2A - Maternal Health Mortality | Conjunto de Fichas

Pregunta	Respuesta
Obstetric complications	Assessment skills are vital for identifying probelms: Involves all senses observation, palpatation, percussion, auscultation thorough history taking of women and her family
Maternal mortality	death of a pregnant woman or within 42 days of delivery termination
What to do	access to quality care skilled professional workforce good hygiene access to safe abortion prevent unwanted pregnancies access to contraception oxytocin after birth detection/management of pre-existing conditions address inequalities in access and quality
Australia and SA incidences	Aus 1.1/100,000 births in 2015 SA - 8.9/100,000 births 3 maternal deaths in 2015
Abortion in South Australia	medical termination of pregnancy became legal in SA in 1970 SA was the first legal state to enable this
Abortion in South Australia\ stats in 2014	notifications: 4439 notified, women 20-24 and 25-29 had highest rates, teens reducing over 10 years by 11.9% reasons: mental health 95.6%, serious abnormality 3.8%, maternal condition 0.6% complications: 115 reported cases, 89 retained conception prodcuts, 12 sepsis, 8 haemorrhage, 5 failed procedure, 1 perforation uterus
Maternal complications in SA	remember 56.1% of pregnancies have no complications most arise from diabetes - 10.4% HTN - 7.0% Haemorrhage - 4.4% other 22.10% combined
Gestational diabetes definition:	carb intolerance of variable severity with onset or first recognition during pregnancy at risk of maternal and foetal mortality/morbidity large babies, difficult labour, hypertension, haemorrhage
Risk factors of gestational diabetes	family history obesity previous GDM in pregnancy previous baby weight 4500gms maternal age over 25 years multiple pregnancy
CHO metabolism	glucagon needed to free glucose insulin actively transports free glucose across cell membranes into cells insufficient insulin - BGL increases - glycosuria fats oxidised for energy - ketones a by product
Insulin sensitivity	0-20 weeks progesterone and oestrogen stimulate beta cells in pancreas to increase insulin production - insulin sensitivity increased glycogen synthesis and storage enhanced glucose use in peripheries - leads to lower BGL fat synthesis/storage increases reduced BGL and insulin needs
Insulin resistance	late 2nd and 3rd trimester - pregnancy hormones (prog, prolactin) antagonise the effectiveness of insulin glucose mobilised out of storage peripheral use of glucose reduced which facilitates availability of glucose for foetus increased BGL increased insulin needs
Gestational diabetes cycle	other hormones influence insulin pancreas- low/effective insulin blood stream-raised glucose level high glucose level affects embryo hormonal changes during pregnancy
pathophysiology	insulin secretion does not overcome insulin resistance gestational diabetes (type 3) aggravated pre-existing diabetes mellitis type 1 2)
Diagnosis	OGCT taken 26-28 weeks gestation non-fasting 50 gram glucose drink one hour venous blood is taken one hour blood glucose level of greater than 7.8mmol indicates need for an oral glucose tolerance test (OGTT)
OGTT	oral glucose tolerance test ensure normal diet 300 gm carb at least 3 days before test performed under 8 hr fasting obtain fasting venous blood sample 75 gram glucose drink given measure at 2 hours fasting glucose - less than 5.5mmol or glucose less than 7.8mmol 2 hrs after drink
Management	referral to high risk pregnancy and medical care home blood glucose monitoring education insulin treatment admission for further treatment if BGL over 11mmol or poor compliance with diet
Gestational diabetes follow up	all gestational diabetes women should have a glucose tolerance test at 6-8 weeks post partum education and advice given about risk of type 2 diabetes maintain healthy diet and exercise
Hypertension in pregnancy	arises in pregnancy at 20 weeks gestation pre-eclampsia classic triad of symptoms: HTN 140/90, proteinuria 300mg/24 hours, oedema rapid weight gain is supported
Pre-eclampsia diagnosis	PE is a multisystem disorder potentially affecting both mother and baby usually detected by measurement of an elevated bP
pathophysiology	Intense vasospasm - In pregnancies complication by PE - blood vessel constrict leading to vasospasm and reduction in blood flow causing maternal organ damage damage to endothelium of vessels release of inflammatory factors coagulation factors placental hypoxia
Clinical course of pre-eclampsia	eye- retinal haemorrhage, arteriolar spasm resp - pulmonary oedema, ARDS liver - hepatic rupture, haemorrhage CNS - seizures, CVA Pancreas - ischaemia kidneys - ARF Uteroplacental circulation - Abruption, fetal compromise
Management of mild pre-eclampsia	expectant management at home with visits in hospital bed rest with care of DVT careful checking of BP, urine protein and foetal activity monitoring of liver and renal function
Diagnostic criteria of severe pre-eclampsia	headaches, visual disturbances, pulmonary oedema, oliguria, elevated creatinine, proteinuria, systolic 160-180 diastolic 110 above
Management of severe pre-eclampsia	admit to high dependency, monitor closely prevent seizures lower BP to prevent cerebral haemorrhage assess for delivery, balance mother and baby conditions
Magnesium sulfate	preferred anticonvulsant slows neuromuscular activity and decreased CNS irritability no significant effects on BP 4-6gm load, followed by infusion of 1-3gms/hr levels monitored for toxicity
Antihypertensive medication	goal: diastolic 90/110mm/hg choice of agent - beta blockers, vasodilators oral alternatives (slower onset) - CCB, methydopa
