Is one kidney enough for me?

Well, Iam doing Transplant Nephrology right now. So I though I will chip in with this topic ....that many patients ask about. These are some of the facts that we know about donating a kidney......

Usually donors have be healthy..and ideally free of chronic problems especially Diabetes, cancer, strong family history of renal disease ending on dialysis, and without anatomical abnormalities like Polycystic kidneys.

So we are dealing with a group of healthy people. Consequences of donating may be divided into two...for the ease of explaining..

1. Issues with surgery - The surgery for removing is mostly done laparoscopically these days.(usually left kidney is removed due to ease of removal ). On a recent study in JAMA ,the mortality in the first 90 days is around 3/10,000 patients. Mostly due to bleeding, thromboembolic disease etc. After 1 year the mortality equals the mortality with a comparable healthy cohort.

2. Issues with loss of kidney mass -  Since 50% of the nephron mass is lost, its expected that their left over kidney swells up a little to compensate, and creatinine can theoretically double. But usually creatinine goes back to normal or settles within 40% above baseline. The other theoretical risks that need to be watched for over the next 2 years are 1.Hypertension ( not significantly high than in normal population)
                                       2. Protenuria (significance is not really known)
 As I mentioned above, the mortality is the same for these people as for someone who has 2 kidneys.

One advantage of donating a kidney is...if in case the donor ends on Dialysis either due to trauma, cancer or CKD), then they will be considered as high priority, and will get transplanted (if they dont have a living donor) within 6 months.

So..go ahead ..encourage patients to donate...if they can...!!!!

Hepatitis C and its transmission........something to know!

I came across this article from Yale(presented at the 17th CROI in Feb 2010), where they did a research on the Survival of hepatitis C virus in the syringes ..mainly with respect to intravenous drug users, as the main form of transmission of Hep C in US is intravenous drug abuse(IVDA). Eventhough HIV and HCV almost have the same mode of trasmission, there are differences in their prevalance.For example...in places where HIV prevalance is 1-10 %,the HCV prevalance has been around 40-50%. This is likely due to longer survival of HCV.

Ok...what they studied in Yale is ....loading insulin and tuberculin syringes (both are commonly used by IVDA) with a lab strain of Hepatits C virus, and they stored the syringes at varying temperatures of 4 C(fridge temp), 22 C(room temp), and 37 C(autoclave temp) for up to 63 days. They checked for viability of HCV. The insulin syringes did not show viable HCV beyond day 1 at all temp except 4C where it was viable until Day 7
The tuberculin syringes there was 96%, 71% & 52% viability for HCV at temp of 4C, 22C, & 37C respectively, at 7 days.
This is likely due to the high void volume ( volume left in syringe after injection) in case of the tuberculin syringe.This study gives us some idea about the transmission of HCV on syringes. Since this study has been done on lab strains, it may not apply for the actual HCV. With this ..I will leave you to decide on the final sentence..

This gives us something to add to our history taking skills..when it comes to IVDA. And we can add this to our counselling skills as well (if we have time!!). Preventing needles is the best way to prevent HCV.But if not possible..then may be using an Insulin syringe instead of a tuberculin syringe may help. This will be a advice from me to my patients until we have any further compelling evidence to change this.

Obstructive Sleep Apnea - More than about sleep!!

Sleep apnea has long been considered something that improves the quality of life for patients. However, it's becoming more clearer that OSA obviously has metabolic effects way more important than just helping people sleep and feel better in the morning.

Severity of OSA correlates with diabetes control. According to a study published just last December 2009 at AJRCCM, compared with patients without OSA, the adjusted mean HbA1c was increased by 1.49% in patients with mild OSA, 1.93% in patients with moderate OSA, and 3.69% in patients with severe OSA (P < 0.0001 for linear trend).

Treating heart failure patients with OSA can actually improve CHF. In the first randomized trial involving 24 patients with heart failure (EF < 45%) and moderate to severe OSA, 30 days of CPAP lowered daytime heart rate and systolic BP and increased ejection fraction by 9%. In contrast, there was no change in any of these variables in the 12 patients in the control group.

