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patient should be checked for decreased deep
tendon reflexes, hypotension, somnolence and
heart block; Mg
+2
levels should be re-checked.
Serum K
+
and Ca++abnormalities should be
addressed.
Oral magnesium is limited by the common
side effect of diarrhea; magnesium chloride as an
enteric coated tablet is best tolerated.
1
Doses are
dependent on degree of deficit but are generally
4–6 grams daily.
3
Consideration may be given
toward substituting a potassium-sparing diuretic
such as amiloride or triamterene for furosemide
or a thiazide.
16
(Table 41.5)
Hypermagnesemia
Hypermagnesemia is relatively rare in the ED.
Prominent causes include RI and excessive magnesium intake IV iatrogenically or through use of
antacids and laxatives which contain magnesium,
particularly in the elderly patient. The kidneys are
able to adequately excrete magnesium until glomerular filtration falls below 20 ml/min.
17
Symptoms
generally occur above levels of 4–6mg/dl
(1.74–2.61 mmol/L) and include nausea, vomiting,
hypotension, hyporeflexia, and respiratory
depression.
17
The patient without severe symptoms such as significant bradycardia or complete
AV block, paralysis, or depressed level of consciousness is an appropriate candidate for the
OU. Those requiring consideration of IV calcium
salts or with renal failure requiring hemodialysis
are not appropriate candidates.
Treatment
Workup includes testing for renal function, potassium, and calcium and obtaining a 12-lead ECG.
All exogenous magnesium should be discontinued.
After giving IV normal saline, a loop diuretic such
as furosemide (40–80 mg IV) can be administered
to enhance urinary excretion of magnesium.
3
Sodium
Sodium is normally tightly maintained in a range
of 135–145 mmol/L.
4
Water balance is regulated
through the actions of antidiuretic hormone
(ADH) and requires an intact thirst mechanism,
as well as access to water.
18
Subtle clinical changes
or life-threatening consequences depend not only
on the sodium value but also how acutely the
abnormality occurred. Laboratory testing may
include urine and serum electrolytes, renal function, plasma and urine osmolality to determine
etiology.
19
Hyponatremia
Acute onset of hyponatremia is more likely to
present with encephalopathy including visual
changes, focal neurologic deficits, mental status
changes, and seizures.
20
If the decline in Na+is
more gradual, milder or no symptoms may present.
21
Patients with altered neurologic status,
hemodynamic instability, or seizures are not candidates for observation care. In the hyperglycemic
patient, correction should be made for osmolarity: each 100 mg/dL rise in glucose results in a 1.6
mEq/L decline in serum sodium.
1
Isotonic hypo-
natremia or “pseudohyponatremia” is caused by
hyperlipidemia or hyperproteinemia.
3
Hyponatremia is categorized by whether the
patient is hypovolemic, euvolemic, or hypervolemic. With hypovolemic hyponatremia due to
renal losses, urine [Na
+
] should be > 20 mEq/L.
If fluid losses are predominantly extrarenal with
normal renal function, urine [Na
+
] should be
< 20 mEq/L.
3
A potential candidate for the OU
is the patient with exercise-associated hyponatremia as seen in long-distance runners who drink
excessive water during a race.
20
A reasonable cut-
off for observation care is a serum [Na
+
]of
approximately 120–125 mEq/L and no neurologic
symptoms. Those requiring hypertonic saline for
any reason should be managed in an intensive
care setting.
Table 41.5 Hypomagnesemia Management in the
Observation Unit
Establish adequate renal function
2-4 grams Magnesium sulfate IV over 10–20
minutes as emergency therapy, then up to 6–12
grams MgSO
4
over 8–24 hours.
Discharge home on 4–6 grams per day for 3–4 days
orally: Magnesium chloride or Mag-Tab SR
magnesium lactate 2–4 tablets/day if mild, 6–8
tablets if severe.
Consider diuretic adjustment (potassium sparing):
amiloride or triamterene instead of a loop diuretic
or a thiazide.
