far too clever an organ to eat!
MY COLLEAGUES IN THE ICU are a terrific lot, patient and forgiving. As a group we are extraordinarily tight and I can say, hand on heart, that we genuinely like each other and take an interest in each other’s lives. That is just as well because we spend a lot of time together and rely on each other to provide the 24/7 services our patients demand. Our lives are ones of constant compromise—‘Can you do my Thursday if I do your Saturday?’ ‘One of the kids is sick so could you do my second on today, please?’ The hospital has been a second home and, given the nature of our work, we all have a second family to think about. When I look around at other groups cast together for a lifetime like us, we have done well.
Like all families though, there are times when we drive each other crazy. This worries us because we’re sensitive people and generally attuned to each other’s feelings. I especially worry about it because I’m high maintenance on one or two fronts because of the huge range of things I do and the chaos which comes when I don’t manage them well.
Thankfully, we are all somewhat protected from each other by the regular, six-monthly turnover of registrars. These young doctors are wanting to be specialists in anaesthesia, emergency medicine or general medicine, so they move through different departments every six months to cover off their training requirements. Of course, we try to convert as many of them as possible to become trainees with the College of Intensive Care Medicine.
These young ones are hard-working and conscientious. They are very bright and most are quite savvy in a streetwise kind of way so they’re able to adapt to the intricacies of working in different parts of different hospitals, all of which have their own unique cultures and personalities.
I love hearing the registrars chat, all the while getting a sense of how they see the world—our one and their one. It’s really just gossip most of the time interspersed with occasional deeply philosophical arguments about the purpose of life. Sometimes they make me feel very old, but sometimes they sound old themselves and I feel sorry for them.
These young people bring fresh ideas and as a group we welcome that. Without their banter and our need to teach and supervise them, I am sure some of my colleagues would have given up on me years ago.
For many years I greeted these young doctors with a range of questions. I am genuinely interested in them as people. I’m also keen to learn about why they are doing what they are doing, and what they hope to accomplish in the future. I also like to ask them whether they eat kidneys.
You may think that is a strange question. If you do, I would either invite you to come and spend some time with us in the ICU or it might be slightly simpler if you read on …
I have a habit of anthropomorphising the organs of the body. That’s why I see the heart as reliable and organised in its function but capable of such stupidity in how it keeps going in some and how it stops in others. Contrast that with the unimaginably clever kidney, which some people choose to eat. I simply cannot and will not because I have too much respect for it as an organ and so too should those young kidney-eating doctors! I say the same thing about the brain and the liver of course, although there is a complication there. The liver is so brilliant an organ I know I should feel the same way but I am Jewish and ‘chopped liver’ (chicken livers) is a cultural imperative for me—in much the same way foie gras is to the French. When I explain that to the young doctors, trying to hide my smile, some roll their eyes while others appear dumbfounded.
I asked the same question in Samoa. ‘Yes, of course we do!’ was the answer. It is a sign of respect and honour to be a guest at a Sunday lunch with a Samoan family. Sundays in this proud independent island state are like the Sundays of old where devotion to G-d and family are unparalleled. The day starts early to prepare the umu—Samoa’s equivalent of the Māori hāngı ¯. Traditional foods and delicacies are placed in the earth oven to cook while the family attend church. The pièce de résistance is, of course, the whole pig, named Babe by many. Different parts of the pig are allocated to the assembled diners according to their status. Offal including the liver, heart and kidney are offered to the village chief or matai, as too is the tuala of the pig—that part of the body on the back between the ribs and the pelvis. The belief is that there is power in those organs and that power is assumed by those lucky enough to be offered it.
On occasions I too was offered the tuala of the pig, a potentially tricky situation for a Jewish man like me. Thankfully I was brought up by pork-eating Jewish parents who only ate kosher pork from circumcised pigs killed facing Jerusalem. So out of respect I accepted the honour with grace and a smile.
In the great debate between creationists and scientists over the origins of the world, the former argue that the world and man were created by G-d in seven days; the latter believe that mankind evolved over billions of years. Of course, I am clearly with the scientists on this one. However, in my heart, I would like to think that we are something more than just another form of animal life constantly evolving to become something else again.
