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with dizziness presentations will be discussed
here. As previously discussed, truncal ataxia is a
good predictor of a central lesion. Generally
patients may have difficulty ambulating with a
peripheral lesion, but should be able to do so.
With a central lesion, patients are too uncomfortable to walk and generally will fall if not properly
aided. Cerebellar strokes represent only 3% of
total strokes, but unfortunately will often have
nonspecific findings (nausea, vomiting, unsteady
gait, or headache) or subtle neurological findings
(ataxia, dysarthria, and nystagmus). Usually
superior cerebellar artery ischemia minimally
involves the brainstem and may present with
any of the aforementioned findings.
Ischemia of the anterior inferior cerebellar
artery (AICA) can result in tinnitus, hearing loss,
Horner Syndrome or facial weakness. Hence, care
must be taken to ensure that a misdiagnosis of
Meniere’s disease is not given for AICA ischemia.
Posterior inferior cerebellar artery (PICA)
ischemia is termed lateral medullary syndrome,
also known as Wallenberg syndrome. Characteristic findings of lateral medullary syndrome are
fairly extensive and include contralateral truncal
and extremity sensory, pain, and tem perature deficits, ipsilateral facial sensory, pain, and temperature deficits, and ipsilateral cranial nerve deficits.
This, along with vertebrobasilar ischemia, tends
to have very not able neurological findings.
Vertebrobasilar ischemia often will include
symptoms of pupillary abnormalities, abnormal
ocular movements, facial palsy, hemiplegia or
quadriplegia. Other intracranial differentials to
consider include space occupying lesions, normal
pressure hydrocephalus, and multiple sclerosis.
These can usually be identified by history, physical examination, and the proper imaging.
Integration of data is important for determination of patient diagnosis and disposition. The
clinician should seek out specialist consultation
in cases of increased complexity, special interventions, diagnostic help, or suspected further inpatient evaluation and treatment. Patients with
dizziness complaints are frequently placed in the
OU to rule out cardiac ischemia or to rule out
strokes, so frequently cardiac and neurological
workups are initiated within the OU. These workups are discussed elsewhere in this text.
Causes of Dizziness
Patients presenting with the disequilibrium subtype (unsteady sensation) after complete workup
tend to have mainly orthopedic, neurologic or
sensory problems. Additionally, polypharmacy
may be a consideration and may need to be
checked. Patients presenting with presyncope
subtype tend to have cardiac or vasomotor conditions as their final diagnosis. Patients presenting
with lightheadedness or atypical dizziness also
may have polypharmacy as a cause, but psychiatric conditions should be considered. Some
patients may have multiple causes of their dizziness or have chronic dizziness syndromes, of
which a team approach may help.
Summary
Ultimately, a patient placed in the OU will need a
final disposition within 24 hours. If the patient
requires further workup and treatment, they
should be appropriately placed into an inpatient
bed. Sometimes, the patient symptoms that got
them placed into the OU have not resolved or
improved, so the patient will need to be placed
in an inpatient bed if it is not safe to send the
patient home. Patients may also have all their
testing and consultations completed within the
24-hour period, in which case they can be sent
home for further outpatient treatment. Overall,
the clinical picture will help determine the
patient’s final disposition.
Bibliography
1. Newman-Toker DE, Hsieh YH,
Carmargo CA Jr, et al. Spectum
of dizziness visits to US
emergency departments: crosssectional analysis from a
nationally representative
sample. Mayo Clin Proc 2008;
83:765–775.
2. Kroenke K, Lucas CA,
Rosenberg ML, et al. Causes
of persistent dizziness. Ann
Intern Med 1992;117(11):
898–904.
3. Dros J, Maarshingh O, et al.
Tests used to evaluate dizziness
in primary care. CMAJ Sept
2010; 182 (13):E621–31.
4. Herr RD, Zun L, Mathews JJ.
A directed approach to the
dizzy patient. Ann
Emerg Med 1989;
18(6):664–672.
5. Hoffman RM, Einstadter D,
Kroenke K. Evaluating
dizziness. Am J Med 1999;
107(5):468–478.
Dizziness and Vertigo
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6. Kentala E, Rauch SD.
A practical assessment
algorithm for diagnosis of
dizziness. Otolaryngol Head
Neck Surg 2003;128(1):54–59.
