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20. Middleton P, Kelly AM, Brown
J, et al. Agreement between
arterial and central venous
values for pH, bicarbonate,
base excess, and lactate. Emerg
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21. Hillman K. Fluid resuscitation
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Med, 1987. 13(1): 4–8.
22. Molitch ME, Rodman E,
Hirsch CA, et al. Spurious
serum creatinine elevations in
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23. Kitabchi AE, Murphy MB,
Spencer J, et al. Is a priming
dose of insulin necessary in a
low-dose insulin protocol for
the treatment of diabetic
ketoacidosis? Diabetes Care,
2008. 31(11): 2081–2085.
24. Luzi L, Barrett EJ, Groop LC,
et al. Metabolic effects of lowdose insulin therapy on glucose
metabolism in diabetic
ketoacidosis. Diabetes, 1988. 37
(11): 1470–1477.
25. Brown PM, Tompkins CV, Juul
S, et al. Mechanism of action of
insulin in diabetic patients: a
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Med J, 1978. 1(6122): 1239–1242.
26. Umpierrez GE, Cuervo R,
Karabell A, et al. Treatment of
diabetic ketoacidosis with
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27. Hillier TA, Abbott RD, Barrett
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the correction factor for
hyperglycemia. Am J Med,
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29. Okuda Y, Adrogue HJ, Field
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in diabetic ketoacidosis. J Clin
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314–320.
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Hyperglycemia
043
21:05:56
Subpart IVE
Chapter
40
Clinical – Metabolic, Endocrine
Hypoglycemia
Pawan Suri, MD
Taruna Aurora, MD
Introduction
Severe hypoglycemia is defined as an episode that
is undetected by the patient or is detected so late
that intervention by someone else is required to
inject glucagon or take the patient to the hospital
to receive intravenous (IV) glucose.
1
Varying
degrees of hypoglycemia are seen in both type
I and type II diabetics. Type I diabetic patients
on intensive insulin therapy have a greater than
threefold increased risk of severe hypoglycemia.
2
Less commonly, severe hypoglycemia may also
affect patients with type II diabetes who take
either oral antidiabetic medications or insulin.
In the Diabetes Control and Complications
Trial (DCCT), type I diabetics had a 65% incidence of severe hypoglycemia when followed over
6.5 years.
2
In contrast, the cumulative incidence
of hypoglycemia in type II diabetics who were
followed over a period of 6 years was 3.3%
in patients taking sulfonylureas and 11.2% in
patients taking insulin.
3
Thus, hypoglycemia
becomes a progressively more frequent clinical
problem in type II diabetics as they approach the
insulin deficient end of the disease spectrum.
Risk factors for hypoglycemia include patients
over age 65, those taking multiple medications
and those who are frequently hospitalized.
4,5
.
Commonly, patients have inadvertently taken
excessive or ill-timed dose of their insulin or oral
hypoglycemic agent. Decrease in exogenous glucose delivery – as seen with missed meals, delayed
gastric emptying or an overnight state – is another
frequent cause of hypoglycemic episodes. Longacting agents such as chlorpropamide and glyburide are more likely to cause hypoglycemia.
4,6
Renal insufficiency is associated with a fourfold
increased risk for hypoglycemia in patients taking
sulfonylureas. Interaction of gatifloxacin with sulfonylureas can also cause hypoglycemia.
7
This is
unique to gatifloxacin and not a quinolone class
effect. ACE inhibitors increase insulin sensitivity
and glucose disposal, incr easing the risk of hypoglycemia. Nonselective ß-blockers can impair
early warning symptoms and can lead to severe
hypoglycemia.
8,9
One of the best predictors for
developing severe hypoglycemia is a previous episode of severe hypoglycemia. The risk is also
increased in patients with high initial HbA1c
levels that decreased quickly after intensive insulin therapy was begun. Other minor risk factors
include male sex, higher insulin doses and
adolescents.
Pathophysiology
In normal subjects the extrac ellular supply of
glucose is carefully regulated by insulin and glucagon.
5
Insulin acts to restore normoglycemia in
three ways: (a) It decreases hepatic glucose production by inhibiting both glycogenolysis and
gluconeogenesis, (b) Increased glucose uptake by
skeletal muscle and adipose tissue by translocating glucos e transporters from an intracellular
pool to the cell surface, and (c) It reduces the
delivery of gluconeogenetic precursors alanine
and glycerol to the liver via its antiproteolytic
and antilipolytic actions. Insulin also inhibits glucagon secretion by direct inhibition of the glucagon gene in the pancreatic alpha cells,
10
which
further diminishes hepatic glucose production.
The ability to suppress insulin release is an
important component of the normal response to
hypoglycemia. Another defense against hypoglycemia is the increased release of counter-regulatory
hormones, which raise plasma glucose concentration by stimulating glucose production and by
antagonizing insulin induced increase in glucose
utilization. In diabetics, since insulin is supplied
exogenously and cannot be suppressed, the release
of conterregulatory hormones becomes the primary defense against hypoglycemia.