When I think about the kidney, knowing what I know about how it functions and has adapted, I am left dumbfounded by its intricacies. There is no way such a complex and reliable thing could have been created in seven days, but it’s also hard for me to accept there is not some divine hand behind its evolution over such a long a time.
For many years, I spent time looking after the health of British tourists injured overseas. When I started, I would do ward rounds to all corners of the world from a small office in West Sussex.
As a guide I used a large white board and then later a new revolutionary tool, an Amstrad computer with its weird alien green font on a black background, to keep track of them all and to make my notes.
My patients, mostly domiciled in the UK, were scattered across all four corners of the world and suffered from a variety of ailments and injuries. It was my job to liaise with their treating medical teams to determine what levels of treatment were appropriate and to help decide when they were safe to travel home. Some of the travellers could do that on their own, others needed medical escorts—sometimes a nurse, sometimes a doctor. A few needed urgent attention so a team would be sent to oversee their care and bring them home on a commercial airliner or in an air ambulance. I did most of those trips and had the chance to witness how differently the same condition was treated in different parts of the world. It was a fun and challenging role and I learned to be extremely resourceful, often doing a lot with not very much.
Whether we are black or white, speak French or English, grew up in the northern hemisphere or on the other side of the world, when we look under the skin, into the blood circulating around our bodies, into our organs and deep down into the protoplasm of each and every cell, we are essentially the same. That came to me as an epiphany in the operating room of a small hospital in Malaysia. My London-based patient was from the Caribbean and had been gravely injured in a car crash on the motorway from Kuala Lumpur to Malacca. Back then I was young and perhaps a bit thoughtless so now feel embarrassed about the epiphany I had on seeing the pink mesentery of his intestine—pink like mine and pink like yours!
Our kidneys all look the same too. We have two, each weighing about 150 grams and running to 12 to 14 centimetres in length. They live in the area behind the abdominal cavity that we call the retroperitoneum, on either side of our bodies just below the level of the ribs. The kidneys have an outer cortex, a medulla and a renal pelvis, where urine begins its journey down the ureter into our bladder and from there, into the loo or under a tree in the garden.
That journey belies the complexity of the process—bulk filtration, selective reabsorption of fluid and molecules, and secretion of wastes. In a series of self-adjusting processes determined by a myriad of feedback loops, normal kidneys work hard to restore us to homeostasis no matter our circumstance.
These horseshoe-shaped organs keep us well by continually cleaning our blood of the rubbish created by the messy business of living. They do this by constantly regulating the fluid and electrolyte balance in our bodies. In order to carry out that task, they receive an enormous blood flow via each renal artery.
Adults have about five litres of blood in circulation at any one time. Of that, two litres are red blood cells and three litres are plasma. Every day the kidneys filter 180 litres of plasma at the staggering rate of 120 millilitres per minute! The functional unit of the kidney that does this is the nephron and each kidney has a million nephrons. If attached end to end, our supply of nephrons would be 160 kilometres long.
Each nephron is a complex little beast made up of different parts. There are a series of buckets and tubes into which fluid flows. The nephron’s interface with the blood is the Bowman’s capsule in which sits the glomerulus. The Bowman’s capsule is located in the outer cortex of the kidney. This glomerulus is a strange tangle of small capillaries where fluid and molecules are forced down a pressure gradient to form what we call the glomerular filtrate. This filtrate enters the Bowman’s capsule then runs into the proximal convoluted tubule, where about 70 per cent of the filtered plasma water and sodium is reabsorbed together with all the glucose and amino acids. From there, the filtrate travels into the ascending and descending loop of Henle, which are located in the medulla of the kidney, water is reabsorbed and our electrolyte balance fine-tuned. This effluent then flows into a final distal tubule deeper in the medulla for more water to be reabsorbed or secreted, a final check and then voilà, we have urine appear in the renal pelvis and soon after in the ureter running down into the bladder and when it suits into the loo—it’s amazing, isn’t it! So no matter how many pints we drink in the pub or how much salt or other minerals we ingest with our food, our kidneys will sort it out for us.
The ability of the human kidney to adjust to changing circumstances is extraordinary, especially when it comes to dealing with cold or hot climates by conserving water when we are dehydrated. But the prize for efficiency of this process goes to the kangaroo rat and the camel. They both have extremely long loops of Henle and are capable of concentrating their urine down to the point it is almost solid.