Monitor for decreased deep tendon reflexes (may
lead to bradycardia, prolonged intervals on ECG,
heart block, paralysis or apnea). Recheck serum
Mg
++
periodically.
Electrolyte Abnormalities
045
21:05:58
Treatment
Unless it is completely clear that the patient’s
symptoms developed acutely, it is unsafe to correct
sodium rapidly due to risk of osmotic demyelination syndrome (ODS), which may be irreversible.
Neurologic examinations for fluctuating consciousness, dysarthria, convulsions, and disturbed
consciousness should be performed.
22
It is recommended that [Na+] be increased by
no more than 10 to 12 mEq/L during a 24-hour
period, aiming for a discharge sodium in the
125–130 mEq/L range.
20
Diuresis of dilute urine
can increase [Na
+
] more rapidly than anticipated,
and overcorrection of serum [Na
+
] > 125–130
mEq/L should be avoided.
20
Patients at high er
risk for ODS include alcoholics with malnutrition, hypokalemic patients, and elderly women
on thiazide diuretics.
4
Patients with hypovole mia and clinical signs
of dehydration should have an initial infusion
of 500–1000 cc/hr of isotonic 0.9% saline to
restore volume.
20
After correction of dehydration, a hypotonic fluid (such as 0.45% saline)
may be given to avoid a too rapid elevation of
[Na
+
], as in the patient with diuretic-induced
hyponatremia.
21
Patients with euvolemic hyponatremia such as SIADH will generally respond
to fluid restriction but may require long-term
salt tablets to help excrete water.
21
The patient
with hypervolemic hyponatremia requires both
fluid restriction and diuretics and is better suited
to inpatie nt management.
Hypernatremia
Hypernatremia, defined as serum sodium [Na+]
> 145 mEq/L, usually results from impaired water
intake (dementia, mental illness, hepatic encephalopathy, or critically ill patient) or massive
sodium load.
18
Initial symptoms may be nonspecific and may be masked by concomitant disease.
22
While many patients will have acute
symptoms with serum [Na
+
] > 158 mEq/L, the
rate of change of sodium and water balance is
important.
3
Correction of free water deficits
should take place over at least a 48-hour period
to prevent rapid fluid shifts and cerebral edema.
1
Patients with hypernatremia are generally not
appropriate for care in the OU. A possible exception is the acutely dehydrated patient who is
otherwise neurologically intact, with access to free
water in his or her living environm ent.
Treatment
If hypovolemia is present, isotonic 0.9% saline
should be given until hemodynamically stable
and tissue perfusion restored. At that time IVF
may b e changed to hypotonic 0.45% saline solution.
22
The goal is to decrease serum [Na+]byno
more than 0.5 mEq/L each hour until the
patient’s sodium is 145 mEq/L.
4
Oral or enteral
hydration with free water is generally safest.
23
Phosphate
Phosphate is the most abundant intracellular
anion. Less than 1% of total body phosphate is
found in plasma. Norma l levels are generally
cited as 2.5–4.5 mg/dl. It is regulated by PTH
and vitamin D.
1
Phosphate is essential for every
intracellular reaction through the body’senergy
source of adenosine triphosphate.
24
Phosphate
should be checked in patients if an abnormal
serum potassium, magnesium, or calcium is
found.
25
Hypophosphatemia
Hypophosphatemia is rela tively rare except in
specific populations: DKA, chronic obstructive
pulmonary disease (COPD), asthma, malignancy,
long-term total parenteral nutrition, infl ammatory bowel disease, anorexia nervosa, and alcoholism.
25
The most common cause of renal
phosphate loss is diuretic therapy including thiazides, loop diuretics, and acetazolamide.
1
Hypo-
phosphatemia is classified as mild 2.5–2.8 mg/dL,
moderate 1.0–2.5 mg/dL, and severe < 1.0 mg/
dL.
