbent treatment position with an aimed backrest elevation of 45° is not feasible for mechanically ventilated patients.

Another interesting question raised in discussion of first study: Is semirecumbent positioning itself a risk for VAP ? !!!, as pooling of colonized oropharyngeal fluids above the inflated cuff of the endotracheal tube is common in mechanically ventilated patients and it is possible that the semirecumbent position (and all movements to keep it) stimulates leakage of oropharyngeal fluid by means of gravity. Whether ETT with continuous aspiration of subglottic secretions (CASS) will be more effective than semirecumbent positioning?

References: Click to get article/abstract
1. Feasibility and effects of the semirecumbent position to prevent ventilator-associated pneumonia: A randomized study - Critical Care Medicine. 34(2):396-402, February 2006.
2. Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomised trial - Lancet.1999 Nov 27;354(9193):1851-8.
3. Elevation of the Head of the Bed - Institute for Healthcare Improvement

2006-06-30T07:57:00.000-06:00

Friday June 30, 2006
Double the dose of mucomyst ?

A noteworthy study came out yesterday in The New England Journal of Medicine1 regarding protective effect of N-Acetylcysteine in Contrast-Induced Nephropathy in primary angioplasty. When the cumulative dose of N-Acetylcysteine was doubled from 3000 mg (a 600mg IV bolus before angioplasty followed by 600 mg orally twice daily for the 48 hours after angioplasty) to 6000 mg (a 1200 mg IV bolus followed by 1200 mg orally twice daily for the 48 hours after intervention), it showed

significant decrease in increase of serum creatinine concentration (15 percent vs 8 percent)
overall decrease in in-hospital mortality in patients with contrast induced nephropathy (4 percent vs 3 percent).
When the combined end point of death, acute renal failure requiring temporary renal replacement therapy, or the need for ventilator during the acute phase of myocardial infarction was considered, the rate was 7% in the standard dose group, and 5% in the high dose group.

In study there were 3 groups - placebo, standard dose and double dose.

It appears that, the benefit of high-dose N-acetylcysteine is greater in patients receiving a larger or more than regular volume of contrast.

Conclusion: N-acetylcysteine reduced the severity of contrast medium induced nephropathy in patients with acute myocardial infarction treated with primary angioplasty. The effect appears to be dose dependent and is accompanied by a significantly improved in-hospital outcome.

Related previous pearls:
Contrast induced Nephropathy and
Preventing contrast-Induced Nephropathy

Reference: Click to get article/abstract
1. N-Acetylcysteine and Contrast-Induced Nephropathy in Primary Angioplasty - Volume 354:2773-2782, Number 26, June 29 2006
2. Contrast Nephropathy Prevention With N-Acetylcysteine in Acute Myocardial Infarction - clinicaltrials.gov

2006-06-29T18:03:00.000-06:00

Thursday June 29, 2006
ICU Index Spider Diagram

The Society of Critical Care Medicine’s (SCCM) Coalition for Critical Care Excellence (CCCE) has developed The ICU Index™ (click to get more details) as a measurement tool that can be used at the individual ICU level to baseline a series of performance variables and then track progress. It look into 16 important measures and can either be approached in a regular bar chart form or as a spider diagram.

Goal is to move the said measure as much as possible inside the spider to central target. Comparing spider diagrams every few months can tell improvements in ICU in just one glance. See the diagram above. You may wish to change, add, substract measures like you can track VAP rate, LOS etc as per your local ICU need.

If you would like more information, or would like to participate in the pilot project, please email ICUIndex@sccm.org.

Diagnostic criteria of Delirium

2006-06-28T14:40:00.000-06:00

Wednesday June 28, 2006
Diagnostic criteria of Delirium

Q: What are 4 basic criteria to label patient as having Delirium?

A: Per American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders. 4th ed. (DSM-IV), Patient is having delirium if

1. Disturbance of consciousness (eg, reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention.
2. A change in cognition such as memory deficit, disorientation, language disturbance (or the development of a perceptual disturbance that is not better accounted for by a preexisting, established, or evolving dementia).
3. The disturbance develops over a short period of time (usually hours) and tends to fluctuate during the course of the day.

4. Disturbance caused by a general medical condition or substance intoxication or medication use.

Related website:

www.icudelirium.org (must see for intensivists)

Related previous pearls:
Zolpidem-Induced Delirium ,
SEROTONIN SYNDROME ,
Amiodarone Neurotoxicity

References: click to get abstract/article

1. An Empirical Study of Different Diagnostic Criteria for Delirium Among Elderly Medical Inpatients - J Neuropsychiatry Clin Neurosci 15:200-207, May 2003
2. Delirium in Elderly Patients - Focus 3:320-332 (2005)
3. Delirium in Older Persons - N. Engl. J. Med., March 16, 2006; 354(11): 1157 - 1165
4. Delirium - emedicine.com
5. Delirium - American Family Physician® Vol. 67/No. 5 (March 1, 2003)

2006-06-27T15:22:00.000-06:00

Tuesday June 27, 2006
We will need more intensivists !!

Currently in USA, only 37% of critically ill patients are cared for by intensivists and an estimated 360,000 deaths occur each year in ICUs not managed by intensivists. In 2003, the US Senate asked Health Resources and Services Administration (HRSA) to work with the American College of Chest Physicians (ACCP) to update critical care workforce models in order to more accurately assess the adequacy of supply for critical care physicians. In the newly released US Department of Health and Human Services Report to Congress: The Critical Care Workforce: A Study of the Supply and Demand for Critical Care Physicians, it has been predicted that the demand for critical care services will increase rapidly, while the intensivist supply would not be able to care for a greater proportion of critically ill patients. The shortage is will be exacerbated by the year 2020 due to the aging population and the increased utilization of intensivists.

By 2020, the demand for intensivists would likely increase by 129 percent above the current supply.

Some Suggestions include:
Increase role of eICU
Possible rationing of critical care services or regionalization of ICU services like trauma system
Restructuring current Medicare reimbursement system
Expanding National Health Services Corps and J-1 waiver program
Only deserving patients getting admission to ICU
Decreasing care for know futile outcomes by more public/physician education

Read full report: HRSA Report to Congress. The Critical Care Workforce: A Study of the Supply and Demand for Critical Care Physicians

2006-06-26T20:29:00.000-06:00

Monday June 26, 2006
Thrombelastography - TEG

TEG was first introduced about 60 years ago by Hartert . TEG monitors hemostasis as a whole dynamic process and measures the viscoelastic properties of blood. The strength of a clot is graphically represented over time in a cigar shape figure. With little practice, just a glance at shape and size of cigar, it provides clue to underlying disease process. It is an underutilized tool in ICU. See picture for self explanation:

Read review on Thromboelastography/thromboelastometry here (pdf file) (ref: Clin. Lab. Haem. 2005, 27, 81–90)

2006-06-25T13:12:00.000-06:00

Sunday June 25, 2006
Introducing iCritical Care Podcasts

www.sccm.org/podcast

iCritical Care Podcasts from Society of Critical Care Medicine is a kind of radio which you can listen on your home computer, or your portable media player (iPod and others). The iCritical Care Podcast is a novel way for you to keep up-to-date with the latest in Critical Care. Site get frequently updated with talks on recent breakthrough articles carrying interviews with authors of these articles as well as talks on non-academic but critical care related issues. So far upto 34 talks have been added including but not limited to:
Lorazepam vs. Propofol
Catheter-Related Bloodstream Infections
Prophylactic Antimicrobial Use in the ICU
Hospital Mortality Assessment
Rationing in the ICU
Morbid Obesity and the Surgical Critical Patient
Dopamine's Influence on the Outcome of Shock
Defining and Treating Abdominal Compartment Syndrome
Early Indicators of Sepsis Survival
Getting Our ICU Language Straight
Critical Care Pharmacists
Implementing the Surviving Sepsis Campaign

Host is Richard H. Savel, MD, Associate Director, Surgical Intensive Care Unit at Maimonides Medical Center, Brooklyn, NY, and Assistant Professor of Medicine at Mt. Sinai School of Medicine, NY.

Again site is www.sccm.org/podcast

Related previous themes:
Introducing Resident ICU Course and
PACT - Critical Care distant learning course

fenoldopam

2006-06-24T07:56:00.000-06:00

Saturday June 24, 2006

Case: 39 year old male admitted with hypertensive emergency after he ran out of his prescriptions. "ED Doc" started patient on IV cardene (nicardipine) drip and resumed patient's home med for BP which consist of Toprol (metoprolol) XL - first dose given in ER. On review of CXR you noticed some pulmonary edema and decide to switch to Fenoldopam to get dual effect of lowering BP as well as dopaminergic effect to resolve pulmonary edema. Patient dropped his BP precipitously and coded.

Probable cause: It is not advisable to start fenoldopam on patients with B-blocker or atleast close caution should be maintained. Concomitant use of beta-blockers in conjunction with fenoldopam may cause life threatening hypotension from beta-blocker's inhibition of the sympathetic reflex response to fenoldopam 1.

Related previous pearl: Renal dose Fenoldopam ?

References: click to get abstract/article1. Corlopam - fda.gov

2. Fenoldopam — A Selective Peripheral Dopamine-Receptor Agonist for the Treatment of Severe Hypertension - Volume 345:1548-1557, Number 21, Nov. 22,2001

2006-06-23T15:30:00.000-06:00

Friday June 23, 2006

Case: 24 year old male admitted with left thigh cellulitis and abcess. I and D was performed and cefazolin (ancef) was initiated. Patient did not respond to cefazolin and antibiotic was changed to vancomycin after availability of sensitivity from micro lab. Patient showed marked improvement over next 3 days except patient complaint of new rash on his body which you attributed to "Red man syndrome" and wrote an order to infuse vancomycin slowly and with increase dilution. Next day, as you reached hospital, you were informed by outgoing intensivist that patient deteriorated overnight and required intubation. You were baffled and as you examine the patient, you find extensive dermal exfoliation along with axillary and inguinal lymphadenopathy. On lab, LDH and liver enzymes were markedly elevated and kidney funtion deteriorated from normal to anuria. CBC showed eosinophilia.

Vancomycin-induced Stevens-Johnson syndrome

Stevens-Johnson syndrome is an acute mucocutaneous process characterized by severe exfoliative dermatitis and mucosal involvement of the gastrointestinal tract and conjunctiva. Pathogenesis is unclear, but an immunological mechanism, probably cell-mediated, has been suggested. Clinical diagnosis of Stevens-Johnson syndrome is based on the presence of "target" or "iris" lesions involving the skin and erosive lesions of two or more mucosal surfaces. Associated findings include extensive dermal exfoliation, nephritis, lymphadenopathy, hepatitis, and multiple serologic abnormalities. Vancomycin, a glycopeptide antibiotic, has case reports in literature produceing immunologically mediated adverse reactions such as interstitial nephritis, linear IgA bullous dermatosis, exfoliative erythroderma, necrotizing cutaneous vasculitis and toxic epidermal necrolysis. The treatment consists of cessation of vancomycin and administration of antihistamine and/or steroid.

See pic here

References: click to get abstract/article

1.Vancomycin-induced Stevens-Johnson syndrome Allergy Asthma Proc. 1996 Mar-Apr;17(2):75-8.

2.Stevens-Johnson-type reaction with vancomycin treatment. - Ann Pharmacother. 1992 Dec;26(12):1520-1

3 Uncommon Vancomycin-Induced Side Effects - Brazilian Journal of Infectious Diseases - 2002;6(4):196-200

2006-06-22T16:29:00.000-06:00

Thursday June 22, 2006
Imipenem and Primaxin

Q: What advantage we have when we add cilastatin with Impenem ?

OR in other words, What is the difference between Imipenem and Primaxin (Imipenem plus Cilastatin) ?

A: Imipenem get metabolized in the kidneys by enzyme called dehydropeptidase I and cannot achive therapeutic level in urine. Addition of Cilastatin inhibit the enzyme in kidney's renal tubules so that when imipenem and cilastatin are given concomitantly, increased imipenem levels are achieved in the urine.

