Monday July 31, 2006
What's the right length of endotracheal tube (ETT) for oral intubation?
a gold standard the only way to make sure that tip of ETT is atleast 2 cm away from carina (or at appropriate place) is via
chest X-ray. But there are many bedside quick tricks/formulae described in literature. One such formula 1 which also found to have good clinical correlation, is
ETT length (incisors to midpoint of trachea, cm) = patient's height
Like, if patient's height is 170 cm, ETT should be taped at
170/10 + 5 = 22 cm
Another trick is to have ETT's cuff palpable at sternal notch, a technique
described about 40 years ago ! 2 .
1. Anaesthesia Intensive Care 1992;
2. Anesthesiology 1964; 25:169
Sunday July 30, 2006
When to "trach" patient?
It is a common understanding that if prolong ventilation is anticipated, its better to provide tracheostomy to
patient but so far there is no standard time period and it all depends on case to case basis and physician-in-charge's
1. One study
recently looked into a total of 163 relevant ICU patients 1 and study suggests
that: "Tracheostomy after 21 days of intubation
is associated with a higher rate of failure to wean from mechanical ventilation, longer ICU stay and higher
2. One meta-analysis of five
studies with 406 patients was recently published in BMJ 2 and
found that " In adult ICU patients, who require prolonged mechanical ventilation,
performing a early tracheostomy, may shorten ventilator days and length of stay in ICU but does not alter mortality or the risk of pneumonia".
Early tracheostomy - anywhere 1 - 7 days
Late (or no) tracheostomy - anywhere after 8 days but mostly after 14 days
Editors' note: It appears that jury is still
out on the timing of tracheostomy and present practice will continue till more studies get publish.
Related: Read this very interesting ground round
/all round review:
Adult Tracheostomy from Romaine F. Johnson, M.D. (March 6, 2003 at Baylor College of Medicine,
Bobby R. Alford Department of Otolaryngology-Head and Neck Surgery )
References: Click to get article
Saturday July 29, 2006
What Dig. level makes you happy ?
Digoxin is known to provid reduction in hospitalizations among patients with heart failure and depressed left
ventricular systolic function without improving mortality (DIG trial -The Digitalis Investigation Group trial) 1. Very interesting
work published in JAMA about 3 years ago (about 3800 patients) as a followup of above trial - looking into mortality
association with different Digoxin level 2 . What they found:
* SDC = serum digoxin concentration
* Patients were divided into 3 groups based on SDC at 1
Patients with SDCs of 0.5
to 0.8 ng/mL had a 6.3% lower mortality rate compared with patients receiving placebo.
No reduction in
mortality among patients with SDCs of 0.9 to 1.1 ng/mL,
Study suggested that the effectiveness of digoxin therapy
in men with heart failure and a left ventricular ejection fraction of 45% or less may be optimized
in the SDC range of 0.5 to 0.8 ng/mL.
References: Click to get abstract
Friday July 28, 2006
PICC line removal
Case: As you recently started your
critical care fellowship, you have been called to remove PICC line (Peripherally
Inserted Central Catheters). You successfully pulled the PICC line. What one thing you should document
in chart before throwing away the used PICC line?
Answer: As PICC line need to be trimmed at the tip on insertion, depending on the length of patient's arm, it is a good practice
to document in chart the length of PICC line at removal with length at insertion time. Obviously, they should be same.
Length of PICC on removal ______ cm = Length of PICC on
insertion ______ cm
See educational insertion brochure on PICC insertion here (pdf file)
(Bard Access Systems, Inc.)
Thursday July 27, 2006
Case: You have been called to 'code blue' with patient in PEA (pulseless electrical
activity). You tried rounds of epinephrine and atropine beside IVF wide open, without any success. While in that chaos you
heard 2 suggestions - one for 'soda-bicarb' and other for 'calcium chloride'. You decide to try both !. What would be other
advise you will give with order ?
Answer: First of all calcium is not recommended in PEA unless there is a specific indication like evidence
or suspicion of hyperkalemia (as in renal failure patients) or hypocalcemia or calcium channel-blocker overdose. It may have
potential serious complications 1.
Also, routine administration of sodium bicarbonate is discouraged because it worsens
intracellular and intracerebral acidosis and failed to show any improvement in mortality rate. It should be reseved
for patients with severe systemic acidosis, hyperkalemia, or a tricyclic antidepressant overdose.
In case, for above reasons, if you decide to use both sodium bicarbonate and calcium
- Give order with advise - "Use different lines for both". It's a simple chemistry.
NaHCO3 and CaCl in the same line will form together CaCO3. Also, it is advisable
to give soda-bicarb before calcium to avoid above reaction and to avail the benefit of soda-bicarb and once utilized, give
|1. Critical Care Medicine: The
Essentials - Marini and Wheeler, Page 335|
Wednesday July 26, 2006
Bedside tip ! - What to do if G-tube falls out !!
Case: You get call, in middle of the night that patient's gastric (PEG) tube
accidentally fall out. What would you do till gastroenterology service evaluates patient?
Answer: The stoma (opening in the skin from where PEG is inserted) close up very quickly, actually
as early as within 2 hours. First evaluate the area and examine the whole abdomen to rule out peritonitis, bleeding, infection
etc. If 'belly is benign', ask
for foley catheter at bedside. After lubrication or just wetting with tap water, insert the foley catheter about 3 inches
into the hole. Tape the catheter to the skin. If PEG is fresh, advise is not to inflate the baloon as whole purpose is
to keep the stoma open. If its an old and healed PEG, you may inflate the baloon and tape to skin. Don't use the catheter till ok given by GI service.