1
Patients unsuitable for the OU include those
with mental obtundation, seizures, coma, respiratory failure, encephalopathy, or ileus. Phosphate
disorders will seldom be the primary cause for an
OU stay.
Treatment
For mild or moderate hypophosphatemia, oral
replacement with potassium phosphate is
1200–1500 mg/daily given in divided doses.
3
If
severe total body deficit, one may need to dose
as high as 3000 mg/daily with the oral form.
25
The
parenteral form of potassium phosphate IV is
administered using a weight based regimen with
0.08–0.16 mmol/kg over 6 hours. Except for
DKA, it is unlikely that IV phosphate will be used
in the observation setting.
Kimberly A. Ressler and Jonathan Glauser
045
21:05:58
Hyperphosphatemia
Hyperphosphatemia, serum phosphate > 5.0 mg/
dL, is most commonly seen in RF but also occurs
with rhabdomyolysis, tumor lysis syndrome, or
hemolysis.
1
Tetany and ventricular dysrhythmias
should preclude observation stay.
25
Treatment
Hyperphosphatemia can initially be treated
with isotonic saline infusion if renal function
is intact, which can enhance excretion of phosphate but may further decrease calcium.
4
For the
CRF patient, hyperphosphatemia is managed
with dietary restrictions and phosphate-binding
salts of aluminum, magnesium, or calcium.
25
Patients deemed to require acetazolamide or
dextrose/insulin are better managed in another
setting.
Summary
Patients with a variety of electrolyte abnormalities
are suitable for 24-hour admission into an OU.
Treatment considerations include the underlying diagnosis and the patient’s comorbidities.
Whether a patient is appropriate for observation
care should be considered on an individual basis
taking into account severity and possible etiology
of the electrolyte abnormality.
Bibliography
1. Gibbs MA, Tayal VS.
Electrolyte disturbances. In:
Marx JA, Hockerberger RS,
Walls RM, editors. Rosen’s
Emergency Medicine
Concepts and Clinical Practice.
6th ed. Philadelphia:
Mosby Elsevier; 2010.
pp. 1615–1632.
2. Unwin RJ, Luft FC, Shirley DG.
Pathophysiology and
management of hypokalemia: a
clinical perspective. Nat Rev
Nephrol. 2011;7:75–84.
3. Kelen GD, Hsu E. Fluids and
electrolytes. In: Tintinalli JE,
Stapczynski JS, Ma OJ, Cline
DM, Cydulka RK, Meckles,
editors. Tintinalli’s Emergency
Medicine a Comprehensive
Study guide. 7th ed. New York:
The McGraw-Hill Companies,
Inc; 2011. pp. 117–129.
4. Weiss-Guillet EM, Takala J,
Jakob SM. Diagnosis and
management of electrolyte
emergencies. Best Pract Res
Clin Endocrinol Metab. 2003;17
(4):623–651.
5. Alfonzo AV, Isles C, Geddes C,
et al. Potassium disorders–
clinical spectrum and
emergency management.
Resuscitation. 2006;70(1):
10–25.
6. Nyirenda MJ, Tang JI,
Padfield PL, et al.
Hyperkalemia. BMJ. 2009;339:
b4114:1019–1024.
7. Weisberg, LS. Management of
severe hyperkalemia. Crit Care
Med. 2008;36:3246–3251.
8. Elliott MJ, Ronksley PE, Clase
CM, et al. Management of
patients with acute
hyperkalemia. CMAJ. 2010;182
(15):1631–1635.
9. Khanna A, White WB.
Management of hyperkalemia
in patients with cardiovascular
disease. Am J Med.
2009;122:215–221.
10. Pepin J, Shields C. Advances in
diagnosis and management of
hypokalemia and hyperkalemic
emergencies. Emerg Med Pract.
2012;14(2):1–17.
11. Cooper MS, Gittoes NJ.
Diagnosis and management
of hypocalcaemia. BMJ. 2008;
336:1298–1302.