Bonus Pearl: Primaxin is hemodialyzable so dose may be unreliable in such patients or preferably should be given after hemodialysis session. Dose in dialysis dependent patient is either 250 mg q 12 hrs or 500 mg after each dialysis.

When Imipenem was introduced, it get reputed with nick name of "Jesus water" due to its broad coverage and to kill most bugs.

2006-06-20T22:06:00.000-06:00

Wednesday June 21, 2006
Normosol is NOT just Normal Saline

Being an intensivist, the most important thing to know - what is infusing in patient. There is some misconception that Normosol is just another name of Normal Saline, which is not true.

Contents of Normal Saline:

Na = 154 mEq/L
Cl = 154 mEq/L
PH = 5.4

Contents of Normosol:

Na = 140 mEq/L
Cl = 98 mEq/L
K = 4 mEq/L
Mg = 3 mEq/L
Acetate = 27 mEq/LGluconate = 23 mEq/L
PH =6.6

Normosol contains added K and Mg which may be unsuitable for some patients like patients with renal failure.

Bonus Pearl: If it says R on IVF bag, it means manufacturer recommends bag for replacement therapy and if it says M on IVF bag , it is meant for maintenance IV. Contents may be little different. Most "M" bags contain extra dextrose.

Related Previous Pearl: Difference between LR and Normal Saline

Labetolol dose

2006-06-20T17:14:00.000-06:00

Tuesday June 20, 2006

Labetolol dose

Q: What is the usual guided dose of labetalol in hypertensive emergency ?

A; Loading dose of 0.25 mg/kg followed by 0.5 mg/kg every 15 minutes but total dose should remain less than 3.25 mg/kg.

Advantage of Labetalol:

Action within 5 minutes and
combined alpha and beta blocker effect
Disadvantage of Labetalol:

It decreases both SVR (Systemic Vascular Resistance) and CO (Cardiac Output).

(From Dr. Joseph Varon's lecture "Hypertensive Emergencies in the Perioperative Cardiovascular Setting" at Hypertensive Crisis: Strategies To minimize End-Organ Damage With Focus On The Heart and Brain - symposium during Chest 2005)

Anemia in ICU

2006-06-19T20:19:00.000-06:00

Monday June 19, 2006
Anemia in ICU

Q: If you admit a patient with Hb of 10 g/dL and draw 100 ml of blood for various lab works. How much will be the drop in Hb ?

A; Hb will drop from 10 to 9.3 g/dL. With each 100 ml of blood draws, Hb drop by 0.7 g/dL 1. Remember ! phlebotomy (blood draws) is the major of cause anemia in ICUs.

Bonus pearl: In anemic patients, if blood workup is necessary, use pediatric tubes.

Related previous pearl: ICU anemia score

Reference: click to get abstract
Blood testing causes anemia - J Gen Intern Med 2005; 20:520–524

pre-ICU care

2006-06-19T14:48:00.000-06:00

Sunday June 18, 2006
To decrease ICU mortality - fix pre-ICU care !!

Team from Cooper University Hospital, Camden, NJ (Raquel Nahra, MD, Christa Schorr, RN and David R. Gerber, DO) - addressed a very important and often ignored issue at ACCP meeting of november 2005 : PRE–INTENSIVE CARE UNIT LENGTH OF STAY AND OUTCOME IN CRITICALLY ILL PATIENTS 1.

Patients were divided into 4 groups:

Group M1 - medical patients HLOS less than / = 5 days
Group M2 - medical patients HLOS more than / = 6 days
Group S1 - surgical patients HLOS less than / =5 but more than 1 day

Group S2 - surgical patients HLOS more than / = 6 days

*HLOS = hospital length of stay and data was obtained from the Project Impact database.

Study found that: ICU admission from a general care floor after more than / = 6 days is associated with poor outcome(Group M2). Suboptimal care prior to ICU admission is the reason for poorer outcomes. Probable reasons:
Poor organization,
Insufficient knowledge,
Failure to appreciate clinical urgency,
Inadequate supervision and
Failure to seek advice

Editors note: Lessons to be learned include intensivists' early involvement in care outside ICU, formation of rapid response team, close working of floor team (hospitalist) and intensivist and more inservices/training for floor staff.

Related previous pearl: Rapid Response Team
Related Sites: IHI's RRT - getting started kit and SCCM's RRT/ MET forum

Reference: click to get abstract

PRE–INTENSIVE CARE UNIT LENGTH OF STAY AND OUTCOME IN CRITICALLY ILL PATIENTS - Critical Care Outcomes, ACCP meeting November 2, 2005

EKG changes in Hyperkalemia

2006-06-17T15:51:00.000-06:00

Saturday June 17, 2006
4 EKG changes in Hyperkalemia

The first EKG sign of hyperkalemia is peaked T waves and usually appears once K level go around 6 meq/L.

Second sign is prolongation of PR interval which can be seen with K level going around or above 7 meq/L.

Absent P wave with widen QRS complex is the third manifestation and is a very dangerous sign. It means that atrial activity is lost and stage is set for ventricular tachycardia/fibrillation. It is usually seen at level around 8-9 meq/L.

Ventricular tachycardia/fibrillation is the price you pay of ignoring above changes on monitor.

Above are just rough rules of thumb. Read a good review

Recognising signs of danger: ECG changes resulting from an abnormal serum potassium concentration (source: Emerg Med J 2002; 19:74-77)

2006-06-16T15:05:00.000-06:00

Friday June 16, 2006
Carvediol (Coreg)

Q: How Carvediol (Coreg) is different from other B-blockers?

A; Coreg is a triple blocker. It blocks beta-1, beta-2 and alpha-1 receptors. Alpha-1 blockade provides vasodilation and so protection in congestive heart failure (CHF). U.S. Carvedilol Heart Failure Study with 1094 patients showed 65% lower risk of death than placebo patients 1. Dose should be started at 3.125 mg BID and titrated (as tolerated) upto 25 mg BID. Obese patients may require higher dose.

Extended release Metoprolol (Toprol XL) is another B-blocker approved from FDA for use in CHF. MERIT-HF study showed 34% reduction in mortality than placebo in patients taking Toprol XL 2.

FDA approves only Toprol-XL and Coreg for CHF.

References: Click to get article/abstract

1. The Effect of Carvedilol on Morbidity and Mortality in Patients with Chronic Heart Failure - N Engl J Med. 1996;334:1349-1355.

2. MERIT-HF Study Group. Effect of metoprolol CR/XL in chronic heart failure: metoprolol CR/XL randomised intervention trial in congestive heart failure. Lancet. 1999;353:2001-2007

IV Dig

2006-06-15T08:19:00.000-06:00

Thursday June 15, 2006
IV Digoxin

Q: You wrote an order: Digoxin 0.25 mg IV x 1.
What is missing in this order?

A; Rate: Digoxin IV should be given over at least 5 minutes. Rapid infusion of Digoxin (digitalis) may cause coronary arteriolar constriction, which may induce cardiac ischemia or make it worse. Also, it is not advisable to administer digoxin simultaneously in the same intravenous line as with other drip/drug, if possible. Another important reminder - Digoxin level should be measured just before the next scheduled dose (trough) or at least 6 to 8 hours after the last dose, to allow adequate time for equilibration of digoxin between serum and tissue.

Related previous pearl: Why sometime IV vasotec (enalapril) does not work?

2006-06-14T08:58:00.000-06:00

Wednesday June 14, 2006
Swan is still very in !!

Lately we had some constant negative studies for pulmonary artery catheter like ESCAPE trial, PAC-MAN study and recently published ARDSnet's FACTT trial 2.

This month Critical Care Medicine published retrospective database analysis of 53,312 trauma patients 1. After all adjustments following groups showed benefit:

Patients aged 61-90 yrs,
with arrival base deficit worse than -11 and
Injury Severity Score of 25-75.

It was found that it was associated with a protective effect in patients with severe shock, regardless of age, and in older patients with moderate shock.

Also note negative outcome: Highest risk of death associated with PAC use was in younger patients who arrived at the ED without a significant base deficit. Moreover, no survival benefit was detected with PAC use in patients arriving at the ED without evidence of shock.

Conclusion: PAC insertion is associated with

improved outcome in critically injured patients with severe shock at admission, regardless of age, and
in elderly patients with moderate shock.

Related previous pearls: PAC-MAN study ! and ESCAPE Trial

Reference: Click to get article

1. Pulmonary artery catheter use is associated with reduced mortality in severely injured patients: A National Trauma Data Bank analysis of 53,312 patients - Critical Care Medicine. 34(6):1597-1601, June 2006.
2. Pulmonary-Artery versus Central Venous Catheter to Guide Treatment of Acute Lung Injury - Volume 354:2213-2224, NEJM, May 25, 2006

CVP via PICC

2006-06-13T20:08:00.000-06:00

Tuesday June 13, 2006

Can we measure CVP (central venous pressure) with PICCs (peripherally inserted central catheters) ?

YES: PICC lines can be used to measure CVP, if situation arise. CVP recorded via PICC lines are about 1 mm Hg higher than CVP from centrally inserted venous catheters. PICC lines need to be hooked to continuous infusion with heparinized saline at 3 mL/hr to overcome the resistance of longer length and narrower lumen of PICC line. Trend should be followed for better perception as first PICC measured CVP is reported higher, probably due to microthrombi which get flushed later on.

Dr. Black and coll. from Pennsylvania State University College of Medicine, Hershey, PA studied 77 data pairs from 12 patients with measurements recorded at end-expiration. 19-gauge dual-lumen PICCs were used and were zeroed/levelled at right atrium. To overcome the longer length, narrower lumen an so higher inherent resistance, continuous infusion device is used with heparinized saline at 3 mL/hr (like in arterial lines) 1.

Reference: Click to get article

1. Central venous pressure measurements: Peripherally inserted catheters versus centrally inserted catheters - Critical Care Medicine. 28(12):3833-3836, December 2000.

2006-06-12T16:13:00.000-06:00

Monday June 12, 2006

While you are carrying 'code beeper' as an intensivist, you heard 'code blue in cafeteria'. On arrival you found 36 year old female who was in cafeteria after visiting allergy clinic, where according to daughter she received her 'expensive asthma shot'. While you were resuscitating patient from what appears to be anaphylactic shock, you keep wandering about that 'expensive asthma shot'.

Xolair: Omalizumab (xolair) is the subcutaneous injection treatment for allergic asthma that works by blocking immunoglobulin E (IgE). Anaphylaxis is rare but the tricky part is it may cause anaphylaxis even after months of successful and uneventful treatment. There is an indication in atleast one case report that polysorbate present in omalizumab may be responsible for it 1.

Per month cost of treatment is about 500 - 2000 US $.

Reference: Click to get article

1. Late-Onset Anaphylaxis to Omalizumab Reported - from acep.org site

IV to PO conversion

2006-06-11T14:10:00.000-06:00

Sunday June 11, 2006
IV to PO conversion - check med list everyday !!

58 year old male admitted with atrial fibrillation with RVR (rapid ventricular rate) and required intravenous (IV) Diltiazem (cardizem). Now patient is stable at 7 mg/hr dose. What would be the equivalent PO dose?

Diltiazem CD 240 mg po qd 1.

Usual IV to PO Cardizem is as follows:

3 mg/h = Diltiazem CD 120 mg po qd
5 mg/h = Diltiazem CD 180 mg po qd
7 mg/h = Diltiazem CD 240 mg po qd
11 mg/h = Diltiazem CD 300 mg po qd
15 mg/h = Diltiazem CD 360 mg po qd

Using this question as an excuse, the objective is to highlight the point that many times PO medications are as effective as IV (See reference # 1). Good intensivist always remain in the quest to simplify the medication list. It always help to have a savy critical care pharmacist in the team !.

Related: Sample INTRAVENOUS TO ORAL/ENTERAL (IV TO PO) MEDICATION SWITCH PROGRAM from American Society of Health-System Pharmacists' site

Reference: click to get abstract/article
1. Intravenous to Oral Conversion Table: source nih.gov

Feeding in ventilated patients

2006-06-10T04:58:00.000-06:00

Saturday June 10, 2006
Yes ! Feed Critically Ill Mechanically Ventilated Medical Patients early despite risk of VAP

There is some hesitancy in literature about early feeding for critically ill mechanically ventilated medical patients due to increase risk of ventilator-associated pneumonia (VAP) 1.

