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Disseminated Intravascular Coagulation due to Sepsis Following Therapeutic Abortion: A Case ReportJody M. DawsonTrent University 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. 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 ValuesTestNormal valuesPamInterpretationPartial thromboplastin time (PTT)28-38 seconds63 secondsProlonged PTTProthrombin time (PT)10-13 seconds27 secondsProlonged PTFibrin degradation products2-10 ug/ml35 ug/mlIndicative of DICFibrinogen175-400 mg/dL105 mg/dLHypofibrinogenemiaHemoglobin (Hb)120-160 g/L80 g/LReflects loss of bloodPlatelet count150-400 (x 109/L)90 (x 109/L)ThrombocytopeniaLeukocytes5-10 (x 109/L)3.5 (x 109/L)LeukopeniaNote. Normative values adapted from “Laboratory and Diagnostic Tests with nursing implications” by J. L. Kee, 2005. Upper Saddle River, N.J.: Prentice Hall. DICThe 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.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). 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 (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 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 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 ConsiderationsResearch 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 (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., 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 (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 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 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). 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. ConclusionThe 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. ReferencesBaldwin, K. (2006). From Inflammation to MODS: Stopping Sepsis in its Tracks. LPN 2009. 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