12. Shepard MM, Smith JW.
Hypercalcemia. Am J Med Sci.
2007;334(5):381–385.
13. Makras P, Papapoulos SE.
Medical treatment of
hypercalcaemia. Hormones.
2009;8(2)83–95.
14. LeGrand SB, Leskuski D, Zama
I. Narrative Review:
Furosemide for Hypercalcemia:
An unproven yet common
practice. Ann Intern Med.
2008:149:259–263.
15. Assadi F. Hypomagnesemia:
An evidence-based approach to
clinical cases. Iran J Kidney Dis.
2010;4(1):13–19.
16. Topf JM, Murray PT.
Hypomagnesemia and
hypermagnesemia. Rev
Endocr Metab Disord. 2003;4:
195–206.
17. Musso CG. Magnesium
metabolism in health and
disease. Int Urol Nephrol.
2009;41:357–362.
18. Archinger SG, Mortiz ML,
Ayus JC. Dynatremias: Why
are patients still dying?
South Med J. 2006;99(4)
353–362.
19. Adrogue HJ, Madias NE.
Hypernatremia. N Engl J Med
2000;342(20):1493–1499.
20. Verbalis JG, Goldsmith SR,
Greenberg A, et al.
Hyponatremia treatment
guidelines 2007: Expert
panel recommendations.
Am J Med. 2007;120(11A):
S1–S21.
21. Vaidya C, Ho W, Freda BJ.
Management of hyponatremia:
Providing treatment and
avoiding harm. Cleve Clin
J Med. 2010;77(10):715–726.
22. Lin M, Liu SJ, Lim IT.
Disorders of water imbalance.
Emerg Med Clin N Am.
2005;23:749–770.
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23. Wakil A, Atkin SL.
Serum sodium disorders:
Safe management. Clin
Med. 2010 ;10(1):
79–82.
24. Assadi F. Hypophosphatemia:
An evidence-based problemsolving approach to clinical
cases. Iran J Kidney Dis. 2010;4
(3)195–201.
25. Shiber JR, Mattu A. Serum
phosphate: Abnormalities in
the emergency department.
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395–400.
Kimberly A. Ressler and Jonathan Glauser
045
21:05:58
Subpart IVF
Chapter
42
Clinical – Hematologic
Sickle Cell Disease
Matt Lyon, MD FACEP
Leah Taylor, MA
Robert W. Gibson PhD, MSOTR/L
Introduction
Vaso-occlusive crisis (VOC) is the most common
complication resulting from sickle cell dise ase
(SCD) in adults.
1
VOC is caused by ischemic
tissue injury as a result of occlusi on of microvascular beds from abnormal, sickle -shaped red
blood cells. SCD patients display a host of complications associated with micro- and occasionally macrovascular occlusion, including stroke,
leg ulcers, spontaneous mis carriage, and renal
insufficiency. However, the acute pain crisis is
the most common reason sickle cell patients seek
medical care in emergency departments (EDs).
2
Due to the recurrent nature of the acute pain
crisis, possible inadequate knowledge by health
care providers of this disease and the intensity of
treatment needed, patients with VOC m ay be
undermedicated in the ED.
3
This leads to low
patient satisfaction, low provider satisfaction
and increased costs of care. Through the use of
an ED observatio n unit (ED OU) clinica l pathway, patients suffering from VOC can be effectively managed to improve outcomes, improve
satisfaction and decrease cost of care.
4
Pathology and Clinical Presentation
SCD is a genetic disorder, which results in abnormal hemoglobin synthesis and abnormally shaped
red blood cells (sickle-shaped red blood cells)
when the red blood cell becomes deoxygenated.
SCD is inherited in an autosomal recessive
manner with heterozygous patients only rarely
expressing clinical symptoms (sickle cell trait)
under extreme conditions. In homozygous
patients (SS) both hemoglobin genes are abnormal and express the sickle cell mutated hemoglobin. This results in the clinical syndrome of
sickle cell anemia. Other sickling disorders, which
are clinically similar in presentation, though milder
in severity, include hemoglobin SC and hemoglobin Sβ-thalassemia disease.
