Re: Potassium Cyanide Rash?
From: Harry (paminifarm3_at_netscape.net)
Date: 03/29/05
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Date: 29 Mar 2005 14:01:57 -0800
Hello, Sbharris,
Oh, Yes, i do know what iam talking about!!!!
Do you?
Remember, while reading the following, Michael was
reported to the police for injecting Terri with insulin, then
couple that with the red rash, his RN knowledge, insane
desire for her demise and $1.2 million, plus his sparkling-new,
2-inch-wide, intricately designed, gold bracelet on his right wrist.
I suspect the bracelet was on his right wrist, because he was
hiding from audience view, something in the nature of a watch
on the left wrist- Everyone in Pennsylvania, wears their watch
on their left wrist, as itis all but sacrilegious to do otherwise,
and considering the bracelet, the watch must be a $dozzie$.
Considering the small brain of the man, his lawyer was lucky
he was able to get him to at least hide the watch during his
coming-out, tv debut.
http://bdubinmededcom.ezhostsite.com/latest_information.html
Diabetic Ketoacidosis (DKA):
Insulin-dependent diabetes mellitus (IDDM) is a disorder that results
from the autoimmune destruction of the pancreatic beta cells. These are
the insulin producing cells of the body and their destruction causes a
chronic disorder for which there is no cure. In the United States, the
prevalence of IDDM by the age of 20 years is approximately 0.26%, but
the disease can occur at any point in an individualÕs lifetime. DKA is
one of the most serious complications occurring in this population and
has a 2-5% mortality in developed countries.
DKA is a metabolic disorder consisting of three major abnormalities:
elevated blood glucose level, high ketone bodies, and a metabolic
acidosis with an elevated anion gap. Dehydration and hyperosmolarity
may be present as well. It is important to understand that any
individual patient may present with a range of clinical findings not
clearly meeting the above criteria
PATHOPHYSIOLOGY:
To understand what happens in DKA, it is helpful to understand the
normal process of glucose metabolism. After absorption of food glucose
concentrations in the blood increase and then slowly fall over a period
of several hours. Under normal circumstances the body is able to
maintain blood glucose within a narrow range during both these feeding
and fasting states due to a complex interplay between insulin and a
catabolic hormone called glucagon. In the period between meals there is
a relative insulin lack, which allows a mobilization of free fatty
acids from adipose tissue. When this occurs, metabolism shifts slightly
so that the lipids are used by peripheral tissues for energy rather
than glucose. This allows the remaining glucose to be available to
tissues such as the brain. It is important to be aware that brain cells
are both insulin insensitive (they do not require insulin for transport
of glucose into the cells) and primarily use glucose for energy. This
means that the brain continues to use glucose as its fuel, even during
fuel deprivation, starvation, and DKA. Some of the fatty acids released
are taken up by the liver and converted to ketones which can be
oxidized in the brain to provide backup fuel should hepatic glucose
production fail. These changes are typical of the post-parandial phase
and would usually end at the next meal. If the fasting period is
extended the ketone levels will begin to rise, but usually are limited
by the fact that ketones stimulate insulin release which prevents
further breakdown of adipose tissue. Obviously, in severe starvation
conditions this mechanism can be overridden so that adipose stores can
be used.
DKA can be viewed as a state of absolute or relative insulin deficit
and increased levels of counter-regulatory hormones (glucagon,
catecholamines, cortisol, growth hormone). As discussed above, under
normal conditions these hormones balance out their actions on the fat
cells and the liver allowing for well regulated management of glucose
and lipids within the liver and adipose tissues. In cases where the
counter-regulatory hormones outweigh the effects of insulin, for
whatever reason, DKA supervenes. In some ways, DKA can be seen as
starvation in the midst of plenty. Clearly, there is an excess of
glucose, the normal substrate used for energy production.
Unfortunately, without the presence of insulin, the glucose goes
largely unused since most cells are unable to transport glucose into
the cell without the presence of insulin. Many of the cells in the body
feel as though they are starving and they innocently activate
homeostatic mechanisms to provide even greater quantities of glucose,
thus resulting in greater hyperglycemia. In response to the sense of
starvation, other alternative fuels, such as ketoacids and fatty acids,
are produced. Despite these fuels, the majority of cells remain
ÒhungryÓ and continue to order more food production. The manner in
which this ÒfoodÓ production is undertaken in this pathological
situation is discussed below.
