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nursing management of obstetrical emergencies

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Information about nursing management of obstetrical emergencies
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Published on March 13, 2014

Author: rubshoyan

Source: authorstream.com

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Nursing management of obstetrical emergencies: Mrs.M . Amutha Shoba Ruban , M.sc (N)., Assistant Professor, Dept of OBG, Vinayaka Mission’s College of Nursing, Puducherry. Nursing management of obstetrical emergencies INTRODUCTION:  INTRODUCTION Uterine bleeding associated with an obstetric complication can lead to severe hemorrhage, hypovolemic shock, infection and coagulation disorders. Not only is the pregnant patient at risk for increased morbidity and mortality, but the fetus may also be adversely affected. obstetrical emergencies: obstetrical emergencies DEFINITION: Obstetrical emergencies are life-threatening medical conditions that occur in pregnancy or during or after labor and delivery. obstetrical emergencies: obstetrical emergencies Vasa praevia Cord presentation and cord prolapse Shoulder dystocia Rupture of the uterus Amniotic fluid embolism /anaphylactoid syndrome of pregnancy Acute inversion of uterus Shock DEFINITION OF SHOCK : DEFINITION OF SHOCK It’s critical and life threatening medical emergency / complex syndrome results from acute, generalized, inadequate perfusion involving reduction in blood flow to the tissues below that needed level to deliver the oxygen and nutrition for normal tissue function leading to dysfunction of organs and cells. AETIOLOGY: AETIOLOGY The Major Classes of Shock Include: Hypovolaemic shock Septic shock Cardiogenic shock and Distributive shock Hypovolaemic shock : Hypovolaemic shock Hemorrhage – Associated with postpartum/ postabortal hemorrhage, ectopic pregnancy, placenta previa , abruptio placenta, rupture of uterus and obstetric surgery Fluid loss shock – Associated with excessive vomiting, diarrhea, diuresis or rapid removal of amniotic fluid. Supine hypotensive syndrome- associated with compression of inferior vena cava due to pregnant uterus Shock associated with DIC- intrauterine dead fetus syndrome and amniotic fluid embolism. Burns Peritonitis Diabetic Keto -acidosis Septic shock : Septic shock Endotoxic shock associated with Septic abortion, chorio amnionitis , pylonephritis , and rarely postpartum endometritis . CARDIOGENIC SHOCK: CARDIOGENIC SHOCK Massive pulmonary embolus Cardiomyopathies - myocardial infarction, hypertrophic obstructive cardio myopathy , cardiac amyloid , myocarditis . Obstructive non-structural- pulmonary embolism, cardic tamponade , pulmonary hypertention , constructive pericarditis PowerPoint Presentation: Obstructive structural- valvular aortic stenosis , valvular mitral stenosis,coarctation of the aorta, left atrial myxoma . Regurgitant lesions- mitra l regurgitation, aortic regurgitation, ventricular septal defect, left ventricular aneurysm, ventricular wall rupture. Blunt cardiac trauma - contusion Dysrhythmias Cont’d Distributive shock : Distributive shock Neurogenic shock- spinal injury Drug induced- reginal anesthesia anaphylaxis Chemical injury- associated with aspiration of gastrointestinal contents during general anesthesia specially in caesarean section ( Mendelson’s syndrome ) PATHOPHYSIOLOGY : PATHOPHYSIOLOGY If untreated shock progress through three stages. Inadequate management allows shock to progressively worsen passing through these stages until death occurs. Stage 1- compensated : Stage 1- compensated Changes in blood pressure and cardiac output compensated by adjustment of homeostatic mechanism. In healthy patients this category of shock may not require fluid replacement if the cause is removed. Stage 2- decompensated : Stage 2- decompensated Maximal compensatory mechanism is acting but tissue perfusion is reduced . Vital organ (cerebral, renal, and myocardial) function becomes impaired. Stage 3-irreversible: Stage 3-irreversible Vital organ perfusion is impaired. Acute tubular necrosis, severe acidosis, decreased myocardial perfusion and decreased myocardial contractility occurs. The profound decrease in perfusion leads to cellular damage and death. CLINICAL FEATURES OF SHOCK : CLINICAL FEATURES OF SHOCK Hypovolaemic shock Early phase ( compensatory phase) Normal blood pressure Tachycardia Diaphoresis Extremities remain warm Patient appears restless and anxious. This phase can easily managed with fluid replacement. PowerPoint Presentation: Intermediate phase (Reversible phase ) Patient progressively becomes pale Tachycardia persists Periphery becomes cold Sweating Patient remains conscious Urine output within normal