Friday, 7 December 2007

Dr Aoki's Visit

Dear Bloggers

Yesterday saw the great Dr Aoki visit our institution again to impart his wisdom to us all.

He was presented with a most unusual case of a patient with multisystem problems including confusion, pneumonia, and skin rashes.

The patient had a varied and extensive history and the sexual and social histories provided for many areas of thought for considering different diseases.

The session went very well and a lot was learnt by all who attended.

At the end of the session, Dr Aoki was presented with a number of the second edition of his own book on infectious diseases to sign for the residents!

Tuesday, 4 December 2007

Dehydration-- How To Recognise It and Avoid Disaster.

Dear Bloggers

Today I would like to discuss about inpatients and one of the biggest problems that can cause morbidity and mortality -- Dehydration !!

Yes, dehydration. Patients who are admitted with severe illness usually have a deterioration over several days before being admitted to the hospital. In that time, they may have stopped eating and drinking and have already started to dehydrate. Moreover, with the onset of confusion, they may have abolition of thirst and be unaware of the fluid loss. Addition of fever and a warmly heated hospital ward all year round means that fluid loss from sweating can become a real problem.

We as doctors have to acknowledge that dehydration can occur in patients and that it can even occur in hospital.

How to recognise dehydration and how to deal with the problem requires knowing what to look for and communicating with the nursing staff. For example, asking the nurses whether the patient is drinking by themselves and the total quantity is a basic question but useful as it indicates that the patient is alert and whether they have an intact thirst mechanism.

Asking how much urine the patient has been passed is equally as important because low urine output is a red flag danger sign that no doctor should miss.

Examining the patient is very important. The fingers should be felt for reduced temperature which can indicate vasoconstriction. Next the pulse for assessment of tachycardia followed by checking the skin turgor. The finding of 'tenting', where the skin pulled up into a fold, usually on the forearm, taking several seconds to flatten can also indicate dehydration. In the elderly, with loss of connective tissue, the sign is not entirely accurate, but it should be interpreted in the context of the clinical situation. Checking the mouth mucous membranes and tongue to assess how wet it is (dehydration cause salivary glands to cease production of saliva) is again a reasonable sign although it can be misleading if the patient is mouth-breathing. Obviously, knowing the blood pressure and assessing if there is a drop in blood pressure (>20/10mmHg) when sitting or standing is an indicator of hypovolaemia or sympathetic dysfunction. In children, looking for sunken eyes and reduced pulsation of the anterior fontanelle is a good indicator of volume depletion.

Examining the peripheral lower limbs can also reveal skin mottling which is a purple discolouration of the lower limbs in a non-specific lace-like pattern that ascends from the feet to the thighs with reduced skin temperature indicates reduced circulatory volume, although by this time, the patient can be severely unwell.

Finally, checking the urine volume and colour in a catheter bag can be helpful. Dark coloured urine is usually indicative of the concentrating ability of the kidneys and if working normally, a small volume, highly concentrated volume is produced. It can be dark for other reasons such as jaundice, anti-TB drugs, glomerulonephritis, fistula from bladder to bowel, myo- or haemoglobuniuria, alkaptonuria (only on standing in air for oxidization) etc..

Hence, there are many indicators of dehydration and hypovolaemia. These cannot be identified by CT or MRI scan and require the physician to examine in some detail at the bedside.

Of course, blood and urine analysis can give extra information such as the severity, but actually going to the bedside for making an assessment is essential.

I have heard of many cases in Japan and the UK, where the renal function begins to deteriorate and things such as infection, drugs and collagen-vascular disease are thought to blame, and in some circumstances, that may be so. However, in several cases, when going to the bedside to examine the patient, an element of dehydration and hypovolaemia is invariably present.

There is a constant concern that too much IV fluid can cause heart failure from 'fluid overload'. Yes, too much fluid can cause heart failure, but too little fluid will cause hypovolaemia, multi-organ dysfunction and especially, pre-renal failure. Which is the worst of both evils, heart failure or renal failure??

Well, if too much fluid is given to a patient, there are several therapies to treat heart failure such as loop-diuretics, nitroglycerine, CPAP, and even haemodialysis if necessary. However, for pre-renal failure from dehydration, there can only be one therapy and that is WATER. Haemodialysis will not resolve pre-renal failure. All haemodialysis does is remove toxins but it does not change the causative problem. That can only be sorted with fluid administration.

Hence, the worst problem in my view is renal failure rather than heart failure. Therefore, the concern of giving too much fluid and causing heart failure is unfounded. In fact, these sorts of patients with dehydration and hypovolvaemia may have several litres of fluid deficit and require significant replacement.

In a recent case reported to me from another institution, a patient had developed a pneumonia in hospital and it had been noticed that the BUN and creatinine were rising. There was concern that the drugs were causing the renal failure or the sepsis. However, when going to the bedside, it was clear that the problem was severe dehydration from the signs described above. The patient was having 1.5 litres of fluid in per day but only 500ml out in urine. The doctor was concerned about giving more fluid without obvious reason as the patient had no signs of heart failure.

The in-out volumes were unbalanced because of the concentrating ability of the kidney in response to hypovolvaemia through increased Vasopressin release and upregulation of the renin-angiotension-aldosterone axis and hence, it was no surprise that this was the clinical picture.

It was suggested to double the daily input (at the very least), and after several days, the patient's kidney function had normalised from the replenishment of water.

Water makes up 70-80% of the human body and depletion of it can kill.

Common things are common -- dehydration in the elderly is very common and should never be forgotten or ignored. Giving adequate fluid replacement can make the difference between your patient improving quickly or developing worsening renal failure. This can be completely avoided.

Please do not be scared giving IV fluid.

There are several equations available for assessing the estimated weight of a patient and working out the fluid loss by calculating measured Na against target Na, which may all be very helpful. However, we are not machines. We are biological organisms and one equation does not fix all. Sometimes, giving fluid and reviewing the urine output, blood pressure, chest sounds for new crackles [assessing for heart failure] and pulse rate can determine whether your iv fluid replacement strategy is on target, under- or overshooting.

At the beginning and the end of the day, it comes back to being around the bedside and examining the patient using your clinical skills of assessment to see if your treatment is working and adjusting it accordingly.

Please consider.... :-)