5
The hallmark of SCD is the VOC (aka Sickle Cell
Crisis or pain crisis) in which there are recurrent
episodes of severe pain affecting most commonly the
back, legs, knees, arms, chest, and abdomen. Commonly the pain is bilateral, symmetric and usually
affects the same body areas or regional distribution
in subsequent attacks. VOC is the most common
reason for hospitalization in patients with SCD.
6
Factors associatedwith the onset of VOC include
any activity that increases the requirement for
oxygen, such as illness, physical stress, psychological
stress and/or locations with decreased oxygen tension such as highaltitudelocations. However,in half
of all episodes the precipitating factors are unknown.
The typical VOC lasts from 3 to 14 days with a
crescendo/decrescendo type pattern. Typically, the
pain crisis of SCD often has an abrupt onset.
7,8
Despite oral medication treatment regimens that
may begin at home, many patients require parenteral opioids for relief, and many consider the pain
associated with VOC to be similar to the pain associated with bone metastasis from cancer.
Many patients with SCD experience chronic
pain. VOC pain is distinctly different and occurs
independently of this baseline chronic pain. How
each patient is affected by his or her chronic pain
as well as the VOC episodes is quite variable.
6,9
This variation is due to differences in the type of
SC disease and its genetic expression, how the
patient expresses or internalizes pain, his or her
prior interaction with the health care system, his
or her opioid tolerance, and his or her prior
experience with VOC and chronic pain. Generally, patients with SCD can resume a relatively
normal life in between crisis, although the chronic
pain can lead to disability in some cases.
6
Other complications from SCD may occur
besidesVOC. Since vaso-occlusion results in splenic
046
21:12:36
infarction at a young age, the majority of patients
with SCD do not have the protection from encapsulated bacteria resulting in a suppressed immune
system. Thus SCD patients are susceptible to overwhelming sepsis. VOC may also occur in the lungs
resulting in Acute Chest Syndrome, which includes
hypoxia and dyspnea, and may progress to death if
not recognized and treated appropriately. As a
result of the sickle-shaped red blood cells, the red
blood cells have a shortened life span, leading to a
chronic anemia. During a VOC, the rate of destruction of red blood cells may increase, leading to a
rapid decline in the hemoglobin (hyperhemolysis)
and the possibility of severe complications.
5
Current Management
Many patients with SCD have a relationship with
a primary care physician or a hematologist who
can manage the VOC with oral home medications
or throug h infusion therapy in specialized sickle
cell centers. However, many patients are remote
from these centers and do not have access to
specialized care, particularly when experiencing
a VOC. The sudden onset of pain combined with
an elevated opioid tolerance often leads to treatment in an ED setting.
10
While the vast majority of sickle cell patients
seek care in an ED on a limited or infrequent basis,
a small subset of SCD patients utilize the ED on a
frequent basis. The use of the ED on a frequent basis
by this small subset of patients is usually due to poor
social support, limited specialist or primary care,
patients who have developed a more chronic form
of the disease and those with a true addiction. While
the proportion of sickle cell patients with an opioid
addiction is similar to the general population,
11,12,13
many of these frequent users of EDs are often
grouped together as exhibiting a drug-seeking
behavior.
1
This perception, combined with a lack
of objective measurement of the severity of thevasoocclusion, may lead to skepticism from health care
providersas to the amount or severity of pain that is
associated with VOC.
3,14,15
Combined with the typical duration of a VOC of up to 2 weeks, undertreatment of pain in many cases leads to multiple
ED visits during a single VOC episode, further
reinforcing the stereotype of drug-seeking behavior.
16
Consequently, sickle cell patients are often
distrustful of emergency physicians and may appear
hostile, demanding and disruptive in the ED.