limit Still adequate management shock state may be reversed. Cont’d PowerPoint Presentation: Late stage- irreversible Hypotension continues Extremities becomes cold and clammy Color of the skin becomes ashen gray Metabolic acidosis Coagulopathy and thrombocytopenia are associated Oliguria and mental confusion –expected Treatment of any kind is practically useless in this phase and mortality varies between 3% to 100% Cont’d PowerPoint Presentation: Neurogenic shock Compensatory phase- Transient Irreversible phase pallor is absent Flushed face Temperature remains normal Cont’d Septic shock: Septic shock Initial phase Patient remains alert Marked flushing of the face The skin feels warm Temperature->38°C (or) <36°C Bounding pulse Heart rate >100beats/ mt Respiratory rate >20 breaths/ mt WBC >12000/ml 3 If state of shock persists Intense constriction of sphincters at either end of capillary bed Pale and profuse sweating Extremities are cold and clammy Urine output is reduced DIAGNOSIS : DIAGNOSIS No laboratory Test -but high index suspicion and physical signs of inadequate tissue perfusion and oxygen are base to initiate treatment. Complications : Complications Haemorrhagic shock Fetal - changes to the uteroplacental blood flow can cause fetal hypoxia, acidosis, placental abruption, intracranial haemorrhage and death Maternal - acute renal failure,  Sheehan's syndrome , disseminated intravascular coagulation (DIC), death Septic shock Acute respiratory distress syndrome Arrhythmias DIC Hepatic and renal failure Fetal and maternal death Prevention: Prevention PPH is much reduced with an actively managed 3rd stage of labour Women at high risk of haemorrhage should not be delivered in isolated units or facilities without immediate access to specialist consultant care, blood products or intensive care. Any problems that may lead to sepsis should be communicated to the community carers at the time of discharge so that appropriate follow-up can be instituted Identification of women with risk factors for venous thromboembolism (VTE) should occur prior to pregnancy or in early pregnancy, with implementation of appropriate thromboprophylaxis . Reassessment of risk should take place prior to delivery . Women with BMIs >35 should be referred for specialist assessment. INITIAL MANAGEMENT:  INITIAL MANAGEMENT Successful management of shock patient requires team work . Senior team of anesthetist, obstetrician, hematologist, and midwife other support staff like neonatologist, radiologist, theatre team and dedicated porter. To be in contact. Maternity unit must have established protocol PowerPoint Presentation: Management should start once diagnosis made aiming for prompt restoration of tissue perfusion and oxygenation. Management of underlying etiology is next step until resuscitation is initiated. Cont’d PowerPoint Presentation: NURSING MANAGEMENT PowerPoint Presentation: ABC AIRWAY Airway-high flow oxygen (15lts/min by mask with reservoir bag) Protected by tracheal intubation if there is potential compromise BREATHING ventiation should be checked and supported if inadequate CIRCULATION insert two widebore peripheral intravenous canulas Initial circulatory management aims to restore circulating volume and reverse hypotension with crystaliod . keep ready blood for transfusion (6 units) Samples can be drawn for full blood count, coagulation screen, urea, electrolytes and cross matching. continuously monitoring the response. Cont’d SPECIFIC MANAGEMENT: SPECIFIC MANAGEMENT Hemorrhagic shock: Infusion and transfusion Blood transfusion is must Crystalloids- Normal saline has to be infused initially for immediate volume replacement. colloids- polygelatin solutions ( Heamaccel ) are iso -osmotic with plasma maintenance of cardiac efficiency. 6liters of crystalloids may be needed for loss of 1liter of plasma volume. Hemodynamic monitoring should be aimed to maintain systolic BP>90mmhg , mean arterial pressure > 60mmhg , CVP 12-15cm H2O and pulmonary capillary wedge pressure 14-18 mmHg . PowerPoint Presentation: Administration of oxygen to avoid metabolic acidosis In the later phases, ventilation by endo - tracheal intubation may be necessary. Oxygen delivery should be continued to maintain O2 saturation>92%, PaCO2 30-35mmHg and PH<7.35 Cont’d PowerPoint Presentation: Control of hemorrhage Specific surgical and medical treatment for control of hemorrhage should start along with the general management of shock. 