ONE NIGHT AT A reception, in a place 4000 kilometres from home, a lovely thing happened to me. Another guest, someone I recognised but couldn’t quite place, thanked me for looking after his wife when she had been desperately ill. He was especially grateful for the time that I devoted to him and his family throughout that ordeal. That was twenty years ago when she was pregnant and suffering from a life threatening complication of pregnancy called the HELLP syndrome—a condition related to pre-eclampsia, whose name is an acronym of its three main features: haemolysis, elevated liver enzymes, and low platelet count.
Their child, their only child as it turns out, was delivered by caesarean section as much as anything to save the mother’s life as well as that of the baby. That infant is now a student—tall and handsome too by the look of the photo he showed me. His wife, Wendy, is well and they are happy. Not long after her recovery, Wendy joined forces with another woman to start a support group to help other women in the same condition and to raise awareness of the warning signs of this condition. It was lovely to be reminded of that time.
It’s always been hard to get into medical school and most students do so on the basis of their grades at college and their performance in an interview. The cut-off grade to get an interview is now so high that only the smartest and hardest working students get through. Once accepted these bright young things are separated from their peers and continuously fed with fact after intoxicating fact about physiology, anatomy, neuroscience, organ systems and their diseases, the heart, lungs and, yes, the kidney! They start early in the day and finish late at night. They study for exams and, because they don’t meet anyone else, they often end up marrying each other. They go down roads others don’t, take turn after turn into the middle of a maze that some never leave or recover from. This, combined with the extraordinary workload of many doctors, is the excuse I make when patients and their families complain about poor communication from medical staff, which leaves them feeling like they don’t know what’s going on.
It is easy to forget or not think about the impact we have on those we see on a daily basis. I have been stopped in supermarkets, on trains and planes, and in the street by people who I thought I had long forgotten about but, in the end, almost always remember. They remember me not primarily for my technical skills but for how I made them feel. More often than not, theirs are sad stories of loss that have, in time, become accepted. They remember that they were treated with dignity and respect, and they were listened to. Strangely, it is the sad stories that stay with me too. Probably because my emotional investment there is always so much greater.
I first saw Jake propped up on two beds in the emergency department. He had been brought into hospital with the help of the Fire Service who had to cut a bigger opening in the doorway of his house to carry him to the ambulance. He was only eighteen but weighed 280 kilograms.
Jake had been particularly unwell for three days with laboured breathing, most likely a consequence of a skin infection on his tree trunk-like legs. When I first saw him I struggled to get past a deluge of unhelpful thoughts about how he had come to be so big in order to concentrate on doing the right thing by this young man and his family. He was barely conscious, only mumbled when spoken to, and was not able to follow simple commands. Because his arm was twice the size of my thigh, getting a reliable recording of his blood pressure was difficult despite using the biggest cuff in the hospital. All the readings though were in the dangerously low range, as too was the level of oxygen in his blood measured by the pulse oximeter. As we made our assessments I had a brief but important conversation with his parents about the seriousness of the situation, learning more about Jake’s life.
He was born with a rare but well-described condition called Prader-Willi syndrome, the result of a complex genetic abnormality in one of his chromosomes. Like many with the syndrome he suffered from polyphagia, an obsessive desire to eat, as well as a range of other behavioural and physical issues. Despite therapies and treatments throughout his childhood and adolescence, his obsessive behaviour became increasingly difficult to control and his weight gain accelerated.
Because of his size the paramedics couldn’t find a vein to put in an IV line so that was left to me. As I lowered the head of Jake’s bed to 30 degrees to put a line into the internal jugular vein in his neck, he quite suddenly stopped breathing and very quickly died. My lowering the bed, just a bit, was the final straw; ‘expiratory airflow obstruction’, we call it, or, to put it in layman’s terms, Jake was effectively crushed by his own weight. Being so sick and so heavy, he simply didn’t have the strength or drive to be able to activate and move his own respiratory muscles to breathe. When that happened we didn’t try to resuscitate him. There was nothing we could do. It was an awkward and strange moment for those of us there trying to help him. Instead we immediately brought his family into the room to be with him as he faded away.