7. White J. Benign paroxysmal
positional vertigo: How to
diagnose and quickly treat it.
Cleveland Clinic Journal of
Medicine Sept 2004; 71(9):
722–728.
8. Bronstein AM, Lempert T,
Seemungal BM. Chronic
dizziness: a practical approach.
Pract Neurol 2010; 10:129–139.
9. Dizziness in the elderly. British
Journal of Hospital Medicine
Jan 2011, 72(1):M4–7.
10. Barin K, Dodson E, Dizziness
in the elderly. Otolaryngol Clin
NAm2011; 44 437–454.
11. Thabet E, Evaluation of
patients with acute vestibular
syndrome. Eur Arch
Otorhinolaryngol 2008;
265:341–349.
12. Wetmore S, Eibling D, Goebel
J, et al. Challenges and
opportunities in managing the
dizzy older adult.
Otolaryngology–Head and Neck
Surgery 2011 144(5) 651–656.
13. Labuguen, Ronald H. Initial
evaluation of vertigo. Am Fam
Physician. 2006 Jan 15;
73(2):244–251.
14. Rubin D, Cheshire W.
Evaluation of “dizziness” in the
neurology office. Semin Neurol
2011;31:29–41.
15. Kerber K. Vertigo
presentations in the emergency
department. Semin Neurol
2009;29:482–490.
16. Kulstad C, Hannafin B. Dizzy
and confused: A step-by-step
evaluation of the clinician’s
favorite chief complaint. Emerg
Med Clin N Am 2010;28:
453–469.
17. Kerber K, Morgenstern L,
Meurer William. Nystagmus
assessments documented by
emergency physicians in acute
dizziness presentations:
A target for decision support?
Academic Emergency Medicine
2011;18:619–626.
18. Post R, Dickerson L. Dizziness:
A diagnostic approach. Amer
Fam Phys 2010;82(4): 361–368.
19. Drachman DA, Hart CW. An
approach to the dizzy patient.
Neurology 1972;22(4):
323–334.
20. Kerber KA, Fendrick AM. The
evidence base for the
evaluation and management of
dizziness. J of Eval in Clin Prac
2010;16: 186–191.
21. Kentala E, Rauch S. A practical
assessment algorithm for
diagnosis of dizziness.
Otolaryngology: Head and Neck
Surgery 2010;128(1): 54–59.
22. Swartz R, Longwell P.
Treatment of Vertigo. Amer
Fam Physician; Mar 15, 2005;
71(6):1115–1122.
23. Bhattacharyya N, Baugh RF,
Orvidas L, et al. Clinical
practice guideline: Benign
paroxysmal positional vertigo
Otolaryngology–Head and
Neck Surgery 2008;139:
S47–S81.
24. Tarnutzer AA, Berkowitz AL,
Robinson KA, et al. Does my
dizzy patient have a stroke?
A systematic review of bedside
diagnosis in acute vestibular
syndrome. CMAJ, June 14,
2011;183(9):E571–E592.
25. Kattah JC, Talkad AV, Wang
DZ, et al. Three-step bedside
oculomotor examination more
sensitive than MRI diffusionweighted imaging. Stroke, 2009;
40:3504–3510.
26. Savitz SI, Caplan LR, Edlow JA.
Pitfalls in the diagnosis of
cerebellar Infarction. Academic
Emergency Medicine 2007;
14:63–68.
27. Chan Y. Differential diagnosis
of dizziness. Curr Opin
Otolaryngol Head Neck Surg.
2009 Jun;17(3):200–203.
Saurin Bhatt
041
21:05:18
Subpart IVD
Chapter
38
Clinical – Neurologic
Central Nervous System (CNS) Shunts
Mark G. Moseley, MD, MHA, FACEP
Miles P. Hawley, MD, MBA
Introduction
Intracranial hypertension has many different
causes including brain mass, infection, hydrocephalus, cerebral venous thrombosi s and idiopathic intracranial hypertension, or pseudotumor
cerebri. Patients with intracranial hypertension
are frequently treated with shunt placement.
Shunt placement is often done to improve symptoms including headache and vision changes.
1
Shunt placement is usually performed by a neurosurgeon after medical treatment has failed. The
most common types of shunts placed to relieve
intracranial pressure include ventriculoperitoneal
shunts and lumboperitoneal shunts.