Dr. Artinian and coll. from Division of Pulmonary and Critical Care Medicine, Henry Ford Health System, Detroit, MI recently looked into about 4000 patients requiring mechanical ventilation for more than 2 days 2. Those patients who received enteral feeding within 48 hours of mechanical ventilation were labeled as the "early feeding group" otherwise as "late feeding group." Results showed that
The overall ICU mortality was 18.1% vs 21.4%
The overall hospital mortality was 28.7% vs 33.5%
In substudy, three separate models were done using APACHE II, simplified acute physiology score II, and mortality prediction model at time 0. In all models, early enteral feeding was associated with
an approximately 20% decrease in ICU mortality
a 25% decrease in hospital mortality
The lower mortality rates in the early feeding group were most evident in the sickest group

The truth was found that in all adjusted analysis, early feeding was found to be independently associated with an increased risk of ventilator-associated pneumonia (VAP).

Study concluded that early feeding significantly reduces ICU and hospital mortality mainly in the sickest patients and should be instituted in medical patients receiving mechanical ventilation especially in patients at high risk of death, despite being associated with an increased risk of VAP developing.

Related previous pearls:
Where is my food dude !! and Is post pyloric feeding absolute ?

Reference: click to get abstract/article
1. Early versus late enteral feeding of mechanically ventilated patients: results of a clinical trial - Journal of Parenteral and Enteral Nutrition, Vol 26, Issue 3, 174-181
2. Effects of Early Enteral Feeding on the Outcome of Critically Ill Mechanically Ventilated Medical Patients - Chest. 2006;129:960-967

2006-06-09T19:38:00.000-06:00

Friday June 9, 2006

Case: 76 year old female, admitted 3 days ago to your ICU with possible aspiration pneumonia. Review of report from nursing home also mention of increase diarrhea. You decide to add metronidazole (flagyl) and start the workup. Patient responded well to treatments and appears to be back to her baseline. You decide to keep patient overnight before transferring to floor in AM. Patient complaint of epigastric abdominal pain during night and on-call physician added pancreatic enzymes for AM and lipase is noted to be 1254 (was normal on admission). You could not find any apparent reason of acute pancreatitis. As C.diff came back negative you stopped the Flagyl and pancreatitis resolved.

Metronidazole Induced Pancreatitis: Acute pancreatitis is a potentially serious adverse effect of metronidazole. Any patient while on metronidazole develops nausea, vomitting and epigastric pain should be evaluated for acute pancreatitis. Acute pancreatitis may develop upto 5 weeks after metronidzole exposure and drug intake in previous weeks should be evaluated carefully particularly in long term care facility residents. Diagnosis can be confirmed with rechallenge with metronidazole but obviously it should be avoided. The mechanism of metronidazole-induced pancreatitis is not known but unlike many other antibiotics metronidazole penetrates well into pancreatic tissue and explains atleast part of the problem.

Reference: click to get abstract/article
1. Metronidazole Induced Pancreatitis. A Case Report and Review of Literature - JOP. J Pancreas(Online) 2004; 5(6):516-519
2. Metronidazole-associated pancreatitis - The Annals of Pharmacotherapy: Vol. 34, No. 10, pp. 1152-1155
3. Acute pancreatitis caused by metronidazole - Ned Tijdschr Geneeskd. 1996 Jan 6;140(1):37-8.

2006-06-07T22:09:00.000-06:00

Thursday June 8, 2006
What if plasma exchange is not available as treatment of TTP

Q: You just diagnosed a patient with thrombotic thrombocytopenic purpura (TTP) but you were informed by the nursing supervisor that plasma exchange with fresh frozen plasma is not available in hospital due to technical reason and it will take time before patient can be transferred to a facility where the said services are available. What would be your alternate plan to bridge that time?

A; High-dose plasma infusion with rate of 25-30 mL/kg per day. When immediate plasma exchange with fresh frozen plasma is not available, simple plasma infusion can be performed until transfer to a higher care facility is available. There is always a substanial risk of fluid overload with such high plasma infusion and you have to weigh risks and benefits of the clinical decision or to watch patient closely while plasma is infusing.

Reference: click to get abstract/article

High-dose plasma infusion versus plasma exchange as early treatment of thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome - Medicine. 82(1):27-38, January 2003.

acetazolamide for metabolic alkalosis

2006-06-07T09:26:00.000-06:00

Wednesday June 7, 2006
Dose of acetazolamide (diamox) for metabolic alkalosis

Many times we use acetazolamide for metabolic alkalosis in mechanically ventilated patients when nothing else is making it better. What dose should we use?. Mazur and coll. from Henry Ford Health System, Detroit, MI looked into 40 mechanically ventilated patients with a metabolic alkalosis (arterial pH more/= 7.48 and serum bicarbonate concentration more/= 26 mEq/L) which were resistant to other therapies such as fluid infusion or potassium therapy.

Study found that a single IV 500-mg dose of acetazolamide is as effective as multiple doses of IV 250 mg of acetazolamide.

Reference: click to get abstract/article

Single versus multiple doses of acetazolamide for metabolic alkalosis in critically ill medical patients: A randomized, double-blind trial. Critical Care Medicine. 27(7):1257-1261, July 1999.

Wells Score of DVT

2006-06-06T12:56:00.000-06:00

Tuesday June 6, 2006
Wells Score of DVT

Pulmonary embolism from deep venous thrombosis remains a leading killer. Many times intensivists are faced with the question of proceeding or not with further radiological workup. Although Wells score is not the absolute score to rule out DVT and subsequently the risk of PE (some literature argue against its validity), it still remains a strong quick tool while differential diagnosis with other conditions. It has been said that if the score of low-probability is combined with negative d-dimer, the negative predictive value is 99.5% 1. In other words, you can safely hold on further radiological workup.

3 points if objective signs like localized tenderness, asymmetric calf swelling.
1.5 points if Heart Rate more than 100 beats/min
1.5 points if bedridden for more than 3 days or major surgery within 4 weeks
1.5 points if previous 'documented' diagnosis of DVT or PE
1 point if hemoptysis
1 point if active cancer
3 points if high clinical suspicion of PE (on overall clinical and lab. findings).
0 - 2 low probability,
2-6 moderate probability,
3-6 high probability

Remember,

low-probability + negative d-dimer = -ve predictive value of not having DVT is 99.5%

Related previous pearl: What if even thrombolysis fails in massive PE ?

Reference: click to get abstract/article
Excluding Pulmonary Embolism at the Bedside without Diagnostic Imaging: Management of Patients with Suspected Pulmonary Embolism Presenting to the Emergency Department by Using a Simple Clinical Model and D-dimer Philip S. Wells and coll.,Ann Intern Med 2001;135:98-107

Four generations of Quinolones

2006-06-05T06:53:00.000-06:00

Monday June 5, 2006
Four generations of Quinolones

The classification of the fluoroquinolones on the basis of generations (imitating from cephalosporins) is not officially standardized, but it is now commonly use to classify them by their spectrum of action.

1st generation - Gram negative coverage but not pseudomonas (example: Nalidixic acid)

2nd generation - Gram negative coverage with pseudomonas and some gram postive coverage including s.aureus but not strep pneumoniae. (example: Ciprofloxacin, Ofloxacin, Norfloxacin)

3rd generation - Gram negative coverage with pseudomonas. More gram postive coverage including penicillin sensitive and resistant s. pneumoniae. (example: Levofloxacin, Sparfloxacin, Gatifloxacin (tequin), Moxifloxacin (avalox)). Avalox has been said to be the most effective in this generation.

4th generation - Same as 3rd generation but with anaerobic coverage (example: Trovafloxacin (Trovan) ).

Read comprehensive review on Quinolones (Source: Am Fam Physician 2002;65:455-64, authors: CATHERINE M. OLIPHANT, PHARM.D., University of Wyoming School of Pharmacy and GARY M. GREEN, M.D., Kaiser Permanente, California)

Quinolones in UTI

2006-06-04T01:52:00.000-06:00

Sunday June 4, 2006
Quinolones in UTI

Q; Name atleast one quinolone which should not be used for UTI in ICU ?

A: Moxifloxacin (avelox) - as it doesn't reach sufficient level in the urine. On the flip side, the advantage is that you don't need to adjust dose in renal insufficiency unlike other quinolones if use for other reasons. Similarly, Sparfloxacin (Zagam) and trovafloxacin (Trovan - almost off the market due to severe hepatic side effects) should not be used as these 3rd and 4th generation quinolones are more metabolized through liver.

Urinary tract infection (UTI) is a common and many time an isolated or accidental finding in ICU. Rememeber ! Bactrim (TMP/SMX) is still a first line, cost-effective and preferred antibiotic for uncomplicated UTIs. You should jump to quinolone only if your hospital's antibiogram shows local resistance higher than 20% or if patient is allergic to sulfas. Even in this instance nitrofurantoin is a very valid choice. If you decide to use quinolone - ciprofloxacin, ofloxacin, or norfloxacin is a better choice. Levofloxacin is also commonly prescribed but technically it is not really needed for UTI and just contribute to increase resistance in ICU by overuse.

Previous related pearls:

1. Quinolones and errant glycemic reaction

2. Epidemic of new fluoroquinolone induce strain of C. Diff.

2006-06-03T16:40:00.000-06:00

Saturday June 3, 2006

Q; Which one electrolyte you will be worried most in patients on TPN (Total Parenteral Nutrition) ?

A; Phosphate. About 33% of patients on TPN develop hypophosphatemia despite supplemented in solution. Patients who require insulin during TPN, or have a history of alcoholism, chronic weight loss, cancer and on diuretic therapy are at increased risk of hypophosphatemia, which also may manifest as "Refeeding syndrome". Serum phophate level below 1.5 mg/dl ( .5 mmol/L), can manifest symptoms of refeeding syndrome.

Read interesting editorial, Refeeding syndrome, Is underdiagnosed and undertreated, but treatable , from BMJ. ( BMJ 2004;328:908-909 )

References: click to get abstract/article

1. Refeeding syndrome: life-threatening, underdiagnosed, but treatable, QJM, April 1, 2005; 98(4): 318 - 319.

4 Ts of HIT

2006-06-02T21:59:00.000-06:00

Friday June 2, 2006
4 Ts of HIT

Continuing our theme of Heparin-Induced Thrombocytopenia (HIT) from yesterday, lets talk today about "4 Ts" of HIT.

Thrombocytopenia - more than 50% fall

Timing of platelet count fall - Days 5 to 10, or less than/= 1 day if heparin exposure within past 30 days

Thrombosis or other sequelae - Proven thrombosis, skin necrosis, or, after heparin bolus, acute systemic reaction

Other cause for thrombocytopenia - None

American Society of Hematology has developed a full HIT score which can be seen by clicking here. 1

References: click to get abstract/article

1. When Heparins Promote Thrombosis - Review of Heparin-Induced Thrombocytopenia - Circulation. 2005;111:2671-2683

2006-06-01T08:10:00.000-06:00

Thursday June 1, 2006
Argatroban Therapy in Hepatic Dysfunction

Argatroban is a second line anti-coagulation as well as remained one of the drug of choice in patients affected with Heparin-induced thrombocytopenia (HIT). Argatroban improve outcomes in patients with HIT, by reducing new thrombosis 1 . Also reported its safety with no increase risk of bleeding 2 .

Argatroban is primarily metabolized in the liver and its dosing need to be adjusted in hepatic dysfunction. Dr. Levine and coll. from Texas has reported in this month of chest after retrospectively analysing data of 82 argatroban patients and 34 historical control therapy patients with hepatic impairments (all HIT patients) 5. Their results concluded following points:

1. In hepatic impairment 0.5 µg/kg/min is a reasonable, conservative initial dosage of argatroban.

2. serum bilirubin level appears to be a better indicator than ALT or AST of argatroban dosing requirements and argatroban should be initiated at a dose of 0.5 µg/kg/min if a patient’s serum total bilirubin level is 1.5 mg/dL.