The cause of Jake’s obesity was well known and with that came an acceptance by his parents of what might one day happen to their son. So, although a sad and tragic story for Jake and his family, the end was not unexpected. Nor did the family have unrealistic expectations of what we could do for him in hospital. At best, all we would offer was always going to be limited support with oxygen, fluids and antibiotics—that was our agreement. In the end, Jake was spared even the indignity of that, choosing to take himself off, hopefully to some better place.
While we can attribute the cause of Jake’s size to a well-described genetic predisposition, what is fuelling the obesity epidemic worldwide is more complex. It is driven by a mix of factors that reflect changes in lifestyle—the burgeoning market economy, the advent and rapid spread of high-fat, high-sugar foods and drinks, mass marketing, urbanisation, changes in the labour market and much more. All these changes have swept across the world and they have effectively overwhelmed us. In many ways we have benefited by the massive global shifts of the late twentieth century and early twenty-first century, but in others, we have lost out.
Few countries or governments have been immune and fewer still have adapted to maximise the benefits of these changes and minimise their harms. Most have been simply swept along by them. We are, as a world, forever changed and to unpick some of this has become simply too hard for many to contemplate. However this epidemic, an unintended consequence of this post-industrial modern revolution, causes immense harm to individuals and creates huge costs for society. It simply must be addressed.
Seleni is a case in point. She, like millions of others, is enormous, weighing in at 160 kilograms, however, she was not born enormous. In fact, her mother remembers her as a slim child. When Seleni’s hit adolescence that changed, when the impact of her diet and lifestyle began to take its toll. If she was thirsty, it was cool to drink a fizzy drink loaded with enormous amounts of sugar. If she was hungry, she would eat food high in carbohydrates and rich in fats. She would snack all day and at mealtimes eat large portions of whatever was being served. In the family home, the cupboards and shelves offered few healthy food choices, as did the shops nearby where she bought her food. Occasionally she would eat fruit and vegetables, but they were much more expensive to buy.
By the time Seleni was a teenager she weighed 120 kilograms. When she finished school at sixteen, she took a job as a seamstress. It suited her well because, by then, walking was uncomfortable and she got tired quickly.
Her mother, a big woman herself, remembers it was about then that she began to snore at night and nod off during the day. The snoring and daytime somnolence are signs of something we call sleep apnoea, a condition that results from a partial obstruction of our airway as we breathe.
It is common in overweight people and is characterised by cycles of loud snoring, periods of apnoea when no breathing occurs for short periods, and then commonly a very loud snore or grunt associated with the intake of another cycle of breaths. As unpleasant as this sounds for the sufferer, it is also deeply annoying for those forced to listen. If that was all it was, wearing earplugs, putting a pillow over your head, or sleeping in another room might help others put up with this. But the consequences for the sufferer are more sinister.
During these cycles of obstructed breathing and especially when Seleni’s breathing stopped altogether, the oxygen saturation in her blood dropped to extremely low levels. Potentially dangerous in the moment, the cumulative effect of this degree of hypoxaemia causes physical changes in the arteries of the lung, leading to an increased resistance to blood pumped into the lungs by the right ventricle to pick up oxygen and dispose of carbon dioxide. In response, the right side of the heart becomes increasingly bulky, making it difficult for it to do its job. This cycle of increasing pulmonary vascular resistance and hypertrophy of the right side of the heart leads to a condition called pulmonary hypertension and, eventually, heart failure.
As bad as this sounds, it gets worse. Because of the weight of her chest wall whenever Seleni slept on her back she struggled to breathe adequately and couldn’t effectively get rid of the carbon dioxide her body produced, a condition called obesity related hypoventilation, which accelerated her heart failure.
Like others with the same condition, Seleni complained about always being tired. She couldn’t remember the last time she woke in the morning feeling refreshed or a time when she didn’t doze off during the day. Just as well then that Seleni was a seamstress and not an airline pilot or bus driver.
Unfortunately her tiredness had other consequences too, making things much worse for her. Many of us will have had occasions where, through work or play, we’ve had a big night and not much sleep, leaving us tired the next day. With that often comes a ferocious appetite, usually for something hot and greasy like fish and chips—that’s my weakness—or a meat pie. In my career as an intensivist, I have had many of those and know that the more tired I feel, the hungrier I become. There’s a reason for that and it’s called grehlin, ‘the hunger hormone’.