The complication rate from shunting is high.
In addition, shunts do not often completely alleviate symptoms.
2
For these reasons, patients with
intracranial hypertension and ventriculoperitoneal or lumboperitoneal shunts frequently present
to the emergency department (ED) with symptoms. Symptoms commonly include headache
and vision changes. It can be difficult to determine on initial evaluation if the symptoms are
related to shunt malfunction, underlying intracranial hypertension or another process. These
patients can often complete an evaluation in the
observation unit (OU).
Discussion
There is very little evidence to guide the evaluation
of patients with potential shunt malfunction.
Shunt failure is the most common complication
of shunt placement. Shunt failure in patients with
lumboperitoneal shunts occurs in 48 to 86% of
patients.
2–8
Some patients will require multiple
revisions. Other shunt complications include shunt
infection, abdominal pain, back pain and CSF leak.
Shunt infection occurs in approximately 10% of
patients.
9
Rare complications include subdural
and subarachnoid hemorrhage, cerebellar tonsillar
herniation and syringomyelia.
10–13
In addition to the known complications of
ventriculoperitoneal or lumboperitoneal shunts,
these patients often have symptoms from their
underlying disease process. Patients with idiopathic intracranial hypertension often have persistent headache and vision changes despite shunting.
2
The goal of evaluating these patients when they
present to the ED is to exclude life-threatening
causes of their symptoms, provide symptom relief
and set up an appropriate treatment plan. For
these patients this often includes excluding infection, shunt malfunction and elevated intracranial
pressure.
Patient Criteria
Inclusion criteri a
Ventriculoperitoneal or lumboperitoneal
shunt placed for elevated intracranial
hypertension.
Presenting complaint that may be related to
shunt malfunction or elevated intracranial
pressure.
Expectation that diagnostic work-up can be
completed in under 24 hours.
Exclusion criteria
High likelihood of shunt infection or
meningitis.
New abnormality on head CT or MRI.
Other medical conditions that make discharge
in under 24 hours unlikely such as severe
dehydration, uncontrolled diabetes, and
uncontrolled hypertension.
Management
Patients with ventriculoperitoneal or lumboperitoneal shunts who present with symptoms such
as headache or blurred vision need a complex
diagnostic workup and often therapeutic treatment
042
21:05:20
as well. The goal of the diagnostic workup is to
exclude shunt malfunction, shunt infection and
elevated intracranial pressure. Initial testing
should be a noncontrast head CT scan. This is
often performed in the ED prior to placing the
patient in the OU. The purpose of this test is to
rule out new brain mass, bleeding and significant
hydrocephalus. Following a head CT, a shunt
series can be obtained to look for any kinking or
discontinuity in the shunt. If any abnormalities
are found on the shunt series then neurosurgery
should be contacted immediately to determine
if urgent surgery should be performed. These
patients will normally require a lumbar puncture
to obtain an opening CSF pressure and CSF fluid
for analysis. This often will need to be done by
radiology under fluoroscopy. An opening pressure will help determine if the shunt is functioning appropriately and if the patient’s symptoms
are likely to be related to elevated intracranial
pressure. CSF is often sent for cell count, protein,
glucose, culture and gram stain. Infection can
usually be ruled out based on CSF studies. Ophthalmology consultation may be necessary to
evaluate for papilledema. Neurosurgical consultation is often required to assist in evaluation and
adjustment of the shunt.
In addition to diagnostic evaluation, these
patients also present with headache, dehydration
and hypertension. Many of the principles for
treating general headache apply to this patient
population – quiet, hydration, darkness, rest,
and anti-emetics. These patients may require
opioid pain medications initially to control their
symptoms. Caution should be used when using
opioids, given analgesic rebound headaches and
the possibility of narcotic abuse. These patients
often present dehydrated due to nausea and
vomiting. They will benefit from hydration
with IV fluids and treatment with anti-emetics.
This patient population often has comorbid
hypertension. They frequently present with elevated blood pressure. This can occasionally be
treated by prescribin g home medications or
giving oral medications. However, given that
these patients frequently have nausea as a presenting symptom they often require treatment with
IV medications. Blood pressure should be monitored closely during their evaluation, as uncontrolled hypertension may be contributing to their
symptoms.
