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One evening, writing drug charts at the nurses’ station, I looked up to find a woman smiling at me. She was wearing a cashmere sweater over her pyjamas. “Gin and tonic, please,” she said, placing a glass on the counter. We both looked at it for a minute. “I’m afraid we’re out,” I said. “Can I fetch you some water? Tea?” “Tea,” she said. “Do you have any Earl Grey?”

Fluid (although possibly not alcohol) is essential to health. But it’s amazing how difficult it can be to meet basic needs in hospital, even when patients aren’t disoriented. Most patients need to drink – unless they are “nil by mouth” – and they need to urinate. But even simple things aren’t necessarily as easy as they are at home. To drink enough fluid, you need to be aware of your thirst, and not vomiting or nauseous or drowsy or confused. You need to be strong enough to get yourself upright, and have enough power and co-ordination in your hands and lips to manage a cup. Pouring from a jug takes further balance and strength.

Drinking a quarter of a pint may entail calling for help – and any intake will eventually become output, which means pressing the buzzer again to get the commode or asking for help to reach the toilet. “Encourage oral intake,” the doctors write in the notes, not realising what a formidable task this can sometimes be. Ensuring that a frail or demented or post-operative patient has enough to drink is a vital and time-consuming job; it’s labour-intensive, although it’s not the kind of labour that ever seems to count when the staffing ratios are devised.

At the end of last year, the National Institute for Health and Care Excellence, which decides which drugs are used by the NHS, published new guidelines regarding acute kidney injury (AKI), a condition in which your kidneys undergo a sudden deterioration in function (which is usually reversible). The guidelines, and subsequent reports, make it clear that we are failing to monitor and treat AKI appropriately. We fail to notice and react to dehydration, and we continue to use potentially nephrotoxic drugs such as non-steroidal anti-inflammatories (ibuprofen etc) in patients with compromised renal function.

Patients entering hospital are in a vulnerable state, their physiology strained by infection or surgery; it is easy to push their kidneys into decline. AKI causes an estimated 1,000 deaths a month: more than blood clots or the so-called superbugs such as MRSA. It has many causes, and usually arises from a combination of factors. Some can’t be helped; we are failing to stay on top of those that can.

In AKI, the kidneys work less efficiently. Waste products accumulate in the blood and the serum creatinine (a blood marker of kidney function) starts to climb. AKI is pretty much symptomless – other than a fall in urine output – until the kidneys are in a very bad way indeed. The key is to realise that AKI is happening. We can’t control every contributing factor but if we spot it in time, we can at least stop things getting worse and create the right conditions to allow recovery.

We can start intravenous fluids, pause any harmful drugs and avoid investigations that might injure the kidneys further. All the while we must monitor the urine output and creatinine level closely, until the former starts to rise and the latter to fall. Part of the treatment is to ensure the patient is well-hydrated. It’s not complicated but it is frustratingly difficult.

Sophie Harrison is a hospital doctor in South Yorkshire. This column appears fortnightly

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