Grehlin is released from the lining of the stomach as a response to this sort of tiredness. It works in the brain to increase our appetite as well as determining how quickly our hunger will return. Under normal circumstances, the effects of grehlin to stimulate appetite are matched by the impact of another hormone, leptin, which suppresses appetite. However, the impact of constant tiredness and a diet of high-sugar and high-fat food, both of which increase grehlin levels, are simply too much and we lose our balance.
Against this combination of market forces and physiology, Seleni didn’t have a chance. She piled on more and more weight. Soon she weighed 140 kilograms. As that happened, her unwillingness to walk and exercise became a permanent disability, because of pain in her knees and a gnawing backache that never went away. By now she had high blood pressure. She was also diagnosed with diabetes when she had her first episode of cellulitis, a skin infection, in her fluid filled legs. Despite taking pills and testing her blood three times a day, Seleni’s body was overwhelmed and she struggled to keep her blood pressure and sugar levels in the normal range.
The first time I met her was in the emergency department of my hospital. She weighed in at 160 kilograms and had come in with another bout of leg cellulitis, but this time complicated by a much more serious set of problems as a result of her diabetes.
To this point, obesity had been the defining feature of Seleni’s life. Not only did it create health problems for her, it had an overwhelming influence on how she viewed herself as a person and it determined much of what she could and couldn’t do in her everyday life. Obesity, then, had totally defined the quality of her life but now with the added complication of diabetes, it was the quantity of her life that was under direct threat.
Diabetes is a disease of our metabolism that is related to high levels of glucose in the blood. There are two common types of diabetes—type 1, or early onset diabetes, is most commonly diagnosed in children and teenagers, and type 2, or maturity onset diabetes, that usually affects those in middle age and the elderly. It is the latter form that is so common in people like Seleni.
Under normal circumstances, when we eat, our digestive tract breaks down carbohydrates—sugars and starches found in many foods—into glucose, a form of sugar that enters the bloodstream. That glucose is the fuel that keeps our cells alive and it is the hormone insulin, secreted from our pancreas, that allows us to absorb it and use it for energy. Diabetes develops when the body doesn’t make enough insulin, or is not able to use insulin effectively, or both.
There is no doubt that obesity was the cause of Seleni’s diabetes. Yes, perhaps she also may have had some kind of genetic predisposition to the disease but to overplay that card—as some do—is irresponsible and dangerous.
Like most people, Seleni was diagnosed when she presented to hospital with an inter-current infection although it is most likely that she would have had the disease for many months prior to that. If the cells of her body could talk, they would have told her far earlier than her doctor did because full-blown diabetes is usually preceded by a period of insulin resistance—a time when the cells of the body respond less and less to the effects of insulin. As a result, the pancreas pumps out more insulin in an attempt to overcome that resistance until finally it can’t keep up and high blood sugar levels result. For Seleni and millions of others with this disease, the importance of protecting the body from high sugar levels cannot be overstated because the consequences of not doing so are dire.
Hyperglycaemia directly damages our major blood vessels: the aorta, carotid arteries, our coronary arteries and iliac and femoral vessels. It dramatically increases our risk of heart attack and stroke. It slowly wrecks the smaller arteries that take blood to the retinae of our eyes, resulting in what we call retinopathy; to our nerves, limiting their ability to transmit sensation—neuropathy; and to our kidneys—nephropathy. Diabetes is like a form of human rust slowly destroying us. Like many others before her, Seleni was rusty well before her diagnosis was made.
Weight loss, exercise and lifestyle changes will work for some and return their blood sugar levels to a more normal range. A select group might be offered more direct help to lose weight and undergo bariatric surgery, a range of different surgical procedures that have proven to be very effective in promoting significant weight loss among committed individuals, which can slow and, in some cases, cease the corrosion that diabetes causes. However, even if all the bariatric surgeons in the world operated 24 hours a day, seven days a week, this would hardly make a dent in the enormity of this problem. Hence most obese patients don’t get this chance even though they simply cannot or will not be able to lose weight on their own. Seleni was one of those people. Her only realistic option was to continue on a course of therapy with drugs to control both her sugar levels and blood pressure in an attempt to minimise ongoing damage to her vessels and end organs, especially her kidneys.
On her most recent admission, the result of a severe infection in the soft tissues of her massive left leg, Seleni was much sicker than she had ever been. She was febrile, had low blood pressure and came in with a significant deterioration of her renal function due both to the progression of her diabetes and the impact of this acute infection.