In the setting of insulin deprivation three organs are primarily
affected, the liver, the fat cell, and the muscle. When insulin levels
decrease in DKA, large quantities of fatty acids are released from the
fat cell, into the blood. These free fatty acids are taken up by the
liver where, in the setting of decreased insulin and increased
glucagon, become the precursors for ketoacid production. In addition,
the elevated free fatty acid levels increase gluconeogenesis within the
liver, increasing the glucose levels even more. If there were no free
fatty acids there would be no DKA.
Pathological Changes Within the Liver:
Many of the pathological changes seen in DKA are less the result of an
absolute lack of insulin, as they are the result of an alteration in
the balance of insulin and the other counter-regulatory enzymes. When
the balance is working appropriately, insulin normally works to promote
synthetic and storage pathways in the following ways: (1) stimulates
hepatic glycogenesis, (2) stimulates pyruvate production which is used
in the synthesis of amino acids, lipids, and ATP production, (3)
simulates lipogenesis. Glucagon, as mentioned previously, does exactly
the opposite of insulin and when glucagon is present in excess it
multiplies the problems that were initiated by the lack of insulin. For
example, glucagon stimulates the breakdown of glycogen into glucose.
Additionally, it increases glucose formation from pyruvate and inhibits
lipogenesis. The inhibition of lipogenesis allows a cascade of other
reactions to occur which has the end result of increasing the flow of
free fatty acids into the liver mitochondria where they not used
properly and are instead oxidized into ketoacids (acetoacetate and
beta-hydroxybutyrate).
Changes in Other Organs:
While all these actions are occurring within the fat cells and the
liver, other detrimental changes are also occurring. When the serum
glucose level rises above 300 mg/dl it exceeds the ability of the
kidney to reabsorb it and glucose begins to appear in the urine.
Glucose is an osmotically active molecule and when it is present in the
urine it pulls with it water and electrolytes. The ketoacids are also
released into the urine as nonreabsorbable anions of sodium and
potassium salts which adds to the loss of electrolytes. The increased
glucose levels affect the serum in a manner similar to that seen in the
kidneys. The glucose is restricted to the extracellular space and acts
to pull water from the intracellular space to the extracellular space.
Initially, this fluid shift helps maintain the extracellular volume
that is being lost in the urine. However, as the osmotic diuresis
continues, severe intracellular and extracellular dehydration result.
Those patients with normal kidney function, and an ability to remain
well hydrated, can excrete large amounts of glucose within the urine
without becoming markedly dehydrated. Their glucose levels in DKA may
be only moderately elevated. Those patients with severe vomiting,
inability to take in adequate urine eventually become markedly
dehydrated which results in decreased glomerular filtration rates and a
considerably increased serum glucose level.
Potassium deserves special attention in the patient with DKA. As a
rule, the total body potassium levels in the patient with DKA are
decreased. However, the patient may be hyperkalemic or have a normal
serum potassium level at presentation. This falsely normal or elevated
plasma potassium level is multifactorial. First, the osmotic pull of
the extracellular fluid shifts water and potassium out of the
intracellular fluid of the muscle cells. The shift is then further
increased by the breakdown of intracellular protein which liberates
more potassium. Additionally, potassium moves out of cells in exchange
for hydrogen ions which are present in excess during DKA. Finally, in
the absence of insulin potassium is unable to move back into cells once
it has been pulled out. All of this potassium that is pulled from the
intracellular arena is initially brought to the kidneys, where it is
lost in the osmotic pull present due to the extreme glucosurea. When
the patient finally becomes so dehydrated that they cannot maintain
adequate glomerular filtration, the potassium present in the
extracellular fluid appears as a normal or increased amount, despite
severe total body depletion.