These hormones are, in order of importance,
glucagon, epinephrine, cortisol, and growth
044
21:05:54
hormone.
5,11
Glucagon acts only on the liver,
increasing glucose production by stimulating
both glycogenolysis and gluconeogenesis from
amino acids, glycerol, and pyruvate. Epinephrine,
acting via ß-adrenergic receptors has similar hepatic effects. It also increases the delivery of gluconeogenic substrates from the periphery, inhibits
glucose utilization and via alpha-2 receptors
inhibits insulin secretion. In addition, epinephrine induces early warning symptoms of hypoglycemia including anxiety and sweating. If the
hypoglycemia is severe and persists for several
hours, there is increased secretion of cortisol and
growth hormone, which limit glucose utilization
and enhance hepatic glucose production. It is
important to understand that the actions of insulin and glucagon are interdependent. In the pancreatic islets of Langerhans, the insulin producing
ß-cells form the core, surrounded by glucagon
producing alpha cells. Arterial blood enters
the core of each islet, delivering substrates and
information first to the beta cells and then
to alpha and delta cells.
12
The alpha cells rely
heavily on the presence of functioning beta cells
in order to function,
13
a situation that is disturbed
in diabetes.
Glycemic thresholds in normal subjects
– 80 mg/dl – Insulin secretion falls to very
low levels
– 65–70 mg/dl – Release of glucagon and
epinephrine, early protective response:
sweating, anxiety, palpitations and tremors
– < 60 mg/dl – Early cognitive dysfunction and
release of cortisol and growth hormone
– 45–50 mg/dl – Letha rgy and obtundation
– < 30 mg/dl – Coma and convulsions
Response to Hypoglycemia in
Diabetic Patients
The protective response to hypoglycemia is
impaired in many diabetic patients.
14
This is particularly true when hypoglycemia is induced
either directly from exogenous insulin injection
or indirectly from sulfonylurea stimulation. In
these patients insulin release cannot be turned
off and therefore glucose utilization and inhibition of hepatic glucose production continues.
Further, both glucagon and epinephrine response
to hypoglycemia are impaired in many diabetic
patients. Diabetic patients who are well controlled
(HbA1c levels < 8%) may have few warning
symptoms when their plasma glucose concentration falls below 60 mg/dl. The absence of epinephrine induced early warning symptoms can often
lead to dangerously low blood glucose levels.
The concept of hypoglycemia associated autonomic failure (HAAF) in type I diabetes mellitus
(DM),
15–17
posits that recent antecedent hypoglycemia causes both defective glucose counterregulation and hypoglycemia unawareness, setting
up a vicious cycle. Hypoglycemic episodes may
lead to up regulation of glucose transport in the
brain resulting in the maintenance of glucose
uptake and therefore the prevention of warning
symptoms of hypoglycemia. The compensatory
increase in cortisol production during the first
hypoglycemia episode may also play a critical role
in minimizing the protective hormonal response
during a subsequent episode.
18,19
As few as 2–3
weeks of scrupulous avoidance of hypoglycemia
reverses hypoglycemia unawareness and improves
the reduced epinephrine component of defective
glucose counter regulation.
Hypoglycemia is less common in type II DM
because deficits in glucagon and epinephrine are
much less prominent
20
and strict glycemic con-
trol is much more difficult to achieve.
21
However, when hypoglycemia does occur in older
patients, the glucose threshold for the onset of
cognitive dysfunction may overlap with the onset
of symptoms, thus limiting the time to initiate
self treatment and increasing the risk of severe
neurological events.
22
Patient Selection
Hypoglycemic patients on long-acting insulin or
oral hypoglycemic agents who fail to respond to
oral or parenteral glucose or show recurrence of
hypoglycemia in the emergency department (ED)
are often hospitalized for further management.
While most of these patients can be successfully
managed in an ED observation unit (ED OU),
some may require inpatient admission. These
include patients with intentional insulin or oral
antidiabetic medication overdose, patients with
acute or chronic renal or hepatic insufficiency,
persistent mental status changes despite glucose
administration or those with an acute precipitating
illness like sepsis, chronic heart failure, and others.
Hypoglycemia
044
21:05:54
Observation Unit Management
A thorough history is essential in determining the
cause of hypoglycemia. The amount, timing and
reason for any ingestion, what drug was taken,
and coingestants including other diabetic medications must be noted. Laboratory tests should
include a basic metabolic panel and renal function
with further testing as deemed necessary.
Hypoglycemia will respond rapidly to IV Dextrose (D-glucose) 0.5–1 gm/kg available in 50 ml
ampoules containing 25 g glucose in a 50% solution (D50). If thiamine deficiency from alcoholism or other forms of malnutrition is suspected,
parenteral thiamine, 100 mg IV is given in conjunction with glucose.
Glucagon 5 mg, given IM raises serum glucose
levels slightly and is often used in pre-hospital
setting as a temporizing measure
23
when IV
access has not been established. The efficacy of
glucagon is dependent upon hepatic glyco gen
stores, which may be depleted in the setting of
prolonged hypoglycemia.
