Running head: DISSEMINATED INTRAVASCULAR COAGULATION
Disseminated Intravascular Coagulation due to Sepsis Following Therapeutic Abortion:
A Case Report
Jody M. Dawson
Trent University
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DISSEMINATED INTRAVASCULAR COAGULATION
Disseminated Intravascular Coagulation due to Sepsis Following a Therapeutic Abortion:
A Case Report
The number of induced abortions performed in Canada is approximately 100 000
per year (Canadian Institute for Health Information [CIHI], 2010). According to the CIHI
2010 report, 2.3% of abortions performed in Canadian hospitals result in complications.
The most frequently reported complications include retained products of conception,
hemorrhage, and infection (CIHI, 2010). While these complications are rare, the
associated morbidities can be life threatening. It is critical that healthcare providers are
able to recognize early stages of complications from abortion and provide timely
treatment (World Health Organization, 2012). The purpose of this paper is to provide an
in-depth discussion of the complications and nursing implications in the case study of
Pam, a 35-year-old female who was diagnosed with disseminated intravascular
coagulation [DIC] secondary to sepsis following her therapeutic abortion.
Recognition of Acute Post-Abortion Distress
Early recognition of complications associated with pregnancy termination is vital
for decreasing the risk of maternal morbidity and mortality (Bamfo, 2013). Nurses can
promote improved patient outcomes by continuously monitoring trends in vital signs and
contributing to prompt management of the signs and symptoms that are associated with
rapid deterioration (Wagner, 2010). In the present case study, Pam presented to the
emergency department in a state of acute distress, as evidenced by her assessment
findings of hyperthermia, tachycardia, tachypnea, hypotension, and impaired perfusion.
Her vital signs were: temperature 41°C, heart rate 105 beats/min, blood pressure 90/55
mm Hg, and respiratory rate 24 breaths/min. Pam had cold, mottled fingers and toes
along with severe vaginal bleeding and evidence of nasal and oral bleeding.
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3
It is important for nurses to understand the specific laboratory tests that are
monitored in patients who present with severe complications. In order to interpret Pam’s
laboratory values, the findings of her tests were compared with normative values adapted
from Kee’s Laboratory and Diagnostic Tests with Nursing Implications (2009), as
presented in Table 1. Pam’s tests revealed the following abnormal results: leukopenia,
anemia, thrombocytopenia, prolonged prothrombin time (PT), prolonged partial
thromboplastin time (PTT), hypofibrinogenemia, and the presence of fibrin degradation
products. Interpretation of Pam’s signs and symptoms and laboratory results led to her
diagnosis of DIC secondary to sepsis.
Table 1
Adult DIC Diagnostic Tests: Comparison of Case Study with Normative Values
Test
Normal values
Pam
Interpretation
Partial thromboplastin time
28-38 seconds
63 seconds
Prolonged PTT
Prothrombin time (PT)
10-13 seconds
27 seconds
Prolonged PT
Fibrin degradation products
2-10 ug/ml
35 ug/ml
Indicative of DIC
Fibrinogen
175-400 mg/dL
105 mg/dL
Hypofibrinogenemia
Hemoglobin (Hb)
120-160 g/L
80 g/L
Reflects loss of blood
Platelet count
150-400 (x
90 (x 109/L)
Thrombocytopenia
3.5 (x 109/L)
Leukopenia
(PTT)
109/L)
Leukocytes
5-10 (x 109/L)
Note. Normative values adapted from “Laboratory and Diagnostic Tests with nursing
implications” by J. L. Kee, 2005. Upper Saddle River, N.J.: Prentice Hall.
DISSEMINATED INTRAVASCULAR COAGULATION
DIC
The scientific subcommittee on DIC of the International Society of Thrombosis
and Hemostasis defines DIC as “an acquired syndrome characterized by the intravascular
activation of coagulation” (Taylor, Toh, Hoots, Wada, & Levi, 2001, p. 1327). The
committee describes DIC as an acute problem of hemostasis. Under normal physiologic
conditions, the coagulation cascade is controlled locally by clot stimulating and inhibiting
factors (Wagner, 2010). In the clinical syndrome of DIC this balance is lost, leading to
activation of systemic coagulation pathways (Wagner, 2010). Systemic activation of the
coagulation cascade causes excessive intravascular thrombus formation with
simultaneous hemorrhaging due to the exhaustion of platelets and coagulation factors
(Wagner, 2010). If DIC is severe it can progress to a life-threatening state of ischemia
with multiple organ dysfunctions secondary to a compromised blood supply (Taylor et
al., 2001).