17
Current ED management in most hospitals
involves a trial of parenteral opioids and then a
disposition decision. In some hospitals this involves
a set number of parenteral injections, and in other
hospitals this involves a specified total dose of
opioids.
18
In either case, this type of treatment is
labor intensive on both the nursing staff as well as
the physician staff. Further, the opioid delivery is
not only limited in amount and customization to the
individual patient, there are usually long delays in
treatments, decreasing the efficacy of treatment. As
a result, undertreatment of VOC is common,
leading to frequent ED visits, higher admission rates
to the hospital and a high cost of care.
3
Management Goals
Guidelines for the management of VOC in SCD
have been available since 1999.
19
However, most
physicians are not familiar with the treatment
guidelines, and some physicians do not believe
in the need for opioid therapy or the dose necessary to control the pain associated with VOC.
20
There are four essential features outlined by the
pain management guideline for VOC: 1) rapid
initiation of opioid therapy within 15 to 30 minutes of arrival in the ED, 2) use of adequate opioid
starting dose, 3) frequent repeated doses of
opioids (every 15–30 minutes) until pain is significantly improved, and 4) the need to select
treatment regimens based on an individual’s prior
opioid-response history. Evidence to support this
approach was described in the recently published
Evidence-Based Management of Sickle Cell Disease: Expert Panel Report, 2014.
13,21
While these
goals may be difficult to achieve in the typical ED
setting, they are easily accomplished in the OU
setting. By utilizing a setting that allows for
extended treatment and evaluation and a clinical
care pathway, all of the management goals can be
met in addition to limiting many of the biases of
the patient and the physician from prior ED
experiences.
20
This allows the health system to
realize several advantages, including decreased
variability in treatment for this group of patients,
increased patient satisfaction, decreased admission,
improved pain control, a decrease in repeat patient
ED visits during the same VOC episode, and
decreased discharge of SCD patients having a lifethreatening complication.
4,22
Matt Lyon, Leah Taylor and Robert W. Gibson
046
21:12:36
Meeting Analgesia Guidelines
Clinical Pathway
To meet the analgesia guidelines, a clinical pathway
for the evaluation and management of VOC is
imperative.
23
Since patients with VOC have a similar clinical course, a pathway is a method of standardizing treatment for this disease, while also
decreasing and possibly eliminating any bias or
disparity on behalf of the health care provider.
The use of an observation pathway allows for rapid
initiation of therapy as well as decreased ED
resource utilization. By using a Patient Controlled
Anesthesia (PCA) delivered opioid, the patient is in
control of his or her therapy, removing the bias as
well as delays associated with bolus infusions of
opioid. Because PCA delivery of medication is
gradual, use of a PCA rarely results in the opioid
high, consistent with rapid bolus infusions of narcotics. By eliminating the bolus opioid infusions,
patients with opioid abuse behavior are readily
identified due to resistance in use of the PCA and
can be identified for alternative treatment, such as
drug addiction intervention. Specific information
regarding how to implement the clinical pathway
while meeting the analgesia guidelines follows.
I. Rapid Initiation of Opioid Therapy
To meet the rapid initiation of opioid therapy
goal, patients can be identified and initiated into
the treatment protocol from the ED triage.
Patients presenting to triage are initially evaluated
for the presence of SCD and VOC. Many of the
complicating factors of SCD can be discovered at
triage, including hypoxia and hypotension. If any
of these factors are discovered at triage, the
patient should be treated in the ED with an appropriate triage level. However, when a patient presents with the usual VOC pain crisis, the patient
can be placed directly into the ED or OU, eliminating a long wait. Once in the OU, oral or possibly
parenteral opioid regimens can be started via a
nurse-initiated treatment protocol. In our OU,
time to triage of SC VOC averages less than 15
minutes, and time to treatment with opioids averages less than 30 minutes.