Causes of High Anion Gap Metabolic Acidosis
CATMUDPILES
C= CO, CN
A= Alcoholic ketoacidosis
T= Toluene
M= Methanol
U= Uremia
D= DKA
P= Paraldehyde
I= Iron, INH
L= Lactic acidosis
E= Ethylene glycol
S= Salysilates and strychnine
Usually the diagnosis can be assumed by the combination of history and
laboratory tests. Briefly, some of the other diagnosis to consider are
as follows. Carbon monoxide and cyanide often have a traceable source
of exposure as well as multiple victims. Drugs such as iron give very
pronounced gastrointestinal symptoms and pill fragments which are
visible on abdominal radiograph. Isoniazid is associated with
intractable seizures, and it is these seizures that result in the
acidosis. Paraldehyde has an odor of vinyl which may help make this
diagnosis. The acidosis is not usually too severe and ketones may be
present in the urine. Toluene is an aromatic petroleum distillate that
is commonly used as a solvent in paint, pharmaceutical, and chemical
companies. This agent may have associated pulmonary complaints if any
of it was aspirated, however, the most common route of exposure seen in
drug abusers. These people inhale toluene and may present with GI
disturbances, weakness, and neuropyschiatric problems. These patients
may have paint on their hands, or smell of paint products when they
present. Methanol and ethylene glycol can cause mild abdominal
discomfort as well as apparent intoxication. Methanol may also present
with visual complaints and specific findings on physical exam.
Initial tests to consider are those that are likely already available
since electrolytes, BUN, creatinine, and glucose are often ordered
early in the evaluation of ill patients. If the BUN, creatinine, and
glucose are normal then uremia and DKA (unless the patient has
euglycemic DKA) have been removed from the differential. Alcoholic
ketoacidosis usually causes a mild to moderate acidemia and moderate
elevation of the anion gap. Commonly, the patient has a negative
ethanol level and has complaints of abdominal pain. They classically
have a long history of significant drinking. Also, they are unlikely to
have rapid hemodynamic compromise. Clearly, this patient has an
elevated glucose, ketones, and an acidosis.
At this point, a urinalysis will likely be helpful. The urine dipstick
can evaluate for glucose and ketones. This will help further evaluate
for DKA as well as be a marker for the other sources of ketonuria
(ketones may be present in exposure to salycilates, alcoholic
ketoacidosis, and in toluene overdoses). If there is any suspicion of
ethylene glycol exposure then the urine should be exposed to a WoodÕs
lamp. If the patient ingested fluorescien-containing antifreeze
(ethylene glycol) then their urine will fluoresce under the lamp. Also,
ethylene glycol is metabolized in such a way that calcium oxalate
crystals may be present in the urine (the absence of these findings
does not rule out ethylene glycol exposure). Another useful bedside
test or urine is the ferric chloride test. This is a qualitative test
to measure whether the patient has had exposure to salycilates. If the
test is positive, a serum salycilate level must be sent.
If the patient presents comatose, then the causes of acidosis and coma
should be considered. These include starvation, DKA, lactic acidosis,
uremic acidosis, alcoholic ketosis, salicylate intoxication, toxic
alcohol ingestion, NKH, and hypoglycemic coma. Again, with careful
history, physical, and directed laboratory testing the diagnosis can
usually be made.
In addition to the above differential diagnosis, it is important to
understand special instances when the patient has DKA, but does not
meet the usual diagnostic criteria. There are three cases that should
be considered:
Euglycemic DKA: In cases where a patient maintains good hydration, or
has an increased glomerular filtration rate (as seen in a pregnant
patient), ketoacidosis may occur with minimal hyperglycemia. It may
also be seen in patients who are taking insulin, but the amount of
insulin is not adequate for a ketogenic process, such as acute illness.
A careful history, can usually explain the minimal elevation of glucose
and lead to appropriate treatment.
Alkalemic DKA: This is a condition of the expected primary metabolic
acidosis, being mixed with a primary metabolic alkalosis. A markedly
elevated anion gap is generally present. This condition most commonly
occurs in a patient with DKA who develops severe, protracted vomiting.
It may also be seen in those on diuretics, or those with Cushing's
syndrome. The laboratory results come from DKA, which lowers the
bicarbonate, and vomiting which lowers the chloride. Taken together
there is a marked elevation of the anion gap, but the pH is not as low
as predicted by the PCO2.
Nonketotic DKA: In normal conditions there is approximately a 1:5 ratio
of acetoacetate to beta-hydroxybutyrate. In conditions that cause
tissue hypoxemia (such as sepsis, shock, severe hypotension) this
reaction gets driven toward beta-hydroxybutyrate and the ratio may
reach 1:20 (acetoacetate to beta-hydroxybutyrate). This situation
leaves little acetoacetate to be measured by the nitroprusside reaction
and can make the diagnosis of DKA less clear. These patients still have
an elevated anion gap and, usually, and elevated glucose.