3. Conservatic dose should be the starting point if combined hepatic/renal dysfunction is present.

4. As steady-state anticoagulation will be delayed in many patients with hepatic dysfunction, check the aPTT atleast 4 to 5 h after drug initiation or dose change.

5. Argatroban should be stopped for a more extended period in hepatic dysfuntion if an invasive procedure is planned.

Related: Sample Argatroban Protocol For HIT (from The George Washington University Hospital )

References: click to get abstract/article

1. Argatroban Anticoagulation in Patients With Heparin-Induced Thrombocytopenia - Arch Intern Med. 2003;163:1849-1856
2. Argatroban Anticoagulant Therapy in Patients With Heparin-Induced Thrombocytopenia - Circulation. 2001;103:1838
3. The Pharmacokinetics and Pharmacodynamics of Argatroban: Effects of Age, Gender, and Hepatic or Renal Dysfunction - Pharmacotherapy 2000;20,318-329
4. Argatroban Dosing in Patients with Heparin-Induced Thrombocytopenia The Annals of Pharmacotherapy: Vol. 37, No. 7, pp. 970-975.
5. Argatroban Therapy in Heparin-Induced Thrombocytopenia With Hepatic Dysfunction Chest. 2006;129:1167-1175

2006-05-31T17:20:00.000-06:00

Wednesday May 31, 2006
Bedside tip ! - Tracheal Tube Tolerance

Some intubated patients wake up and cough on the tracheal tube, but may not be ready for extubation and you may be reluctant to re-sedate them. Consider a trial of intravenous Lidocaine. Administer 1 mg/Kg slowly over about two minutes. There is a good chance that the patient will experience immediate and dramatic relief from irritation caused by the tracheal tube (some may even sleep for a while). If the patient has a good response to the bolus, you may even start an intravenous infusion of Lidocaine at 2mg/ min. This can buy you the 1 – 3 hours the patient may need to be able to extubated the patient safely.

Capnography in CPR

2006-05-30T08:51:00.000-06:00

Tuesday May 30, 2006
Use of Capnography in Assessment of CPR Adequacy

Myocardial blood flow is determined by the difference between aortic diastolic and right atrial pressures. Because both aorta and atrium experience the same intrathoracic pressure change during cardiopulmonary resuscitation (CPR), myocardial blood flow is very poor during cardiac resuscitation. Even high compression forces that may generate acceptable systemic and pulmonary artery pressures yield only small coronary perfusion pressures.

The arterial blood gas values during CPR manifest complex abnormalities. The reduction in cardiac output, and thus tissue perfusion, promotes anaerobic metabolism and lactic acidosis. However, arterial blood samples reflect either a normal or low PCO2 during CPR, while venous blood gases manifest both a respiratory and metabolic acidosis.

When perfusion is absent in the presence of ventilation, the primary influence on arterial acid-base status is alveolar ventilation. Venous acidosis develops as tissue beds drain CO2 and lactate is produced by anaerobic metabolism. The PCO2 in pulmonary veins increases due to reduced pulmonary blood flow and a resulting decrease in CO2 excretion.

With effective CPR or return of spontaneous circulation, pulmonary blood flow is improved and arterial pH decreases as more of the venous acid load (CO2 and lactate) reaches the arterial side. Aerobic and anaerobic metabolism produce carbon dioxide that is transported in venous blood to the lung and eliminated from the lung by minute ventilation. End-tidal CO2 is a measure of the partial pressure of carbon dioxide at the airway opening at the end of expiration.

During cardiac arrest, the abrupt decrease in cardiac output results in reduction of carbon dioxide transport from the tissues to lung and, hence, decreased carbon dioxide. More recently, capnography has been used to determine the adequacy of cardiopulmonary resuscitation.

There are 2 good sources to understand capnography:

1. capnography.com , educational site on subject from Bhavani-Shankar Kodali MD, Department of Anesthesia, Brigham and Women's Hospital, Harvard Medical School, Boston, USA

2. See concise INTERPRETATION OF CAPNOGRAPHIC WAVEFORM
(from biotel.ws website)

Blumberg's sign

2006-05-29T13:35:00.000-06:00

Monday May 29, 2006
Blumberg's sign

Q: You received call from an old fashioned experienced ER physician to consult a patient with hypotension and positive Blumberg's sign ?

Do you know what is Blumberg's sign ?

A; Sudden release of steadily applied pressure on a suspected area of the abdomen cause sudden stab of pain - an indication of peritonitis. Yes its another name of rebound tenderness. Ideal technique requires to watch patient's face to assess severity of pain while doing above maneuver (there is an innocent tendency to watch abdomen).

Historically this maneuver was described to assess peritoneal inflammation as an early sign of appendicitis by pressing hands over McBurney's point *. Sign was first described by a german surgeon and gynaecologist, Jacob Moritz Blumberg (1873 -1955).

* McBurney's point is located one third of the distance along a line from the front of the right pelvic bone and the belly button (click to see image).

MEDiC Bill

2006-05-28T14:22:00.000-06:00

Sunday May 28, 2006
MEDiC bill

Senators Hillary Rodham Clinton and Barack Obama have coauthored the proposed MEDiC bill. (National Medical Error Disclosure and Compensation Bill).

Main ideas of the bill:

1. This legislation would create an Office of Patient Safety and Health Care Quality within the Department of Health and Human Services. The director of this office will be responsible for establishing a National Patient Safety Database, conducting data analyses to inform policy and practice recommendations, establishing and administering the National Medical Error Disclosure and Compensation (MEDiC) program, and supporting studies related to MEDiC and the medical liability system.

2. The MEDiC program would provide federal grant support and technical assistance for doctors, hospitals, and health systems that disclose medical errors and problems with patient safety and offer fair compensation for injuries or harm. Participants would submit a safety plan and designate a patient-safety officer, to whom these disclosures and notices of related legal action would be reported.

3. If a patient was injured or harmed as a result of medical error or a failure to adhere to the standard of care, the participant would disclose the matter to the patient and offer to enter into negotiations for fair compensation. The terms of negotiation for compensation ensure confidentiality, protection for any disclosure made by a health care provider to the patient in the confines of the MEDiC program, and a patient's right to seek legal counsel; they also allow for the use of a neutral third-party mediator to facilitate the negotiation.

4. Any apology offered by a health care provider during negotiations shall be kept confidential and could not be used in any subsequent legal proceedings as an admission of guilt if those negotiations ended without mutually acceptable compensation.

Is it a fantasy land OR another bureaucratic hurdle ?. OR a real geniune workable idea as argued by senators by citing experiences and studies from University of Michigan Health System and Veterans Affairs (VA) Hospital in Lexington, Kentucky ?. Read by yourself the full article (available free by clicking link below) published by senators in The New England Journal of Medicine, Volume 354:2205-2208, Number 21. May 25, 2006

Making Patient Safety the Centerpiece of Medical Liability Reform

RT or Iced Saline

2006-05-27T17:44:00.000-06:00

Saturday May 27, 2006
Room temperature or Iced Saline ?

Critical Care literature is not clear, actually controversial, regarding the suitable temperature of the solution use as injectable to measure cardiac output via thermodilution. Let see what is the major pro & con of iced saline.

Advantage: Iced injectate gives a higher signal/noise ratio and more reliability in the measured cardiac output. Signal-to-noise ratio is an engineering term for the power ratio between a signal (meaningful information) and the background noise.

Disadvantage: Iced injectate may affect heart rate and cardiodynamics 5.

But practically does it matter ?. Also, iced solution may not be as cold as we think after it passes through the operator's hand and long port.

Overall literature favours room temperature or atleast does not show any major advantage of using iced saline 1-4.

Related: Thermodilution Cardiac Output Measurement Protocol
(sample from Univ. of Carolina Hospitals)

References:

1. Cardiac output measured by thermal dilution of room temperature injectate. - Evonuk E, Imig CJ, Greenfield W, et al: J Appl Physiol 1961; 16:271-275

2. Cardiac output by thermodilution technique. Effect of injectate's volume and temperature on accuracy and reproducibility in the critically Ill patient - Chest, Vol 84, 418-422, 1983

3. Effect of injectate volume and temperature on thermodilution cardiac output determination - Anesthesiology.1986 Jun;64(6):798-801.

4. Iced versus room temperature injectate for assessment of cardiac output, intrathoracic blood volume, and extravascular lung water by single transpulmonary thermodilution - J Crit Care. 2004 Jun;19(2):103-7.

5. The slowing of sinus rhythm during thermodilution cardiac output determination and the effect of altering injectate temperature. Anesthesiology 1985; 63:540-541

CO Pitfalls

2006-05-26T17:19:00.000-06:00

Friday May 26, 2006
Cardiac Output Pitfalls

Determination of cardiac output by thermodilution has several technical pitfalls. Any deviation in technique can produce inaccurate and inconsistent results.

Basis of thermodilutional cardiac output: The method relies on an injection of a known volume of fluid (5-10 mL) into the right atrium. This fluid, either normal saline or D5W is at room (or iced at known *) temperature and therefore cooler than blood. The cooler injectate mixes with blood, thus lowering its temperature. The cooled blood is ejected into the pulmonary artery and flows past a thermistor located in the distal end of the PA catheter. The thermistor generates a change in temperature to time curve. The area under this curve is calculated by integration and is inversely proportional to the flow past the thermistor. In other words, the longer it takes for this change in temperature to “wash out,” the slower the flow past the thermistor. The converse is also true. The greater the flow, the faster the temperature “wash out,” and therefore the smaller the area under the curve. Anything that can disrupt the “washout” of this temperature change can affect the accuracy of this measurement.

* iced saline has been said to provides a better "signal-to-noise" ratio but controversy continues in literature regarding iced vs room temperature solution.

Clinical pitfalls:

1. Severe tricuspid regurgitation causes the injectate to recycle back and forth across the valve falsely lowering cardiac output.

2. An injectate volume that is too large will also falsely lower cardiac output.

3. Intracardiac shunts can falsely elevate cardiac output. In a right-to-left shunt, part of the injectate escapes through the shunt and decreases the amount of time required for washout of the temperature change. An injectate volume that is too small will cause an abbreviated washout and therefore falsely elevate the cardiac output.

Also see Pulmonary Artery Catheter Primer from American Thoracic Society (About 100 MCQ questions covering almost all aspects of PAC).

Related previous pearl: Arterial pressure-based continuous cardiac output

open abdomen

2006-05-25T20:37:00.000-06:00

Thursday May 25, 2006

Q; What is the antibiotic of choice for prophylaxis in "abdomen left open"?

A; The open abdomen (or abdomen left open after damage control) does not require antibiotic prophylaxis (unless there is an evidence of infection).

Keep as reference, nice bedside management review article:

Role of ICU in the management of the acute abdomen.

Kapadia F. Indian J Surg 2004;66:203-208

Reference:

Management of the patient with an open abdomen: techniques in temporary and definitive closure. Curr Probl Surg. 2004;41:815-876.

Hydrocortisone and Dexamethasone

2006-05-24T07:43:00.000-06:00

Wednesday May 24, 2006
Hydrocortisone and Dexamethasone

What are the 3 major differences between Hydrocortisone and Dexamethasone ?

1. Potency of Hydrocortisone and Dexamethasone is 20:1 (precisely 20 : 0.75) - means .75 mg of dexamethasone is equal to 20 mg of hydrocortisone.

2. Mineralocorticoid : Glucocorticoid activity is 1:1 in hydrocotisone but dexamethasone has negligible mineralocorticoid activity as well it does not effect cortisol level.

3. Half life of Hydrocortisone is 8-12 hrs and of dexametasone is 36-54 hrs.

See nice review Relative Adrenal Insufficiency: Case Examples & Review from Bradley J. Phillips, M.D. , Boston Medical Center, Boston Univ. Schl of Med. (ref: The Internet Journal of Endocrinology. 2005. Volume 1 Number 2)

Acute Liver Failure

2006-05-22T22:21:00.000-06:00

Tuesday May 23, 2006
Acute Liver Failure

Q; The chances of survival with medical management in acute liver failure is 26%. How much difference liver transplant can make ?

A; It goes upto 90% !!