24
II. Adequate and Repeated Opioid Until Pain Control
Utilization of opioids via a PCA protocol de livers
medication on demand to the patient. This has
several advantages: 1) the patient is in control of
his or her opioid usage as well as the delivery rate;
2) the nursing staff is freed from rapid reassessments and intensive opioid injection schedules;
and 3) the delivery of the opioid is gradual and
dose-sustaining leading to a more rapid, even (less
peaks and troughs) arrival at an opioid steady
state. Patients are also treated with oral opioids
and consideration should be given to the use of
oral or parenteral nonsteroidal anti-inflammatory
pain medications such as ibuprofen and ketorolac. The use of these oral medications helps to
transition the patient to outpatient treatment of
his or her pain crisis. Further, these medications
decrease the parenteral opioid requirements.
Other medications such as transdermal fentanyl
should also be considered as this may be continued once discharged from the hospital.
The observation pathway for VOC is a
patient-directed pathway. The patient is questioned on an hourly basis for changes in pain
scale as well as the perception that he or she can
manage his or her pain at home. Typically, the
length of stay in our observation unit for SC VOC
is 14 hours or less (depending on the time of year)
with less than 16% of patients requiring admission at 24 hours of observation time.
19
III. Individualized Treatment Regimens
Because of the variable presentation and variable
opioid tolerance of each individualized patient,
utilizing an individual treatment regimen improves
the efficiency of the pathway. We developed an
observation-specific, individualized, treatmentcompliant database for monitoring the individual
PCA dosages and adjunct medications for each of
the sickle cell patients that utilize our hospital. This
consists of the preferred opioid type, optimal initial
PCA settings, preferred antiemetic and antihistamine, and adjunct medications such as long-acting
transdermal or oral opioid. The database results in
more consistency in treatment of individual
patients regardless of who is caring for the patient
in the ED. Outcome results from this intervention
are not available currently, however the trend has
been a lower admission rate and shorter length of
stay, presumably because the opioid steady state
is reached in less time due to a higher starting PCA
dosage.
IV. Sickle Cell Consults and Admission Criteria
Utilizing a standard protocol with regards to
admission criteria and consults, such as hematology
Sickle Cell Disease
046
21:12:36
or internal medicine, also improved the care of
SC patients. Admission criteria are similar to
exclusion criteria for use of the pathway: 1) development of fever or signs of infection, 2) development of hypoxia or hypotension, and 3) lack of
adequate pain control after 24 hours of treatment.
If any of these conditions develop, the patient
should be evaluated for admission to the hospital.
In our institution, the observation nurse notifies
the physician if any of these conditions are met.
The physician should be consulted when the
patient’s pain scale has not changed within 6
hours. Some physicians may be reluctant to utilize
higher opioid doses during treatment as many of
these patients are on large doses from initiation.
Hematologists/oncologists are often more comfortable with larger doses of opioids as they often
use them in oncology settings. By involving the
consultant when the pain is not improving, the
consultant may be able to make recommendations that may eliminate the need for admission.
Pathway coordination between the admitting service and the OU assures that the patient’s care is
not adversely affected due to the change in physicians providing care.
Observation Protocol Implementation
and Maintenance
Implementation of an observation protocol for
VOC can be challenging as the goal of this
pathway is to standardize care and limit variability in the patient’s care. Initially, some physicians may b e resistant to protocol-directed
patient care. However, once established, care of
the SC patient is nearly automated, yielding less
physician interaction time and improving the
efficiency of the ED. As with most OUs, the
protocols are nurse-driven. Thus, nurse training
with regards to SCD and VOC is imperative.
The nursing staff of the OU is typically limited
in nu mber, so familiarity between the nu rse and
the sickle cell patients utilizing the OU for VOC
is common.
Measures of efficacy of this pathway are determined using SC VOC metrics. Suggested metric
goals are listed below in Table 42.1. These metrics
are based on sickle cell analgesia guidelines and
have been modified to observation medicine
practice.