Pathophysiology of DIC
DIC can be triggered by different underlying acute conditions that activate the
clotting cascade. The most common risk factor for the development of DIC is infection
(Davis & Kessler, 2014). Both surgical and medical abortion procedures place women at
a risk of infection secondary to operative injury (i.e. uterine perforation), retained
products of conception, or through spread of endogenous bacterial species of the genital
tract (Rahangale, 2009; Kaponis, Papatheodorou, & Makrydimas, 2010). Infection can
also be introduced into the uterus after an abortion through sexual intercourse or from
pelvic infections such as urinary tract infections (Mary & Mahmood, 2010). The
following is a discussion of the progression of infection to sepsis and DIC.
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The immune system responds to endotoxins by releasing host proteases,
cytokines, and hormones (Taylor, Toh, Hoots, Wada, & Levi, 2001). If the infection is
not contained locally it may travel to the bloodstream and trigger the systemic
inflammatory response syndrome [SIRS] (Baldwin, 2006). When the progression of SIRS
is initiated by an infection, the condition is known as sepsis (Fischerova, 2009). The
overwhelming release of immune mediators from the cytokine cascade can lead to
systemic vasodilation of the vascular system and increased permeability of capillaries
(Taylor et al., 2001). This progression can lead to a state of hypovolemic shock (Taylor et
al., 2001). As a result, systemic hypotension can cause hypoxia, decreased level of
consciousness, and altered perfusion to vital organs (Rahangdale, 2009).
In addition to causing severe hypotension, a systemic inflammatory response can
cause extensive damage to endothelial tissue due to excessive cytokine production
(Taylor et al., 2001). Vascular damage triggers coagulation (Baldwin, 2006). Coagulation
involves platelet aggregation into thrombi that are reinforced by fibrin. Platelet
aggregation is initiated when platelets come in contact with exposed collagen from an
injured blood vessel (Kam, Kuar, & Thong, 2005). This results in the release of platelet
mediators (i.e. thromboxane A2 and adenosine diphosphate), which recruit additional
platelets (Kam et al., 2005). Normally, the effects of platelet mediators are moderated by
prostacyclin that is released following injury to the epithelium (Wagner, 2010). In DIC,
platelet aggregation occurs systemically and the amount of platelet plugs formed is
extensive and unable to be counteracted by prostacyclin (Levi, Toh, Thachil, & Watson,
2009). Eventually the available platelet supply becomes exhausted, as evidenced by
thrombocytopenia and bleeding (Wagner, 2010).
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In the second step of coagulation the platelet plug is reinforced with fibrin (Kam
et al., 2005). Fibrin is a protein that is produced through activation of either the intrinsic
or extrinsic pathway of the coagulation cascade (Sultana, Begum, & Khan, 2011). The
intrinsic pathway is activated when blood contacts collagen that has been exposed as a
result of tissue damage (Lehne, 2013). The intrinsic pathway is also activated by
infection as a result of the ability for gram positive and negative bacteria to bind to
contact factors (King, Bauza, Mella, & Remick, 2014). The extrinsic coagulation
mechanism is activated by tissue factor, which is exposed with damage to the vascular
wall (King et al., 2014). Like infection, placental abruption can also cause damage to
vascular integrity and stimulate the release of tissue factor (Sultana et al., 2011).
Ultimately, stimulation of both the intrinsic and extrinsic pathways promotes the
conversion of prothrombin to thrombin. Thrombin catalyzes the conversion of fibrinogen
to fibrin. Fibrin binds to platelets, white blood cells [WBCs], and red blood cells [RBCs]
to reinforce the platelet plug (Kam et al., 2010).