Please see / keep in file video lecture

Acute Liver Failure: The Critical Team Approach

Dr. Lorenzo Rossaro, Chief of Gastroenterology and Hepatology and Head of the Liver Transplant Program at University of California Davis Medical Center.

(Total time: 42 minutes). Please click on above link.

You will need Real Player to see the lecture

PACT

2006-05-22T06:49:00.000-06:00

Monday May 22, 2006
PACT - Critical Care distant learning course

The European Society of Intensive Care Medicine (ESICM) has designed a multidisciplinary distance-learning programme PACT, Patient-centred Acute Care Training.

Eventually, the whole programme will have 45 modules divided into 4 major areas -
CLINICAL PROBLEMS,
SKILLS AND TECHNIQUES,
ORGAN SPECIFIC PROBLEM and
PROFESSIONALISM.
The content of each module is based on real life in the ICU. Each module describes a clinical scenario in which the user is asked to interpret the nature of problems and make management decisions. At the end of each module there are self-assessment multiple-choice questions (MCQs). 12 modules are already available
ACUTE RENAL FAILURE
ALTERED CONSCIOUSNESS
ARRHYTHMIA
BASIC CLINICAL EXAMINATION
CLINICAL IMAGING
COPD and ASTHMA
HOMEOSTASTIS
MAJOR INTOXICATION
NUTRITION
PYREXIA
QUALITY ASSURANCE AND COST EFFECTIVENESS
TRAUMATIC BRAIN INJURY

Click here to get more info.

For USA intensivists, it carries CME via SCCM. See the PACT Newsletter

icuroom.net or its editors have no relationship with PACT and introduction provided here is solely for educational purpose.

Intrahospital transport and VAP

2006-05-20T23:18:00.000-06:00

Sunday May 21, 2006
Intrahospital transport - a risk factor for VAP ?

Interesting study published about 6 months ago in Critical Care Medicine1 from france where 118 ventilated patients who were transported out of the ICU were matched with 118 ventilated patients who did not undergo intrahospital transport. Adjusting all variables, the ventilator-associated pneumonia (VAP) was 26% in transported patients compared with 10% in the matched untransported patients.

Please read full article to see all inclusion criteria, methods and measurements.

The following interventions were recommended by the group to minimize VAP before transportation:

1. a written protocol focusing on the prevention of aspiration during transport of intubated patients.

2. check material and devices necessary for transport for normal working status,

3. aspirate the endotracheal tube,

4. verify endotracheal tube adequate position,

5. check the endotracheal cuff pressure,

6. fit the ventilatory circuit with a filter,

7. stop enteral nutrition,

8. aspirate gastric contents before and sometimes during transport,

9. if possible, transport the patient in semirecumbent position,

10. if necessary, sedation to obtain a Ramsay score less than 4,

11. verify the availability of the area to which the patient has to be transported.

References: click to get abstract/article

1. Intrahospital transport of critically ill ventilated patients: A risk factor for ventilator-associated pneumonia-A matched cohort study Critical Care Medicine. 33(11):2471-2478, November 2005.

Hypoproteinemia and cosyntropin test

2006-05-20T07:08:00.000-06:00

Saturday May 20, 2006
Hypoproteinemia and cosyntropin test

43 year old malnourished patient admitted with septic shock. You started early goal directed therapy protocol. Patient blood pressure remained low despite showing signs of clinical improvement. You suspected adrenal insufficiency and ordered cosyntropin test. Patient failed to respond. You started low dose hydrocortisone. Next day you received call from lab that they also performed 'free cortisol' response to cosyntropin and found it appropriate to label patient as responder ?

Severe hypoproteinemia (as in this malnourished patient) may give false results and responders may get wrongly labelled as non-responders. In blood, about 90 percent of cortisol is bound to protiens (20 percent of cortisol is loosely bound to albumin and 70 percent is tightly bound to cortisol-binding globulin). Only 10 percent cortisol is in the free state. This is a major pittfall and deception to fall in while prescribing steroids in septic and hypoproteinemic patient under presumption of 'nonresponder'.

An important study reported about 2 years ago from Cleveland 1, looked into 66 critically ill patients with 36/66 had hypoproteinemia (albumin 2.5 g/dl or less) and 30/66 had near-normal serum albumin concentrations (above 2.5 g/dl). Baseline and cosyntropin stimulated serum total cortisol level as well as baseline and cosyntropin stimulated serum free cortisol level were measured. Study found that, nearly 40 percent of critically ill patients with hypoproteinemia had subnormal serum total cortisol levels, even though their adrenal function was normal as measured by free cortisol level.

Related previous pearl: Low dose steroid, yes or no ? - responder or non-responder ? - low-dose corticotropin stimulation test or high dose?

References: click to get abstract/article

1. Measurements of Serum Free Cortisol in Critically Ill Patients - Volume 350:1629-1638, April 15, 2004, NEJM
2. Septic Shock and Sepsis: A Comparison of Total and Free Plasma Cortisol Levels - The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 1 105-114
3. Adrenal Insufficiency - Roberto Salvatori, MD JAMA. 2005;294:2481-2488

HIDA, DISIDA and BRIDA scan

2006-05-18T22:54:00.000-06:00

Friday May 19, 2006
HIDA, DISIDA and BRIDA scan

Hepatic 2,6-dimethyliminodiacetic acid (HIDA) and Diisopropyl iminodiacetic acid (DISIDA) are nuclear studies to assess the function of the gallbladder and obstruction of the Common Bile Duct (CBD) in cholecystitis, cholangitis, billiary leak and atresia. These tests are ordered when ultrasound is equivocal. When you will order HIDA Scan or DISIDA scan ?

Nuclear Medicine literature is vast in this regard but to be short and simple, HIDA scan is used when serum bilirubin is less than 5-7 mg/dl and DISIDA scan is used when serum bilirubin is more than 7 mg/dl. DISIDA scan is now largely used instead of HIDA scan. The basis of this difference is relatively higher hepatic extraction. HIDA scan can be falsely positive when the gallbladder is not filling despite absence of cholecystitis like in severe liver disease (hyperbilirubinemia), patients on TPN or patient NPO for more than 24 hours, alcohol and opiate abuse. In case, serum bilirubin is extremely high (> 30 mg/dl), you can call for Mebrofenin (BRIDA) scan. Mebrofenin has even higher hepatic extraction than DISIDA scan.

Related Previous pearl: Acute acalculous cholecystitis in ICU

RSBI Rate

2006-05-18T12:35:00.000-06:00

Thursday May 18, 2006
RSBI Rate - Not only RSBI !

The Rapid Shallow Breathing Index (RSBI) remained an integral part of ventilator weaning parameter. Dr. Segal and coll. from Morristown Memorial Hospital, NJ went one step forward and looked into "RSBI Rate" (rate of change in the RSBI) with the question that as respiratory failure is a dynamic phenomenon - should serial followup of RSBI would be a more accurate predictor of weaning outcome, instead of one RSBI at a given time ?. In a prospective cohort study, patients with following criteria has been included:
requiring mechanical ventilation for more than 48hrs,
ET tube size no smaller than 7.5 in the ICU,
cleared by an intensivist (independent of study investigators) as an appropriate candidate to undergo weaning,
on hospital respiratory therapist driven weaning protocol.
Spontaneous Breathing Trial (SBT) for up to two hours given and parameters were measured periodically at SBT. The RSBI Rate was calculated by the formula:
RSBI rate: (RSBI2 - RSBI1)/ RSBI1 × 100

Out of 30 patients, 21 were successfully extubated, 3 were re-intubated within 24 hours and six were intolerants to the SBT. The RSBI on the failure plus Intolerance group was 40.2 (SD 14.7) but RSBI rate on every patient that failed or had intolerance to SBT had a RSBI Rate greater that 20%. It was concluded that the RSBI Rate less that 20% has a sensitivity of 90.4% and specificity of 100% in predicting weaning success.

Reference:

USE OF THE RATE OF CHANGE OF THE RSBI DURING SPONTANEOUS BREATHING TRIAL AS AN ACCURATE PREDICTOR OF WEANING OUTCOME - Critical Care Medicine: Volume 33(12) Abstract Supplement December 2005 p A20

Calcium in Dig toxicity

2006-05-17T08:17:00.000-06:00

Wednesday May 17, 2006
Treating Digoxin toxicity

Case: 74 year old male has been found to have arrhythmia with runs of wide complex ventricular tachycardia. Patient so far remained hemodynamically stable. You request crash cart near bed, applied pads to chest and send STAT labs and start reviewing patient's chart. You noticed 4 days ago digoxin level was 1.9 and since then his serum creatinine is steadily rising from 1.6 to 2.8. You suspected "Dig. toxicity" and called lab to run STAT dig. level. Indeed Dig. level is back with 3.4 and accompanying labs showed K+ level of 6.9. You ordered "Digi-bind" (Digoxin Immune Fab). Pharmacy informed you, "it will take time before Digi-bind gets to ICU". Interim you started treating hyperkalemia with IV insulin, D-50, IV bicarb., IV calcium and albuterol neb. treatments.

Where did you go wrong ?

Answer: Calcium has shown to make digoxin toxicity worse. It may be more wise to avoid calcium in management of hyperkalemia from digoxin toxicity. Some literature has shown the similar membrane stabalizing effect from magnesium and may be used instead of calcium.

Caution should be taken not to go very aggressive in treating hyperkalemia, or atleast potassium should be followed very closely if DigiFab is planned. With administration of DigiFab (Digibind), potassium shifts back into the cell and life threatening hypokalemia may develop rapidly. Digoxin causes a shift of potassium from inside to outside of the cell and may cause severe hyperkalemia but overall there is a whole body deficit of potassium. With administration of Digi-bind, actual hypokalemia may manifest which could be equally life threatening.

Read related interesting review: Recognising signs of danger: ECG changes resulting from an abnormal serum potassium concentration: A Webster, W Brady and F Morris (reference: Emerg Med J 2002; 19:74-77)

References: click to get abstract/article

1. Calcium for hyperkalaemia in digoxin toxicity - Emerg Med J 2002; 19:183
2. Using calcium salts for hyperkalaemia - Nephrol Dial Transplant (2004) 19: 1333-1334
3. Slow-release potassium overdose: Is there a role for magnesium? Emergency Medicine 1999;11:263–71

K level via A-line

2006-05-16T07:42:00.000-06:00

Tuesday May 16, 2006
Potassium level via A-line

Potassium level via arterial line may not be as reliable as through peripheral venous punture. See this interesting case report (click reference) published in British Journal of Anaesthesia, where radial arterial line consistently showed K level of 7.4 - 9.3 mEq/L without any clinical signs. Simultaneous venous sample level was 4.4 mEq/L. When cannula was slightly withdrawn, arterial potassium level came back as 4.1 mEq/L (c/w venous sample).

It was postulated that the tip of the cannula could have impinged against the vessel wall so that during withdrawal of the sample a high shear rate could have caused haemolysis of red blood cells leading to an increased potassium concentration in the blood samples.

References: click to get abstract/article

1. Apparent hyperkalaemia from blood sampled from an arterial cannula - British Journal of Anaesthesia 2004 93(3):456-458

Pseudothrombocytopenia

2006-05-15T07:20:00.000-06:00

Monday May 15, 2006

Case: 52 year old male is back from cardiac angioplasty with abciximab (ReoPro) infusion. Pre-cath labs were normal. CBC was send per protocol after 4 hours of abciximab infusion and lab call with critical platelet level of 62. Abciximab was stopped and hematology consulted. Hematology advised to restart abciximab !!

Pseudothrombocytopenia:

Pseudothrombocytopenia is a common phenomenon with patients on abciximab (ReoPro). It is a benign condition and is not a real thrombocytopenia as platelets actually clump in collecting tubes containg EDTA. It is an important diagnosis to make as it may leave patient without an appropriate treatment. Diagnosis can be made by reviewing peripheral blood film or drawing blood in citrated or heparinized tube. It is not clear why abciximab cause more EDTA-induced platelet clumping.

* EDTA (Ethylenediaminetetraacetic acid) is a commonly used anticoagulant in sampling tubes for blood counts.