To determine the extent and depth of the infection in her leg, Seleni went to the operating theatre where she was carefully anaesthetised. Once she was asleep, the surgeons did what we always ask them to do and assessed the viability of the tissues beneath the skin, starting at her ankle and working their way steadily to above her knee. What we saw was not pretty. Beneath the red and swollen skin, the subcutaneous fat and the muscles were a sick grey colour and they did not bleed when cut. This was the case from the ankle to the knee. In effect, her leg was dead so, to save her life, it was amputated above the knee.
During this time Seleni was in poor shape. She was asleep on a ventilator and receiving large volumes of resuscitation fluid and high doses of drugs to maintain an acceptable blood pressure. As soon as the surgery was over, she came back to the ICU where she immediately went onto a kidney dialysis machine to do the job of her failing kidneys.
Seleni eventually recovered, but although only 40, her kidneys—fatally damaged by uncontrolled diabetes and high blood pressure—never did. She was in hospital for several months before going home in a wheelchair to be cared for by her family and tied forever to the dialysis centre three times a week for the rest of her life.
Managing people of this size is difficult beyond description. On a practical level, everything is hard. Getting in an IV line, measuring blood pressure, doing a simple bedside examination, putting in a urinary catheter are all challenging and, in some cases, impossible. Moving the patient from one bed to another takes an army of people; getting appropriate investigations done can be limited by weight restrictions on CT and MRI tables and, even if you can get the scans done, the images can be hard to interpret. In addition there are personal prejudices that clinical staff need to acknowledge and overcome. There is a tendency to blame the patient for their condition and an acceptance that what will be will be, limiting the potential of what we might do to help and the success of any therapeutic intervention. These are real concerns best overcome by getting to know more about the person rather than being put off by their size.
Obesity and its consequences have become a public health emergency in much of the world. Recognised as a form of malnutrition, this crisis is more indolent but more lethal and costly than the malnutrition we are more used to seeing in poor nations across the world.
In many middle income nations, we now have in the same localities, notably our cities, both ends of that spectrum—babies transitioning from the breast who become increasingly malnourished because their food is of poor quality with few real nutrients, anorexic adolescents and young adults, and an increasing number of the morbidly obese.
People flock to urban areas in the Pacific, including those in New Zealand, in search of work, leaving their lands and their traditional family and cultural supports. These are the areas in which infant malnutrition and morbid obesity are on the rise. They bring with them a range of medical complications that are difficult to manage, as well as ethical and moral dilemmas about how our health and social services best respond.
Obesity is defined as an excessively high amount of body fat (adipose tissue) in relation to lean body mass and this is associated with a substantially increased risk of a number of health conditions.
Body mass index (BMI) is the most commonly used measure to classify underweight, overweight and obesity in both children and adults. BMI is a measure of weight adjusted for height and is calculated by dividing your weight in kilograms by your height in metres squared (kg/m2).
| International cut-off points for adults aged 18 years and over | ||
| Classification | BMI score (kg/m2) | Risk of multiple diseases |
| Underweight | <18.50 | Risk of other clinical problems increased |
| Normal range | 18.50–24.99 | Average risk |
| Overweight | 25.00–29.99 | Increased risk |
| Obese | ≥30.00 | High risk |
| Obese (class I) | 30.00–34.99 | High risk |
| Obese (class II) | 35.00–39.99 | Severe risk |
| Obese (class III) | ≥40.00 | Very severe risk |
For children aged two to seventeen years, a similar set of BMI cut-off points have been developed by the International Obesity Task Force (IOTF).
People with an exceptionally low BMI from malnutrition are at risk from a wide range of clinical problems because they have little reserve to ward off illnesses and to heal themselves once they become sick or need an operation. That was shown to be the case in my own ICU when we looked at outcomes for patients admitted with a surgical diagnosis. Among surgical patients, those with a very low BMI generally do worse than those who have a very high BMI admitted for similar problems. At first I was surprised by that but the reason for it relates to the nature of the patients themselves—morbidly obese surgical patients are generally carefully selected and are coming for a specific surgical concern. Most won’t have the advanced complications of end organ disease like Jake or Seleni and, if indeed they are admitted with organ failure as a result of their obesity, their treatment options are limited and their outcomes exceptionally poor.