Lastly treating OSA actually helps with atherosclerosis! A small Brazilian study of 24 patients published in AJRCCM showed that 4 months of CPAP in people with OSA made a significant decrease occurred in carotid intima-media thickness, pulse-wave velocity , C-reactive protein , and catecholamines after 4 months of CPAP.

The impact of OSA on cardiovascular disease and stroke is so profound that the AHA/ACC actually produced a consensus statement about this.

So, treating OSA should be as much of a priority as those pills everybody likes prescribing!!

Some more indications for Statin

As we all know, we are getting more and more new information on the benefits of Statins independent from their ability to inhibit HMG CoA reductase and reduce LDL cholesterol. 

There has been a great interest in high CRP levels and their relation to increased coronary events, even in the absence of hyperlipidemia. The study done on nearly 500 patients who had MI showed nicely that Pravastatin reduced the median and mean CRP levels significantly, compared to placebo, over a period of 5 years.(E.Braunwald - same person who contributed a lot to Harrison's Textbook). With this background, PROVE IT-TIMI 22 trial recruited nearly 4000 pts, and showed that pts with low CRP levels after statin therapy have a better clinical outcome than if CRP level is high. 
Given these stimulating results, investigators tried to apply this in the primary prevention of CAD. And guess what...two studies with slightly different population (AFCAPS- low risk pts, and JUPITER- intermediate and high risk ...due to 10% 10 yr Framingham risk score) showed significant reduction in the first coronary event in patients whose CRP level decreased while on statin. All the participants didn't have hyperlipidemia. The Canadian Heart Guidelines have already included CRP in risk stratifying pts for primary prvention. 


Statins also reduce the incidence of DVT/PE as shown in a meta analysis of nearly 1 million pts done at U Conn. JUPITER trial was included in this meta analysis, as this is the only randomised trial to show reduction in DVT ( but not significant for reduction in PE).


Now this is the latest on the list of benefits from Statin ---- A meta analysis looking at incidence of ventricular arrhythmias(VF/VT) among pts with CAD on a statin Vs no statin, has shown a 31% reduction in ventricular arrhythmic events in the statin group. This has previously been shown in a subgroup from MADIT-II trial.
So ...what about Atrial Fibrillation. Well there were many studies on Statins and maintaining sinus rythm in A fib...with conflicting results. A recent meta analysis showed that Statins does not help maintain sinus rythm in patients who underwent elective DC cardioversion. 


This list of benefits might increase every day....... keep checking!!

Confounded by Delirium

Ok so not everybody is interested in this, but there was an excellent review in JAMA recently which went over the evidence on the accuracy of several instruments in diagnosing delirium in adults.

As we all know, delirium is an indepenent marker for increased mortality, longer hospital stay, increased complications, persistent cognitive devicits and increased discharge rates to long term care.

So when you get a patient who is clearly "out of it".. what does the regular intern reflexively do. MMSE right? NO! According to the review, the MMSE was the LEAST useful for identifying patients with delirium (LR 1.5 for a score of less 24> better than guessing).

The study included 11 bedside delirium instruments. One instrument stood out: the Confusion Assessment Method (CAM) which has a +LR of 7.3 and -LR 0.08 and may be the most convenient because it can be performed in less than 5 minutes, and can be applied by nongeriatricians.

Some training is recommended and an instruction manual is available online. The algorithm is based on only 4 elements of the DSM-III-R criteria: acute onset and fluctuating course, inattention, disorganized thinking and altered level of consciousness(see inset).

ACE-i - a wonder drug for Heart failure

ACE-inhibitors have long been used in heart failure due to their many beneficial effects.  Angiotensin II has shown to activate growth factors in myocardium. So blocking the RAAS with ace-i helps with regression of LV hypertrophy. As we all know, LVH is associated with increased incidence of heart failure, MI or sudden cardiac death. ace-i as we all know....are related to cough due to to inhibition of bradykinin degradation. But this is also the reason how it improves insulin sensitivity, as bradykinin increases Insulin dependent glucose uptake by cells.