24
Once the initial hypoglycemia is corrected, blood glucose should be
measured twice more at 30-minute intervals and
if patient remains euglycemic, serum glucose can
be checked every 4–6 hours thereafter. If the
patients respond to initial therapy with IV glucose
based on clinical symptoms and serum glucose of
more than 60 mg/dl, they should be fed a calorie
rich meal.
If the hypoglycemia is due to an oral hypoglycemic medication, then holding the medication,
feeding calorie rich meal and observation will
suffice for the majority of patients. The role of
octreotide in the observation setting is less clear.
If the patient develops a second episode of hypoglycemia, the authors have on occasion safely
administered octreotide, which is a somatostatin
analog that inhibits insulin release from pancreatic beta islet cells.
25
The drug is rapidly and
completely absorbed when given subcutaneously,
reaching 100% bioavailability within 30 minutes.
26
In adults, the dose of octreotide is 50–150
mcg administered by IM or SQ injection every
6 hours. It may also be given as an IV bolus over
several minutes or by continuous infusion.
When discharging a diabetic patient with
hypoglycemia from the OU, consider consulting
with the patient’s primary care provider or endocrinologist to determine the need for modification
to the current antidiabetic regimen. Since the
patient is at risk for recurrence of severe hypoglycemia following the initial episode, it is important
to avoid tight blood sugar control for 1–2 subsequent weeks. Consider insulin regimens that minimize the risk of hypoglycemia.
15
In a split mixed
insulin regimen, moving the dose of NPH insulin
to bedtime has been reported to decrease the
incidence of nocturnal hypoglycemia. Another
alternative is the use of basal-bolus insulin regimen that involves the use of a long-acting basal
insulin analog once a day with rapid acting insulin analog with meals.
Observation Unit Outcome
Goh et al. performed a prospective observational
study of consecutive patients with diabetes admitted to the ED OU for severe hypoglycemia. Out of
203 patients admitted, 170 were discharg ed and
33 transferred to an inpatient team for a longer
period of treatment. The median length of stay
for discharged patients was 23 hours. Of the
170 patients discharged, 151 were contacted at
7 and 28 days after discharge. Six patients had
symptoms of recurrent hypoglycemia of which
two returned to the ED and were admitted. This
study showed that selected patients with hypoglycemia and be effectively and safely treated in an
observation unit.
27
In our experience, carefully
selected patients are ideally suited to observation
management and can be safely discharged from
an ED OU. The controlled environment of the ED
OU also provides an excellent opportunity to
further educate the patients on their disease process as well as tips to avoid future hypoglycemic
episodes. There could be potential cost saving for
the hospital if the ED OU can demonstrate earlier
disposition as opposed to inpatient admission.
References
1. Workgroup on Hypoglycemia,
American Diabetic Association
(A.D.A.), Defining and
reporting hypoglycemia in
diabetes: a report from the
American Diabetes Association
Workgroup on Hypoglycemia.
Diabetes Care, 2005. 28(5):
1245–1249.
2. Lasker RD. The diabetes
control and complications trial.
Implications for policy and
practice. N Engl J Med, 1993.
329(14): 1035–1036.
Pawan Suri and Taruna Aurora
044
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3. U.K. prospective diabetes study
16. Overview of 6 years’
therapy of type II diabetes: a
progressive disease. U.K.
Prospective Diabetes Study
Group. Diabetes, 1995. 44(11):
1249–1258.
4. Krentz AJ, Ferner RE, Bailey
CJ. Comparative tolerability
profiles of oral antidiabetic
agents. Drug Saf, 1994. 11(4):
223–241.
5. Shorr RI, Ray WA, Daugherty
JR, et al. Incidence and risk
factors for serious
hypoglycemia in older persons
using insulin or sulfonylureas.
Arch Intern Med, 1997.
157(15): 1681–1686.
6. Stahl M, Berger W. Higher
incidence of severe
hypoglycaemia leading to
hospital admission in Type
2 diabetic patients treated with
long-acting versus short-acting
sulphonylureas. Diabet Med,
1999. 16(7): 586–590.
7. Menzies DJ, Dorsainvil PA,
Cunha BA, et al. Severe and
persistent hypoglycemia due to
gatifloxacin interaction with
oral hypoglycemic agents. Am
J Med, 2002. 113(3): 232–234.
8. ter Braak EW, Appleman AM,
van de Laak M, et al. Clinical
characteristics of type
1 diabetic patients with and
without severe hypoglycemia.
Diabetes Care, 2000. 23(10):
1467–1471.
9. Pedersen-Bjergaard U,Reubsaet
JL, Nielsen SL, et al.
Psychoactive drugs, alcohol,
and severe hypoglycemia in
insulin-treated diabetes:
analysis of 141 cases. Am
J Med, 2005. 118(3): 307–310.
10. Gerich JE. Oral hypoglycemic
agents. N Engl J Med, 1989.
321(18): 1231–1245.