19,20
Meetings between the hematology or other
appropriate consultants, the observation staff,
and the observation director on a regular basis
to review the metrics is useful in meeting the
metric goals. Sharing of information between the
ED staff and the consultant staff helps identify
problems with individual patients. Often patients,
who have an increased frequency of use of the
pathway, have a social, psychiatric, or non-sicklecell-related medical problem, which increases
their use of the ED. These problems can be identified and addressed through using this multidisciplinary approach.
Adjunctive Therapy
IV hydration is another area of potential controversy. Risk factors for the onset of a VOC include
dehydration. However, there is little evidence that
IV fluids decrease severity of VOC, length of stay,
intensity of the pain, or improve outcomes. Some
patients with SCD can develop pulmonary edema
due to aggressive fluid intake. For example,
patients with severe cardiomyopathy due to iron
overload from chronic transfusion may not be
able to tolerate bolus fluid orders associated with
the pathway. However, many patients are dehydrated on presentation because of decreased oral
intake prior to presenting to the ED. These
patients should be hydrated to euvolemia shortly
after admission to the OU. Continuous IV fluids
at a maintenance rate are also suggested. Because
patients on a PCA opioid infusion may be sleepy
due to the side effects of the opioids, they may not
be able to maintain adequ ate fluid intake while on
the pathway. Further, nonsteroidal inflammatory
medications (NSAIDS) may lead to decreased
renal perfusion through their prostaglandin
inhibitory effects, leading to renal damage when
given to patients who are already dehydrated.
NSAID medications are also a useful adjunct
to the opioid PCA. The effect of NSAIDS has
been shown to be additive and when an oral
Table 42.1 Suggested Sickle Cell Pathway Metrics
and Goals
Metric Goal
Time to ED or ED OU from Triage 15 minutes
Time to physician evaluation 30 minutes
Length of stay 12 hours
Consult rate < 30%
Admission rate < 15%
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formulation is used, patients can continue the
medication after discharge to maintain the pain
relief achieved on the pathway.
The goal of the pathway is to achieve a level of
pain relief that can be maintained on oral medications at home. For this reason, oral oxycodone,
hydrocodone, or hydromorphone should be part
of the observation pathway. The pathway must
be designed as not to exceed the maximum dose
of acetaminophen in a 24-hour period. The strategy
we utilize is one oxycodone (5 mg)-acetaminophen
(325 mg) every 2 hours while on the pathway. This
adjunct to the pathway should not be utilized with
patients who have liver disease in order to avoid
possible liver toxicity.
Home medications, particularly oral or transdermal long acting opioids, should be continued
while the patient is on the observation pathway.
This will help with the transition from inpatient
care to home care as well as aid in achieving an
opioid steady state. If the patient’s long acting
opioids are not continued while on the pathway,
the dosage of the PCA opioids will need to be
increased to account for this overall decrease in
opioid delivery.
Pitfalls in Observation Management
in SC VOC
As with all observation pathways, some situations may arise that lead to poor outcomes.
Populations that may not be appropriate for
the sickle cell observation pathway include
sickle cell patients who are pregnant or have
other serious medical conditions such as cancer,
severe cardiomyopathy, liver disease, or lung
disease. With each of these conditions, variabilityinhowthepatientwillreactateachpresentation to the treatment protocol can be variable,
leading to uncertain outcomes from the
pathway.
A multidisciplinary team consisting of the
observation staff (nurse), the observation director,
and consultant staff, such as hematology/oncology
or internal medicine, should be considered to discuss variations in pathway design and to monitor
for efficacy. This team can develop contingencies
for patients who exhibit opioid abuse behavior or
other psychosocial behavior detrimental to the
observation pathway. Occasionally including a
pain management specialist or a behavioral therapist for individual patients can help solve even some
of the most challenging cases.
Conclusion
The individual with sickle cell VOC is an ideal
candidate for an observation clinical pathway.
Factors such as p rovider bias and individual
patient variation to the disease can lead to variable outcome. The pathway provides for uniform
treatment that leads to better outcomes, cost
savings, and better patient outcomes.
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