Outcome
There are two primary end points in this patient
population: ruling out life-threatening pathology
and controlling symptoms. When life-threatening
pathology has been adequately ruled out then the
patient needs to be evaluated for discharge. This
evaluation includes ensuring that symptoms are
manageable, the patient is able to tolerate PO and
the patient has good follow-up. When all of these
goals have been met then the patient is appropriate for discharge from observation status.
Conclusion
Management of patients with ventriculoperitoneal
or lumboperitoneal shunts can be complicated.
These patients often present with symptoms that
could be related to shunt malfunction, infection
or underlying disease process. These patients
require an extended workup to rule out lifethreatening pathology. In addition, these patients
also require significant symptom control. With
appropriate planning, this patient population
can be safely managed in an OU.
References
1. Corbett JJ, Thompson HS. The
rational management of
idiopathic intracranial
hypertension. Arch Neurol
1989; 46:1049.
2. McGirt MJ, Woodworth G,
Thomas G, et al. Cerebrospinal
fluid shunt placement for
pseudotumor cerebriassociated intractable
headache: predictors of
treatment response and an
analysis of long-term
outcomes. J Neurosurg 2004;
101:627.
3. Burgett RA, Purvin VA,
Kawasaki A. Lumboperitoneal
shunting for pseudotumor
cerebri. Neurology 1997;
49:734.
4. Eggenberger ER, Miller NR,
Vitale S. Lumboperitoneal
shunt for the treatment of
pseudotumor cerebri.
Neurology 1996; 46:1524.
5. Johnston I, Besser M, Morgan
MK. Cerebrospinal fluid
diversioninthetreatmentof
benign intracranial hypertension.
J Neurosurg 1988; 69:195.
6. Chumas PD, Kulkarni AV,
Drake JM, et al.
Lumboperitoneal shunting: a
retrospective study in the
pediatric population.
Neurosurgery 1993; 32:376.
7. Rosenberg ML, Corbett JJ,
Smith C, et al. Cerebrospinal
Mark G. Moseley and Miles P. Hawley
042
21:05:20
fluid diversion procedures in
pseudotumor cerebri.
Neurology 1993; 43:1071.
8. Lundar T, Nornes H.
Pseudotumour cerebrineurosurgical considerations.
Acta Neurochir Suppl (Wien)
1990; 51:366.
9. Mayhall CG, Archer NH, Lamb
VA, et al. Ventriculostomyrelated infections.
A prospective epidemiologic
study. N Engl J Med 1984;
310:553.
10. Chumas PD, Armstrong DC,
Drake JM, et al. Tonsillar
herniation: the rule rather than
the exception after
lumboperitoneal shunting in
the pediatric population.
J Neurosurg 1993; 78:568.
11. Sell JJ, Rupp FW, Orrison WW
Jr. Iatrogenically induced
intracranial hypotension
syndrome. AJR Am
J Roentgenol 1995; 165:1513.
12. Padmanabhan R, Crompton D,
Burn D, Birchall D. Acquired
Chiari 1 malformation and
syringomyelia following
lumboperitoneal shunting for
pseudotumour cerebri. J Neurol
Neurosurg Psychiatry 2005;
76:298.
13. Suri A, Pandey P, Mehta VS.
Subarachnoid hemorrhage and
intracereebral hematoma
following lumboperitoneal
shunt for pseudotumor
cerebri: a rare complication.
Neurol India 2002;
50:508.
Central Nervous System (CNS) Shunts
042
21:05:20
Subpart IVE
Chapter
39
Clinical – Metabolic, Endocrine
Hyperglycemia
Pawan Suri, MD
Taruna Aurora, MD
Introduction
The clinical presentation of hyperglycemia in the
emergency department (ED) varies greatly and
can range from nonketotic hyperglycemia on the
one end of the spectrum to diabetic ketoacidosis
(DKA) on the other extreme. While some patients
present with new-onset diabetes, most patients
with hyperglycemia will have a prior history of
Type I or Type II diabetes. Nonketotic hyperglycemia is also known as hyperosmolar hyperglycemic state (HHS) and differs from DKA due to
the absence of ketoacidosis and the degree of
hyperglycemia.
1
Approximately 33% of patients
with hyperglycemia will have features of both
DKA and HHS.
