I See You? Si Si You! Knee Cue? Pack You!
A resident physician's life is broken up into four week chunk. And just like this post, residency seems like it could go on forever. These four weeks find me in the ICU.
My fourth year of medical school was spent thinking I wanted to be an intensivist; a fancy term for the doctor who runs the ICU. I was keen on going through an internal medicine residency then match into a critical care fellowship. Many intensivists make their way via a pulmonary-critical care residency.
All these things are processes which when caught and managed well early on, have strikingly different outcomes.
Something like dementia is a process that, at very best, can only barely be slowed. In this case, preparing for the inevitable by making sure the patient is in a safe environment and that the family is well informed and prepared, as well as can be, to see their loved one forget who they are, is important.
Diabetes, as discussed in a previous post, is a process in which the deleterious effects can be ameliorated by controlling blood sugar.
In this, the seventh edition of Doctor, Doctor, Give Me The News we will discuss the most common reasons for being admitted to the intensive care unit. Some in general terms and others in detail.
Let us first ponder the very telling diagnosis that is "Post-Intensive-Care-Syndrome" in that it even exists at all. There is no "Post-Office-Visit-Care-Syndrome" that I'm aware of.
This may lead you to think that bad things happen to people in the ICU, and you'd be right. The alternative, however, is often death, or severe long term sequelae. That should not stop efforts from being made to minimize harmful aspects of staying in the ICU. In other words, bad things have already happened to have a patient land in the ICU.
Being in the unit can be terrifying. Often, however, the patients are sedated and they will have no memory of the worst parts of their stay. Their loved ones, however, have no such magic salve to block what they witness.
Tubes everywhere and going in and out of multiple orifices. Central lines and a veritable quandary of IV medications all hanging from the tree of life, slowly dripping their wondrous charms into the vein of the unaware patient.
Most of us say we don't want to be kept alive by machines. When people say this, I sometimes press to see what exactly they mean. What if they had to be mechanically ventilated for one day? After that they healed and went on to have a normal life. Most would be fine with that. Vented for two weeks? Months?
Of course, the longer the course of life support the grimmer the prognosis. Miracles happen, sure. But they're only miracles because they happen so rarely. Perhaps an examination and exploration of narcissistic tendencies and it's correlation with refusing to sign a DNR for a loved one is in order. I suspect it is a positively correlated phenomenon.
Any of us can have a turn of bad luck and end up in the unit. Overwhelmingly, however, it is people who have known risk factors and are already very sick. I couldn't find any statistics, but I would venture to guess that a large number of patients admitted to the ICU have been in the ICU previously.
This population is of course, self limiting, in that as ICU admissions become more frequent, a "celestial discharge" is looming large.
Diabetic Ketoacidosis
My fourth year of medical school was spent thinking I wanted to be an intensivist; a fancy term for the doctor who runs the ICU. I was keen on going through an internal medicine residency then match into a critical care fellowship. Many intensivists make their way via a pulmonary-critical care residency.
In the ICU, I am reminded why I was so intrigued by critical care medicine. I am also reminded why I am not planning on a career that involves the ICU. Rare is the Family Medicine doc who would manage a patient in the ICU, these days, anyway.
It important to see and gain experience managing diseases at all points in the spectrum.
It important to see and gain experience managing diseases at all points in the spectrum.
Managing a patient at the beginning of their liver failure journey patient takes on a different urgency once seeing what the ending looks like.
Cancer. Renal failure. Dementia. Debilitating stroke. Heart failure. COPD. Diabetes.
All these things are processes which when caught and managed well early on, have strikingly different outcomes.
Something like dementia is a process that, at very best, can only barely be slowed. In this case, preparing for the inevitable by making sure the patient is in a safe environment and that the family is well informed and prepared, as well as can be, to see their loved one forget who they are, is important.
Diabetes, as discussed in a previous post, is a process in which the deleterious effects can be ameliorated by controlling blood sugar.
In this, the seventh edition of Doctor, Doctor, Give Me The News we will discuss the most common reasons for being admitted to the intensive care unit. Some in general terms and others in detail.