DIAGNOSIS:
History and Physical: Patients with DKA usually present with complaint
of fatigue, malaise, thirst, and polyuria. Depending on the length of
symptoms the patient may be able to report weight loss. As the patient
becomes increasingly ill they may begin to vomit and complain of
abdominal pain. The exact cause of abdominal pain that is associated
with DKA is not known. The abdominal pain is disturbing since it may be
secondary to the DKA, or be from the pathologic process that initiated
the crisis, such as pyelonephritis, pancreatitis, etc. Usually,
abdominal pain secondary to DKA will begin to resolve with treatment.
The physical signs of DKA can be variable. Most patients will have some
degree of tachycardia, but the blood pressure is often normal. Evidence
of dehydration, such as loss of skin turgor, and dry mucus membranes
may be present. The patient may be febrile, and extreme elevations of
temperature should not be assumed to be the result of dehydration.
Hypothermia may also be seen. The respiratory rate may be normal or
somewhat rapid, but if the patient is examined closely the deep
breathing typical of ÒKussmaulÓ respirations may be noted.
Laboratory Abnormalities: In general, the laboratory diagnosis of DKA
is based on an elevated blood glucose (usually above 250mg/dl), a low
serum bicarbonate level (usually below 15 mEq/L), and elevated anion
gap, and demonstrable ketonemia. Individually, all of these values may
vary considerably, but taken together they help make the diagnosis of
DKA. In addition to the above there are several calculations that are
important in the evaluation and therapy of the patient with DKA.
Serum Osmolality: Mental status changes can occur in DKA and may be the
result of DKA, or some underlying process that may have caused the
patient to develop DKA. Obviously, it is critical to determine the
cause of the patientÕs altered mental status. It has been well
documented that mental status changes in DKA correlate with the
effective serum osmolality. Thus, a patient with mental status changes
can only have this decompensation explained by the elevated glucose
level if the serum osmolality is significantly elevated. The effective
serum osmolality is calculated as follows:
Serum Osmolality = 2(Na+) + glu/18 + BUN/2.8
Calculated total osmolalities of greater than 340 mOsm/kg H2O are
associated with stupor and coma. Calculated values below this level
would not explain a patient with coma and an additional cause such as
meningitis, or stroke should be considered.
Corrected Serum Sodium Levels: Despite volume depletion, serum sodium
may be low, normal, or elevated. This variation has several causes.
First, dehydration from an osmotic diuresis may result in excess loss
of water compared to sodium, this may give increased values of serum
sodium despite total body sodium depletion. On the other hand, serum
sodium level frequently appears low. Recall that insulin deficiency
results in reduced clearance of triglycerides. The presence of
triglycerides displaces plasma water and cause a low reading for the
sodium concentration (this is pseudohyponatremia). It is possible to
recognize this clinically by noting that the plasma is milky or cloudy
appearing. Finally, Sodium levels often appear artificially low due to
the osmotic pull of the elevated serum glucose levels. The presence of
the increased glucose causes water to shift into the extracellular
space resulting in a dilutional reduction on the serum sodium. When
trying to determine the degree of dehydration in a patient it is best
to use corrected serum sodium level. This can be calculated using the
following formula:
Corrected Na+ = [Na+] + 1.6 x [glu in mg/dl] - 100
100
Often, the initial serum sodium appears low, but when the above
calculation in performed, the final value is elevated. This indicates a
marked intracellular dehydration.
Anion Gap: The differential of an elevated anion gap associated with a
metabolic acidosis has been discussed. This section will simply give an
explanation for the anion gap seen in DKA. The ketoacids produced
during DKA are buffered by the serum bicarbonate and then excreted in
the urine. This causes a loss of bicarbonate which is a measured anion.
As the bicarbonate is lost the anion gap increases.
The three ketone bodies are beta- hydroxybutyrate, acetoacetate, and
acetone. Only acetoacetate and acetone are measured in the
nitroprusside reaction, but the formation of these ketone bodies favors
the development of beta-hydroxybutyrate. Thus, the test for ketone
bodies may be only weakly positive even when large amounts of total
ketones are present. Acetone does not contribute to the anion gap, but
it is measured in the nitroprusside reaction and is a precursor for the
regeneration of bicarbonate. It is not uncommon for the patient to be
improving clinically, but to have the nitroprusside test become more
strongly positive since acetone is being produced. At this point, the
anion gap should be narrowing, even as the nitroprusside test is
getting stronger.