11. Eliasson L, Renstrom E,
Ammala C, et al. PKCdependent stimulation of
exocytosis by sulfonylureas in
pancreatic beta cells. Science,
1996. 271(5250): 813–815.
12. Spiller HA, Management of
sulfonylurea ingestions. Pediatr
Emerg Care, 1999. 15(3):
227–230.
13. Dizon AM, Kowalyk S,
Hoogwerf BJ. Neuroglycopenic
and other symptoms in
patients with insulinomas. Am
J Med, 1999. 106(3): 307–310.
14. Hepburn DA, Deary IJ, Frier
BM, et al. Symptoms of acute
insulin-induced hypoglycemia
in humans with and without
IDDM. Factor-analysis
approach. Diabetes Care, 1991.
14(11): 949–957.
15. Cryer PE. Hypoglycaemia: the
limiting factor in the glycaemic
management of Type I and
Type II diabetes. Diabetologia,
2002. 45(7): 937–948.
16. Cryer PE, Davis SN, Shamoon
H. Hypoglycemia in diabetes.
Diabetes Care, 2003. 26(6):
1902–1912.
17. Dagogo-Jack SE, Craft S, Cryer
PE. Hypoglycemia-associated
autonomic failure in insulindependent diabetes mellitus.
Recent antecedent
hypoglycemia reduces
autonomic responses to,
symptoms of, and defense
against subsequent
hypoglycemia. J Clin Invest,
1993. 91(3): 819–828.
18. Davis SN, Shavers C, Davis B,
et al. Prevention of an increase
in plasma cortisol during
hypoglycemia preserves
subsequent counterregulatory
responses. J Clin Invest, 1997.
100(2): 429–438.
19. Davis SN, Shavers C, Costa F,
et al. Role of cortisol in the
pathogenesis of deficient
counterregulation after
antecedent hypoglycemia in
normal humans. J Clin Invest,
1996. 98(3): 680–691.
20. MacLeod KM, Hepburn DA,
Frier BM. Frequency and
morbidity of severe
hypoglycaemia in insulintreated diabetic patients. Diabet
Med, 1993. 10(3): 238–245.
21. Abraira C, Colwell JA J, Nuttall
FQ, et al., Veterans Affairs
Cooperative Study on glycemic
control and complications in
type II diabetes (VA CSDM).
Results of the feasibility trial.
Veterans Affairs Cooperative
Study in Type II Diabetes.
Diabetes Care, 1995. 18(8):
1113–1123.
22. Saudek CD, Duckworth WC,
Giobbie-Hurder A, et al.
Implantable insulin pump vs
multiple-dose insulin for noninsulin-dependent diabetes
mellitus: a randomized clinical
trial. Department of Veterans
Affairs Implantable Insulin
Pump Study Group. JAMA,
1996. 276(16): 1322–1327.
23. Schwartz NS, Clutter WE, Shah
SD, et al. Glycemic thresholds
for activation of glucose
counterregulatory systems are
higher than the threshold for
symptoms. J Clin Invest, 1987.
79(3): 777–781.
24. Brelje TC, Scharp DW,
Sorenson RL. Threedimensional imaging of intact
isolated islets of Langerhans
with confocal microscopy.
Diabetes, 1989. 38(6): 808–814.
25. Weir GC, Bonner-Weir S. Islets
of Langerhans: the puzzle of
intraislet interactions and their
relevance to diabetes. J Clin
Invest, 1990. 85(4): 983–987.
26. White NH, Skor DA, Cryer PE,
et al. Identification of type
I diabetic patients at increased
risk for hypoglycemia during
intensive therapy. N Engl
J Med, 1983. 308(9): 485–491.
27. Goh HK, Chew DE, Miranda
IG, et al. 24-Hour observational
ward management of diabetic
patients presenting with
hypoglycaemia: a prospective
observational study. Emerg
Med J, 2009. 26(10): 719–723.
Hypoglycemia
044
21:05:54
Subpart IVE
Chapter
41
Clinical – Metabolic, Endocrine
Electrolyte Abnormalities
Kimberly A. Ressler, MD, MSN
Jonathan Glauser, MD, FACEP
Introduction
Patients with electrolyte abnormalities may
be appropriate for the observation unit (OU)
depending on the severity of the disturbance, the
patient’s comorbidities, and the suspected etiology of the imbalance. Optimal management of
specific electrolyte problems must take into
account acid-base status, patient-volume status,
underlying disorders, and measurements of other
electrolytes. Especially as regards the intracellular
cations: potassium and magnesium, serum levels
may not be an accurate indicator of total body
stores. Patients with the potential for requiring
lifesaving interventions or prolonged treatments
are better suited for admission to higher levels
of care.
Potassium
Potassium is responsible for the resting membrane potential for electrical impulses and is critical in the body’s acid-base homeostasis. Buffering
an acute acidosis or alkalosis entails the exchange
of K
+
and H+across the cell membrane. A general
rule is that for a change of 0.1 pH unit there is an
inverse change of 0.5 mEq/L in the serum K
+.1
Hypokalemic patients who are acidotic may
require vigorous repletion.