Let us first ponder the very telling diagnosis that is "Post-Intensive-Care-Syndrome" in that it even exists at all. There is no "Post-Office-Visit-Care-Syndrome" that I'm aware of.
This may lead you to think that bad things happen to people in the ICU, and you'd be right. The alternative, however, is often death, or severe long term sequelae. That should not stop efforts from being made to minimize harmful aspects of staying in the ICU. In other words, bad things have already happened to have a patient land in the ICU.
Being in the unit can be terrifying. Often, however, the patients are sedated and they will have no memory of the worst parts of their stay. Their loved ones, however, have no such magic salve to block what they witness.
Tubes everywhere and going in and out of multiple orifices. Central lines and a veritable quandary of IV medications all hanging from the tree of life, slowly dripping their wondrous charms into the vein of the unaware patient.
Most of us say we don't want to be kept alive by machines. When people say this, I sometimes press to see what exactly they mean. What if they had to be mechanically ventilated for one day? After that they healed and went on to have a normal life. Most would be fine with that. Vented for two weeks? Months?
Of course, the longer the course of life support the grimmer the prognosis. Miracles happen, sure. But they're only miracles because they happen so rarely. Perhaps an examination and exploration of narcissistic tendencies and it's correlation with refusing to sign a DNR for a loved one is in order. I suspect it is a positively correlated phenomenon.
Any of us can have a turn of bad luck and end up in the unit. Overwhelmingly, however, it is people who have known risk factors and are already very sick. I couldn't find any statistics, but I would venture to guess that a large number of patients admitted to the ICU have been in the ICU previously.
This population is of course, self limiting, in that as ICU admissions become more frequent, a "celestial discharge" is looming large.
In broad strokes, the most common categories of primary diagnoses upon admission to the ICU are as follows:
- Cardiac
- Respiratory
- Neurologic
- Gastrointestinal
- Renal and Metabolic
- Burns
More specifically, and more morbidly, the causes of death in critically ill patients overall, meaning whether they are in ICU or not, are as follows:
- Acute, refractory multiple organ dysfunction syndrome
- Refractory cardiovascular failure
- Refractory, chronic multiple organ dysfunction syndrome
- Central nervous system failure
- Acute cardiac arrest
- End stage tumour disease
- Acute hemorrhage
- Intractable intestinal ischemia
- Pulmonary failure
- Acute or chronic liver failure
You may say to yourself, what the hell is an "acute refractory multiple organ dysfunction syndrome" anyway? Think sepsis, in this case, as a major cause of ARMODS (we don't really call it that, but it sounds cool and I kinda wanna start throwing around ARMODS during rounds) although any disease process advanced far enough can kick off the cascade of organ failure leading to death. We'll start by examining the leading cause of death in ICU.
Sepsis
It seems somewhat unfair, and perhaps a design flaw that the body's inflammatory response associated with a progressing infection, one that is usually in the blood, whether it be bacterial, viral, fungal or even protozoan is such an indiscriminate killer.
A lot of human suffering is due to our bodies response to exposures in the material world. Even simple seasonal allergies are a part of this. While sepsis is not an autoimmune disease, per se, it is our bodies response via immune and inflammatory cascades that plays a major part in our demise.
The most common cause of sepsis is from a bacterial infection. Often it is due to a urinary tract infection that has spread to the kidneys (we call this pyelonephritis) and being a place where blood interfaces with an infectious nidus is of concern. The same applies for the lungs, which actually are approximately where 50% of cases arise from. In one third to one half of sepsis patients an infectious source is not found.
In bacterial sepsis, things can progress rapidly and sepsis protocol management is all the rage in hospitals these days.
Gotta get an IV in and start dumping fluid into the circulatory system.
Next: get blood for a blood culture to identify what buggers are growing in the blood -- if any. We also get urine cultures and sputum if necessary. Sometimes wound cultures are gained but often these are relatively useless.