References: click to get abstract/article

1. Occurrence and clinical significance of pseudothrombocytopenia during abciximab therapy J Am Coll Cardiol. 2000 Jul;36(1):75-83.
2. Abciximab-Associated Pseudothrombocytopenia - Circulation. 2000;101:938
3. EDTA dependent pseudothrombocytopenia caused by antibodies against the cytoadhesive receptor of platelet gpIIB-IIIA - Journal of Clinical Pathology 1994;47:625-630
4. Pseudothrombocytopenia Volume 329:1467 Nov. 11, 1993

In Hyperkalemia

2006-05-14T16:13:00.000-06:00

Sunday May 14, 2006
In Hyperkalemia !!

Q; Nurse call you with K+ level of 7.8 (lab confirmed - no hemolysis). You ordered 10 units of IV insulin with 2 ampules of D-50, 1 ampule of calcium gluconate and 2 ampules of sodium bicarbonate in series. RT was requested to give 2 nebulizer treatments of albuterol. The final order set is followed ultimately by PO Kayexalate/sorbitol.

What is wrong in above orders for the management of hyperkalemia?

A; In the management of hyperkalemia, sodium bicarbonate should be given before calcium. Administrating bicarbonate after calcium will bind calcium and will render it ineffective. This is another reason, we don't prepare "bicarb drip" in LR (Lactated Ringer’s) as it contains calcium which will bind bicarbonate and will make the whole management ineffective.

Related previous pearls:

Difference between Lactate Ringer's and Normal Saline solutions

Colonic Necrosis - unusual complication of Kayexalate-Sorbitol

Hyperbaric oxygen in CO poisoning

2006-05-12T22:07:00.000-06:00

Saturday May 13, 2006
Hyperbaric oxygen in CO poisoning

Q; What is the role of hyberbaric oxygen in the management of lethal Carbon-monoxide (CO) poisoning ?

A; It decreases the half life of CO from 5 hours to half hour and so the possible complications. It prevents lipid peroxidation in the brain and preserve ATP levels in tissue exposed to carbon monoxide. It has shown to decrease the cognitive sequelae by 46 % when compared with 'normobaric' group at 6 weeks 2.

Limitations: Hyperbaric oxygen in CO poisoning has its own limitations. It may induce "hyperoxic" seizures (rare) 3. Other adverse effects of hyperbaric oxygen includes reversible myopia, rupture of the middle ear, barotrauma to lungs 4. Hyperbaric oxygen should be reserved for lethal cases of CO poisoning.

Alternate: If hyperbaric oxygen is not available, apply 100% oxygen, high PEEP and if needed high-frequency ventilation. 100% O2 reduces half life of CO effectively to about one and half hour.

Reference: (click to get abstract)
1. Diagnosis and treatment of carbon monoxide poisoning - Respir Care Clin N Am. 1999 Jun;5(2):183-202.
2. Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning - Volume 347:1057-1067, oct. 3, 2002
3. Central nervous system oxygen toxicity during hyperbaric treatment of patients with carbon monoxide poisoning - Hampson NB, Simonson SG, Kramer CC, Piantadosi CA - UNDERSEA & HYPERBARIC MEDICINE 23 (4): 215-219 DEC 1996
4. Hyperbaric-Oxygen Therapy - Volume 334:1642-1648, june 20, 1996

vasopressin/norepinephrine ratio

2006-05-12T07:32:00.000-06:00

Friday May 12, 2006
vasopressin/norepinephrine ratio in septic shock

Role of vasopressin in septic shock seems promising but we don't have enough data yet to support its regular use. Interesting study in Taiwan was done by Lin and co. and published 6 months ago in Am J Emerg Med. 182 patients (consecutive patients visiting the emergency department), who met the inclusive criteria were divided into 3 groups (per standard guidelines):
septic shock,
severe sepsis, and
sepsis.
30 healthy subjects were included as control.

The plasma vasopressin level at baseline was drawn early in course in emergency department. The plasma vasopressin level was significantly lower for those who finally developed septic shock (3.6 +/- 2.5 pg/mL) than severe sepsis (21.8 +/- 4.1 pg/mL) and sepsis group (10.6 +/- 6.5 pg/mL) - kind of bell curve.

Simultaneouly norepinephrine level was measured in the same groups. Norepinephrine level was highest for septic shock group, (3650 +/- 980 pg/mL) in comparion to severe sepsis (3600 +/- 1000 pg/mL) and sepsis group (1720 +/- 320 pg/mL).
The vasopressin/norepinephrine ratio (very early in the course) was significantly lower for the patients with final diagnosis of septic shock (P less than .001).

This study lead us to logical question: Should we use vasopressin early in septic shock instead later ? but probably it is still early to jump on vasopressin, atleast till we get results from evidence based studies such as pending VASST (Vasopressin Vs. Norepinephrine in Septic Shock) study.

*VASST is an ongoing multi-centre triple-blind randomized controlled trial being conducted in Canada and Australia to determine the effectiveness of Vasopressin compared to Norepinephrine (28-day and 90-day survival).

Previous related pearl: Vasopressin .07 units/min ?

Reference: (click to get abstract)
Low plasma vasopressin/norepinephrine ratio predicts septic shock. Am J Emerg Med. 2005 Oct;23(6):718-24.

Auto-PEEP

2006-05-11T18:20:00.000-06:00

Thursday May 11, 2006
Auto-Peep

Q; What level of extrinsic PEEP should be applied to counter act (intrinsic) auto-PEEP?

A; 75 - 85% of auto-PEEP.

Keeping extrinsic PEEP lower than auto-PEEP not only effectively counter acts auto-PEEP but also any ciruclatory depression or lung hyperinflation is unlikely to occur at extrinsic PEEP slightly lower than intrinsic PEEP value.

Read precise review on auto-peep:

Auto-positive end-expiratory pressure: Mechanisms and treatment
M.M. MUGHAL, D.A. CULVER, O.A. MINAI, and A.C. ARROLIGA - CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 72 • NUMBER 9 SEPTEMBER 2005

TTKG

2006-05-10T11:48:00.000-06:00

Wednesday May 10, 2006
The TransTubular Potassium Gradient - TTKG

TTKG is an index reflecting conservation of potassium by Kidney.

TTKG = (Urine-K / Plasma-K) / (Urine-Osm / Plasma-Osm)

Normal value is 8-9 in normokalemic patient and should be 10-11 in hyperkalemic patient.

Clinical significance:
1. In hyperkalemia if TTKG remains less than 7, most probable cause is hypoaldosteronism. Diagnosis can be confirmed by challenging patient with 0.05 mg of fludrocortisone, which should increase the TTKG. (Mineralcorticoid increases TTKG).

2. In hypokalemia - kidney try to conserve potassium and TTKG should fall to less than 2 (like in GI source). If TTKG remains higher, it suggests renal loss of potassium (like in diuretics).

Limitations:
1. Always check urine sodium simultaneouly. TTKG is unreliable if urine sodium is less than 25 mmol/l.
2. TTKG is unreliable if urine osmolality is less than the serum osmolality.

References: click to get abstracts/articles
1.Potassium excretion indices in the diagnostic approach to hypokalaemia - Q J Med 2000; 93: 318-319
2. Transtubular potassium concentration gradient (TTKG) and urine ammonium in differential diagnosis of hypokalemia - J Nephrol. 2000 Mar =Apr;13(2):120-5
3. Diseases of Potassium metabolism: Atlas of disease of the kidney by Robert W. Schrier, Professor and Chairman, Department of Medicine, University of Colorado School of Medicine, Denver, Colorado

Contrast induced Nephropathy

2006-05-08T22:21:00.000-06:00

Tuesday May 09, 2006
Contrast induced Nephropathy

Q: What is the cut off point to suspect Contrast induced Nephropathy ?

A; Unfortunately there is no consensus defination yet to define Contrast Induced Nephropathy but its better to be safer than sorry. The most conservative general rule is to suspect some component of contrast induced nephropathy whenever there is a 25% increase in serum creatinine concentration from the baseline, or an increase of at least 0.3 mg/dL within 48-72 hours, when no other cause could be find.

We found 2 good review articles for further reading :

1. Contrast-Induced Nephropathy, Tadhg G. Gleeson; Sudi Bulugahapitiya, dublin, Ireland. (ref.: Am J Roentgenol 183(6):1673-1689, 2004). This article is available with free registration at medscape.com

2. Radiocontrast-Induced Nephropathy, Resident Grand Rounds by Jeff S. Rose, MD at Wake Forest University School of Medicine, Winston-Salem, NC

Previous related Pearl: Preventing contrast-Induced Nephropathy

Heparin Induced HyperKalemia

2006-05-08T08:27:00.000-06:00

Monday May 08, 2006
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

Our failures !!!

2006-05-06T21:46:00.000-06:00

Sunday May 07, 2006
Our failures !!!
Some big gurus from Critical Care Medicine (all names below in reference) have penned a cumulative article on progress of Intensive Care and Emergency Medicine over the past 25 Years in recent issue of chest 1. The whole article is worth reading but the most interesting part is where authors have pointed out "Our Failures" with following mentions:

Excessive antibiotic use
Iatrogenic IV fluid overload
Excessive administration of inotropic agents
Ventilation with unnecessarily large tidal volumes
Excessive, continuous IV sedation
Unnecessary use of antiarrhythmic agents
Excessive caloric intake
Liberal blood transfusions
Traumatic effects of endotracheal intubation and airway management
Excessive ventilation in low flow states

Frequent interruption of chest compressions during CPR

Reference: Click to get abstract

1. Intensive Care and Emergency Medicine - Progress Over the Past 25 Years: Jean-Louis Vincent, MD, PhD; Mitchell P. Fink, MD, FCCP; John J. Marini, MD; Michael R. Pinsky, MD, FCCP; William J. Sibbald, MD, FCCP; Mervyn Singer, MD; Peter M. Suter, MD; Deborah Cook, MD; Paul E. Pepe, MD and Timothy Evans, MD Chest. 2006;129:1061-1067

ABCDEF of CXR

2006-05-06T09:11:00.000-06:00

Saturday May 06, 2006
ABCDEF of CXR

There are many mnemoics we use in medicine. One mnemonic easy to teach house staff so they don't miss things on chest x-ray is

A (Abnormal) Air and Aqua - (like pneumothorax, pulmonary edema, pleural effusions or even free air below right diaphragm).

B Bone

C Cardia (like pericardial effusion, vena cavae, aortic knob and other cardiac contours)

D Densities (infiltrates, masses and lesions - also include hilar area)

E Elevation of diaphragm (should also take care of atelactasis)

F Foreign bodies (lines, tubes, devices etc).

Dialysis disequilibrium syndrome

2006-05-05T08:09:00.000-06:00

Friday May 05, 2006

Case: 57 year old female, newly hemodialysis patient, transferred from floor to ICU after she developed seizure at the end of her dialysis session. No significant risk factor could be find otherwise. Nurse reports patient appear irritable and restless before episode and complain of headache, nausea and blurred vision. While resident was called to evaluate as patient also noticed to have muscular twitching and confusion, symptoms progressed and seizure was witnessed.

Answer: Dialysis disequilibrium syndrome.

Dialysis disequilibrium syndrome is common during hemodialysis particularly patient’s first few dialysis sessions. It is characterized by neurologic symptoms of varying severity and actually may lead to herniation and death. The rapid reduction in BUN lowers the plasma osmolality, creating a transient osmotic gradient that promotes water movement into the cells, causing cerebral edema and consequently acute neurologic dysfunction. With better understanding of the process and newer dialysis techniques, severe form of syndrome is now not commonly seen. This not only explains that why our nephrology colleagues start with gentle but frequent sessions but also explains one of the several benefits of mannitol during dialysis. Read interesting article from University of Calgary, Alberta, Canada :

Dialysis Disequilibrium Syndrome: Brain death following hemodialysis for metabolic acidosis and acute renal failure - A case report followed with discussion and different management modalities (Ref.: BMC Nephrol. 2004; 5: 9.)

Swan in Amniotic fluid embolism

2006-05-04T08:31:00.000-06:00

Thursday May 04, 2006
Pulmonary Artery Catheter in Amniotic fluid embolism !!