Hypokalemia
Hypokalemia, a serum level < 3.5 mmol/L, most
frequently follows potassium (K
+
) losses or intracellular shifts. Diureti c therapy, both loop and
thiazide, is the commonest cause. The most frequently seen extra-renal cause of hypokalemia is
severe or chronic diarrhea from both volume
depletion and direct K
+
losses in the stool.2In
the presence of metabolic alkalosis, K
+
ions shift
into the cells in exchange for hydrogen ions to
maintain normal pH of the extracellular fluid.
Respiratory acid-base abnormalities do not have
this same effect on potassium.
3
Low serum magnesium may contribute to hypokalemia through
renal wasting. Typically patients have no symptoms with mild hypokalemia at serum levels of
3.0–3.5 mmol/L, but patients with underlying
heart disease have an increased risk of dysrhythmia even within this range.
4
Patients appropriate for the OU include those
with serum K
+
> 2.0, without severe symptoms
such as ileus, rhabdomyolysis, respiratory muscle
weakness, or ascending paralysis, not on digitalis
and without ventricular dysrthymias. Typically,
these will be patients taking a thiazide or loop
diuretic, or have an acute GI fluid loss. Classic
EKG changes of hypokalemia with U waves,
T wave flattening, and ST segment changes should
not preclude an OU stay. ECG monitoring for
ventricular dysrhythmia is required during intravenous (IV) potassium replacement.
5
Treatment
For mild and asymptomatic hypokalemia, oral
replacement is preferred over IV supplementation. If oral medication is tolerated, K
+
supple-
ments can be given as an oral dose of 20 mEq KCl
every 30–60 minutes or 40–60 mEq every 4–6
hours until the goal level is reached.
3
Liquid solutions are more absorbable but tablets are better
tolerated.
If hypokalemia is symptomatic or causes ECG
changes, patients should be treated with IV KCl
and continuous ECG monitoring. KCl is generally
given as 10–20 mEq mixed in 50–100 ml sa line
infused over 1 hour through a large bore peripheral IV. A dose of 20 mEq should increase the
serum K
+
by approximately 0.25 mEq/L.3After
IV dosing of K
+
, a maintenance IV can be given
that should contain no more than KCl 40 mEq
per liter bag. If the solution causes burning, it
should be diluted with saline preferentially to
slowing the rate of potassium repletion. Potassium phosphate can be used instead of KCl in
045
21:05:58
those patients thought to have hypophosphatemia
such as those in diabetic ketoacidosis (DKA).
1
In
this specific population, insulin administration
should be delayed if serum K
+
is < 3.5. Decreased
magnesium levels should be addressed simult aneously; combined deficiency with hypokalemia
can increase the risk for cardiac dysrhythmias.
5
Laboratory monitoring should be done every 2–4
hours to determine the response to the potassium replacement. Consideration for causes of
hypokalemia should be given while the patient
is in the OU. For example, measures may include
adding or substituting a potassium sparing diuretic for a current loop or thiazide diuretic in consultation with the patient’s primary care provider.
(Table 41.1)
Hyperkalemia
Hyperkalemia, a serum potassium (K+) > 5.5
mEq/L, mandates that hemolysis during phlebotomy, extreme elevations of platelets or of white
blood count first be ruled out. Acidosis, β-blockade, and digital is toxicity can cause hyperkalemia
by shifting K
+
from inside the cells to the extra-
cellular space.
1
Tissue injury or necrosis from
rhabdomyolysis, tumor lysis or severe burns can
cause life-threatening hyperkalemia from release
of intracellular K
+.6
Medications including potassium sparing diuretics, angiotensin converting
enzyme (ACE) inhibitors, and angiotensin receptor blockers (ARBs) can precipitate increased K
+
in those with renal insufficiency (RI). A history
of β-blocker or nonsteroidal anti-inflammatory
drug (NSAI D) use should be noted. Patients with
chronic renal insufficiency (CRI) are generally
able to excrete K
+
normally unless their kidney
disease is severe (GFR < 15– 20 ml/min).
6
While there are classic ECG findings associated with hyperkalemia, some patients will have a
relatively normal EKG even with severe hyperkalemia yet develop potentially fatal ventricular
arrhythmias without warning.
7
The rate of the
rise in serum K
+
may be more important than
the absolute value. There is much inter-patient
variability in clinical presentation and response
to treatment.
8
A patient with a serum K+> 6.5
mEq/L, on digoxin, with acid-base abnormalities,
wide QRS complex or absence of P waves may be
inappropriate for the OU. A stable chronic renal
failure (CRF) patient without ECG changes and a
K
+
< 7 mEq/L without those ECG abnormalities
may be appropriate for stabilization in the OU as
a bridge to hemodialysis within the next 12 hours.