After, and only after the culture blood is on it's way to the laboratory should antibiotics be given. If for some reason there is an unreasonable delay in getting cultures, fine -- better to be alive without good cultures than dead with a speciation and sensitivity. Broad spectrum antibiotics are given first. As culture results return we can narrow the coverage. Antibiotic stewardship is really all of our responsibility, by the way. DO YOU WANNA DIE? Then fine, get your z-pack for the common rhinovirus, you jerk.
The facility where I work as a physician uses 30ml/kg fluid bolus guidelines. 100 kg is 220 lbs. A 100kg patient in sepsis who presented to the ED would get 3L in a bolus. That same 100 kg person has between 7 and 9 liters of blood in total!
Imagine this: the bacterium are partying. They are populating their world -- your blood stream. In doing this they produce toxins which inhibit our mitochondria (powerhouse of the cell) in their ability to use oxygen for fuel.
So, our cells use anaerobic respiration (fancy words for burning fuel that doesn't involve oxygen -- it is relatively inefficient and produces lactate) which can only go on for so long before cells involved die.
This, in conjunction with the dilation of the vascular system, which can cause a low blood pressure, which we call "hypotension" serves to limit the oxygen that is available to serve the cells that haven't been forced into anaerobic respiration.
This may seem quite obvious, but often the obvious is taken for granted and it is not addressed. With that in mind, the pressure in our arteries which is regulated by three main things: Heart rate, the heart's inotropic capability (how hard it can pump) and the contraction or dilation of the arteries.
Even a high blood pressure can't keep you out of danger if there is no oxygen to deliver. Oxygen must be able to pass through a small and thin layer of "skin" in the lungs in order to dissolve into the blood. Simplified but nevertheless true. Once in blood, the O2 comes across a hemoglobin.
That hemoglobin is looking hot and the feeling is mutual. The O2 and the hemoglobin join together in a lover's embrace. Of course the honeymoon ends when the O2 gets dumped off, left at the altar of the mitochondrial furnace.
In the blood these things must be present to stay alive: dissolved oxygen, hemoglobin and yes, blood pressure.
If our arteries dilate, this means that functionally there is more room in the tubes, and that means a lower pressure. The heart will start beating faster trying to maintain a good pressure. If a person has a heart that don't pump none too good, well, problems they are a brewing.
Now lactic acid is building up in the blood. It is from the anaerobic respiration and the lack of oxygen delivery due to hypotension. The patient is now dealing with an acid-base issue from the lactic acid.
The pH will start to drop. The first response is to start breathing faster to blow of carbon dioxide, which is also acidic in the blood -- carbonic acid, specifically.
The heart is racing. The diaphragm is working overtime. This does not help the oxygenation of the blood, which, functionally is compromised by the hypotension and things just get worse as the cycle continues.
Accessory muscles of respiration start to be used. These muscles are all the muscles that we use besides our diaphragm to breathe when we need to expedite the loss of CO2 and the gain of O2.
Soon enough the muscles become tired, exhausted even. They seize, cramp -- and this means that breathing is over, and this has a low correlation with the continuation of life as we know it.
This is one way to end up in the ICU from sepsis. If the heart doesn't get the fuel it needs to beat, well, then it may stop before respiratory failure. Really, at the end of the day, all death is defined as cardiac arrest.
Sepsis
It seems somewhat unfair, and perhaps a design flaw that the body's inflammatory response associated with a progressing infection, one that is usually in the blood, whether it be bacterial, viral, fungal or even protozoan is such an indiscriminate killer.
A lot of human suffering is due to our bodies response to exposures in the material world. Even simple seasonal allergies are a part of this. While sepsis is not an autoimmune disease, per se, it is our bodies response via immune and inflammatory cascades that plays a major part in our demise.
The most common cause of sepsis is from a bacterial infection. Often it is due to a urinary tract infection that has spread to the kidneys (we call this pyelonephritis) and being a place where blood interfaces with an infectious nidus is of concern. The same applies for the lungs, which actually are approximately where 50% of cases arise from. In one third to one half of sepsis patients an infectious source is not found.