2
Regardless of the type of clinical
presentation, the basic principles of hyperglycemia management are very similar.
While milder forms of DKA and HHS can be
managed in an observation unit (OU), serious
presentations carry significant morbidity and
mortality and require inpatient admission and
occasionally intensive care unit admission. Newonset diabetics who do not have a primary care
physician or health insurance coverage pose a
unique disposition dilemma for the treating
emergency physician. While these patients often
do not meet acute inpatient admission criteria, it
is unsafe to discharge them without proper diabetic teaching and resources to manage their disease. We find the OU especially useful for this
cohort of hyperglycemia patients.
Clinical Presentation
Significant hyperglycemia classically presents
with polydipsia, polyuria, and polyphagia, with
or without weight loss. DKA tends to develop
rapidly over the course of a few hours to a day.
The cardinal feature of DKA is the presence of an
anion gap metabolic acidosis and ketonemia, both
of which are absent in HHS.
1
Due to the metabolic acidosis, patients with DKA will often present with hyperventilation, abdominal pain and
vomiting.
3
The abdominal pain seen in DKA is
thought to be due to delayed gastric emptying and
ileus associated with metabolic acidosis and electrolyte abnormalities. It is rare to see abdominal
pain in the absence of acidosis.
In contrast, patie nts with HHS are not acid-
otic as evidenced by a pH of > 7.30, negative
urine and serum ketones and serum bicarbonate
of > 20 meq/dl. While serum glucose concentration can exceed 1000 mg/dl in HHS, it is
usually less than 800 mg/dl in DKA.
1,5–6
Patients
with HHS are much more likely to exhibit neurologicsymptomslikelethargy,confusionand
obtundation because of higher plasma osmolality.
2,5,6
These symptoms do not develop until
plasma osmolality exceeds 320–330 mosmol/kg.
Therefore the presence of neurological deficits in
diabetic patient with plasma osmolality below
320 mosmol/kg should prompt the search for
alternate causes. Some patients with HHS can
even have focal neurologic signs like seizures or
hemiparesis.
7
When evaluating a patient with hyperglycemia
for a possible admission to the OU, it is helpful to
consider potential precipitating causes. The two
most common reasons for hyperglycemia in the
ED are noncompliance with antidiabetic regimen
and infections.
2,5,6
Other causes include cerebrovascular accident (CVA), pancreatitis, acute myocardial infarction (MI), drugs like glucocorticoids,
atypical antipsychotics, and thiazide diuretics and
insulin pump malfunction. Psychological problems associated with eating disorders that lead to
poor compliance with insulin regimens and
cocaine use may require additional resources such
as psychiatric consultation and substance abuse
counseling.
8
043
21:05:56
The serum osmolality can be calculated using
the formula:
Effective Plasma Osmolality ¼½2×Na ðmEq=LÞ
+ ½glucose ðmg =dLÞ18
+ ½BUN ðmg=dLÞ2:8
There are two main reasons for the increased
plasma osmolality seen in DKA and HHS. The
first is a rise in serum glucose and the second,
more important reason is the loss of free water
due to glucose osmotic diuresis.
4
Anuric endstage renal disease patients with severe hyperglycemia do not exhibit the rise in plasma osmolality
and rarely develop neurologic symptoms.
9
On physical exam, patients with DKA may
have the classic Kussmaul respirations (rapid,
deep breathing) and a “fruity breath” due to
ketone production. The extent of dehydration in
both DKA and HHS can be gauged from the
physical examination, specifically looking for
dry mucous membranes, decrease in skin turgor,
dry axillae, and hypotension.
In DKA, there are three ketone bodies
produced: acetone, acetoacetic acid, and betahydroxybutyric acid. In severe DKA, betahydroxybutyric acid is the predominant ketone.
The commonly used nitorprusside test detects
only acetone and acetoacetic acid and in rare
circumstances it is possible to have a negative
nitorprusside test in the presence of severe ketosis.
2
Some hospital labs offer beta-hydroxybutyric
acid testing, but it is not widely available.
Serum sodium tends to decrease with rising
serum glucose due to dilution from osmotic water
movement out of the cells. Serum sodium concentration falls by approximately 1.6 meq/L for every
100 mg/dL rise in serum glucose.