When the coagulation cascade is stimulated, thrombi are dissolved through the
digestion of fibrinogen and fibrin by plasmin. Placental abruption can also contribute to
fibrinolysis through intrauterine consumption of fibrinogen during the formation of
“retro-placental clot” (Sultana et al., 2011, p. 69). The three activities of platelet
activation, clot formation and fibrinolysis contribute to the hemostasis of the coagulation
process. When an underlying pathology such as sepsis results in systemic activation of
the clotting cascade, these three activities contribute to coagulopathy (Wagner, 2010).
The result is an exhaustion of platelets and coagulation factors which can lead to
simultaneous widespread hemorrhage and tissue necrosis from occlusive thrombi
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(Baldwin, 2006). These paradoxical manifestations are the defining characteristics of DIC
(Sultana et al., 2011).
Diagnosis of DIC
One of the most important components of the management of DIC is recognizing
the symptoms before it evolves into a catastrophic condition. The diagnosis of DIC
should utilize both clinical and laboratory information (Levi et al., 2009). The 2011
report from the Centre for Maternal and Child Enquiries identifies pyrexia, tachycardia,
dyspnea, and significant vaginal discharge as ‘red flag’ signs and symptoms of sepsis that
need to be promptly attended to. Cold and mottled extremities with tachycardia and
hypotension are associated with hypovolemic hemorrhagic shock (Butt and Saydain,
2012). Bleeding from the nose and mouth are indicators of widespread hemorrhage
(Guha, 2011). Each of these clinical findings of acute distress are present in Pam.
It is important to use a combination of laboratory tests in order to diagnose the
disorder with reasonable certainty (Levi et al., 2009). Laboratory tests for the diagnosis of
sepsis are selected to reflect the impaired oxygenation that occurs with hypoperfusion
(Henry & Johnson, 2010). When oxygen delivery is not meeting cellular demands, it can
result in lactic acidosis secondary to anaerobic metabolism (Henry & Johnson, 2010).
Serum lactate levels as well as arterial blood gases can be used measured to identify
acidosis secondary to hypoperfusion in sepsis.
Laboratory tests for the diagnosis of DIC are selected to reflect the characteristic
changes in hemostatic function of this condition (Levi et al., 2009). DIC is associated
with prolonged PT, prolonged PTT, low platelet counts, low fibrinogen, and elevated
products of fibrin breakdown (Kee, 2005). The PT is prolonged in about 50–60% of cases
of DIC at some point during the course of illness (Levi et al., 2009). The results of these
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tests reflect the consumption of coagulation factors. Thrombocytopenia is a feature in up
to 98% of DIC cases (Levi et al., 2009). The decreased number of platelets is due to
thrombin-induced platelet aggregation (Levi et al., 2009). Fibrinolytic activity is
increased in patients with DIC, as evidenced by the presence of fibrin degradation
products and low fibrinogen counts (Levi et al., 2009). Each of these abnormal findings
that are associated with DIC are present in Pam’s laboratory results.
Pam’s laboratory testing also reveals leukopenia and diminished hemoglobin.
These results can be attributed to her infection and complications of hemorrhaging.
Decreased WBC count reveals the compromised state of her immune system, as her
leukocytes are being depleted as a result of immune cell exhaustion as well as
lymphocyte apoptosis in the acute phase of sepsis (King et al., 2014). It is anticipated that
Pam’s blood cultures will indicate bacteremia as the source of her infection (Rahangdale,
2009).
DIC is an extremely dynamic situation. When interpreting laboratory results, the
tests should be repeated in order to monitor the changing scenario associated with DIC
(Levi et al., 2009). A scoring system that uses simple and widely available laboratory
tests has been established for the diagnosis of DIC by the Scientific and Standardization
subcommittee on DIC of the International Society on Thrombosis and Haemostasis
(Taylor et al., 2001, p. 1327). The authors’ scoring system uses platelet count,
prothrombin time, fibrinogen, and fibrin degredation products to diagnose DIC (Taylor et
al., 2001).