With regards to clinical outcomes in patients with Heart failure, how do ace-i perform?
In 1987, CONSENSUS trial was published in NEJM. 260 patients with NYHA class 3 & 4 heart failure were randomised to enalapril Vs placebo. Cardiovascular mortality was reduced by 30% in enalapril group. There was also a significant decrease in cardiac size, and in NYHA symptoms. 7 pts in enalapril group had to stop it due to hypotension Vs none in placebo arm.

In 1991, SOLVD trial was published in NEJM. 2500 pts with LVEF < 35% and NYHA class 2 & 3 were randomised to enalapril Vs placebo. Follow up for 3.5 years. Enalapril had a 15% reduction in mortality compared to placebo. But in this study patients with creatinine >2 mg/dl or who had a tendency to increased creatinine during the run-in phase ,were excluded from the study.
In both the above studies ..the reduction in deaths were largely due to reduction in deaths due to pump failure.

In 1992, AIRE study was published in LANCET. 2000 pts were randomised to receive Enalapril Vs placebo 3-10 days after an acute MI and showing signs of Heart failure. F/U for 6 mon - 1 year. There was a 27% risk reduction in mortality, with enalapril compared to placebo. The beneficial effect was evident as early as in 30 days. An AIRE extension study (AIREX) found that the benefit extended upto 3 years after the study.

Then in 2000, HOPE trial was published in NEJM! 9000 high risk pts (age > 55) with evidence of vascular disease( CAD, PVD, stroke) or diabetes with 1 additional risk(HTN, hyperlipidemia, smoking ) were randomised to Ramipril Vs placebo. F/U for 5 years. There was a 22% reduction in cardiovascular mortality with Ramipril compared to placebo. Note that 7% of Ramipril patients stopped it due to cough.

All these studies(and many more) have shown beyond doubt, the usefulness of ACE- inhibitors along the whole spectrum of heart failure. As we all are aware of, they also have a renoprotective effect (thats an extensive topic!!). It has become such a wonder medication for Cardiologists, Internist, nephrologist, endocrinologists.........

metformin and lactic acidosis- How strong of a relation?

How much should we be worried about.I felt that lactic acidosis has been hyped a little by everyone in clinical practice. In fact I am yet to see a case of lactic acidosis that can be attributed to Metformin use.
The relation between the two is a legacy of Phenformin, which was taken out of market in 1978 due to high incidence of lactic acidosis.It is still prescribed in Brazil ,Greece, China & Portugal.
Metformin also possesses this risk, but to a lesser extent, mainly because it is not metabolised in the liver(as phenformin).


Lets recap lactic acid metaboism....
Lactic acid is the a dead end product beacuse pyruvate, its immediate precursor is also its only route of metabolism. Lactate is buffered by equal amount of HCO3, and the liver's job is to oxidise the lactate and replace the HCO3.This is a formidable task, as 1400 mmol of lactate are produced everyday, but the plasma concentration is maintained around 1 mmol. The kidneys are responsible for excretion of 10 -20% of lactate. If we look at the picture above, increase in NADH (from alcohol) or pyruvate(from glycolysis) would shift the reaction towards lactate. Metformin may inhibit oxidative metabolism and increase NADH, and thus worsen lactic acidosis. But this happens usually if excretion or buffering is deficient.


Lets look at some data. Of the first one million patients who took Metformin in US, 47 developed lactic acidosis. Of them 43 had renal failure or CHF. Only 4 didn't have any other reason apart from Metformin, and these were not fatal (NEJM 98). Based on this observation, CHF was included in the CI list for Metformin.
Another study done my Bristol Meyers (COSMIC study) comparing 1 year treatment of 7200 pts on Metformin Vs 1500 pts on other antdiabetics showed no cases of lactic acidosis. A meta analysis in 2003, of 194 studies didn't reveal any case of lactic acidosis in 36,893 pt years in Metformin group Vs 30,109 pt years in non-metformin group. Many of the studies in this analysis were of short duration, and included very few number of patients though.
The most recent Cochrane review 2008 on this subject concluded "There is no evidence from prospective comparative trials or from observational cohort studies that metformin is associated with an increased risk of lactic acidosis" . 