20 years ago it was suggested by Mason that probable diagnosis of Amniotic fluid embolism can be made by analyzing pulmonary artery blood with the logic that amniotic fluid does not ordinarily enter the maternal circulation, and the identification of large numbers of fetal squamous in the postpartum pulmonary microvasculature is of clinical significance. (He applied similar argument for other similar diseases such as fat embolism). Diagnosis becomes more probable if other fetal debris such as mucin or hair is present.

Technique described: Obtain blood from the distal lumen of a pulmonary artery catheter (in wedged position). After discarding the first 10 ml of blood, draw an additional 10 ml, heparinize and analyze utilizing Papanicolaou's method.

Above technique is only suggestive of amniotic fluid embolism and not a gold standard.

References: Click to get abstract/article
1. Pulmonary microvascular cytology. A new diagnostic application of the pulmonary artery catheter - Chest, V. 88, 908-14
2. Amniotic fluid embolism - Masson RG - Clin Chest Med.1992 Dec;13(4):657-65.

Massive PE

2006-05-03T14:13:00.000-06:00

Wednesday May 03, 2006
What if even thrombolysis fails in massive PE ?

For intensivists massive pulmonary Embolism (PE) is a dreaded situation, especially when even thrombolysis fails. Meneveau and coll. from france have studied such group of 40 patients who did not respond to thrombolysis. Results were published recently in chest.

14/40 patients who were treated by rescue surgical embolectomy were compared with 26/40 patients who were treated by repeat thrombolysis.

There was a trend for higher mortality in the medical group than in the surgical group (10 vs 1 deaths).
Also, there were significantly more recurrent PEs in the repeat thrombolysis (35% vs 0%).
While no significant difference was observed in number of major bleed, all bleeding events in the repeat-thrombolysis group were fatal.

Study concluded that rescue surgical embolectomy led to a better in-hospital course when compared with repeat thrombolysis in patients with massive PE who have not responded to thrombolysis.

See comprehensive review, Pulmonary Embolism just updated 2 days ago at emedicine.com by Craig Feied M.D.

References: Click to get abstract/article
1. Management of Unsuccessful Thrombolysis in Acute Massive Pulmonary Embolism - Chest. 2006;129:1043-1050

Phosphate level in Tylenol toxicity

2006-05-02T12:36:00.000-06:00

Tuesday May 02, 2006
Is serum phosphate level better than King’s College Hospital criteria ?

One study of 125 patients published in 'Hepatology' in 2002 looked into relation of serum phosphate level and survival in Acetaminophen-induced hepatotoxicity 1. Study found that Phosphate concentrations were significantly higher in nonsurvivors than in survivors at 48 to 72 hours after overdose as well as at 72 to 96 hours after overdose.

A threshold phosphate concentration of 3.71 mg/dL (1.2 mmol/L) at 48 to 96 hours after overdose had sensitivity of 89%, specificity of 100%, accuracy of 98%, positive predictive value of 100%, and negative predictive value of 98%. The serum phosphate level had higher sensitivity, accuracy, and positive and negative predictive values than the King’s College Hospital criteria, and it identified patients significantly earlier.

References: Click to get abstract/article
1. Serum Phosphate Is an Early Predictor of Outcome in severe Acetaminophen-Induced Hepatotoxicity Hepatology - 2002;36:659-665 -Full article available with free registration

IVF Bolus

2006-05-01T21:32:00.000-06:00

Monday May 01, 2006
How to write order for IVF bolus !!

What we have learnt from guru and professor Jean-Louis Vincent is that the most important thing in Critical care Medicine is to master the 'basic and simple things'. Few months back he taught us the art of everyday rounding in ICUs with simple mnemonic of "Fast Hug" 1. In this month issue of Critical Care Medicine he precisely explains the art of fluid challenge. First he busted 5 myths about fluid bolus. Enjoy !!

* Fluid should be withheld because the CVP is high (myth).

* Fluid should be withheld because there is lung edema on the CXR (myth).

* Fluid should be withheld because the patient has already received a large volume in a short time interval (myth).

* Tachycardia is due to fluid deficit and should prompt fluid(myth).

* I gave fluids to increase the central venous pressure to 12 mm Hg to exclude an underlying hypovolemia (myth).

(Read full article to read details on each).

And now 4 parameters need to be written for IVF bolus order:

Type of Fluid.
Rate of Fluid Administration.
Goal to be Achieved.
Safety Limits.

Like NS 500 cc over 30 minutes with clinical goal of MAP of 70 mm Hg. Hold if CVP is 15 with assessment every 10 minutes !!

References:

Click to get abstract
1. Give your patient a fast hug (at least) once a day - Critical Care Medicine. 33(6):1225-1229, June 2005. - Vincent, Jean-Louis MD, PhD, FCCM
2. Fluid challenge revisited. Critical Care Medicine. 34(5):1333-1337, May 2006. Vincent, Jean-Louis MD, PhD, FCCM; Weil, Max Harry MD, PhD, ScD (Hon), FCCM

Post fellowship shock syndrome

2006-04-30T08:32:00.000-06:00

Sunday April 30, 2006
Post fellowship shock syndrome

Q; What is Post fellowship shock syndrome ?

A; Post fellowship shock syndrome is a kind of culture shock for young graduates when they transit from big tertiary care academic centers to regular community based medical practice. Transit from high tech, literature oriented, academic based and superior nursing quality to business oriented, "thats how we do things here" practice, no house staff support, no billing experience and wide spectrum of nursing quality - caught unprepared young graduates with mental and culture shock and may leave them frustrated with present situation. Its important to prepare graduating residents and fellows for future practice of medicine.

Read related article The Realities of the First Year of Practice ( NEJM CareerCenter )

(Post fellowship shock syndrome is a term invented by editors of this web-site)

Nasogastric tube syndrome

2006-04-29T07:48:00.000-06:00

Saturday April 29, 2006
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.

Iodide in Thyroid Storm

2006-04-28T21:13:00.000-06:00

Friday April 28, 2006
Iodide in Thyroid Storm

Q; How long should you wait to administer iodide after giving antithyroid medication in the management of thyroid storm ?

A; Atleast one hour.

Oral or rectal iodide compounds block release of thyroid hormones after starting antithyroid drug therapy. But if given early in management (before antithyroid medication become effective) it can get utilize in the synthesis of new thyroid hormone. Read nicely written review on Thyroid Storm (and Myxedema coma) by Nikolaos Stathatos, MD, and Leonard Wartofsky, MD from Washington Hospital Center in Washington, D.C. - ref.: emedmag.com, 02/15/2003 issue.

IV steroid in postextubation stridor

2006-04-26T22:16:00.000-06:00

Thursday April 27, 2006
IV steroid to reduces postextubation stridor

Interesting study came out in May' 2006 issue of Critical Care Medicine regarding intravenous injection of methylprednisolone to reduce the incidence of postextubation stridor in intensive care unit patients. 128 patients who were intubated for more than 24 hrs with a cuff leak volume less than 24% of tidal volume but met weaning criteria were studied. 128 patients were divided into 3 groups.
placebo group (n = 43) with four injections of normal saline every 6 hrs,
4 INJ group (n = 42) with four injections of methylprednisolone (40 mg every 6 hours)
1 INJ group (n = 42) with one injection of the methylprednisolone (40 mg) followed by three injections of normal saline.

Extubation done one hour after last injection. Postextubation stridor was confirmed by examination using bronchoscopy or laryngoscopy.

Results shows that:
The incidences of postextubation stridor were lower both in the 1 injection (11.1%) and the 4 injections groups (7.1%) than in the control group (30.2%,). The side effects of steroids over 24 hrs were minimal with no obvious complications such as GI bleed, hyperglycemia, or increased risk of infection.

Please read full study for inclusion exclusion criteria, all outcomes, comparision with non-intervention group of 193 patients and discussion of study by authors.

Related previous pearl: Cuff leak tests

References: click to get abstract
1. Intravenous injection of methylprednisolone reduces the incidence of postextubation stridor in intensive care unit patients - Critical Care Medicine. 34(5):1345-1350, May 2006

LaSRS

2006-04-25T22:13:00.000-06:00

Wednesday April 26, 2006

LATE STERIOD RESCUE STUDY (LaSRS): The Efficacy of Corticosteroids as Rescue Therapy for the Late Phase of Acute Respiratory Distress Syndrome.

Finally the results of ARDSnet's LaSRS trial are published. Out of 180 patients with ARDS of atleast 7 days, 91 were randomly assigned to the placebo group and 89 to the methylprednisolone group. Some outcomes are very unexpected :

1. There was no significant difference in the 60-day hospital mortality rate, with 26 deaths in each group.

2. At 180 days, 29 patients had died in the placebo group and 28 had died in the methylprednisolone group.

3. The methylprednisolone group had significantly more ventilator-free days than the placebo group during the first 28 days as well as at 180 days.

4. As compared with the placebo group, the methylprednisolone group also had significantly fewer days in the ICU during the first 28 days but not at day 180 !!.

5. Ventilatory assistance was resumed: 6 in the placebo group and 20 in the methylprednisolone group. Also 8 of the 20 methylprednisolone-treated patients who resumed receiving assisted ventilation died, as compared with 3 of 6 patients in the placebo group.

6. The mean serum glucose level was not significantly different between groups at baseline but was significantly higher in the methylprednisolone group than the placebo group on days 1, 2, and 4.

7. Forty-three serious infections were diagnosed in 30 patients in the placebo group, as compared with 25 serious infections in 20 patients in the methylprednisolone group.

8. There were 17 episodes of septic shock among 15 patients in the placebo group and 6 episodes among 5 patients in the methylprednisolone group.

9. Prospectively, serious neuromyopathy were reported in nine patients, all of whom were in the methylprednisolone group but interestingly retrospective chart review found no significant difference in the incidence of neuromyopathy: 21 in the placebo group and 27 in the methylprednisolone group. Also, Exposure to neuromuscular-blocking agents was not significantly more common among patients who were identified as having neuromyopathy.

10. Patients who were enrolled at least 14 days after the onset of ARDS and who were randomly assigned to receive methylprednisolone had a significantly higher case fatality rate than similar patients who were assigned to receive placebo.

Study conclusion: These results do not support the routine use of methylprednisolone for persistent ARDS despite the improvement in cardiopulmonary physiology. In addition, starting steroid therapy more than two weeks after the onset of ARDS may increase the risk of death.

Editor note: Please read whole article to be aware of limitations of study.

References:
1. Efficacy and Safety of Corticosteroids for Persistent Acute Respiratory Distress Syndrome - Volume 354:1671-1684, Number 16, April 20,2006
2. Protocol of study: ARDSnet.org
3. Late Steroid Rescue Study (LaSRS): The Efficacy of Corticosteroids as Rescue Therapy for the Late Phase of Acute Respiratory Distress Syndrome - clinicaltrials.gov

Esophageal Pressure Measurements and compliance

2006-04-25T04:12:00.000-06:00

Tuesday April 25, 2006
Esophageal Pressure Measurements and compliance

At bedside compliance is measured as

Cs = Vt / Ppl - (PEEP + autoPEEP)

Where Cs = compliance of static thorax, Vt = tidal volume, Ppl = plateau pressure and PEEP is postive-end-expiratory pressure

or in more precise terms

C stat = Vt / (Pao end'inhalation - Pao end'exhalation)

Where Pao = pressure at the airway opening. Pao end'inhalation is same as Ppl. and Pao end'exhalation is same as TotalPEEP.

This compliance measures the whole thorax including chest wall and lungs. Normal Cs is ideally 100 ml/cm H2O or practically 50 to 80 ml/cm H2O is acceptable.

Placement of esophageal catheter can give lung compliance (CL) and chest wall compliance (Ccw) separately. Formulae are

CL = Vt / (Pao - Pes) end'inhalation - (Pao - Pes) end'exhalation
and
Ccw = Vt / (Pes - Patm) end'inhalation - (Pes - Patm) end'exhalation
or practically done simply as Ccw = Vt / Pes end'inhalation

Where Pes = Esophageal pressure and P atm = Atmospheric pressure

Normal CL and Ccw is 200 ml/cm H2O.