Additional Laboratory Evaluation: When the patient arrives in the
Emergency Department some initial labs should be sent. Many of these
common tests will give the data needed to do the above important
calculations. A tube should be sent for exact glucose determination,
but a bedside test can me used to determine gross blood sugar levels.
To determine the degree of acidosis and bicarbonate loss, an ABG should
be sent early in the evaluation of a patient considered to have DKA.
The complete blood count often shows an elevation of the white blood
cells. This may be, in part, due to hemoconcentration secondary to
dehydration. Thus, WBCÕs of 20,000 occur commonly. Those patients with
WBCÕs greater than 30,000 who have a bandemia on peripheral smear
should be assumed to have an infectious process. Additional evaluation
should take into consideration the best tests to help determine the
potential cause of the patientÕs decompensation into DKA. Urinalysis,
chest radiograph, and electrocardiogram should be done on most
patients.
TREATMENT:
The treatment goals of the patient with DKA are as follows: (1) improve
hypovolemia and tissue perfusion, (2) decrease the serum glucose, (3)
reverse ketonemia and acidemia at a steady rate, (4) correct
electrolyte losses and imbalances, (5) find and treat the underlying
cause of the patients DKA.
Hydration Therapy: Patients with DKA are invariably dehydrated and
foremost in the treatment of DKA is restoration of the intravascular
volume. Estimates of fluid deficits in the decompensated diabetic is 4
to 10 liters (usually 5-6 liters). Enough fluid should be given to
approximate this amount. Remember to keep track of net fluid needs,
which means the total fluid deficit as well as ongoing urine and
insensible losses. In addition to improving tissue perfusion, fluid
therapy lowers the hyperglycemia by dilution and increased glomerular
filtration rate. A significant decrease in serum glucose can be
achieved in the absence of any insulin therapy, simply by adequate
hydration.
There are several recommendations for the amount of fluid, type of
fluid, and over what time period the fluid should be given over. The
use of normal saline is well established, and its use avoids rapid fall
in extracellular osmolarity. Lactated ringers has less chloride and
some buffers from hyperchloremic, acidotic patients. However, it
contains potassium and must be used with care in patients with elevated
potassium levels. Half-normal saline with two ampules of bicarbonate
can be used for severe acidosis. As stated, the usual initial fluid
recommendation is normal saline. Although the patients are in a state
of hypertonic dehydration, the initial need is intravascular repletion,
which is why normal saline or lactated ringers is initially
recommended.
Initially, one to two liters of normal saline is given within the first
hour followed by 1 L/hour for the next several hours. This initial
management should be guided by the patientÕs general condition and
response, with more or less fluid as indicated. After the first 3-4
hours, as the clinical condition of the patient improves, with stable
blood pressure and good urine output, fluids should be changed to 1/2
normal saline at 250-500cc an hour for 3-4 hours. Ongoing reassessment
is critical. When dehydration does not appear severe, rehydration rates
one-half as fast as the above regimens have been studied with good
results and less electrolyte disturbance. This may be considered in
those patients who appear only minimally dehydrated.
Insulin: Insulin has several actions in managing DKA. These include
decreasing glucagon release from the pancreas and limiting glucagonÕs
effect on the liver. This decreases gluconeogenesis and ketogenesis in
the liver. Additionally, the insulin allows glucose uptake and
utilization by peripheral tissues.
In the past, large doses of insulin were used in the early stages of
DKA therapy. At this point different methods of giving insulin have
been studied and large doses of subcutaneous insulin are no longer
recommended. Most recent recommendations suggest that more modest
amounts of insulin should be given and that the intravenous or
intramuscular routes are best. If the patient has evidence of decreased
tissue perfusion, even intramuscular routes may be inadequate and in
these case intravenous routes should be used. The intravenous route is
preferred in the initial management of the patient with DKA because it
allows smoother control of blood glucose, and fewer hypoglycemic or
hypokalemic events. When patients initially present they have a
relative insulin resistance due to the elevated levels of
counterregulatory hormones. This explains why the insulin requirements
during DKA are usually significantly higher than the patientÕs normal
needs. Elderly people usually will do well with half the amount of
insulin than most younger adults will need.