Kidney failure is a disaster and, depending on the cause, can either be temporary or permanent. In the acute setting, kidney failure is usually caused by a constellation of factors including the impact of the disease process and how well (or not) the kidneys function normally. However in this setting, which is very different to that of patients with longstanding diabetes or other diseases specifically of the kidney, if the patient survives their acute illness or injury, the kidneys will usually recover their function within a period of two to four weeks. I say if the patient survives, because no matter the nature of the underlying problem, if it results in acute kidney failure there is an increased likelihood of death resulting. The reason for this is not obvious—acute kidney failure can be treated effectively with dialysis, so the increased mortality associated with it must be related to the severity of the disease process causing renal failure as well as a lot more damage to other body systems.
If the kidneys do fail acutely, without an interim period of dialysis, patients will usually die as a result of the metabolic effects associated with a loss of kidney function. Although it is life-saving, dialysis can be tricky in this unstable patient group.
Last century, I worked for a few years in one of London’s oldest teaching hospitals. Now called the Royal London, there was nothing royal about it in the mid-1980s when it was just called the London Hospital. Set on the Whitechapel Road in east London, the hospital was one of those dark brick Victorian institutions, whose claim to fame was that it had the skeleton of Joseph Merrick, aka the Elephant Man, in its anatomy museum. It had history, that place, played out in all manner of ways including the plumbing.
Opposite it was the Grave Maurice (pronounced Morreece) pub and another 100 metres east of that, the Blind Beggar, where the Kray Brothers shot Jack ‘The Hat’ McVitie. Further east still was the Mile End Hospital, an annex of the London, not so far away as the crow flies but given the nature of the hospital telephone exchange in times of crisis, it might well have been on the other side of the world.
At Aldgate, just west of the hospital, was Blooms, a Jewish deli where we went for salt beef sandwiches and latkes. Mrs Bloom, hair done in the style of the Iron Lady, guarded the till, her face pinched tight as a snare drum from too many procedures. Just north of there was Brick Lane, famous for its curry houses, bagels and beer. A bit further north was London Fields where we lived.
‘See one, do one, teach one’ was the principle that guided service delivery at the hospital. It was a time when service trumped supervision and when junior doctors learned from their mistakes more frequently than they did from the things they did right. One day I was with a specialist seeing how to anaesthetise a patient for a coronary bypass graft, the next day I was performing the same procedure, and the day after I was an expert. It was crazy stuff. The workload was ferocious and the rosters cruel so every second week I did 134 hours on call.
The people were great though, including most of the double-dipping consultants who spent so much time in Harley St or the Princess Grace, a private hospital in upmarket Marylebone. Often they would ask us to help them. Having another set of hands meant they could get through five or six cardiac cases in a day instead of three. At the end of each procedure, I’d take the still anaesthetised patients to the ICU as the boss started the next one. For my trouble, each time I helped I was given 50 pounds.
I will never forget my first day on my own in the cardiac theatre at the London. The patient was a bus conductor from Newham. He was only 5 foot 3, bald and of a wiry build. He was having a quadruple bypass and a mitral valve replacement because his leaked badly.
Operating theatres are like a stage and the different contributing staff like actors, with each day bringing a new performance. Back then, the performance began in the theatre itself with the anaesthetist inserting an arterial line usually into the radial artery, where you feel for the pulse in the right wrist. This was used primarily to check the patient’s blood pressure and allowed for frequent blood tests to be taken to monitor the patient’s state. The anaesthetic technician then attached the ECG leads and finger probe of the oximeter to measure the oxygen saturation of their blood. Then we put the patient off to sleep, taking great care with our choice and doses of drugs.
The arterial line slid in beautifully, he went to sleep with no change in his blood pressure or heart rate, and when I tipped him head down to insert three long intravenous catheters into his internal jugular vein, they went in first time too. I was on a roll. The different actors played their part, lines were spoken and things that needed to be done were done well.