Read article Esophageal and Gastric Pressure Measurements , including all the basics of how to insert and measure the esophageal catheter pressures by Dr. Joshua O Benditt (ref: Resp. Care, Jan. 2005, vol 50, no. 1)

CURB-65 Score

2006-04-23T22:52:00.000-06:00

Monday April 24, 2006
CURB-65 Score

Lim and colleagues have designed a score called CURB-65 to rate mortality in community acquired pneumonia (CAP) - based on information available at initial hospital assessment. Give one point each for following values

C = Confusion
U = Urea (BUN) if more than 20 mg/dl (7 mmol/l)
R = Respiratory rate if more than / = 30/min,
B = BP if syst. less than 90 mm Hg or diast. less than/= 60 mm Hg,
65 = If age more than / = 65 years

With score 0 expected mortality is 0.7%,
With score 1 expected mortality is 3.2%,
With score 2 expected mortality is 13%,
With score 3 expected mortality is 17%,
With score 4 expected mortality is 41.5% and
With score 5 expected mortality is 57%

References:
1.Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study - W S Lim, M M van der Eerden, R Laing, W G Boersma, N Karalus, G I Town, S A Lewis and J T Macfarlane - Thorax 2003;58:377-382

Hemodynamic variables in septic shock

2006-04-23T13:30:00.000-06:00

Sunday April 23, 2006
Hemodynamic variables to watch in septic shock

Dr Varpula and coll. from Helsinki, Finland tried to identify the most related hemodynamic variables in 111 septic shock patients. Data from 6 hours and 48 hours were analyzed separately. Primary endpoint was 30-day mortality. Following results were found:

1. Univariate analysis showed that lactate level on arrival and MAP-derived variables (average of all MAP values, hypotension time) during the first 6 hours correlated with the 30-day mortality.

2. The best cutoff values for hypotension and hypoperfusion times were found to be MAP of 65 mmHg and SvO2 of 70%, respectively.

In conclusion, data suggest that time spent with low BP and with inadequate CO (decrease SvO2) are the most important hemodynamic variables related to outcome. This study find threshold values in synchrony with values published in recent guidelines.

Related Sites: survivingsepsis.org

Related Previous pearls: Shock alert , ScvO2 or SvO2 ? and EGDT and PAC need

References:
1.Hemodynamic variables related to outcome in septic shock - Intensive Care Medicine, Volume 31, Number 8 , August 2005, Pages: 1066 - 1071

Law of LaPlace

2006-04-22T10:18:00.000-06:00

Saturday April 22, 2006
Law of LaPlace, PEEP and surfactant

Law of LaPlace tells us that "Pressure is always greater in smaller radius".

P = 2T/r

where P = pressure, T = tension and r = radius

So in lungs, smaller alveoli will have greater resistance for air to flow during inspiration because of higher pressure. We use PEEP to keep alveoli open during expiration (prevent derecruitment), as name says positive end-expiratory pressure. High tidal volume cause more shear force damage to smaller alveoli with each breath to overcome this pressure. Thats why, our present approach to ventilator management in ARDS is low tidal volume and optimum PEEP (See ARDSnet

Lower Tidal Volume/ Higher PEEP Reference Card).

Looking at same formula, other approach is to decrease Tension, by nature's method of applying surfactant. One study published in August 2004 looked into 'Effect of Recombinant Surfactant Protein C–Based Surfactant on the Acute Respiratory Distress Syndrome' and found no significant difference in terms of 28 days mortality or the need for mechanical ventilation but also showed that 'Patients receiving surfactant had a significant greater improvement in blood oxygenation during the first 24 hours of treatment than patients receiving standard therapy'. Actually literature suggests that "..Sufficient levels of PEEP will also help to prevent further loss of surfactant in still ‘healthy’ alveoli,"

Read Professor Lachmann's lecture -

Current status of lung protective ventilation in ARDS, discussing Law of LaPlace, surfactant and PEEP. (source: eacta.org - European Association of Cardiothoracic Anaesthesiologists)

References:
1.Effect of Recombinant Surfactant Protein C–Based Surfactant on the Acute Respiratory Distress Syndrome - Volume 351:884-892, Number 9, NEJM Aug. 26, 2004
2. Higher versus Lower Positive End-Expiratory Pressures in Patients with the Acute Respiratory Distress Syndrome - The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network ,Volume 351:327-336, Number 4, NEJM, july 22, 2004

ketek

2006-04-21T11:21:00.000-06:00

Friday April 21, 2006

Case: 74 year old male resident of assisted living facility, admitted to ICU with exacerbation of his myasthenia gravis. He also reports newly devloped symptoms of blurred vision, difficulty focusing, and diplopia which according to him is not typical of his symptoms but you assume it as part of exacerbation of myasthenia gravis. Patient denies stopping his medicine. 3 days ago he was seen by his primary care physician for cough and was given samples of a new strong antibiotic. His neurologist has been consulted who requests you to change his antibiotic. Patient symptoms resolved within 24 hours.

Answer: Ketek (Talithromycin) is a first ketolide (cousin of macrolide), indicated for mild to moderate acute exacerbation of chronic bronchitis, acute bacterial sinusitis and in mild to moderate CAP, atypical and multi-drug resistant strains of S pneumoniae. Talithromycin unlike the macrolides has 2 strong binding sites on the bacterial ribosome and this strong dual binding helps provide coverage against resistant strains of S pneumoniae. Exacerbations of myasthenia gravis have been reported in patients with myasthenia gravis treated with Talithromycin. It cause visual disturbances like blurred vision, difficulty focusing, and diplopia by slowing the ability to accommodate and the ability to release accommodation. Other major side effects include hepatic dysfunction and potential to prolong the QTc interval.

References:
1. FDA Public Health Advisory Ketek (telithromycin) Tablets - fda.gov
2. FDA consumer info. - fda.gov
3. www.ketek.com

Ambien

2006-04-19T10:43:00.000-06:00

Thursday April 20, 2006
Zolpidem-Induced Delirium

Relatively Zolpidem (Ambien) is a safe medicine and recently has been the drug of choice in critical care units to induce sleep. But it is important to be aware of reported cases of Ambien related psychosis, delirium and mania. Atleast one case is reported with visual perception distortion after a single dose of zolpidem. One way to combat the problem is to decrease the prescribing dose particularly in elderly population and in hypoalbuminemia (5 mg instead of 10 mg). Also, female population has been reported to have more plasma level with same dose. Also note that Zolpidem metabolized through liver so it may be necessary to decrease the dose in liver insufficiency.

Related previous pearls: SEROTONIN SYNDROME

References:
1. Delirium associated with zolpidem - The Annals of Pharmacotherapy: Vol. 35, No. 12, pp. 1562-1564
2. Zolpidem-Induced Delirium With Mania in an Elderly Woman - Psychosomatics 45:88-89, February 2004
3. Zolpidem-induced agitation and disorganization. - Gen Hosp Psychiatry. 1996 Nov;18(6):452-3. (pubmed)
4. Zolpidem-induced psychosis. - Ann Clin Psychiatry.1996 Jun;8(2):89-91. (pubmed)
5. Clinical pharmacokinetics of zolpidem in various physiological and pathological conditions, in Imidazopyridines in Sleep Disorders. Edited by Sauvanet JP, Langer SZ, Morselli PL. New York, Raven Press, 1988, pp 155–163
6. Zolpidem-Induced Distortion in Visual Perception - The Annals of Pharmacotherapy: Vol. 37, No. 5, pp. 683-686

US guided radial artery

2006-04-19T07:25:00.000-06:00

Wednesday April 19, 2006
Ultrasound guided insertion of radial artery catheters

Role of ultrasound guidance in central venous catheter (particularly internal jugular vessel) is well known 1 but literature on its efficacy in arterial line insertion is very scant. Levin and coll. from Hadassah University Hospital, Jerusalem, Israel has done a simple but interesting study on the use of ultrasound guidance in the insertion of radial artery catheters 2. A total of 69 patients were randomized - 34 to the ultrasound group and 35 to the palpation group. The following results were found:

* The arterial cannula was inserted on the first attempt in 21 of the 34 patients (62%) in the ultrasound group vs. 12 of the 35 patients (34%) in the palpation group.

* Overall, there were 55 total attempts (1.6 per patient) at arterial catheter insertion in the ultrasound group vs. 110 (3.1 per patient) in the palpation group.

* The mean overall time taken per patient for catheter insertion was 55.5 secs in the ultrasound group vs. 111.5 secs in the palpation group.

* In the ultrasound group, a total of 39 cannulae were used vs. 60 in the palpation group (cost effectiveness).

References:
1 Bedside Ultrasonography in the ICU Part 2 - Chest. 2005;128:1766-1781
2. Use of ultrasound guidance in the insertion of radial artery catheters - Critical Care Medicine: Volume 31(2) February 2003 pp 481-484

Wernicke's Encephalopathy

2006-04-18T16:14:00.000-06:00

Tuesday April 18, 2006
Wernicke's Encephalopathy in ICU

Q: Can Wernicke's Encephalopathy be iatrogenic in ICU ?

A: Yes, it can be precipitated in any patient by glucose (like D-5, D-10 or D-50) administration who is thiamine deficient. It is not limited to alcoholics and can happen in any nutritionally deficient patient. It is always a good idea to add thiamine in D-5 drip in patients who are at risk of Wernicke's Encephalopathy.
Disorder was described about 25 years ago by Carl Wernicke as a triad of
acute mental confusion
ataxia
opthalmoplegia

Read a case of Wernicke's encephalopathy. in a non-alcoholic patient with MRI findings here (Ref.: The New England Journal of Medicine, Kaineg and Hudgins 352 (19): e18, May 12, 2005)

Also full review article Wernicke's encephalopathy from Philip Salen, MD at emedicine.com

Rule of 20s

2006-04-16T23:21:00.000-06:00

Monday April 17, 2006
Progressive rule of 20s

Q: What is "progressive rule of 20s" during Pulmonary Artery Catheter insertion ?

A: During Pulmonary Artery catheter insertion from Right Internal Jugular approach:
Right atrium (or SVC) should be entered within 20 cm from skin
Right ventricle should be entered within 40 cm from skin
Pulmonary artery should be entered within 60 cm from skin

Related Previous Pearl: Procedure Tip - Does that waveform look ‘wedged’?

Tacrolimus

2006-04-15T21:55:00.000-06:00

Sunday April 16, 2006

Case: 34 year old male with recent kidney transplant admitted to your unit with mental status change and family reports witnessed seizure. While evaluating patient, nurse hand over critical lab to you with magnesium of 0.2 mg/dl, your first response is to ask potassium level but it is actually on hyperkalemic side with 5.5 meq/l. As you call his renal transplant physician and reports severe hypomagnesemia and seizure but normal BUN/Cr level, his first question is to read patient's medication list. Why ?

Tacrolimus (FK-506 or Prograf) is a macrolide, an immunosuppressive drug, use in organ transplant to reduce the risk of organ rejection. It causes hyperkalemia due to renal tubular acidosis, Type 4 (RTA-IV) but simultaneously cause hypomagnesemia, unusual to find both together. Other side effects of tacrolimus includes seizures, tremors, hypertension, confusion, calciuria, hyperglycemia, weakness, depression, cramps, and neuropathy. Apart fron side effect of severe hypomagnesemia, seizure and other neural are direct effects of tacrolimus too.

References:
1. Downregulation of Ca2+ and Mg2+ Transport Proteins in the Kidney Explains Tacrolimus (FK506)-Induced Hypercalciuria and Hypomagnesemia - J Am Soc Nephrol 15:549-557, 2004
2. FK 506-induced neurotoxicity in liver transplantation. - Wijdicks EF, Wiesner RH, Dahlke LJ, Krom RA. - Ann Neurol 1994;35:498–501.
3. Prograf Warning Letter - fda.gov
4. Tacrolimus leukoencephalopathy: A neuropathologic confirmation Lavigne et al. Neurology.2004; 63: 1132-1133
5. Progressive neurological disease induced by tacrolimus in a renal transplant recipient: Case presentation - BMC Nephrology 2006, 7:7