10
There is an
overall total body potassium deficit due to gastrointestinal losses, loss of potassium from cells due to
glycogenolysis, urinary losses from glucose osmotic
diuresis as well as hypovolemia-induced hyperaldosteronism. Despite a potassium deficit, the serum
potassium concentration is either normal or may
even be elevated
4
due to solvent drag from water
movement out of the cell as well as insulin deficiency that impedes potassium uptake by cells. Further, acidemia plays a small role through a
transcellular exchange of potassium with hydrogen
ions resulting in a rise in serum potassium. Similarly, serum phosphate concentration is usually
normal or high because of metabolic acidosis and
insulin deficiency despite a total body phosphate
deficit from osmotic diuresis and decreased
phosphate intake.
11
Insulin therapy can unmask
this low phosphate that is usually asymptomatic.
Clinically evident hemolysis as well as rhabdomyolysis with myoglobinuria are rare complications of
hypophosphatemia.
12,13
There may be unexplained elevation of serum
amylase and lipase in DKA without evidence of
acute pancreatitis, therefore a diagnosis of pancreatitis in patients with DKA has to be made by
clinical findings consistent with acute pancreatitis
and abdominal CT scan.
14
Leukocytosis unrelated
to infection often occurs in hyperglycemic
patients but the exact etiology of this nonspecific
leukocytosis is not known. Increase in white cell
count corresponds to the degree of ketosis,
15
though WBCs > 25,000/microL or greater than
10% bands may favor an infectious etiology.
16
The combination of insulin deficiency and
increase in ACTH, glucagon, growth hormone
and catecholamines in DKA and HHS leads to
lipolysis and marked hypertriglyceridemia and
hypercholesterolemia.
17
These abnormalities start
to resolve within 24 hours of insulin therapy.
Patient Selection
Hyperglycemic patients presenting to the ED with
blood glucose level < 600 and a pH > 7.2 can be
successfully managed in an ED OU provided they
do not have new onset DKA, acute mental status
changes, end-stage renal disease, sepsis, acute
CVA, acute MI, or infections, or significant complications. (Both glucose and ph levels for the
indication for ICU admission are an arbitrary
cut off with no support in literature, in general.)
Patients who do not meet the blood glucose and
pH criteria upon ED presentation and have treatment initiated with fluid replacement and insulin
are often able to meet these criteria upon reevaluation if they remain in the ED.
Observation Unit Management
Patientswith hyperglycemiawho are admitted to an
OU are carefully selected to exclude seriously ill
patientswho may require inpatientor ICU management. However, it is imperative to closely monitor
and follow these patients in the OU. This may
include reevaluation in order to identify and treat
any underlying events that may have precipitated
the hyperglycemia and to recognize any complications, as well as to assess the progress of therapy.
Hyperglycemia
043
21:05:56
The primary goals of treatment of both DKA
and HHS are frequent monitoring, administration of IV fluids and insulin therapy to correct
hypovolemia, hyperglycemia, hyperosmolality,
electrolyte abnormalities, and in the case of
DKA, correct the metabolic acidosis.
All patients with hyperglycemia should have a
complete blood count, serum electrolytes including serum glucose, blood urea nitrogen (BUN)
and creatinine, urinalysis and an EKG done. If
there is an anion gap or the presence of ketones
in the urine, patients should have arterial (or
venous) blood gas (ABG)(VBG) and serum
ketones drawn. Optional tests may include a chest
x-ray, blood and urine cultures, cardiac enzymes,
amylase and lipase. For patients with new-onset
hyperglycemia obtain a baseline weight and consider sending HbA1C, liver function tests (for
Type II diabetics), c-peptide and insulin antibodies. Even thoug h these test results may not
be available prior to discharge, they will help
follow-up care.
Most patients will have an elevated BUN and
creatinine. DKA presents with a high anion gap
metabolic acidosis and low serum bicarbonate.
Sometimes DKA can present with serum glucose
that may be only slightly elevated or even in the
normal range. This occurs in patients with poor
oral intake or pregnancy.
18
Check the serum glucose every hour while the
patient is on an intravenous insulin infusion.
Serum electrolytes, blood urea nitrogen, creatinine should be measured every 4 hours.