Treatment
Initial management of the hyperkalemic patient
occurs in the ED prior to the OU. A repeat potassium level should be drawn to verify the level and
an ECG performed. Treatment should be initiated
immediately if hyperkalemia is suspected without
waiting for laboratory confirmation, and continuous ECG monitoring performed. There are three
treatment strategies: stabilization of cell membranes, shifting extracellular potassium into the
intracellular space, and promoting loss of potassium through renal and gastrointestinal systems.
4
The initial treatment of hyperkalemia is 10–20
ml of 10% calcium gluconate IV over 2–5 minutes, which can be repeated in 5–10 minutes.
4
Calcium antagonizes the toxic effects of hy perkalemia on the myocardium, but its protective
effects last only 60 minutes and other interventions must be started simultaneously.
9
Regular
insulin 10 units IV with 50 ml of 50% dextrose
will shift potassium into the cell for an expected
fall in plasma K
+
of 0.5 to 1.5 mEq/L with peak
effect within 30–60 minutes.
4
If the glucose is
above 250, insulin can be given without dextrose.
1
High-dose nebulized albuterol 10–20 mg results
in a shift of extracellular potassium into cells
within 1–2 minutes with peak effect lasting
90–120 minutes.
10
Up to 40% of renal dialysis
patients may not respond to β-agonists even if
not on β-blockers.
4
There is an additive decrease
in serum K
+
if both insulin/glucose and nebulized
albuterol are given together, decreasing serum
Table 41.1 Hypokalemia Management in the
Observation Unit
Oral supplementation (if possible): 10–120 mEq/day
or 40–60 mEq of KCl every 4–6 hours in divided
doses. High potassium foods give more gradual
increase than oral K
+
concentrates
Intravenous KCl 10–20 mEq in 50–100 ml over
1 hour infused through large bore IV. If burning
from the infusion, may need to dilute the solution
rather than slow the repletion rate
If needed, a maintenance IV can contain up to KCl
40 mEq per liter bag
Check and replete magnesium as needed
Monitor K
+
closely during replacement. Continuous
ECG monitoring if administering IV
Electrolyte Abnormalities
045
21:05:58
K+by an average of 1.21 mEq/L.8Research has
not supported the role of bicarbonate in routine
treatment for hyperkalemia, and its use may be
limited to those with hyperkalemia and metabolic
acidosis.
Potassium levels should be rechecked at regular intervals. In the presence of intact renal function, a potent loop diuretic such as furosemide
40–80 mg IV or ethacrynic acid 50–100 mg IV
can be used to remove potassium from the body.
4
Sodium polystyrene sulfonate (SPS, Kayexalate®)
as oral dose or enema exchanges Na
+
for K
+
across the intestinal wall but has not been shown
to increase K
+
excretion in the stool any more
than expected in diarrhea induced by laxatives.
5
A recent review does not support the use of SPS
for hyperkalemia due to lack of evidence and
potential risks.
10
Hemodialysis is the most effective
way to remove potassium from the body. Prevention should be addressed. Medication lists should
be reviewed along with diet discussion including
the use of salt substitutes. Medications that slow
progression of kidney disease such as ACEinhibitors and ARBs may need to have dose adjustment or other agents prescribed.
6
Medication
adjustments may have to be made in patients with
heart failure and hypertension.
5
Changes should
be made in collaboration with the patient’sprimary physician, as ACE inhibitors, beta blockers,
ARBs, and potassium-sparing diuretics may be
lifesaving in heart failure patients, with plans for
close outpatient follow-up. See Table 41.2.
Calcium
Calcium is involved in nerve conduction, muscle
contraction and blood coagulation. Only 1% of
the calcium in the body is in the ECF compartment. Measured serum calcium includes that
which is bound and unbound to albumin, and
should be corrected for low albumin states:
Corrected Ca
þ2
ðmg=dlÞ¼measured
Ca
þ2
ðmg=dlÞþ½0:8×4-albumin ðgm=dlÞ:
Alkalosis increases binding of calcium to albumin
so that for each 0.1 rise in pH the ionized Ca
+2
is lowered by about 3–8%.3Respiratory alkalosis
or hyperventilation can inc rease protein binding,
decreasing ionized calcium. Correction of calcium disorders in the OU mandates measurement of serum magnesium, albumin, creatinine,
and phosphate. Tests such as serum parathormone (PTH) levels, 25-OH D3, and 1, 25-(OH)
2
D3 levels may be helpful in tracking the etiology,
but are of little relevance in the observation medicine setting.
Hypocalcemia
Hypocalcemia, ionized calcium < 2.1 mEq/L
(or < 1.05 mmol/L) in the ambulatory population, is seen in patients with hypoparathyroidism
(primary or iatrogenic) or CRF due to hyperphosphatemia and decreased activated vitamin D.
Hypomagnesemia may exist in conjunction with
low serum calcium in patients with alcoholism,
diuretic use, epilepsy, and renal failure, and
Table 41.2 Hyperkalemia Management in the
Observation Unit
Treatment Onset and Duration
of Action
Calcium gluconate
10 ml of 10% solution
IV over 2–5 minutes.
Calcium chloride as
alternative. Repeat
dose in 5–10 minutes if
no effect.