The main accusations on Metformin and lactic acidosis have been only from case reports, and they still continue to be reported. 
Usually pts on Metformin who develop lactic acidosis are sick, and have other underlying problems.I will go back to my first statement,that this relation has been overhyped, and that Metformin does not seem to cause lactic acidosis IF USED IN THE RIGHT POPULATION.( avoid if CKD 4 & 5, caution in CKD 3, avoid if Creat >1.3 in females, and >1.4 in males, CHF, and any underlying reason that can cause tissue hypoxia--> lactic acidosis)

urinalysis in rhabdomyolysis

Urinalysis is an important part of the evaluation of any renal disorder.It is very simple, easy to perform and gives quick and valuable information. Out of the whole array of information, lets concentrate on the test that need to be done and are useful for diagnosing and managing rhabdomyolysis

Urine volume - ask about this in the history as it may give an idea about the renal involvement while you wait for the Creatinine. Of course it is helpful in monitoring response to fluids and recovery of function.

Color of urine - the myoglobin released from the muscles, turns the urine brown or red due to the heme content.

Ph of urine - Its useful to check Ph as myoglobin has shown to precipitate when Ph drops below 5.5. So check this initially and start with aggressive fluid resuscitation. recheck the Ph after 2-4 L boluses ,and if its still less than 7 , infusing bicarbonate will help increase the urine Ph and prevent precipitation of myoglobin in the tubules.


Blood & RBC count - it is well known to everyone that the urine is positive for blood and negative for RBCs( or has less than 5 cells/hpf) . The dipstix we use is sensitive for picking heme protein and myoglobin breaks down into heme, so is the positive finding of blood ,with no RBC s under the microscope. So in this scenario we assume its due to myoglobin.

Casts - finding of casts are useful diagnostically, as they are in any other case of AKI. In case of rhabdomyolysis, the casts are formed as a result of reaction between Tamm Horsfall protein and myoglobin.The casts are usually pigmented.

Urine electrolytes - In rhabdomyolysis you can calculate the Fractionl excretion of Sodium, and this will give an idea about the likely mechanism of AKI. Both pre renal and ATN can contribute to AKI in rhabdomyolysis.
Hope you all have fun with spinning the urine next time!

osmolality ...or...osmolarity!!

This probably wont interest many of us.But it is interesting to know why ,how and when we use these terms!

Before going to osmolality or osmolarity, lets get the definition of molality & molarity.

High school physics - Mole is a SI unit for amount of substance i.e quantity. The no. of atoms in one mole is Avagadro's consatant and we dont need that here!!

MOLALITY - no. of moles per kg of a solution (mol /kg)

MOLARITY - no. of moles per litre of a solution (mol/L)

So if we apply this ..... Osmolality is no. of osmoles /kg, and Osmolarity is no. of osmoles /L .

One more word we need to remember- DENSITY which is mass / volume.

Lets quickly discuss abt water which has a density of 1. To make it simpler....1L of water will be equal to 1kg of water! So if you apply the definition osmolarity & osmolality to water, then they both would be the same.

Since blood has a density close to water i.e 1 (we know that because the specific gravity of blood is 1.03 - 1.05), now we can say that its osmolality is equal to its osmolarity, and sooooooo they can both be used interchangeably.

Osmolarity & Osmolality can be used interchangeably in case of blood/plasma, only beacuse its density is nearly equal to 1. For fluids whose density is not near 1, then you cannot use these terms to mean the same thing, as osmolality & osmolarity will differ.

Is it still not clear ? !

I have cavities in my lung . Im from South Africa- Can I fly?

We recently had a a lady from South Africa who came to US to visit her daughter.She is a physician in RSA in a TB clinic. She came to our ER c/o dysuria and subjective fevers. She didn't have any other symproms, and she was prescribed bactrim as urinalysis showed leucocytes & nitrites. A clever resident! did a chest Xray which showed 3-4 cavities. She is supposed to fly back to RSA the next day. This raises a few questions.