19
We do
not repeat ABGs during treatment and elect to
rely on serial bicarbonate measurements and the
anion gap to determine the extent of acidosis. If
needed, the venous pH can be checked instead,
which is about 0.03 units lower than arterial pH
and is less painful for the patient.
20
Fluid Replacement – The osmotic diuresis
seen in DKA and HHS leads to significant volume
depletion that can average up to 6 L in DKA and
10 L in HHS.
1
In addition, for each liter of fluid
lost, there is concomitant loss of approximately
70 meq of sodium and potassium. Hence, one of
the most important goals of therapy is to replace
the intravascular volume and electrolytes.
If this is done too rapidly, it can lead to precipitous lowering of plasma osmolality and cause
cerebral edema. Isotonic saline (0.9% sodium
chloride) is the fluid of choice and is given at a
rate of 10–15 mL/Kg per hour, not to exceed
50 mL/Kg in the first 4 hours
19
with a goal of
replacing estimated deficits within the first 24
hours. Response to fluid replacement can be
judged by hemodynamic monitoring and urine
output. As renal perfusion increases, serum glucose is further r educed by increasing urinary loss
of glucose.
21
While isotonic saline is the appropriate fluid for initial hydration, one-half isotonic
saline can be used if the corrected serum sodium
is normal or elevated and if concurrent potassium
replacement is needed.
19
The serum creatinine is initially elevated out
of proportion to the fall in glomerular filtration
rate, because acetoacetate artifactually raises
measured creatinine in the standard colorimetric
assay.
22
With fluid replacement, as the glomerular
filtration rate rises, BUN and creatinine fall to
normal levels.
Insulin Therapy – Insulin remains the corner-
stone of therapy for treating hyperglycemia. For
treating DKA a continuous IV regular insulin
drip can be started at 0.14 U/kg per hour. Alternately, the patient can be given a bolus of 0.1 U/kg
followed by a continuous infusion at 0.1 U/kg per
hour.
23
Both the approaches are equally effective.
Contrary to popular belief, insulin lowers serum
glucose primarily by decreasing hepatic glucose
production rather than enhancing peripheral
utilization.
24
Insulin, in relatively low doses,
exerts a potent antilipolytic effect. Insulin infusion is started after ensuring that serum potassium is above 3.3 meq/L since insulin will worsen
the hypokalemia and may lead to possible
arrhythmias, cardiac arrest, and respiratory
muscle weakness.
19
Initial fluid repletion will reduce serum glucose
by 35–70 mg/dL per hour by increasing urinary
losses and hemodilution. Addition of insulin will
further reduce serum glucose. If the serum glucose
does not fall by 50–70 mg/dL in the first hour, the
insulin infusion should be doubled every hour
until a steady decline in serum glucose is achieved.
Higher doses of insulin will not produce greater
than 50–70 mg/dL fall because the insulin receptors are already saturated.
25
When the serum glucose reaches 200 mg/dL in
DKA or 250–300 mg/dL in HHS, the insulin
infusion rate can be reduced by half to 0.05 U/Kg
per hour and the intravenous saline solution is
switched to dextrose in saline.
2
Any further reduc-
tion in the serum glucose at this time below
200 mg/dL in DKA or 250–300 mg/dL in HHS
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may promote the development of cerebral edema.
Newer insulin analogs like glulisine insulin are
equally effective in treating hypoglycemia. Another
alternative for treating uncomplicated, mild DKA
is the use of subcutaneous insulin analogs (insulin
lispro and aspart).
26
Insulin infusion causes a rapid reversal of
potassium distribution from extracellular to
the intracellular space and it is very important
to carefully monitor serum potassium. If the
serum potassium is ini tially elevated despite substantial total body potassium deficit, repletion is
not begun until the serum potassium concentration falls below 5.3. The use of one-half isotonic
saline is preferred when adding potassium
(20–40 meq/L) since it is osmotically active
and if added to isotonic saline, it will yield a
hypertonic solution that will be unable to correct
the hyperosmolality. The goal is to maintain
serum potassium between 4.0 and 5.0 meq/L.
Reversing the hyperglycemia wi th insulin wi ll
lower the plasma osmolality, which will cause
water to move from the extracellular fluid into
the cells, there by raising the serum sodium
concentration.