In bacterial sepsis, things can progress rapidly and sepsis protocol management is all the rage in hospitals these days.
Gotta get an IV in and start dumping fluid into the circulatory system.
Next: get blood for a blood culture to identify what buggers are growing in the blood -- if any. We also get urine cultures and sputum if necessary. Sometimes wound cultures are gained but often these are relatively useless.
After, and only after the culture blood is on it's way to the laboratory should antibiotics be given. If for some reason there is an unreasonable delay in getting cultures, fine -- better to be alive without good cultures than dead with a speciation and sensitivity. Broad spectrum antibiotics are given first. As culture results return we can narrow the coverage. Antibiotic stewardship is really all of our responsibility, by the way. DO YOU WANNA DIE? Then fine, get your z-pack for the common rhinovirus, you jerk.
The facility where I work as a physician uses 30ml/kg fluid bolus guidelines. 100 kg is 220 lbs. A 100kg patient in sepsis who presented to the ED would get 3L in a bolus. That same 100 kg person has between 7 and 9 liters of blood in total!
Imagine this: the bacterium are partying. They are populating their world -- your blood stream. In doing this they produce toxins which inhibit our mitochondria (powerhouse of the cell) in their ability to use oxygen for fuel.
So, our cells use anaerobic respiration (fancy words for burning fuel that doesn't involve oxygen -- it is relatively inefficient and produces lactate) which can only go on for so long before cells involved die.
This, in conjunction with the dilation of the vascular system, which can cause a low blood pressure, which we call "hypotension" serves to limit the oxygen that is available to serve the cells that haven't been forced into anaerobic respiration.
This may seem quite obvious, but often the obvious is taken for granted and it is not addressed. With that in mind, the pressure in our arteries which is regulated by three main things: Heart rate, the heart's inotropic capability (how hard it can pump) and the contraction or dilation of the arteries.
Even a high blood pressure can't keep you out of danger if there is no oxygen to deliver. Oxygen must be able to pass through a small and thin layer of "skin" in the lungs in order to dissolve into the blood. Simplified but nevertheless true. Once in blood, the O2 comes across a hemoglobin.
That hemoglobin is looking hot and the feeling is mutual. The O2 and the hemoglobin join together in a lover's embrace. Of course the honeymoon ends when the O2 gets dumped off, left at the altar of the mitochondrial furnace.
In the blood these things must be present to stay alive: dissolved oxygen, hemoglobin and yes, blood pressure.
If our arteries dilate, this means that functionally there is more room in the tubes, and that means a lower pressure. The heart will start beating faster trying to maintain a good pressure. If a person has a heart that don't pump none too good, well, problems they are a brewing.
Now lactic acid is building up in the blood. It is from the anaerobic respiration and the lack of oxygen delivery due to hypotension. The patient is now dealing with an acid-base issue from the lactic acid.
The pH will start to drop. The first response is to start breathing faster to blow of carbon dioxide, which is also acidic in the blood -- carbonic acid, specifically.
The heart is racing. The diaphragm is working overtime. This does not help the oxygenation of the blood, which, functionally is compromised by the hypotension and things just get worse as the cycle continues.
Accessory muscles of respiration start to be used. These muscles are all the muscles that we use besides our diaphragm to breathe when we need to expedite the loss of CO2 and the gain of O2.
Soon enough the muscles become tired, exhausted even. They seize, cramp -- and this means that breathing is over, and this has a low correlation with the continuation of life as we know it.
This is one way to end up in the ICU from sepsis. If the heart doesn't get the fuel it needs to beat, well, then it may stop before respiratory failure. Really, at the end of the day, all death is defined as cardiac arrest.
This is the time that a patient is intubated -- meaning a tube connected to a breathing machine is shoved down the throat and into the foyer of the lungs.
What happens if the fluid and the antibiotics aren't enough to stave off the hypotension and build up of lactic acid? We can give drugs called "pressors" which function, essentially, to squeeze the arterial system so that pressure is maintained at a level compatible with life. We can give bicarbonate via IV, which helps to balance out the academia built up from the lactic acid.