The play continued and he went onto the bypass machine without difficulty. This machine that assumes the role of the heart and the lungs is made up of different components including a large cannula inserted into the right atrium of the heart, from where venous or blue blood is drawn into the machine by a centrifugal pump. A set of roller pumps then propels the blood around a circuit made of silicone to an oxygenator, which adds oxygen to the blood and removes carbon dioxide before finally returning that oxygen-rich red blood via another cannula inserted by the surgeons into the aorta. When the perfusionist who operates the bypass machine, the surgeon and the anaesthetist speak together it reminds me of listening to air traffic controllers—there’s a lot of words but there doesn’t seem to be any obvious meaning!
Once on bypass, the surgical team then stops the beating heart by infusing a cold, potassium-rich cardioplegic solution into the coronary arteries. This makes it easier for them to operate on the heart’s bits and pieces, putting new grafts around old blockages and inserting new valves to replace worn-out old ones.
While one surgeon took the large saphenous vein from his leg, another prepped the heart; he received four grafts around obstructions in his coronary arteries and a new mechanical heart valve that would forever go clickety-click inside his chest so long as he lived. All was good until we warmed him up to get his heart started and off the bypass machine. Each time we tried to do this, we failed. His heart was too weak to fully take over. This wasn’t in the script.
The surgeon stared at me as though it was my fault. I spoke to him but he didn’t answer. I called for help and, in the meantime, put up an infusion of drugs to help the patient’s heart. On the fourth attempt, we finally got him off the bypass machine but all was not well.
His heart was limping as we raced to the ICU. It was a Friday afternoon and I was on for the entire weekend. The unit was full—people with overdoses, a couple of victims of a bad car crash, and three other cardiac cases that had been done that day and the day before. My boss for the night had long since gone and would not be back until the next morning but was available by phone.
The bus conductor was struggling. I spoke with his wife and she cried. Over the next few hours, his heart rhythm settled down and his blood pressure improved—but he wasn’t peeing and that was bad. The bag attached to his catheter had only 100 millilitres of urine in it after five hours in theatre. His initial blood tests showed a significant deterioration in his renal function and he was requiring more oxygen from the ventilator than I expected. Most likely this was the result of what had happened toward the end of the case when he had a particularly low cardiac output, injuring his kidneys and also causing fluid to accumulate in his lungs.
I was young and I was worried. I was worried because if his kidneys failed he would need dialysis and, although we could do that, the risk of him dying was significantly increased. I wanted to give him more fluid but thought that his heart might not stand that and his lung function would worsen. I rang the boss for advice and then began to fiddle. A bit more fluid, a bit more pressure from the ventilator, some drugs to ensure he had decent blood pressure, a dose of frusemide—a diuretic to make him pee—and a few other manoeuvres for good measure.
Although the exact detail now escapes me, I know I spent much of that night sitting on a stool beside the bus conductor’s bed counting drops of urine as they leaked one by one into his catheter bag, smiling as the drips slowly turned into a trickle and, by morning, into a torrent. In the end he did well. About a year later, I saw him conducting on the number 22 bus that ran from Hackney to the West End. He recognised me and doffed his enormous conductor’s hat in my direction and I returned the doff with a smile.
Many patients who develop overwhelming organ failure from acute illness or injury will develop kidney failure and, without dialysis, they will die. This happens in the same way as someone who had become hypoxic as a result of extreme breathing difficulties would die without respiratory support, or someone might die from shock if they aren’t resuscitated with intravenous fluid and drugs to support their cardiac function. If we don’t deal with the underlying cause of all that mayhem, people die.
Roger was 51 and normally well. He was married to Rosalie and they had two kids, aged fourteen and sixteen. Roger had no medical issues that he knew about, didn’t smoke and had only been in hospital for a reconstruction of his left knee, which he’d injured playing rugby a long time before. He was a fit guy. I have no real explanation as to why he became so ill and almost died from a simple skin infection; why he got it is still a mystery to me.
Roger was on a plane heading to Auckland from Australia when the redness and pain started. His leg was itchy so he scratched it. By the time he arrived in Auckland he was hot, sweaty and already delirious. Paramedics met him at the gate. Recognising how ill he was, they gave him oxygen to breathe, put in an IV line, and raced him to Middlemore Hospital. I first saw Roger in the resuscitation room of the ED.