Current recommendations for insulin therapy include an initial
intravenous insulin bolus of 0.1 to 0.4 U/kg body weight followed by a
continuous intravenous infusion of 0.1 U/kg/hour. This usually amounts
to 5-10 U/hour in the typical adult. The goal of treatment should be to
lower the serum glucose of the patient by 75-100 mg/dl/hour. The rate
can be doubled every hour if this rate is not achieved. Ongoing severe
difficulty in controlling the glucose levels may indicate the presence
of a severe underlying infection.
The ketosis and acidemia in DKA take longer to resolve than the
elevation of glucose. For this reason, the insulin therapy must be
continued even when the blood glucose levels have improved to near
normal levels. When the glucose levels begin to approach 250 mg/dl,
insulin infusions are continued, but the fluid composition is changed
to include 5-10% dextrose in water to avoid hypoglycemia.
General Guidelines for Treatment of DKA:
Intravenous Fluids: * 500-1000 cc NS or LR/hr for 3-4 hours (adjust as
needed
for elderly patients, or those with profound shock)
* 250-500 cc/hr of 1/2 NS for 3-4 hours
* D5 or D10 as serum glucose begins to normalize.
Insulin Therapy: * 0.1-0.4 U/kg IV push followed by,
* 0.1 U/kg regular insulin, per hour as an insulin drip
* Double dose of insulin every 1-2 hours if glucose not responding
* Reduce insulin drip as glucose approaches 250 mg/dl
Potassium: Regardless of the serum potassium level at the initiation of
therapy, during treatment of DKA there is usually a rapid decline in
the potassium concentration in the patient with normal kidney function.
Patients who have life-threatening elevation of potassium should be
treated in the same manner as any other patient with severe
hyperkalemia. The drop in potassium is a result of hydration and
resolution of acidemia, but in particular is due to insulin
administration. As insulin is given potassium is driven into the
intracellular compartment. Additionally, early in the course of therapy
potassium is usually still being lost in the urine due to ongoing
osmotic diuresis and ketonuria. Since potassium is normally an
intracellular ion, it is not well conserved as these mechanisms begin
to take effect.
While it is not uncommon to have hyperkalemia, the development of
severe hypokalemia is usually a greater threat. Total body deficits are
estimated at 3-5 mEq/kg. When treating the patient with DKA the
clinician should be able to anticipate all of these shifts and maintain
potassium levels at near normal throughout therapy.
General recommendations for potassium replacement are as follows. If
the patient does not have marked elevation of potassium, is not in
renal failure, the ECG does not show evidence of hyperkalemia beyond
peaked T-waves, potassium therapy is initiated once good urine output
has been established. Potassium is usually added to the intravenous
fluids and should not exceed 40 mEq per liter of intravenous fluids.
Some authors recommend spitting the potassium replacement as KCL and
KPO4. The potassium level should be checked every one to two hours
initially since this is when the greatest shift occurs. After the
patient has stabilized the potassium can be checked every 6 to 8 hours.
Bicarbonate Therapy: The use of bicarbonate in the treatment of DKA is
highly controversial. The advocates of bicarbonate suggest that
acidosis is detrimental to cardiac function, while opponents of this
therapy point out several problems. These include: (1) paradoxical
lowering of intracellular pH from diffusion into cells of CO2 which is
produced from the bicarbonate, (2) a decrease in tissue oxygenation
from a shift in the oxygen dissociation curve, (3) sodium overload, (4)
increased chance of acute hypokalemia. There are a limited number of
studies evaluating the use of bicarbonate but those that are present
have found that bicarbonate therapy does not significantly alter the
recovery or outcome in DKA. To date there are not studies looking at
the use of bicarbonate in severely acidotic patients (those with pH
less than 6.9) and it is generally felt that this group should probably
receive bicarbonate therapy.
Current recommendations for bicarbonate therapy are as follows. Use of
bicarbonate is considered unnecessary when the blood pH is greater than
7.1. For those patients with pH between 6.9 and 7.1 there are no clear
guidelines. If the patient is elderly or very debilitated there may be
some benefit to the bicarbonate in this range. If it is given it should
be given with the intravenous fluids and not as IV push. For those
patients with pH below 6.9 bicarbonate should be added to the
intravenous fluids. One ampule of bicarbonate has 44 mEq of sodium
bicarbonate. Attempts should be made to create an isotonic fluid with
the bicarbonate being added to either one-half normal saline or D5W.