Diabetic Ketoacidosis
DKA. Similar to sepsis, in that many people have heard of it, but few understand even the basic physiology and pathology involved.
DKA and HHS (Hyperosmolar Hyperglycemic State) are like two sides of a coin, and represent extremes of the hyperglycemic spectrum.
First, a quick refresher on diabetes. Many still think of it as a "one" vs "two" disease, and while categorization is fast becoming exceedingly outdated with our increased understanding of how and what diabetes is, we will use the nomenclature of DMT1 and DMT2 -- diabetes mellitus type one, and two, respectively. This is for simplification sake.
To be honest, I'm tempted to use "insulin dependent" vs "non-insulin dependent" as this has more of an impact on clinical management and treatment, in acute and clinical settings. And, really, for our porpoises here, DMT1 defaults to "insulin dependent" and DMT2 means "insulin independent, or, non-insulin dependent."
DMT1 is still sometimes referred to as "juvenile diabetes" because it was (and still kinda is) the kind of sugar disease that kids could get. These days, with the "fat-assing" of America, and indeed, now the world, kids can get DMT2 too. A touch of genetic vulnerability combined with too many Turkish Delights (shout out to Edmund Pevensie who just couldn't say no to that tasty treat -- I get you, fam) will cause the insulin resistance, and eventually, full blown diabetes, type two.
I recommend reading the first effort in this ongoing series, Diabetes, Cha Cha Cha, which has fun analogies involving keys and locks! Fun!
HHS, or HONK (Hyperosmotic Hyperglycemic NonKetotic State, and a name that is infinitely more enjoyable to say than "HHS") is much, much less common than DKA. In fact, it accounts for less than 1% of all DMT1 and DMT2 related hospital admissions. However, the mortality rate for HONK (yeah, I'm just going with that now) is around ten times higher than DKA! The reason for this is because the precipitating factors that drive a patient to HONK are usually very terrible, and the deaths in HONK patients are not related to the metabolic derangements seen in DKA.
HONK, in general, is a DMT2 kinda thing. More specifically, it happens in patients who have some insulin lying around. DMT1 have no insulin. Some people with longstanding DMT2 have no insulin because they burned their pancreas beta-cells out.
Sidenote: Medicine, perhaps more than any other endeavor I know of has so many caveats and exceptions that writing these things can become difficult. On one hand, I strive to simplify, yet on the other, I feel driven to stay true to the pathophysiology and explain all the catches, anomalies, peculiarities and remonstrations. Just know that behind every concept exists an unbelievable amount of nuance and subtle influences. This is why a computer won't take my job in the near future.
Back to HONK. Like DKA, it is usually kicked off with an infection or other acute illness, such as myocardial infarction (heart attack) or CVA (stroke.) A relative insulin deficiency leads to way too much sugar in the blood, we say "hyperglycemia" and this makes the blood thick. Not the good kinda Instagram model "thick" but a viscous blood thick -- we say, "hyperosmolar."
Thick blood makes the kidneys wanna make the pee pee, in an effort to pee out the stuff making the blood thick. Bad idea, if the kidneys were to ever ask me. This leads to volume depletion, and for those of you with foreskin -- haha, I mean foresight, can see that this only leads to increased hyperglycemia, and so it goes. Until it doesn't, and you die.
The difference in DKA lies in the fact that there is no insulin. Pancreatic cells that make the insulin have been nuked from orbit and that is why DMT1 patients are forced to stab themselves with a needle in the belly. Their insulin is exogenous.
HONK ain't gonna give you ketoacidosis because the presence of even small amounts of insulin inhibits hormone-sensitive lipase mediated fat tissue breakdown. And you thought I wasn't gonna simplify this.
The HONK-y Talk take home point boils down to the fact that uncontrolled diabetes puts you at risk for just about everything, with decreased ability to bounce back from everything, including HONK.