1. What is the significance of the finding of cavities in this lady ?
2. Does it need to be investigated now?
3.Can she fly back home?
4.Is there a higher chance of TB spread in a flight?

                    She is a high risk for TB ( based on work and she is from RSA). The finding of cavities in this lady is incidental. The most important point to remember is that SHE IS ASYMPTOMATIC (esp without a cough),as with regards to TB, it spreads through respiratory droplets. Cavitary TB is more infectious than other forms of TB.
As she does not have any respiratory symptoms she does not need to be investigated right now.But has to be evaluated soon ..first with a CT chest and a PPD, and then if needed, a brochoscopy.

Third....as she is asymptomatic, she is safe to fly back home. Have a look at the WHO recommendations on flying - In short.. you should not fly....if your sputum is +ve for AFB. If positive, then you should be treated for 2 weeks , and for 4 weeks in case of MDR TB before you can fly.

Forth... In 2005, CDC diagnosed 6 cases of TB in air travellrs and cabin crew, and trace down all possible contacts.This included 2900 travellers in 191 carriers.followed for a period of 3 years, only 2 of them developed TB(one was another cabin crew member, and other was a person sitting on the back row to the person with TB). So it looks like the chances of spreading TB in a flight is same as in any confined space(like in a elevator or car), and spreads only to close contacts. In both cases of TB, the flight duration was 12 hours.

So, if someone with TB has to travel, then they can do so with a little isolation, and if the flight duration is less than 8 hours.......well...provided Public Health Department is aware of this!!

cell phones and brain tumors

Cellular telephones, which include handheld or mobile telephones, car telephones, and portable or bag telephones, operate on radiofrequency (RF) signals in the 800- to 900-MHz range
.
Cell phones are dangerous 
They emit microwaves.
They produce heat.
Source of the emission is close to your brain.
There are claims that people have had brain tumors in the exact size, shape and position as the antenna on their cell phone!!

Cell phones are safe
Cell phones use a very, very low level of radio frequency (rf) energy - too low to cause damage.
The type of energy emitted is non-ionizing - meaning it doesn't cause damage dna.
Hundreds of millions of people have been using cell phones and cordless phones for years. If there were a problem, we would have seen it by now.


A case control study from JAMA looked at 470 patients with primary brain cancer and matched them with a similar cohort without brain cancer. No association of cancer was found for a follow up period of 2.8 years.Interestingly cerebral tumors occurred on the same side of the head as cell phones were used.In temporal lobe tumors , a greater proportion of tumors occurred on the contralateral side. Both these findings failed to achieve significance.

The latest study published in March 2010 -  INTERPHONE was a international case control study which looked at 4 types of cancer - glioma, meningioma, acoustic neuroma and parotid tumors, and their association with cell phone usage. They included 2708 glioma and 2409 meningioma cases and matched controls. Overall, no increase in risk of brain cancer was found in cell phone users over a period of greater than 10 years. 


We need studies with even longer follow up, considering the fact that radiation changes in tissues take a long time to develop .As for as now, we can safely tell our anxious i-phone users ! that there is no association between cell phones and brain cancer over a 10 year period of use.

Preventing the first variceal bleed

Once a person has been diagnosed with Cirrhosis due to any etiology, then the next question would be if they are compensated or decompensated? Signs of decompensation are ascites, jaundice, encephalopathy, variceal bleeding. The median survival of pts with compensated cirrhosis is about 9 yrs.
So...... after someone has been diagnosed with compensated cirrhosis, they all need a screening for varices and hepatocellular caner. Lets discuss varices and its management,as its present in 50% of cirrhotics. If varices are found on screening endoscopy, there are two options available for managing them.
1. Non selective beta blockers (NSBB)
2. Endoscopic Variceal ligation (EVL)
 For management purpose varices can be divided into small (<6mm) and large (>or = 6mm).