Effects within 1–3
minutes, duration 30–60
minutes. Start other
treatment
simultaneously.
10 U regular insulin
with 50 ml 50%
dextrose (hold the
glucose if BS > 250).
Effects within 15–30
minutes, lasts 4–6 hours.
Produces fall in K
+
of
0.5–1.5 mmol/L.
Beta-2 agonists:
albuterol high-dose
10–20 mg via high flow
nebulizer which may
be repeated in 2 hours.
Onset within several
minutes, lasting 1–2
hours. Lowers K
+
0.6-1
mmol/L.
Furosemide 40–80 mg IV or ethacrynic acid 50–100
mg IV if renal function intact.
Sodium polystyrene sulfonate: 20–50 grams with
100 ml of 20% sorbitol every 4–6 hours. May give
50 g as enema with 50 ml of 70% sorbitol and
100–150 ml water, retained for 1–2 hours.
Consider need for
dialysis. Address access
and consult
nephrology.
Immediate effect but
may have rebound
hyperkalemia from
intracellular K
+
shifts.
Monitor K
+
closely during interventions. Address
potential causes including medications that
increase serum potassium: ACE inhibitors, NSAIDs,
K
+
-sparing diuretics, ARBs, β-blockers.
Kimberly A. Ressler and Jonathan Glauser
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induces PTH resistance and decreased secretion of
PTH.
3
Symptoms of hypocalcemia due to the
neuromuscular excitability depend on the absolute
level of serum calcium and how rapidly the decline
occurred. Chvostek’s or Trousseau’ssigns,myalgia,
cramps, and paresthesias should not preclude
observation care.
11
Patients with symptoms such
as hypotension, psychosis, confusion, or ventricular dysrhythmias are inappropriate candidates for
observation care. The differential diagnosis of
hypocalcemia is broad, and often impractical to
accomplish in a 24-hour stay. Following thyroid
or parathyroid surgery, the cause may be obvious.
Treatment
Correction of hypocalcemia is dictated by symptoms and underlying etiology. ED OU workup
should include renal function, electrolytes including magnesium, ionized calcium level, and albumin. PTH and vitamin D levels may be obtained
to guide further workup as an outpatient. IV
calcium replacement should be used if symptoms
are present or the hypocalcemia is severe (ionized
Ca
+2
< 1.3 or 0.65 mmol/L).
3
Calcium is given as chloride (360 mg of elem-
ental calcium in 10 ml) or gluconate (93 mg of
elemental calcium in 10 ml over 2–5 minutes) for
an initial adult dose of 100–300 mg of calcium
diluted with 5% dextrose.
1
Calcium gluconate is
preferred over calcium chloride because of less
local tissue irritation and lower risk of tissue
necrosis with extravasation. A continuous infusion may be needed to prevent further episodes
and is achieved by mixing ten 10 ml ampules of
10% calcium gluconate in one liter of 5% dextrose
or 0.9% saline infused at 50 ml/hr and titrated to
level of calcium.
11
Patients receivin g IV calcium should have
continuous ECG monitoring to evaluate for
bradycardia or heart block. Oral supplementation should be started i n the OU with 1000–2600
mg of calcium carbonate or calcium citrate daily
in divided doses between meals.
4
If the patient is
on digitalis, calcium administration should
be done cautiously and more slowly. Hypomagnesemia if present should be addressed. See
Table 41.3.
Hypercalcemia
The two most common causes of hypercalcemia
are hyperparathyroidism and malignancy, notably
myeloma, breast, renal, and non-small cell lung
cancer. Hypercalcemia from malignancy is a poor
prognostic sign.
12
Medications such as thiazide
diuretics, lithium, and calcium-based antacids
can contribute to hypercalcemia, especially in
the dehydrated patient. Granulomatous disorders
including sarcoidosis and tuberculosis cause
hypercalcemia related to excessive 1,25-(OH)
2
Vitamin D production.1Patients appropriate
for the OU include those with trouble concentrating, personality changes, fatigue, weakness,
and nausea. Symptoms may relate to the time
frame of elevation as much as to the actual calcium level. Patients with altered mentation,
stupor, o r coma, or requiring an extensive diagnostic workup are inappropriate for observation
stay. Prior to the OU, the cause for hypercalcemia such as malignancy, sarcoid, or hyper PTH
should be evident.
Treatment
The goals of treatment include identifying the
cause and reducing serum calcium, especially via
rehydration. Laboratory workup should include
calcium, albumin, ionized calcium, renal function
tests, magnesium, and potassium. Isotonic saline
IV should be started with 1–2 liters over the first
hour followed by 4–6 liters in the next 24 hours.
4
Table 41.3 Hypocalcemia Management in the
Observation Unit
Calcium gluconate 10
ml, 10% (93 mg
elemental Ca) diluted in
50 ml of D5 or NS, over
5 minutes. Slow rate of
infusion by half; use
with caution if patient is
on digitalis.
As alternative, may give
calcium chloride, but it
has increased risk of
tissue irritation and
tissue necrosis with
extravasation.