5,10,19,27
Bicarbonate therapy is usually not needed in
the stable hyperglycemic patients admitted to an
OU, though it may be indicated in severe cases
with a serum pH < 6.9 or severe hyperkalemia.
Side effects of bicarbonate therapy include
reduced respiratory drive, increase in pCO2 and
paradoxical CNS acidosis.
28
Bicarbonate administration can also slow down the rate of recovery of
the ketosis
29
and lead to a post-treatment meta-
bolic alkalosis.
Despite the hypophosphatemia accompanying
insulin therapy, routine use of phosphate replacement is not recommended because of potential
side effects like hypocalcemia and hypomagnesaemia. Phosphate replacement in the form of 20–30
meq/L of potassium phosphate added to replacement fluids is reserved for patients with a serum
phosphate of < 1.0 mg/dl or patients who show
signs of cardiac dysfunction, hemolytic anemia,
or respiratory depression.
Cerebral edema and noncardiogenic pulmonary edema are rare complications of the treatment of DKA an d HHS. Most cases of cerebral
edema are seen below the age of 20.
30
OU management should include looking for symptoms
like headache that may develop within 12 hours
of therapy. Once developed, cerebral edema can
progress rapidly to obtundation, seizures and
death, with an overall mortality between 20%
and 40%.
19
Ensuring that initial fluid replacement does not exceed 50 mL/Kg in the first
4 hours and not letting the blood glucose fall
below 200 by switching replacement fluids to
dextrose (see earlier) are two strategies used to
prevent cerebral edema. Both mannitol and
hypertonic saline have been used to treat cerebral
edema.
30
New-onset Diabetics – All the new-onset dia-
betics in our OU get a literacy test. We use
REALM-R (Rapid Estimate of Adult Literacy in
Medicine, Revised) available at adultmeducation.
com to gauge the ability of English-speaking
patients to understand diabetes teaching packet
instructions. Low Literacy instruction pamphlets
are available. Patients also get a visual acuity to
determine if they are able to measure insulin
accurately. Insulin pens are preferred for visually
impaired patients. If available, a diabetes educator
(usually a nurse or a midlevel provider) are excellent resources and should be involved in patient
management.
For all Type I diabetics, who are usually thinner and insulin sensitive, we start insulin at a total
daily dose of 0.3 units/kg/day
31
and recommend
an endocrinology consult. We use a single daily
subcutaneous injection of the long-acting Glargine insulin (Lantus) along with 4 units of Humalog at the largest meal. If the patient is unable to
afford the Lantus, we start NPH insulin twice a
day in divided doses of 0.15 units/kg/day. We
ensure the patient can perform self-glucose-monitoring and is able to self-administer insulin and
provide the patient with a blood glucose meter or
a prescription to get one.
For Type II diabetics, who are typically obese
and insulin resistant, we use oral antidiabetic
medications and insulin, either alone or in combination. For patients with blood glucose < 200,
start monotherapy with metformin 500 mg twice
a day unless there is a contraindication (serum
creatinine > 1.5, congestive heart faillure [CHF],
elevated liver enzymes, alcohol abuse or IV contrast within 48 hours). Patients with blood glucose > 200 can s tart once daily Lantus at 0.4
units/kg/day and metform in 500 mg twice a
day. Another option is to start NPH insulin 0.2
units/kg twice a day along with metformin
500 mg twice a day.
32
All patients must have
access to a glucose meter and be able to use it.
Hyperglycemia
043
21:05:56
Observation Unit Outcome
Tokarski et al. conducted a retrospective observational study of 101 pediatric and adult patients
admitted to an OU with mild to moderate DKA
over the course of a year. OU patients had a mean
arterial pH of 7.3 and a mean blood glucose of 489
mg/dl. Sixty percent of patients were discharged
from the OU after a mean total ED OU stay of
22.8 hours. Complications included hypoglycemia
(6%) and recurrent hyperglycemia or ketosis
requiring reinstitution of the insulin infusion
(22%).
33
Patients with uncomplicated DKA or
HHS respond well to OU management with fluid
replacement and insulin and can be safely discharged. The OU also provides an opportunity
for diabetic teaching that includes self-monitoring
of blood glucose and insulin administration.
There could be potential cost saving for the hospital if the OU can demonstrate earlier disposition
as opposed to inpatient admission.
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