For varices which are small, have any red wale marks on them, or child Pugh class B/C then NSBB are the right options.They reduce the incidence of first bleed by 10% over 2 years.Actually the effect is more evident in pts with large varices than in small varices.(Gastro 2004). NSBB should be titrated to a HR of 55 - 60/min.( but remember there is no correlation between reduction in HR and reduction in portal pressure)
NSBB are not useful if endoscopy does not show varices, as they dont prevent development of varices, but delay the growth of varices. Once you begin treatment with NSBB there is no need to repeat endoscopy.


For those with large varices,red wale marks, idependent of Child Pugh class either EVL or beta blockers can be used, and both are equally effective in preventing the first variceal bleed and reducing mortality. Randomised trials have shown EVL to have a small but significant reduction in variceal bleed than NSBB. But these trials were of very short duration. And recent metaanalysis have shown that both therapies are equally effective. Check this excellent report.Hepatology 2008 . Again if NSBB is started there is no need for a repeat endoscopy, whereas EVL is done every 1-2 weeks until obliteration, and needs surveilance every 6 months.


Well, a combination of EVL and NSBB has also been tested in a few studies with no significant difference between combination and each agent used alone.In fact there were more side effects with combining them.

Is MONA in MI....evidence based..

Do I need this anymore !

Im referring to the mnemonic we all learned in our medical school, for management of Acute Myocardial infarction...........MONA standing for Morphine, Oxygen, Nitrates and Aspirin respectively.
We will discuss about the usefulness of Oxygen supplied through a mask or a cannula in the setting of an acute MI.

Although it is biologically plausible that oxygen is helpful, it is also biologically plausible that it may be harmful. Potentially harmful mechanisms include the paradoxical effect of oxygen in reducing coronary artery blood flow and increasing coronary vascular resistance(McNulty et al demonstrated this in a study on 29 pts during cardiac acth 2005 ) and also reperfusion injury from increased oxygen free radicals( AJP 2007)


A recent review by Wijesinghe (Heart 2009) looked at 2 controlled trials and  concluded that  routine use of high-flow oxygen in uncomplicated MI may result in a greater infarct size and possibly increase the risk of mortality. 
Subsequently, the most recent Cochrane review 2010 concluded that there was no evidence to support the use of supplemental oxygen. In fact, there were  3 times more likelihood of death in patients given O2 than not.(Since the total mortality was very low, this finding may be due to a chance)


Its surprising that the major evidence for the benefit of oxygen therapy in MI comes from studies of experimental coronary occlusion in animal models( AHJ 1995 ). 
The current AHA guidelines puts use of O2 in MI as level C evidence. In the accompanying text it says that it is ‘‘not known whether this therapy limits myocardial damage or reduces morbidity or mortality’’.


So it looks like..the age old mnemonic needs to be altered, as does the AHA guidelines !! 

Is an IVC filter as safe as a thermometer ?

According to FDA ,it is !

The FDA has classified and described over 1,700 distinct types of devices and organized them in the Code of Federal Regulations (CFR) into 16 medical specialty "panels" such as Cardiovascular devices or ENT devices. The devices are classified into class I, II, or III.

class I, II, or III, depends upon the degree of regulation necessary to provide reasonable assurance of their safety and effectiveness. The class into which a device is placed determines the requirements that must be met before a manufacturer may distribute the device.
Class I includes  devices with the lowest risk and Class III includes those with the greatest risk.
Given these, lets look at some commonly used devices and their classification.


Class I - tongue depressor, gown, manual stethoscope, nasogastric feed tube, lead jacket used in radiology. 


Class II - EKG, EEG, clinical thermometer, IVC filter, x-ray machine, electronic stethoscope, iv canula, blood pressure cuff, left & right heart catheters, low energy DC defibrillator (that we use), trancutaneous cardiac pacer, occult blood test kit.


Class III - implantable pacemakers, heart valves, intra aortic balloon pump, hip joint prosthesis.


These are some examples. Looking at the list, it does not make much sense to have such a broad classification, as a occult blood test kit and a defibrillator has to go through the same process of approval before being released in the market!

Now with reports of adverse events with IVC filters (Arch of Int Med 2010), may be FDA need to consider altering their classification system,as this does not serve the purpose of classifying the devices according to their use and risk profile.
Does anyone have an explanation for this?? 