The cornerstone management of DIC is detection and elimination of the primary
cause (Sultana et al., 2011). Persistent bleeding following an abortion is an indication of
retained products of conception (Davis, 2006). In cases that present with persistant
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bleeding, the nurse should anticipate the prompt use of an ultrasound for evaluating the
presence of retained products of conception (Rahangdale, 2009). Once the diagnosis has
been established, the health team can initiate action towards the comprehensive
management of the underlying condition and it’s clinical manifestations.
Treatment of DIC in Pam and Nursing Considerations
Research from the departments of Emergency Medicine and Critical Care
Medicine at Vancouver General Hospital illustrates the effectiveness of a sepsis protocol
in a Canadian Centre (Sweet, Jaswal, Fu, Bouchard, Sivapalan, Rachel, & Chittock,
2010). The authors’ findings demonstrate that the implementation of an empirical sepsis
protocol is associated with improved patient outcomes. Again, the first step in
management is detection and elimination of the primary cause (Sultana et al., 2011). The
second step in management is supportive measures to control major complications such
as compromised perfusion, bleeding, and thrombosis (Sultana et al., 2011). The
following is a comprehensive discussion of recommendations and nursing implications
for the acute management of sepsis and DIC in Pam.
Correction of underlying cause. After being examined in the ICU, Pam was
taken to the operating room where a large segment of placenta was removed. She
received two antibiotics, vancomycin and gentamycin. According to the Induced
Abortion Guidelines created by the Society of Obstetricians and Gynaecologists of
Canada, surgical intervention by repeat curettage and possibly laparoscopy should be
performed immediately in the event of retained products of conception to remove the
source of infection (Davis, 2006). High-dose, broad-spectrum intravenous antibiotics
should be administered within the first hour of recognizing severe sepsis and septic shock
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(Bamfo, 2013). Blood cultures should be obtained before antibiotic administration
(Dellinger et al., 2012).
Post-abortal sepsis is known to be polymicrobial (Mary and Mahmood, 2010).
The recommended antimicrobial therapy for infections caused by multiple organisms is a
synergistic combination of vancomycin and gentamycin (Fischerova, 2009). Pam is
administered IV vancomycin (1 g over 60 minutes) and IV gentamycin (2 mg/kg).
Vancomycin is a bactericidal antibiotic that inhibits cell wall synthesis of Gram-positive
bacteria (Jia, Zhu, Ma, Cao, Li, & Chen, 2009). Vancomycin also selectively inhibits
ribonucleic acid synthesis and alters permeability of the cell membrane (Jia et al., 2009).
Gentamycin is an aminoglycoside. Aminoglycosides promote bacterial cell death by
inhibiting protein synthesis and disrupting the integrity of the bacterial cell membrane
(Shakil, Khan, Zarilli, & Khan, 2008). Gentamycin is used primarily to treat serious
infections caused by gram-negative bacteria (Lehne, 2013). The ability of vancomycin to
alter cell-membrane permeability enhances the ability of gentamycin to penetrate into
bacterial cells, and increases the bioavailability of gentamycin (Jia et al., 2009). The use
of these medications combined promotes the broad-spectrum destruction of gram-positive
and gram-negative bacilli, as recommended for the antimicrobial treatment of sepsis
(Banfo, 2013).
A major concern with the combined use of vancomycin and gentamycin in Pam is
the increased risk for ototoxicity and nephrotoxicity (Bisht & Bist, 2011; Wong-Beringer,
Joo, Tse, & Beringer, 2011). Damage to the ear can occur due to accumulation of
vancomycin and gentamycin within the inner ear, impairing hearing and balance (Bisht &
Bist, 2011). Renal failure is a major toxicity associated with the concurrent use of
nephrotoxic medications such as vancomycin and gentamycin (Wong-Beringer et al.,
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2011). Accumulation of these medications in the proximal tubular cells leading to cellular
necrosis may be the underlying mechanism of nephrotoxicity (Wong-Beringer et al.,
2011). The risks associated with toxicities of these medications necessitates the
monitoring of safe serum levels as well as renal function, as these medications are
excreted in the urine (Karch, 2014).