If needed, can use continuous infusion of Calcium
Gluconate: 10 ampules (930 mg) in 1000 ml bag of
5% dextrose or 0.9% NS given over 24 hours.
Consider administration of parenteral calcium until
serum calcium reaches 7–7.5 mg/dL.
Continuous ECG monitoring while giving IV Ca
++
.
Evaluate and treat for hypomagnesemia.
Oral calcium supplements 1000–1500 mg/day in
divided doses 2–4 times daily with calcium
carbonate or citrate between meals.
Consider Vitamin D supplementation if
replacement: Calcitriol 1,25 (OH)
2
D 0.25-2 mcg/day.
Electrolyte Abnormalities
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Rates should be adjusted to degree of hypercalcemia, fluid status, and ability to toler ate volume
expansion.
1
The role of loop diuretics in the management of hypercalcemia should be limited to
management of volume overload, which generally
is not present.
13
After saline hydration, bisphosphonate ther-
apy is the pharmacologic treatment of choice.
14
Bisphosphonates are given as a single IV infusion
over 15 minutes to 4 hours, with an expected
ensuing reduction in Ca
++
after 24–72 hours.
Recommended doses are pamidronate 90 mg or
zoledronate 4 mg as a single infusion.
13
For severe symptoms, subcutaneous calcito-
nin (4 U/kg) can be given every 12 hours, which
should decrease the calcium level within 12–48
hours, and as quickly as 2 hours.
14
Calcitonin
can be given simultaneously with the bisphosphonates.
13
If hypercalcemia is due to excessive
Vitamin D production, as in patients with granulomatous diseases such as sarcoid or lymphoma, glucocorticoids should be administered.
1
(Table 41.4)
Magnesium
Magnesium is mostly intracellular with only 1%
present in the serum for a normal value of
0.74–0.95 mmol/L (1.7–2.2 mg/dL).
4
It is a cofactor in cell metabolism, protein synthesis, and
neuromuscular activity.
3
It plays a role in the
body’s regulation of potassium and calcium, and
a low serum magnesium may not accurately
reflect total body deficit.
Hypomagnesemia
Magnesium depletion typically is due to renal
wasting (alcohol, diuretics) or GI losses (diarrhea,
malabsorption, fistula) and is frequently seen in
patients with alcoholism, poor nutrition, cirrhosis, pancreatitis, or chronic diarrhea.
3
It is the
most common electrolyte abnormality in the
ambulatory diabetic patient and is frequently seen
in DKA.
1
Proton pump inhibitors may contribute
to hypomagnesemia by increasing GI losses of
magnesium.
2
Correction of low magnesium may
be necessary to treat refractory hypokalemia and
hypocalcemia. With the exception of those
with life-threatening dysrhythmias, tetany, and
seizures, patients with hypomagnesemia are often
good candidates for correction in the OU. For
diagnostic purposes, the fractional excretion of
magnesium can distinguish renal wasting from
GI loss:
FEMg
þ2
¼fðUrine Mgþ2times plasma
creatinineÞ=0:7 times ðplasma Mg
þ2
times urine CrÞg times 100
If FEMg+2> 2%, one can generally assume
renal magnesium wasting.
4
Treatment
Clinical signs and symptoms usually do not occur
unless magnesium is below 1.2 mg/dL (0.49
mmol/L), at which point the patient should be
treated with IV magnesium.
15
Adequate renal
function should be confirmed prior to replacement of magnesium (Mg
2+
), with dose reductions
of 50–75% for RI.
16
The initial dose is 2–4 grams of 50% magne-
sium sulfate in saline or dextrose given over
30–60 minutes.
1
Consensus statements recom-
mend 6–12 grams of magnesium sulfate IV over
the first 24 hours.
16
During treatment, the
Table 41.4 Hypercalcemia Management in the
Observation Unit
Treatment Comments
Saline fluid bolus by
giving 1–2 L of 0.9%
saline IV over first hour
followed by 4–6Lof
saline over 24 hours at
rate of 200–300 ml/
hour. Keep urine at
100–150 ml/hour.
Monitor for fluid status
with hydration especially
in the elderly. Use
furosemide only if
volume overload
present.
Bisphosphonates:
Zoledronic acid 4 mg IV
over 30 minutes (at
least 15 minutes) or
Pamidronate 60–90 mg
IV over 2–4 hours.
Effects within 1–3 days.
Usually well-tolerated,
may cause arthralgias,
fever, myalgia, fatigue.
Slow rate or decrease
dose in renal failure.
Salmon calcitonin
4 IU/kg subcutaneously,
may be repeated in
6–12 hours for Ca
+2
> 14.
Lowers Ca
+2
in 12–48
hours, short-term use
only due to
tachyphylaxis.
Steroids: prednisone
40–60 mg/day for 3–7
days or hydrocortisone
100–300 mg daily.
Use if 1, 25-(OH)
2
Vitamin D mediated
(lymphoma, sarcoid,
myeloma). Effective
within 2–5 days.
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