A ketoacidotic state has gotten more press as of late because of the popularity of the ketogenic diet. Some of the same processes are at play, naimly the our liver turning water into wine -- I mean triglycerides into ketone bodies.
For those of us that wish to use our diet to control our epilepsy or drive muscle sparring weight loss, fat into ketones is almost as good as water to wine. In a patient who is a DMT1, which means that there is no endogenous insulin production -- you get this by now, I'm sure, but feel compelled to refresh your memory. The moves the body makes when it goes to long without insulin, especially while it's stressing about something else, is what makes DKA such a danger.
An infection, or even a bender can push a person into DKA. An MI, stroke -- anything
What two hormones do you think of when you ponder the subtle complexities of extracellular glucose concentration? I hesitate to ask a question of such a personal nature. I'll just tell you me mine in hopes you tell me yours.
Glucagon -- that swarmy, age old driver of gluconeogenesis.
Insulin. Putt'n the sugar in the cells since the pancreas was a twinkle in the blastocyst's eye.
Food chew down gullet acid bath dooawdunum sugar go blood go pancreas insulin squirt sugar go cell human live.
When insulin is around the block, glucagon ain't gonna show his face. When insulin is gone, glucagon tells the liver to make sugar. It can makes sugar from the stored form of sugar, called glycogen, which is easy. It takes a lot more energy to make it out of protein. Understandable that our bodies try to preserve musculature -- it is very hard to build in the first place.
It is this state, where glucagon runs the block that we get into trouble. I mentioned the body under stress. You've probably heard about "stress hormones." These are the stress hormones: catecholamines, cortisol and growth hormone. Adrenalin is a catecholamine.
The liver is cranking out the ketone bodies. It does this because it thinks the body is starving. It takes the protein from the muscles and turns it into sugar. This adds to the rising level of sugar in the blood.
All the sugar which cannot enter the cells because there is no insulin to be found. Okay, fine -- insulin is the key and the door that lets the sugar into the cell has a lock and insulin unlocks the door and without the key the door stays shut and cells starve.
Meanwhile the kidneys have been working overtime to pee out the sugar. It takes water to make the pee pee and this makes everything worse. Ketone bodies are acidic, too.
Now the issue becomes the body trying to regulate the acid base levels in the blood.
I've said it before, and I'll say it again; if people understood the basics of pH control the body works towards, things like alkaline water and acid-base diets, and such would be ridiculed and run out of business.
Initially, the kidneys work to adjust the bicarbonate levels in the blood. HCO3 (bicarb) is alkaline. This process is overwhelmed and the pH continues to drop.
How else to get these excess hydrogen ions -- which is what acid is, out of the body? Kussmaul Breathing is the name we give to what the body does to push out the CO2 -- carbon dioxide, which is acidic.
Where else is there a lot of excess hydrogen ions in the body? Yup -- exactly, the stomach. HCl galore and the body pukes it out.
Often, by the time a DKA patient is breathing like this, they are mentally altered. Confused.
By the time people show up in the ED, they are severely dehydrated, blood thickened with sugar and are depleted in potassium, chloride, magnesium, sodium, phosphate and calcium. All the electrolytes we use to live. Much of these were peed out in an effort to push out the sugar, too. Some of them were pushed into cells, out of the blood.
If left unchecked, the DKA patient can go into sepsis, and septic shock, as the overall stress can trigger an inflammatory cascade response, even in absence of an infection. If that doesn't kill a person, as outlined above, cerebral edema will.
Some argue that the edema is a complication of improper management and fluid resuscitation. There are many cases documenting cerebral edema without any treatment at all, however.
A DKA patient goes to the ICU because they need to be monitored closely and their blood needs to be checked frequently. Fluids. A lot of fluids. Electrolyte replacement. Insulin. Making sure the acidemia is corrected.
Provided a patient survives their DKA journey, the good news is that the prognosis is usually fairly good. Like HONK, prognosis depends primarily on the underlying stressor or reason for embarking on the journey in the first place. If it were a weekend booze binge -- while not good for long term health, all other things being equal, the patient will do well. If it were because of a pneumonia that has run amok, prognosis is a worse.