When administered intravenously, vancomycin has the potential to cause
hypotension related to a histaminergic reaction (Ruggero & Abdelghany, 2012). This
adverse reaction could exacerbate Pam’s current case of impaired oxygen perfusion. It is
important to administer the medication slowly to decrease the risk of sudden profound
hypotension (Karch, 2014). It is also important to monitor Pam’s vital signs very closely
(Karch, 2014). Another risk that is concerning for Pam is the potential for gentamycin to
cause leukopenia and thrombocytopenia (Karch, 2014). The etiology is believed to be the
induction of drug-dependent antibodies, which bind to platelets and white blood cells and
cause their immune-mediated destruction (Visentin & Liu, 2007). These adverse
reactions would significantly exacerbate the problem of Pam’s already depleted levels of
leukocytes and platelets. It is therefore important to monitor Pam’s laboratory tests for
complete blood counts, hepatic function and renal function. The final concern for the
nurse is in administration of these medications. Vancomycin and gentamycin are
incompatible and should never be mixed in the same solution (Karch, 2014).
Optimize oxygen perfusion to tissues. Pam’s oxygen perfusion is being
compromised as a result of her low level of hemoglobin, hypotension, and ineffective
breathing pattern. It is important to continue to monitor Pam’s hemoglobin and
hematocrit. If Pam’s hemoglobin level decreases to less than 70g/L, the nurse should
anticipate the administration of blood products with a red blood cell transfusion
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(Kleinpell, Aitkin, & Schorr, 2013). In addressing patients with hypotension, the primary
focus of the Surviving Sepsis Campaign is initial fluid resuscitation (Dellinger et al.,
2012). The guidelines recommend crystalloids as the initial fluid of choice in
resuscitation of patients with severe sepsis. The nurse should anticipate an order for fluid
resuscitation in order to restore tissue perfusion by increasing cardiac output. In addition,
the nurse should anticipate oxygen therapy, and titrate oxygen according to the
physician’s orders. The nurse can monitor the efficacy of these interventions by
monitoring Pam’s vital signs. Increased respiratory rate and heart rate are signs that the
body is compensating for decreased tissue oxygenation. The nurse should continuously
evaluate Pam’s need for higher levels of oxygen (Bernstein & Lynn, 2013).
An additional intervention to optimize oxygen perfusion involves the use of a
vasopressor to counteract hypotension (Dellinger et al., 2012). Pam is administered IV
phenylephrine (120 mcg/min). When administered parentally, this medication is an
effective first-line agent for the treatment of vascular failure in septic shock (Morelli et
al., 2008). An additional benefit of phenylephrine is that it does not compromise
gastrointestinal and hepatosplanchnic perfusion, as compared with norepinephrine
administration (Morelli et al., 2008). Phenylephrine is a selective alpha1 adrenergic
agonist (Lehne, 2013). It acts on the smooth muscle layer of blood vessels and mimics
the sympathetic nervous system to increase blood flow to vital organs by increasing
blood pressure and cardiac output (Henry & Johnson, 2010).
The most significant adverse effects associated with systemic administration of
phenylephrine relative to Pam is the potential for cardiac arrhythmias and compromised
perfusion if used long-term (Karch, 2014). It is important for the nurse to monitor Pam’s
vital signs closely while Pam receives this medication for signs of decreased cardiac
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output and reflex bradycardia (Henry & Johnson, 2010). It is also important to monitor
Pam’s IV site for infiltration as well as bleeding complications (Henry & Johnson, 2010).
Finally, it is important to avoid prolonged use of this medication, as prolonged use may
increase Pam’s risk of renal complications due to constriction of renal blood vessels
(Karch, 2014).
Decrease oxygen consumption. In addition to optimizing oxygen delivery, it is
important to decrease oxygen demands of the heart by decreasing total body work,
decreasing pain, and decreasing temperature (Henry & Johnson, 2010). The nurse can
decrease Pam’s oxygen consumption by encouraging her bed-rest, monitoring pain and
administering pain medications, initiating cooling measures and providing antipyretics,
and promoting a calm environment (Henry & Johnson, 2010).