Postpartum management	improvement rapid after birth risk of seizures greatest in first 24 hours mag sulfate continued for first 24 hours all monitored and continued for 24 hours watch for signs of fluid overload
Eclampsia	appearance of seizures in a woman with PE aetiology uncertain, cerebral oedema, ischaemia, possible causes BP often significantly elevated can occur berfore, during, after birth develops quickly: facial congestion frothing at mouth period of apnoea deepening loss of consciousness tonic phase of muscular rigidity usually lasts 60-70 secs women regains consciousness quickly
management of eclampsia	more than 50% occur out of hospital if seizure happens: call for help prevent injury/aspiratin give oxygen via hudson mask evaluate airway, pulse, BP, CPR secure IV access ASAP stable plan for birth may need ICU for monitoring respirations and CVS systems
Maternal physiology - cardiovascualr	reduction in blood volume by 30-50% before shock becomes evident HR normally higher BP lower to mask symptoms decreased vascular resistance - may not be clammy reduce ratio of RBC to plasma higher coagulability high clotting factors reflex vasoconstriction - reduced uteroplacental perfusion
Maternal physiology - gastrointestinal respiratory	gastro- reduced motility and emptying, higher risk of aspiration resp - high tidal volume, low PC02, high oxygen requirements, maternal/foetal hypoxia
Physiological changes of pregnancy that affect resuscitation/trauma	uterine blood flow determined by perfusion pressure with drop in maternal BP uterus receives 20-30% of CO Aortocaval compression causes 30% CO to be sequestered to lower body - 27% tilt during resuscitation haemorrhage of 1000-1500mls can occur before the woman shows signs of hypovolaemic shock increased oxygen consumption - maintain above 90%
Primary assessment maternal and foetal	maternal: stabilisation, life support, resuscitation, ABCs, oxygen, fluid support, initial physical examination, baseline maternal VS Foetal: fundal height (gestation), uterine activity (contractions), foetal HR, movement, assess for vaginal bleeding, ruptured membrans, US
Secondary assessments	x-rays, USS, lab investigations, CVP, urine output, complete physical examination
Definitive care	consider need for: emergency delivery ongoing fetal surveillance tocolytics antibiotic cover anti-d
Obstetric haemorrhage	can occur during: antenatal - miscarriage, placenta praevia, placental abruption intrapartum during birth - placental abruption or trauma to birth canal postpartum - post partum haemorrhage
Placenta Praevia	implantation of placenta inside the uterus near or over the opening of the cervix grade 1 - placenta mostly in upper segment of uterus but encroaching on lower segment grade 2 -reaches but doesnt cover the internal os grade 3 - covers internal os when its closed but not completely when its dilated grade 4 - placenta completely covers the internal os
Risk factors for placenta praevia	previous c-section previous instrumental birth older mother smoking multiple gestation
Placenta praevia	painless bleeding - 2/3 trimester or at term often following intercourse, may have preterm contractions on presentation: vital signs, FHS, determine gestation Lab, Gp and X match (have 2 units of whole blood in dept, coags) US to confirm placement management - no intercourse late pregnancy bleeding - assess for premature labour, corticosteriods, tocolysis
Placental abruption	premature seperation of placenta uterine wall -partial or complete, revealed, concealed, mixed foetal compromise, prematurity, restriction, stillbirth
Risk factors for abruption	HTN, smoking, substance use, trauma, MVA, over distension of uterus, chorioamnionitis
placental abruption	vaginal bleeding is usually associated with abdominal pain, uterine contractions, tenderness faint, collapse, signs of haemorrhagic shock * consider consealed abruption if abdominal or back pain is present
Management of abruption	depends on severity maternal resuscitation if needed monitor FHR, pain, contractions management of fluids, IVT 2 lines, oxyegn, USS
Postpartum haemorrhange	bleeding occurs following 2nd stage causes: poor uterine tone tissue present in uterus - membranes trauma from birth (cevix, vaginal tear) primary - within 24 hours of birth secondary - within 7-10 days postpartum
PPH risk factors	antepartum: pre-eclampsia, multiple gestation, previous PPH Intrapartum: lacerations of vaginal, cervical, perineal, assisted birth, forceps, vacuum
Post partum haemorrhage	up to 6% of vaginal births definition over 500mls blood loss 25% of maternal deaths causes: tone 70% tissue trauma thrombin
PPH - management	keep woman warm uterine mssage - encourage uterine contractions inspect lacerations and repair oxytocics -1st line - syntocinon - 2nd line - ergometrine - 3rd line - prostaglandin F2 alpha - intramyometrial surgical intervention - manual placenta, retain products, repair of trauma
Amniotic fluid embolism	occurs in 1 in 2 pregnancies maternal mortality 85% with ICU management 26.4% risk factors: multiparity abruption IUFD
AFE what and when	what: amniotic fluid force into the maternal circulation via uterine sinuses of the placental bed due to increased pressure When: close to term, during labour, immediately post partum
Clinical presentation of AFE	gradual or sudden chest pain, dyspnoea, resp distress, nausea and vomiting, seizures, blood stained sputum, anaphylactic reaction common, DIC, coma, death
AFE maternal assessment	initial event: oxygen 100% intubation ventilation PEEP to avoid alveolar collapse invasive haemodynaic monitoring central line two large bore IV - aggressive fluid replacement urine output monitored CXR and ECG

Siguiente

2A - Maternal Health Mortality

Descripción

Resumen del Recurso

Similar

	Creado por Elizabeth Then hace más de 6 años