1. Management of uterine atony Optimise uterine tone- bimanual massage of the uterus, oxytocin bolus followed by infusion, ergometrine bolus and carboprost (15-methyl prostaglandin F2) Surgery- removal of retained products of conception, intra-uterine balloon tamponade , B-Lynch suture, hysterectomy and arterial embolisation Cont’d PowerPoint Presentation: 2. Lacerations of genital tract (Cervix, Vagina & perineum)- Repair of genital tract, vaginal pack. 3. Uterine rupture Stop oxytocin infusion if running. Continues maternal & fetal monitoring Emergency laparotomy with rapid operative delivery. Caesarean hysterectomy- if hemorrhage is impossible to control. Cont’d PowerPoint Presentation:  4. Uterine inversion Replacement of the uterus quickly Administer tocolytics (nitroglycerin, terbutaline, magnesium sulphate ) to allow uterine relaxation. General anaesthesia is usually necessary. Manual removal of placenta by slowly and steadily pushing upwards, with hydrostatic pressure. Cont’d PowerPoint Presentation: Monitoring Clinical parameters like skin temperature, visible peripheral veins can be helpful to assess the degree of tissue perfusion. Urine output (> 30ml/hr) Arterial blood pressure Central venous pressure (CVP) Pulse oximeter and blood gas analysis are useful to assess tissue perfusion. Measurement of left atrial pressure Cont’d PowerPoint Presentation: Pharmacologic agents Vasopressor drugs Vasoactive drugs eg : phenylephrine (1-5µg/kg) and corticosteroids Cont’d PowerPoint Presentation: Antibiotics Ampicillin (1g I.V.every 6 hours,) gentamicin (2mg/I.V loadingdose followed by 1.5mg/kg I.V every 8 hours) and metronidazole (500mg I.V every 8 hours) is good combination. Alternative regimen is to give ceftazidine 1g I.V. every 8 hours combined with gentamicin. Clindamycin 600mg I.V. infusion (single dose) is an alternative to metronidazole. Intravenous fluids and electrolytes Liberal infusion and blood transfusion Cont’d PowerPoint Presentation: Correction of acidosis Acidosis and hypozaemia depress myocardial contractility. Bicarbonate should be administered to correct persistent metabolic acidosis (pH<7.2) First dose would be 50-100 meq (60-110ml of 7.5 percet ) of sodium bicarbonate solution. Further doses will depend on the clinical state of the patient and blood gas analysis result. Cont’d PowerPoint Presentation: Maintenance of blood pressure Inotropes should be used. Adrenaline, noradrenalin, dopamine and dobutamine have both inotropic and vasoconstrictive effects. Vasodilator therapy Sodium nitroprusside and nitroglycerine could be used. This is done under continuous hemodynamic monitoring Diuretic therapy To reduce fluid over load (pre load) and pulmonary oedema , diuretics should be used. Frusemide is the drug of choice. The dose recommended in septic shock is 50mg of hydrocortisone per kg body weight. Cont’d Septic shock- management : Septic shock- management Transfer to a higher level facility Invasive monitoring is mandatory Obtain blood culture as soon as possible (other sites includes wounds, urine, sputum, or other body fluids like amniotic fluid) Start with antibiotics –broad spectrum Removal of infected tissue after initial intubation ,evacuation of uterus, delivery, drainage of abscess and hysterectomy in case high of myometrial micro abscesses . Delivery may not be indicated if sepsis not related to uterus and may depend up on gestational age. Septic shock- management: Septic shock- management Treatment of diffuse intravascular coagulation-Heparin therapy - as a prophylaxis, Heparin 5000IU subcutaneous (or) IV at 8 hourly interval H2 blockers -ranitidine IV Nutritional support- oral (or) parentral nutrition to provide 20-30Kcal/kg/day with fat and carbohydrate Advances in sepsis management : Advances in sepsis management Goal directed therapy – modify the component of treatment to achieve specific end points (mean arterial pressure>65mmhg , urine output >0.5ml/kg/h, CVP 8-12cmh 2 o , and normal o2saturation ). Insulin therapy- aggressive control of blood sugar has been demonstrated to improve outcome in septic patients. Activated protein C Administration in septic shock has been reported to decrease mortality and reduce organ dysfunction PowerPoint Presentation: Distributive shock 1. basic shock management (ABC) 2. Special aspects in management of high block Support of the cardiovascular system with vasopressor drugs and inotropes to maintain adequate BP. Sedative agents- To reduce the risk of awareness once the initial resuscitation has been effected. Cont’d PowerPoint Presentation: Neurogenic Shock- Management fluid replacement Resuscitation initiation of vasopressor drugs to counteract vasodilatation. Administer atropine if bradycardia occurs Cont’d PowerPoint Presentation: Anaphylactic Shock Management 1 . basic and circulatory management. 