Phosphate: Phosphate is normally an intracellular substance that is
dragged out of the cell during DKA. Similarly to potassium, at
presentation the serum level may be normal, high, or low while the
total body supply is depleted. Despite this depletion, replacement of
phosphate has not been shown to affect patient outcome and routine
replacement is not recommended.
COMPLICATIONS OF THERAPY:
Brain Edema: Clinical brain edema occurs in less than one percent of
the pediatric population and even less frequently in adults. When it
does occur the mortality rate is high. The pathology of this rare
condition is not well understood. Therapy of DKA has several
theoretical factors that could contribute to brain edema, but no single
factor has been identified that can predict this complication. It is
probably prudent to prevent overvigorous correction of severe
hyperosmolarity and hypernatremia.
When this complication does develop it typically has a rapid onset of
severe headache and depression of the mental status. CT scan will show
characteristic changes. Treatment must be started rapidly with
intravenous mannitol and intubation as indicated.
Adult Respiratory Distress Syndrome: This complication usually occurs
during therapy with fluids, insulin, and electrolyte replacement. Fluid
therapy causes an increase in the right atrial pressure and
additionally, decreases colloid oncotic pressure. These conditions
could favor the development of pulmonary edema in a normal patient, but
those with DKA may also have an increased pulmonary capillary
permeability for unclear reasons.
Patients who have a widened A-a gradient or who have rales onlung exam
at the time that they present with DKA seem to be at an increased risk
for developing ARDS. In patients with these risk factors it is probably
wise to use lower rates of fluid replacement.
Hyperchloremic Acidosis: This complication can be recognized by a low
bicarbonate level, low to normal pH, normal anion gap, and an increased
serum chloride level. The cause of this condition is multifactorial:
(1) ketoacid anions are metabolized by the regeneration of bicarbonate.
Therefore, the prior loss of the ketoacids in the urine prevents
regeneration of bicarbonate, This causes a hyperchloremic acidosis, (2)
During the development of ketoacidosis, sodium is lost preferentially
to chloride leaving more of this anion in the body.
Generally, this condition causes no adverse outcome and will usually
resolve on its own with ongoing therapy. It may be minimized by
switching to hypotonic fluids during therapy and by using smaller
amounts of chloride during therapy (KPhos rather than KCl).
Hypokalemia: As the patient is being treated for DKA, the volume
expansion, and insulin therapy can rapidly lower potassium. As long as
these therapies are ongoing, the potassium level will continue to
decline unless it is being aggressively replaced. To avoid sudden
decompensation due to severe hypokalemia, it is prudent to recheck a
serum potassium, following each liter of fluid. If large doses of
insulin are required to control the patientÕs blood glucose, the
potassium level will need to be checked more frequently.
Hypoglycemia: As discussed previously, during DKA therapy, the serum
glucose typically normalizes before the ketotic state has been
corrected. To reverse this state it is necessary to continue insulin
therapy after the glucose levels have improved. Without close
monitoring, this can result in life-threatening hypoglycemia. To help
avoid this, glucose measurements should be done frequently, and as the
glucose level nears 250 mg/dl, the insulin infusion rate should be
slowed, and glucose infusion with D5W should be started.
Nonketotic Hyperosmolarity (NKH):
Another well known complication of diabetes is one that is most
commonly seen in an older population with type II diabetes. This
complication is perhaps best known as hyperglycemic hyperosmolar
nonketotic coma. However, since patients rarely present in coma (less
than 10% of patients) other names have been suggested that might truly
represent the condition in which the patient presents. Thus, this
discussion will use the term nonketotic hyperosmolaritym (NKH).
When considering the patient with NKH there are patients who present
purely with this disorder while others seem to have a combination of
both. Thus, DKA and NKH should be thought of as a continuum of disease.
At one extreme is pure DKA without hyperosmolarity of significant
amount. As noted above these patients may present with more modest
degrees of glucose elevation. At the other extreme is NKH with extreme
elevations of glucose, and hyperosmolarity, but without significant
ketosis (see table below). Finally, there are a range of patients who
will have features of both.