There are many other indications for critical care admission, but some of the more interesting conditions such as myocardial infarction, liver failure, renal failure deserve their own post.
ICU nurses are usually the cream of the crop and are bad ass clinicians. I find that in general they have an understanding of pathophysiology that when combined with the practical and applied knowledge of an RN they have much to teach me.
I see you.
DKA and HHS (Hyperosmolar Hyperglycemic State) are like two sides of a coin, and represent extremes of the hyperglycemic spectrum.
First, a quick refresher on diabetes. Many still think of it as a "one" vs "two" disease, and while categorization is fast becoming exceedingly outdated with our increased understanding of how and what diabetes is, we will use the nomenclature of DMT1 and DMT2 -- diabetes mellitus type one, and two, respectively. This is for simplification sake.
To be honest, I'm tempted to use "insulin dependent" vs "non-insulin dependent" as this has more of an impact on clinical management and treatment, in acute and clinical settings. And, really, for our porpoises here, DMT1 defaults to "insulin dependent" and DMT2 means "insulin independent, or, non-insulin dependent."
DMT1 is still sometimes referred to as "juvenile diabetes" because it was (and still kinda is) the kind of sugar disease that kids could get. These days, with the "fat-assing" of America, and indeed, now the world, kids can get DMT2 too. A touch of genetic vulnerability combined with too many Turkish Delights (shout out to Edmund Pevensie who just couldn't say no to that tasty treat -- I get you, fam) will cause the insulin resistance, and eventually, full blown diabetes, type two.
I recommend reading the first effort in this ongoing series, Diabetes, Cha Cha Cha, which has fun analogies involving keys and locks! Fun!
HONK, in general, is a DMT2 kinda thing. More specifically, it happens in patients who have some insulin lying around. DMT1 have no insulin. Some people with longstanding DMT2 have no insulin because they burned their pancreas beta-cells out.
Sidenote: Medicine, perhaps more than any other endeavor I know of has so many caveats and exceptions that writing these things can become difficult. On one hand, I strive to simplify, yet on the other, I feel driven to stay true to the pathophysiology and explain all the catches, anomalies, peculiarities and remonstrations. Just know that behind every concept exists an unbelievable amount of nuance and subtle influences. This is why a computer won't take my job in the near future.
Back to HONK. Like DKA, it is usually kicked off with an infection or other acute illness, such as myocardial infarction (heart attack) or CVA (stroke.) A relative insulin deficiency leads to way too much sugar in the blood, we say "hyperglycemia" and this makes the blood thick. Not the good kinda Instagram model "thick" but a viscous blood thick -- we say, "hyperosmolar."
Thick blood makes the kidneys wanna make the pee pee, in an effort to pee out the stuff making the blood thick. Bad idea, if the kidneys were to ever ask me. This leads to volume depletion, and for those of you with foreskin -- haha, I mean foresight, can see that this only leads to increased hyperglycemia, and so it goes. Until it doesn't, and you die.
The difference in DKA lies in the fact that there is no insulin. Pancreatic cells that make the insulin have been nuked from orbit and that is why DMT1 patients are forced to stab themselves with a needle in the belly. Their insulin is exogenous.
HONK ain't gonna give you ketoacidosis because the presence of even small amounts of insulin inhibits hormone-sensitive lipase mediated fat tissue breakdown. And you thought I wasn't gonna simplify this.
The HONK-y Talk take home point boils down to the fact that uncontrolled diabetes puts you at risk for just about everything, with decreased ability to bounce back from everything, including HONK.
A ketoacidotic state has gotten more press as of late because of the popularity of the ketogenic diet. Some of the same processes are at play, naimly the our liver turning water into wine -- I mean triglycerides into ketone bodies.
For those of us that wish to use our diet to control our epilepsy or drive muscle sparring weight loss, fat into ketones is almost as good as water to wine. In a patient who is a DMT1, which means that there is no endogenous insulin production -- you get this by now, I'm sure, but feel compelled to refresh your memory. The moves the body makes when it goes to long without insulin, especially while it's stressing about something else, is what makes DKA such a danger.