2. Specific management. Includes immediate and late. Immediate Stop administering suspected agent and call for help Early intubation Client to be placed immediately in supine or Trendelenburg position with leg elevation to increase venous return. Start epinephrine IM. Repeat every 5-15 min. until improvement occurs in blood pressure. if need IV in severe cases. Cont’d PowerPoint Presentation: Replacement with crystalloids solution for rapid intravascular fluid volume expansion. Advanced life support measures if cardiac arrest occurs. Secondary (late)- Management IV epinephrine if hypotension persist. Atropine in cases with significant bradycardia IV salbutamol if brancho spasm persist. If need Anti histamines preferable Refer to critical care centers Cont’d AMNIOTIC FLUID EMBOLISM: DEFINITION An amniotic fluid embolism is a rare but serious condition that occurs when amniotic fluid, fetal material, such as hair, enters the maternal bloodstream. AMNIOTIC FLUID EMBOLISM HISTORICAL PERSPECTIVES: AFE is thought to occur when amniotic fluid , fetal cells, hair, or other debris enter the maternal circulation. Ricardo Meyer (1926); reported the presence of fetal cellular debris in the maternal circulation. Steiner and Luschbaugh (1941) described the autopsy findings of eight cases of AFE. Until 1950, only 17 cases had been reported. AFE was not listed as a distinct heading in causes of maternal mortality until 1957 when it was labeled as obstetric shock. The first well-documented case with ultimate survival was published in 1976 ( Resnik R, et al. Obstet Gynecol 1976;47:295-8). HISTORICAL PERSPECTIVES PowerPoint Presentation: Since then more than 400 cases have been documented, probably as a result of an increased awareness. Overall incidence ranges from 1 in 8,000 to 1 in 80,000 pregnancies. 10% of maternal deaths in USA &16% in U.K. 75 % of survivors are expected to have long-term neurologic deficits. If the fetus is alive at the time of the event, nearly 70 % will survive the delivery but 50% of the survived neonates will incur neurologic damage. INCIDENCE Risk factors of AFE: Risk factors of AFE Advanced maternal age Multiparity Cervical laceration Intrauterine foetal death Very strong frequent or uterine tetanic contractions Sudden foetal expulsion (short labour) Placenta accreta Polyhydramnios Uterine rupture Maternal history of allergy or atopy Chorioamnionitis Macrosomia Male foetal sex Oxytocin (controversial) Pathophysiology : Pathophysiology - Poorly understood. - Cotton (1996), has proposed a biphasic model . Phase 1 : Amniotic fluid and fetal cells enter the maternal circulation biochemical mediators pulmonary artery vasospasm pulmonary hypertension elevated right ventricular pressure hypoxia myocardial and pulmonary capillary damage left heart failure acute respiratory distress syndrome . PowerPoint Presentation: Phase 2 : Biochemical mediators DIC Hemorrhagic phase characterized by massive hemorrhage and uterine atony Cont’d Clinical features : Clinical features The classic clinical presentation of the syndrome has been described by five signs that often occur in the following sequence: (1) Respiratory distress (2) Cyanosis (3) Cardiovascular collapse (4) Hemorrhage (5) Coma. Laboratory investigations in suspected AFE: Laboratory investigations in suspected AFE Non specific • complete blood count • coagulation parameters including FDP, fibrinogen • arterial blood gases • chest x-ray • electrocardiogram • echocardiogram Specific cervical histology serum tryptase PMV analysis Differential diagnosis Obviously depends upon presentation: Differential diagnosis Obviously depends upon presentation Anaphylaxis (Collapse) Pulmonary embolus (Collapse) Aspiration ( Hypoxaemia ) Pre- eclampsia or eclampsia (Fits, Coagulopathy) Haemorrhage (APH ; PPH) Septic shock Drug toxicity (MgSO 4 , total spinal, LA toxicity) Aortic dissection MANAGEMENT OF AFE: MANAGEMENT OF AFE GOALS OF MANAGEMENT: Restoration of cardiovascular and pulmonary equilibrium - Maintain systolic blood pressure > 90 mm Hg. - Urine output > 25 ml/hr - Arterial pO 2 > 60 mm Hg. Re-establishing uterine tone Correct coagulation abnormalities PowerPoint Presentation: As intubation and CPR may be required it is necessary to have easy access to the patient, experienced help, and a resuscitation tray with intubation equipment, and emergency medications. IMMEDIATE MEASURES : - Set up IV Infusion, O 2 administration. - Airway control  endotracheal intubation  maximal ventilation and oxygenation. Cont’d PowerPoint Presentation: LABS : CBC,ABG,PT,PTT,fibrinogen,FDP . Treat hypotension, increase the circulating volume and cardiac output with crystalloids. After correction of hypotension, restrict fluid therapy to maintenance levels since ARDS follows in up to 40% to 70% of cases. Steroids may be initiated. Dopamine infusion if patient remains hypotensive (myocardial support). Vasopressor therapy such as levarterenol may be a drug of chioce (reduced systemic vascular resistance) Cont’d Management of AFE In the ICU: Management of AFE In the ICU Early placement of arterial, central venous, and pulmonary artery catheters to provide critical information and guide specific therapy. Continuously monitor ECG, pO 2 , CO 2 , and urine output. PowerPoint Presentation: Central venous pressure monitoring is important to diagnose right ventricular overload and guide fluid infusion and vasopressor therapy. Blood can also be sampled from the right heart for diagnostic purposes. Pulmonary artery and capillary wedge pressures and echocardiography are useful to guide therapy and evaluate left ventricular function and compliance. An arterial line is useful for repeated blood sampling and blood gases to evaluate the efficacy of resuscitation. Cont’d Management of AFE Coagulopathy: Management of AFE Coagulopathy DIC results in the depletion of fibrinogen, platelets, and coagulation factors, especially factors V, VIII, and XIII. The fibrinolytic system is activated as well. Most patients will have hypofibrinogenemia , abnormal PT and aPTT and low Platelet counts Treat coagulopathy with FFP for a prolonged aPTT , cryoprecipitate for a fibrinogen level less than 100 mg/ dL , and transfuse platelets for platelet counts less than 20,000/mm 3 Restoration of uterine tone : Restoration of uterine tone Uterine atony is best treated with massage, uterine packing, and oxytocin or prostaglandin analogues. Improvement in cardiac output and uterine perfusion helps restore uterine tone. Extreme care should be exercised when using prostaglandin analogues in hypoxic patients, as bronchospasm may worsen the situation. PowerPoint Presentation: Dopamine increases myocardial contractility and systolic BP with little increase in diastolic BP. Also dilates the renal vasculature, increasing renal blood flow and GFR. DOSE: 2-5 µg/kg/min IV; Contraindications: ventricular fibrillation, hypovolemia , pheochromocytoma . Precautions: Monitor urine flow, cardiac output, pulmonary wedge pressure, and BP during infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful Sympathomimetic Vasopressor agent Dopamine Maternal Mortality in AFE : Maternal Mortality in AFE Maternal death usually occurs in one of three ways : ( 1) sudden cardiac arrest, ( 2) hemorrhage due to coagulopathy , ( 3) initial survival with death due to acute respiratory distress syndrome (ARDS) and multiple organ failure For women diagnosed as having AFE, mortality rates ranging from 26% to as high as 86% have been reported. Further issues in the Management: Further issues in the Management Transfer: Transfer to a level 3 hospital may be required once the patient is stable. Deterrence/Prevention: Amniotic fluid embolism is an unpredictable event. Risk of recurrence: is unknown. The recommendation for elective cesarean delivery during future pregnancies in an attempt to avoid labor is controversial. Perimortem cesarean delivery: After 5 minutes of unsuccessful CPR in arrested mothers, abdominal delivery is recommended . NURSING PROCESS:  NURSING PROCESS Nursing diagnosis Ineffective tissue perfusion related to excessive blood loss causing decreased placental circulation to the fetus. Deficit fluid volume in relation to excessive blood loss Anxiety related to unexpected occurrences because of the sudden development of complications. Ineffective individual or family coping related to the transfer of the woman to a tertiary center for more intensive management. Powerlessness related to inability to prevent or control condition and outcomes. Risk for impaired physical mobility related to restriction of movement with monitoring devices. PowerPoint Presentation: Nursing diagnosis Risk for impaired parenting related to separation from infant secondary to treatment regimen. Risk for injury (maternal) related to administration of blood products and operative procedures. Risk for fetal injury related to reduced placental perfusion secondary to vasospasm. Risk for infection related to presence of favourable conditions for infection. Deficit knowledge related to the unexpected emergent nature of care required to ensure maternal and fetal well-being. Cont’d PowerPoint Presentation: Nursing diagnosis: Ineffective tissue perfusion related to excessive blood loss cuasing decreased placental circulation to the fetus. Expected out come: woman will have stable vital signs, oxygen saturation, arterial blood gases and hemoglobin INTERVENTION RATIONALE Monitor vital signs (pulse, respirations, and blood pressure every 15min; apply pulse oximeter and automatic blood pressure cuff as necessary.) level of consciousness. Provides baseline data on maternal response to blood loss Administer oxygen as necessary at 6-10 L/min by face mask. Provides adequate fetal oxygenation despite lowered maternal circulating blood volume Administer