Tuesday July 25, 2006
Criteria for hepatorenal syndrome
The International Ascites Club has defined the specific criteria for
the diagnosis of HRS. All points of criteris need to be fulfilled
1. Low GFR, defined by
2. No systemic etiology
Absence of shock
- Ongoing bacterial infection
- Fluid losses and
- current treatment with nephrotoxic drugs
3. No sustained improvement in renal function as
- decrease in serum creatinine to <1.5 mg/dL or
- increase in clearance to >40 mL/min)
following diuretic withdrawal and plasma volume expansion with albumin
4. Proteinuria less than 500 mg/d
5. Absence of ultrasonographic evidence of obstructive
uropathy or parenchymal disease.
Minor criteria/supportive evidences - but not needed
- Urine volume lower than 500 mL/d
- Urine sodium less than 10 mEq/L
- Urine osmolarity greater than the plasma osmolarity
- Urine blood cells fewer than 50 per high-power field
- Serum sodium concentration lower than 130 mEq/L
Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis
(p 164-176) - Hepatology, Volume 23, Issue 1
Monday July 24, 2006
2 types of Hepatorenal syndrome (HRS)
About 40% of patients with cirrhosis
and ascites develop HRS during the course of their disease. There are 2 basic types of Hepatorenal Syndrome (HRS). Out
of many other names for HRS, few are Flint's syndrome, Frerichs' syndrome, Leber-Nieren-Syndrom, nephrite fonctionelle,
hepatourologic syndrome; hepatic death syndrome; bile nephrosis; urohepatic syndrome; hepatonephritis serosa acuta
as well as the Heyd's Syndrome.
Type 1: It is characterized by rapid and progressive
renal impairment, with marked increase in serum creatinine. Hyponatremia and hyperkalemia are very common. Type 1 is
mainly associated with acute liver failure and cirrhosis and usually get precipitated by subacute bacterial peritonitis
(SBP) even though it is treated. It is so acute that without intervention, most patient dies within few weeks.
Clinical significance: With recognition
and early intervention, disease process can be reversed and patient can be saved.
Type 2: It is characterized by relatively slow reduction
in the glomerular filtration rate (GFR). Without intervention, most patient dies within 3-6 months.
Clinical significance: To recognise type 2
is important as the major hurdle in these patients is resistance to diuretics.
Sunday July 23, 2006
2 most strong Evidence-Based
Practices associated with survival in patients requiring prolonged mechanical ventilation.
A very interesting study recently published in American
Journal of Medical Quality (March/April 2006 issue), looking into 6 Evidence-Based Practices in patients requiring prolonged
mechanical ventilation. End point was in-hospital mortality. 1463 ICU patients (in 38 AMCs -
academic medical centers) receiving continuous mechanical
ventilation for more than 96 hours were reviewed. All
measures were looked on day # 4 of MV except glucose control.
The six measures taken into account to see its association with
in-hospital mortality among patients requiring prolonged mechanical ventilation were
Sedation management - counted if respond to command on Day # 4 of
Stress ulcer prophylaxis - counted if present on Day #
4 of MV,
DVT prophylaxis - counted if present on Day # 4 of MV,
Semi-recumbent positioning (atleast 30 degree), counted if present
on Day # 4 of MV
Glycemic control (70-215 mg/dL), counted for all ICU days and
Spontaneous breathing trials - counted even if first attempt is by day
# 4 of MV
Out of above six, a strong association with survival was seen for only 2 measures: Sedation management
and Glycemic control . Glucose
level was allowed liberally upto 215 mg/dL but despite that it showed association with decreased mortality and similarly with
sedation break, despite its relatively late notice on Day # 4.
Editors' of this website feel that the biggest flaw of this study is: too
much liberty was given to centers in carrying out these measures like all measures were looked relatively late
on Day 4 of mechanical ventilation and it may have impacted the overall outcome of the study and failed to show
any association between improved survival with major interventions like SBTs, DVT and GI prophylaxis, HOB elevation
Related previous pearl:
Reference: Click to get abstract
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.
Friday July 21,
Prohibiting cell phones in ICUs - Are we
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,
surveyed reported using cell-phones as their primary mode of communications and
17.5% used overhead paging (or did not respond to this question)
- 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)
References: click to get abstract/article
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
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).
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.
- 80-100 units of factor VIII, which consists of both the procoagulant activity and the von
- 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
Tuesday July 18, 2006
IV (intravenous) DDAVP (desmopressin) should be given?
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.
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.
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.
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
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.
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
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
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.
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:
- 1:12, and
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
to get article/abstract
Intensivist-to-Bed Ratio - Association With Outcomes in
the Medical ICU - chest. 2005;128:567-572.
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
monoxide, Cyanide, Alcoholic ketoacidosis,
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.
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.
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.
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
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
July 13, 2006
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
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.
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.
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
Continue present settings with followup ABGin 1-2 hours
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,
2. A potential complication of bi-level positive airway pressure
after gastric bypass surgery - Obes Surg. 2004 Feb;14(2):282-4.
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
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.
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
full guidelines here
“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
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 ?
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)
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
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
Friday July 7, 2006
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.
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
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.
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
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
- It fully fits the definition of whole Brain death, showing the absence of whole brain perfusion, down to the foramen
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
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
- 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
References: click to get abstract/article
1. Emergency tracheal intubation: complications
associated with repeated laryngoscopic attempts - Anesth Analg 2004;99:607-613
Monday July 3, 2006
-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
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
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".
time from the onset of pulmonary edema to BNP testing was 3 hrs.
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:
Can BNPs replace Pulmonary Wedge Pressure?,
BNP or Pro-BNP ?
Re. Nesiritide (Netrecor)
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,
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.
of the head of the bed- 30 or 45 degrees ?
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,
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