Lung Nodule... What do I start attacking?

Major changes have been made this year on the staging system for Lung Cancer. This may cause some confusion as to the flow of patient work-up and clinical staging. The staging system is still based on the TNM system. This staging system is now based on a 10 year validation study involving 81,015 patients after exclusion of ineligible cases.

Remember that when dealing with a potential lung tumor, we should always biopsy the one that gives the highest stage. Restaging is always done once surgery has been made. This is the difference between clinical and pathologic staging.

The following changes were made:

• There are new size cut-offs of 2, 3, 5, and 7 cm
• T1 is divided into T1a and T1b
• T2 is divided into T2a and T2b
• Separate tumor nodule(s) located in the same lobe as the primary tumor are reclassified as T3, instead of T4
• Separate tumor nodule(s) located in a different lobe of the ipsilateral lung are reclassified as T4, instead of M1
• Malignant pleural nodules, pleural effusions, or pericardial effusions are reclassified as M1, instead of T4

This means that there are several scenarios:

1. If you have a pleural effusion, tap it. If it's malignant - Stage IV.
2. If you have another tumor on the other lung, or a lymph node on the other side (Basically anything on the other side) - Stage IIIB. No surgery.
3. If you have a tumor that invades the mediastinum, or a lymph nodes in the mediastinum or subcarinal area. - Stage IIIB. Likely not a surgical candidate. (This is where endoscopic endobronchial ultrasound has found some use).
3. Otherwise, assess as a surgical candidate, but do thorough staging first (MRI, CT, PET) to maximize your clinical staging.

Of course, after you do the surgery, you have to reassess the staging to make the staging pathology based. This is an oversimplification, but you get the idea.

Simple.

Doc....do I need to be admitted to ICU for this??

We had a a 48-year-old woman presented to the ER with a 48-hour history of anorexia, fever, chills, and cough and left pleuritic chest pain. On examination she looked acutely ill and seemed to be confused. Her temp was 102.2°F; HR110; RR 30; and BP 90/60 mm Hg. Sats was 89% with an infiltrate on chest xray. So the diagnosis is Community acquired pneumonia.

Can she go home? or needs admission to the floor? or needs ICU monitoring?

2 commonly used prognostic scoring systems for Community acquired pneumonia (CAP) are the Pneumonia severity Index(PSI) and the CURB 65.These were initially developed to predict mortality, but later have been used to triage patients with CAP. while PSI identifies patients with low risk of death, CURB identifies high mortality risk pts.

PSI - includes 20 variables. was developed from a cohort of nearly 140000 pts.(PORT cohort)has been validated in variety of pt. population. It divides pts into 5 classes, with class 1-3 having low mortality( 0.1 to 2.8%). class 4 & 5 had higher mortality. This does not translate into site of care decision making as nearly 27% of class 1-3 pts may end up in ICU(Eur Resp 2001).Also it doesn't take immunosupressed pts, COPD, pts with SOB etc.(e.g -a 30 yo HIV with SOB and smoking history would not be a high risk in PSI) So in triaging pts, PSI can't replace a physician's judgement, but can help to make that decision.

CURB 65 - developed and used widely in Europe,this is easy to use in ER, with scores >3 having a >20% 30-day mortality. Again,this has been translated into triage decision making, with scores 0-1 being managed as outpatients. Eventhough CURB predicted hospitalisation well in some studies(Capelastegui et al.), it can't replace clinical judgement for site of care.

So both these scores are not designed for making triage decisions,but can help clinician by providing an idea about mortality. They also are not very reliable in the elderly population.

Once decided to admit....then the need for ICU monitoring has to be determined, and again these 2 scores are not designed to do that. So ATS & IDSA have come up with a criteria ,which has sensitivity & specificity of 71% & 88% resp. for predicting ICU admission.

www.idsociety.org/WorkArea/DownloadAsset.aspx?id=9974. This is a pocket guide.

Used appropriately, these scores will help care for the needy, and at the same time save unnecessary healthcare spendng!!