Laboratory Evaluation of DKA vs NKH
DKA
NKH
Plasma Glucose
elevated
very high
pH
below 7.3
above 7.3
Bicarbonate
<15meq/l
>20mEq/L
Serum ketones
present
negative
Ketonuria
present
negative
Osmolarity
varies
very high
Insulin levels
very low
can be normal
PATHOPHYSIOLOGY:
The initial steps in the development of NKH are similar to those seen
in DKA. Insulin is present in these patients, however the organs are
insulin resistant and in the relative absence of insulin hepatic
glucose production is markedly increased. The excess glucose is
deposited in the extracellular space where it cannot be appropriately
utilized because of the insulin resistance. However, while there is
insulin present in patients with NKH, this alone does not explain all
the differences seen between DKA and NKH and there are several theories
as to the cause of these differences. One theory is that the
counter-regulatory hormones are not as elevated in NKH as in DKA. Thus,
there is not as great a driving force for the break down of fats and
ketone formation. Additionally, in NKH the extreme hyperosmolarity that
develops actually suppresses lipolysis, so the patient with NKH does
not have the substrate needed to form ketones. Finally, it is thought
that since pancreatic insulin secretion is present in NKH, there is
enough circulating insulin to prevent lipolysis but not enough to
prevent hepatic glucose overproduction. Whatever the exact cause, the
net result in the patient with NKH is the development of severe
dehydration, electrolyte imbalance, and hyperosmolarity, with far less
ketone production.
The precipitating factors that lead to development of NKH in a patient
with type II diabetes are similar to those noted to cause DKA. Illness,
particularly pneumonia, is the most common reason for a patient with
type II diabetes to decompensate. As was the case with DKA, many
medications can precipitate NKH and this should be considered before
starting a diabetic on a new medication.
DIAGNOSIS:
History and Physical: NKH is a slowly progressive disease and it is not
uncommon to have 3-10 day history of increasing thirst, polyuria, and
malaise. Courses of up to three weeks have been described. Symptoms of
an underlying infection may be present, but in some cases there is
little history and the clinician must consider this diagnosis in the
elderly obtunded patient.
Patients usually have evidence of dehydration such as dry mucus
membranes, tachycardia, poor skin turgor, and sometimes a low grade
fever. The blood pressure is usually well preserved unless there is
severe dehydration or infection. Respiratory symptoms are usually
absent unless the patient has pneumonia. Central nervous system
dysfunction is relatively common in patients with NKH. Lethargy and
disorientation are common, but frank coma is rare. It is critical to
remember that these CNS symptoms rarely present unless the effective
osmolarity is greater than 340-350 mOsm/L. Patients with altered
sensorium and osmolarity less than this should have a different
etiology searched for. Any area within the brain can be affected, and
while focal neurologic findings are uncommon in DKA, they are fairly
common in patients with NKH. Seizures may be present in up to
one-fourth of patients and can be focal or generalized. Fortunately,
cerebral edema is very rare in patients with NKH.
Laboratory Abnormalities: In general, NKH is defined as those
individuals with: serum glucose levels in excess of 600 mg/dl, serum
osmolality greater than 330 mOsm/kg, absent or minimal serum ketones,
arterial pH above 7.3, and a serum bicarbonate above 20 mEq/L. Patients
presenting with features of both DKA and NKH are not uncommon. The same
formulas that are useful in patients with DKA to determine osmolarity,
anion gap, and corrected serum sodium are useful in patients with NKH.
NKH is characterized by severe fluid and electrolyte depletion due to
the osmotic diuresis produced by the extreme levels of glucose in the
serum. Patients may lose up to one-quarter of their extracellular
fluid. The diuresis causes a hypotonic fluid loss that eventually
raises serum sodium levels. However, as was the case in DKA, the
increased serum sodium level can be masked by the pseudohyponatremia
secondary to increased glucose and triglyceride levels. Serum potassium
levels can be normal, high, or low, but as was true in DKA the total
body amount of potassium is significantly depleted.
Elevations in white blood cell count are not uncommon in patients with
NKH. Leukocytosis can result simply from the stress of NKH and not
necessarily from infection. However, extreme elevations in WBC should
probably be considered evidence for infection. It is wise to have a low
threshold for doing complete septic workups and for obtaining a head CT
to avoid missing the pathologic process that precipitated the patients
current condition.
COMPLICATIONS:
The complications of NKH are essentially the same as those seen in DKA.
The exception to this is the development of cerebral edema.
Fortunately, this complication is quite rare in NKH.
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