intravenous fluid such as lactated ringer’s Replaces intravascular fluid volume; intravenous line is established if blood replacement will be needed. Place woman flat in bed on her side. Maintains optimal placental and renal function Provide suctioning Clears airway PowerPoint Presentation: Nursing diagnosis: Deficit fluid volume in relation to excessive blood loss Expected outcome: woman will demonstrate fluid balance as evidence by stable vital sings, balanced intake and output. INTERVENTION RATIONALE Monitor vital signs (pulse, respirations, and blood pressure every 15min; apply pulse oximeter and automatic blood pressure cuff as necessary.) level of consciousness. Provides baseline data on maternal response to blood loss Monitor blood hemacrit and Hb Provides baseline data on maternal response to blood loss Insert indwelling catheter and measure hourly urine output Provides baseline data on maternal response to blood loss Administer blood (packed cells, fresh frozen plasma) Provides adequate circulating blood volume Administer intravenous fluid such as lactated ringer’s Replaces intravascular fluid volume; intravenous line is established if blood replacement will be needed. Place woman flat in bed on her side. Maintains optimal placental and renal function PowerPoint Presentation: Nursing diagnosis: Anxiety related to unexpected occurrences because of the sudden development of complications. Expected outcome: women well verbalizes that anxious feelings are diminished INTERVENTION RATIONALE Monitor emotional status of client and family members. Provides baseline data Provide calm, competent attitudes and environment Decreases anxiety Explain all procedures Decreases anxiety Allow the women to verbalize feelings Permits clarification of information Keep family informed of condition. Provides supports PowerPoint Presentation: Nursing diagnosis: Ineffective individual or family coping related to the transfer of the woman to a tertiary center for more intensive management. Expected outcome: women and family will demonstrate coping as evidenced by accepting the conditions. INTERVENTION RATIONALE Monitor coping status of client and family members. Provides baseline data Provide emotional support to women, her partner and her family. Support woman’s self-esteem. Assists problem solving, which is lessened by poor self-esteem Provide calm, competent attitudes and environment Decreases anxiety Explain all procedures Decreases anxiety Allow the women to verbalize feelings Permits clarification of information Keep family informed of condition. Provides supports PowerPoint Presentation: Nursing diagnosis: Risk for impaired physical mobility related to restriction of movement with monitoring devices. Expected outcome: women will be able to change positions and ambulate at intervals. INTERVENTION RATIONALE Discontinue continuous electronic monitoring at intervals Changes position and increase mobility Encourage woman to change position and reposition monitor as needed Decreases complications of immobility Place external monitor manually at intervals Collect data while woman is out of bed PowerPoint Presentation: Nursing diagnosis: Risk for impaired parenting related to separation from infant secondary to treatment regimen. Expected outcome: women begins to bond with newborn with exposure as evidenced by expression of positive feeling toward newborn increasing participation in care of newborn INTERVENTION RATIONALE promote adequate rest and sleep Ensures adequate energy for interaction. Contact family members to participate in care of the newborn Allows mother to rest and recover from infection. Offer praise and positive reinforcement for caretaking tasks Facilitates bonding and attachment. Encourage mother to care for herself first and then the newborn Ensures adequate energy for newborn’s care. Refer to CHN for follow up care of mother and newborn at home Fosters continued development of maternal- infant relationship. CONCLUSION : CONCLUSION The management of emergencies is usually the responsibility of hospital obstetricians. As more maternity care is now given in the community, however, midwives, general practitioners, and paramedics may be involved and must know the outlines of management of emergencies and the possible side effects. TAKE HOME MESSAGE : TAKE HOME MESSAGE Successful management of the shocked patient requires team work Obstetric units should have established protocols for dealing with shock and practice ‘fire’ drills regularly Shock management should commence immediately diagnosis is made aiming for prompt restoration of tissue perfusion and oxygenation . The resuscitation follows the familiar ABC pattern. PowerPoint Presentation: Thank you

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