The 2012/13 New Zealand Health Survey found that in the adult population:
•Almost one in three adults (aged fifteen years and over) were obese (31 per cent), with a further 34 per cent being overweight
•48 per cent of Māori adults were obese
•68 per cent of Pacific adults were obese
•Obesity in males had increased from 17 per cent in 1997 to 30 per cent in 2012/13
•Obesity in females had increased from 21 per cent in 1997 to 32 per cent in 2012/13.
When it comes to children, the same trends are emerging. The same health survey found that:
•One in nine children (aged two to fourteen years) were obese (11 per cent)
•A further one in five children were overweight (22 per cent)
•19 per cent of Māori children were obese
•27 per cent of Pacific children were obese
•Children living in the most deprived areas were three times as likely to be obese as children living in the least deprived areas. This finding is not explained by differences in the sex, age or ethnic composition of the child population across areas of high and low deprivation.
•The obesity rate in children has increased from 8 per cent in 2006/07 to 11 per cent in 2012/13.3
These are disastrous statistics for a small nation like ours struggling to provide health and social services from a small GDP (gross domestic product) that is growing only slowly.
New Zealand is not alone with this problem because obesity is an epidemic spreading largely unchecked across much of the developed world, with a doubling of the world-wide obesity rate since 1980.
According to the World Health Organisation, globally in 2014, more than 1.9 billion adults, eighteen years and older, were overweight. Of those, over 600 million were obese. It is affecting children in staggering numbers too, with 42 million children under the age of five now overweight or obese in 2013.4
This is the case too for most developing nations. It is a particular problem for small nation states like those in the Pacific where obesity rates are soaring and health services are already overwhelmed.
These numbers are now so high that obesity kills more people in the world than starvation or malnutrition, with those deaths being far more costly as nations shift scarce resources from other important public priorities.
Even though the causes of obesity are multiple it is a preventable disease. Proof of that are the many millions of individuals who are not obese and pockets of people who have the knowhow and the resources to organise themselves to stay healthy. Doing that at a national level requires a degree of stewardship that few governments wish to embrace because it requires a long-term commitment to effective public policy, social marketing and help to change the behaviours of communities, families and individuals. Some baulk and say it cannot be done and that we are at the mercy of the market and the media. I say bollocks to that.
Our future is what we are prepared to make it. Road trauma and tobacco use are just two examples of major threats to the health of the public where societies have made massive gains to reduce mortality and costs. The road toll has been lessened through effective public policy by licensing cars and drivers, designing safer roads and getting tough on drink driving. Tobacco-related deaths have been reduced through an increase in price and banning advertising of tobacco products. Certainly in the latter case the combination of regulation with social marketing, the availability of nicotine replacement therapy, and advice through the Quitline have been generally effective in reducing tobacco use among many groups. There is absolutely no reason why the same approach, over time, would not work with obesity. The major barrier to that is the antipathy and ignorance of many governments to use regulation to drive change—it simply doesn’t sit well with their ideological beliefs and it would mean upsetting so many of their friends in the food and fat industry. As it stands, many nations are creating a future for themselves they will never be able to afford.
For Seleni—and so many like her—life as she knew it, or as she once hoped it would be, had gone forever, replaced by an exhausting and dangerous struggle just to stay alive. Perhaps looking on the bright side of life, at least half of those patients with diabetes will die of ischaemic heart disease, heart attack or stroke before their kidneys fail and they need dialysis. So perhaps Seleni has been lucky in that regard but her life on dialysis will be as hard as it will be short, with good odds that she will be dead in a year or two. Infection took out one of Seleni’s legs—diabetes, heart failure and venous stasis from her obesity contributed to that. For many other diabetics, it is their neuropathy and a lack of sensation that leads to injuries to their feet, putting them at risk of infection. It could be something as simple as a tight shoe breaking the skin or a simple cut causing a wound that won’t heal and eventually becoming infected. These small infections can quickly turn into a disaster, with more and more tissue being lost as the bugs spread in the encouraging environment of the diabetic foot and leg. Sometimes, after months of dressing changes and wound debridements, the foot or the leg is lost.
In many low- and middle-income countries where diabetes is endemic and resources and health services limited, wound care is often poor, leading to high rates of amputation. There are few prosthetics in those countries, leaving more and more people crippled and dependent on their families.
Looking in from the outside, it seems to me that obesity and diabetes are a man-made, modern version of the plague and I have no idea where that vortex of misery and cost will end up.