He was now barely conscious, had a temperature of 40 degrees Celsius, was breathing hard, and both the oxygen level in his blood and his blood pressure were dangerously low. So too was his blood sugar level. On his leg was the cause of all this—a spreading redness extending from the shin to the mid-thigh. He had a cellulitis, an infection of the skin causing what we define as septic shock. This is the result of an overwhelming infection from bacteria that have spread into his blood stream now causing havoc with his other organs.
The redness working its way up Roger’s leg was just the tip of something much bigger and more deadly: he was at war with a bacterium called Staphylococcus aureus and the exotoxin it produces. These poisonous substances circulate in our blood stream, destroying cells and disrupting our normal cellular mechanisms. One organ down, another quickly following, Roger was in a bad way.
When people become acutely ill, the immediate threat to their life is from a failure of their respiratory and cardiovascular systems so that’s where we started. Oxygen by mask, soon after via a tube into his trachea, driven by an expensive ventilator; fluids in the vein and high doses of drugs to prop up his flagging circulation; glucose to prevent the disastrous damage to the brain that results from prolonged hypoglycaemia; antibiotics to kill the bugs; low dose hydrocortisone to help everything; and a quick look-see in the operating room to ensure there was no deeper infection or necrotic material that needed to be debrided and removed. All of these interventions are urgent; unless they happen fast, people die. These things are obvious to me and to the people I normally work with; it’s not to less experienced doctors or those who might see something like this once a year or once a lifetime. Delayed resuscitation and treatment not only increase the risk of death, but also lead to a need for more aggressive and protracted organ support. This in turn means a delayed recovery with more profound psychological and physical consequences for the patient on discharge from hospital.
Within an hour, Roger was on close to maximal therapy and off to the operating room for a ‘keyhole procedure’. To define the extent and depth of the infection in his leg, the surgeons make a series of incisions to define the proximal extent of the infection—how far it has spread up the leg. Incisions are also made to determine the depth of infection, whether it is confined to the skin or if it involves deeper areas of the leg, like the subcutaneous fat, the fascia that overlies the muscle, or even the muscle itself. Dead tissue will never be cured by antibiotics alone and must be removed; if not it will be a source of ongoing infection and the patient will not get better. ‘Heal with steel’ and ‘never let the sun go down on undrained pus’ are two mantras for the successful treatment of people like this. The message is that antibiotics alone will not be enough; surgical drainage of pus and debridement of dead tissue is necessary to effect a recovery.
Members of the public and doctors unused to managing critical illness often worry that a patient could be so sick to go to the operating room. I usually reply that they are so sick they must go.
As it happened there was no dead tissue or pus in Roger’s leg so we concentrated our fire on what we were already doing to effectively treat his evolving organ failure while continuing to marinate him in antibiotics. Despite this Roger’s condition continued to get worse.
When I met with his family, they asked me a series of terrific questions including: What more could we do? Would he survive? What would his survival depend on? Why was he still getting worse if we knew what we were doing?
I did my best to explain again using the domino analogy. If our treatments were effective and we did no substantial harm by them, and if we were able to support Roger with our machines, and if he had the physical and physiological reserve and inner strength to withstand what was happening to him, he might get better. The dominoes would slowly stop falling. Then the rate at which we picked them up would start to exceed the rate at which they fell. If he recovered, those dominoes would shuffle themselves into lines again but never quite in the same order they’d been in before.
Roger’s organs were going down fast. He was still on a ventilator and needed high pressures and more and more oxygen. He was still being actively resuscitated with fluid and was on high doses of drugs to improve his circulation. His blood was not clotting and now his kidneys were not working.
Developing renal failure in this setting of acute illness makes recovery impossible without dialysis. In illnesses like this, although the kidneys usually will recover if the patient recovers—that may take two to three weeks—if we don’t correct the worsening biochemical abnormalities in the patient’s blood, the other organs of the body will simply shut up shop and slowly die, and the patient will follow. It’s a bit like swimming in a horribly polluted river—if we stay in there long enough, we will die too.