Prophylaxis of associated complications. Once a protocol for the management
of sepsis has been initiated, the nurse’s responsibility is to then to initiate preventative
measures. Potential complications the nurse should be aware of include the progression
of systemic inflammation to multiple-organ dysfunction syndrome [MODS], as well as
deep vein thrombosis.
Multiple-organ dysfunction syndrome [MODS]. Infection can cause direct
damage to organs by causing widespread microvascular thrombosis (Fischerova, 2009).
Infection can also cause secondary damage by triggering systemic hypotension which
leads to altered perfusion to vital organs (Rahangdale, 2009). The sympathetic nervous
system compensates for ineffective circulating blood volume by shunting blood to the
heart and lungs (Henry & Johnson, 2010). This results in decreased blood flow to internal
organs such as the kidneys, liver, and the gastrointestinal tract (Henry & Johnson, 2010).
In order to decrease the progression of SIRS to MODS, nurses should monitor lab
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evidence as well as signs and symptoms for indications of hematologic, hepatic, renal,
gastrointestinal, respiratory, cardiovascular and neurologic function. Abnormal findings
include the following: elevated liver enzyme levels and serum lactate level about 4
mmol/L, elevated D-dimer level, urine output below 0.5 ml/hr, elevated creatinine level,
ileus, oxygen saturation below 92%, respiratory rate about 24 breaths/minute, heart rate
above 100 beats/minute, systolic blood pressure below 90, altered level of consciousness
(Bernstein & Lynn, 2013).
Thrombosis. Antithrombotic therapy is recommended for the treatment of
clinically evident intravascular thrombosis (Sultana et al., 2011). Although heparin has
been considered as cornerstone management for prevention of thrombosis, Lepirudin is a
good alternative for Pam, as it will minimize her risk of heparin-induced
thrombocytopenia (Kam, Kaur, & Thong, 2005). Pam was treated with IV lepirudin (0.4
mg/kg over 20 seconds followed by 0.15 mg/kg/hr). Lepiruden directly binds and inhibits
thrombin by blocking its interaction with substrates, thus decreasing the risk of deep vein
thrombosis as well as necrosis of organ tissue caused by microthrombi (Cheng-Ching,
Samaniego & Naravetla, Zaidat, & Hussain, 2012). A concerning adverse effect of
lepirudin in Pam is the increased risk of bleeding (Cheng-Ching et al, 2012). While
monitoring this medication, it is important for nurses to be observant for signs of
bleeding and to provide safety measures to prevent injuries from bleeding (Karch, 2014).
Another problem with lepirudin treatment is that it does not have an antidote (Kam et al.,
2005). It is important to monitor aPPT to achieve target lepirudin plasma levels (Kam et
al., 2005).
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Summary of Nursing Priorities for Continuous Management of DIC in Pam
In a comprehensive overview, Kleinpell, Aitkin, and Schorr applied the new
international sepsis guidelines to implications for nursing care (2013). The authors
identified the top four nursing priorities of nurses for managing sepsis within the first
three hours of diagnosis. The authors’ top four priorities for nursing management of
patients with sepsis are 1) measuring lactate levels, 2) obtaining blood cultures before
administration of antibiotics, 3) administering broad-spectrum antibiotics, and 4)
anticipating crystalloids for fluid resuscitation. Additional priorities include applying
vasopressors, controlling glucose, and prophylaxis of DVT.
Conclusion
The adverse outcomes associated with complications of abortion can be reduced
with prompt management (Bamfo, 2013). Nurses play a vital role in the early recognition,
diagnosis, and treatment of complications such as infection leading to sepsis (Kleinpell et
al., 2013). Sepsis is characterized by systemic activation of the cytokine cascade,
coagulopathy, and altered distribution of blood-flow (Rahangdale, 2009; Taylor et al.,
2001). The treatments that were first initiated in Pam are consistent with the
recommendations of the Society of Critical Care Medicine’s 2012 “Surviving Sepsis
Campaign”. This includes the attainment of appropriate cultures, controlling the source of
infection, implementation of broad-spectrum antibiotics, use of a vasopressor, and
prophylaxis of DVT. The implementation of evidence-based recommendations will help
to ensure optimal outcomes for Pam.
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