Given the reluctance of governments to act, we clinicians have both a collective and an individual responsibility to advocate for health policies to prevent the consequences of diseases like diabetes and its causes—especially obesity. Individually, we also have a responsibility to each patient to promote strategies to improve their health, keep them free of disease, and to help them stay well.
Each week, I spend time with a group of medical students. More often than not, my teaching is loosely structured as we talk about the people and the conditions they have seen that week. They are smart, keen to learn and seem to love those conversations.
Some are chatty, some more taciturn; some older, some younger. They vary in all sorts of ways, including their size. Priscilla is a fifth-year student and weighs 42 kilos—I know this not because I asked but because she told me! She weighs a little more than the amount of fluid we gave to Seleni over the first 48 hours of her descent toward death.
Sonny, a chatty, bright, fourth-year student, was exactly five times Priscilla’s weight. He told me that one day after a class in which we had discussed the causes of obesity and its consequences. It was a conversation that I started with the class without initially thinking about him, but as soon as it began his body language quickly told me how uncomfortable it made him. He looked down and did not make eye contact with anyone and no one looked at him. He didn’t say a word, and the conversation became stilted and difficult. Obviously, I should have spoken with him beforehand but I didn’t.
Sonny was 22 and, once we were on our own, he was relieved to have the chance to talk. He lived with his sister, her child and their nanny. All of them in the house were overweight. Sonny had gout and was already a pre-diabetic. He had been admitted to hospital twice with infections related to his weight, but had not yet developed any major signs of organ failure. He had tried to lose weight on numerous occasions, often through starving himself, but always ended up hungry and bingeing on all the wrong foods. Each time he tried to lose weight, he put more on. If he lived somewhere else Sonny might have become a candidate for bariatric surgery but on this island that was impossible.
You don’t get to be 210 kilograms by accident. Every day, he would drink four or five energy drinks, each containing fourteen teaspoons of sugar. In addition to that, he would also drink the same number of soft drinks, each with nine teaspoons of sugar. So each day Sonny would drink the equivalent of 100 teaspoons of sugar or 1600 calories.
He also ate what most people ate because it was available and cheap, foods with high carbohydrate and fat content: cream buns, two to three a day—another 900 calories; bread—520 calories; taro, often steamed then eaten with coconut cream and high-fat fried noodles. In between meals, he would snack on taro chips. His calorie intake was enormous and his energy expenditure through exercise minimal.
Later, I met with him and his sister and together we devised a plan for the household. First to go were the sugary drinks, replaced by water or niu (fresh coconut water). Sonny was a medical student, clever as they come and a master of the internet so with some urging he began to explore healthy food and snack options which he could turn to when he got hungry. With only a few hours research, he found a small range of healthy foods that were available and just affordable so over the next week he and his sister restocked their pantry. He even began to kept carrots and plain popcorn in his bag for emergencies.
Supported by his family and by me, in the first three weeks he lost 11 kilograms. His rate of weight loss has now slowed but he is heading in the right direction. Each week we meet, talk and think about the things that might trip him up. They will likely come from the people, places and things associated with his old lifestyle. They are everywhere and won’t be going away. Sonny’s goal is to get to 100 kilograms but that will be a stretch even if he sticks to his current plan. It will be hard and he will have his relapses but if he can stick with it, in time he will start to feel substantially better and be able to exercise more. With ongoing support, he might just get there and not become another Seleni but the odds remain stacked against that happening.
Looking across my career in medicine I have seen some extraordinary changes, including advances in technology allowing us to do complex things to many more patients safely and effectively. At the same time, the acuity curve of those we now treat in hospitals has shifted dramatically to the right, to the point where extraordinary effort and resources are directed to simply eke out a few more months of life for many already close to death. Seleni is now one of them, crippled to the point where she cannot work and contribute to the well-being of her family, community and society. She has sadly become a burden and a cost to those she loves and to the state for her ongoing care.
While well-off nations fiddle, the diabetes epidemic spreads and we spend more and more on medicines and hospital care to manage the rising tide of its complications. Low- and middle-income countries without the infrastructure or resources to do even this face an even more gruesome task, dealing with the septic complications of diabetes by draining abscesses and amputating limbs. Hospitals in those places are more houses of mutilation than healing. The world is spinning backwards and we are once again in the middle ages.