An infection, or even a bender can push a person into DKA. An MI, stroke -- anything
What two hormones do you think of when you ponder the subtle complexities of extracellular glucose concentration? I hesitate to ask a question of such a personal nature. I'll just tell you me mine in hopes you tell me yours.
Glucagon -- that swarmy, age old driver of gluconeogenesis.
Insulin. Putt'n the sugar in the cells since the pancreas was a twinkle in the blastocyst's eye.
Food chew down gullet acid bath dooawdunum sugar go blood go pancreas insulin squirt sugar go cell human live.
When insulin is around the block, glucagon ain't gonna show his face. When insulin is gone, glucagon tells the liver to make sugar. It can makes sugar from the stored form of sugar, called glycogen, which is easy. It takes a lot more energy to make it out of protein. Understandable that our bodies try to preserve musculature -- it is very hard to build in the first place.
It is this state, where glucagon runs the block that we get into trouble. I mentioned the body under stress. You've probably heard about "stress hormones." These are the stress hormones: catecholamines, cortisol and growth hormone. Adrenalin is a catecholamine.
The liver is cranking out the ketone bodies. It does this because it thinks the body is starving. It takes the protein from the muscles and turns it into sugar. This adds to the rising level of sugar in the blood.
All the sugar which cannot enter the cells because there is no insulin to be found. Okay, fine -- insulin is the key and the door that lets the sugar into the cell has a lock and insulin unlocks the door and without the key the door stays shut and cells starve.
Meanwhile the kidneys have been working overtime to pee out the sugar. It takes water to make the pee pee and this makes everything worse. Ketone bodies are acidic, too.
Now the issue becomes the body trying to regulate the acid base levels in the blood.
I've said it before, and I'll say it again; if people understood the basics of pH control the body works towards, things like alkaline water and acid-base diets, and such would be ridiculed and run out of business.
Initially, the kidneys work to adjust the bicarbonate levels in the blood. HCO3 (bicarb) is alkaline. This process is overwhelmed and the pH continues to drop.
How else to get these excess hydrogen ions -- which is what acid is, out of the body? Kussmaul Breathing is the name we give to what the body does to push out the CO2 -- carbon dioxide, which is acidic.
Where else is there a lot of excess hydrogen ions in the body? Yup -- exactly, the stomach. HCl galore and the body pukes it out.
Often, by the time a DKA patient is breathing like this, they are mentally altered. Confused.
By the time people show up in the ED, they are severely dehydrated, blood thickened with sugar and are depleted in potassium, chloride, magnesium, sodium, phosphate and calcium. All the electrolytes we use to live. Much of these were peed out in an effort to push out the sugar, too. Some of them were pushed into cells, out of the blood.
If left unchecked, the DKA patient can go into sepsis, and septic shock, as the overall stress can trigger an inflammatory cascade response, even in absence of an infection. If that doesn't kill a person, as outlined above, cerebral edema will.
Some argue that the edema is a complication of improper management and fluid resuscitation. There are many cases documenting cerebral edema without any treatment at all, however.
A DKA patient goes to the ICU because they need to be monitored closely and their blood needs to be checked frequently. Fluids. A lot of fluids. Electrolyte replacement. Insulin. Making sure the acidemia is corrected.
Provided a patient survives their DKA journey, the good news is that the prognosis is usually fairly good. Like HONK, prognosis depends primarily on the underlying stressor or reason for embarking on the journey in the first place. If it were a weekend booze binge -- while not good for long term health, all other things being equal, the patient will do well. If it were because of a pneumonia that has run amok, prognosis is a worse.
There are many other indications for critical care admission, but some of the more interesting conditions such as myocardial infarction, liver failure, renal failure deserve their own post.
ICU nurses are usually the cream of the crop and are bad ass clinicians. I find that in general they have an understanding of pathophysiology that when combined with the practical and applied knowledge of an RN they have much to teach me.
I see you.
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