In the late 1980s, Middlemore Hospital was the first intensive care unit in the country to use continuous renal replacement therapy for patients with acute kidney failure. Following the principles of intermittent dialysis—that form of dialysis used for four hours at a time, three to four times a week for patients with permanent end-stage renal failure from diseases like diabetes and glomerulonephritis (the disease suffered by Jonah Lomu)—continuous dialysis is deliberately prolonged, lasting up to eight hours a day and in this setting usually required every day to slowly and steadily clear the waste products generated by the body.
In those days, the technology was very different to what is available today. Back then, we used a system called the Hannover Balance where one large cannulae was placed in the femoral vein in the groin with another in the femoral artery so the flow of blood through the blood filter was effectively driven by the patient’s own blood pressure. The pores on the filter were designed to allow molecules of a certain size to escape from the blood into an overflow while ordinary intravenous fluid was given as a replacement. The balance itself referred to an elaborate mix of weights and measures on a chrome frame to ensure we gave and took off the correct amounts of fluid and electrolytes. Setting it up took hours and the machine and necessary paraphernalia to make it work filled half a room.
Roger needed dialysis as well as those other organ supports to buy time in the hope that he would have the wherewithal to recover. Now dialysis is a simple affair and compared to early models, modern dialysis machines are simple and almost idiot-proof. These machines take blood from one lumen of a large-bore intravenous catheter in an internal jugular vein in the neck, or a subclavian vein in the chest, or a femoral vein in the groin, and return the cleansed blood to the body via a second lumen in the same catheter.
People like Roger are incredibly unstable so great care needs to be taken in doing all of this, especially in getting them on dialysis to avoid a cardiovascular collapse. The machines are smart and interactive and the process is extraordinarily gentle, allowing us to dial up very low flows of blood and dialysate fluid to keep patients stable.
Roger was on that machine for a solid 24 hours before it became evident that we were winning. His descent slowed and the deterioration in his numbers reached a nadir. Then he slowly began to improve.
Over the next few days we whittled away at the levels of support he was on. After a week, although still needing dialysis every second day, his breathing tube came out and he could talk with us. Like most ICU patients as sick as he was, he had few immediate memories of what had happened to him.
I reckon Roger was saved by that machine slowly whirring away in the background; it’s modern, slick and understated and delivers what we call Slow Low Efficiency Daily Dialysis operating at a level well below what would be expected of just one human kidney, but enough to save a life.
The steady whirring of the roller pumps moving his blood at 200 millilitres per minute from the line in his femoral vein, through the filter and back to the same vein through the second lumen of the big catheter. Steadily too ran the dialysis fluid from the machine in an opposite direction to Roger’s blood on the other side of the filter’s membrane. All the time the steady passage of molecules across the filter left Roger’s blood cleansed of the waste products normally cleared by his kidney.
Our organs operate best in the soup in which we were made. They struggle terribly in the poisonous mix that is renal failure so as this process continued, the drugs needed to support his blood pressure steadily reduced. Roger’s fall slowed and after a nervous night it was clear that he was on the up. In his favour, Roger was young and he was healthy. He had been an athlete in his day and was still really fit despite those long sickle-shaped scars on both of his knees. If anyone was going to survive this kind of illness, it should be him.
Over the next few days, we weaned him off all of the drugs supporting his circulation and his requirement for ongoing intravenous resuscitation slowed then eventually stopped. His need for dialysis reduced from almost continuous to just once a day. All was heading in the right direction so we reduced his sedation and allowed him to slowly surface. Still drowsy and stunned he opened his eyes and responded appropriately to us. This was a great time for his family and for us too—for him to have gone so far and now to be seen to be coming back.
During those first few days, as we chased Roger as he tumbled toward death, we gave him 22 litres of fluid to help maintain a half decent blood pressure. If his kidneys had been working he would be peeing that out now but it would take two to three weeks for them to recover so we used our machine to take that fluid off him. Each day we took off between three and five litres. By the end of the week he was off the ventilator and breathing on his own.
A week later, he started to pee. Dilute urine, mostly water, came by the bucketful as his kidneys woke from their unconscious slumber. Slowly learning how to do its business all over again, the quality of his urine improved and its enormous quantities reduced. A week later, they were back on track. Those 12-centimetre fleshy horseshoes—forbidden fruit to me, a delicacy and honour to others—were away, and so too was Roger.