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Midwifery emergencies > Thromboembolic disorders > Flashcards

Thromboembolic disorders Flashcards

1
Q

What is Haemostasis?

A

s is the body’s normal physiological response for the prevention and stopping of bleeding/haemorrhage

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2
Q

Name the three mechanisms that are activated in the process of haemostasis?

A

Constriction of blood vessels – vasoconstriction (to reduce blood flow)

Aggregation of platelets – formation of a plug

Blood clotting – coagulation of the blood

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3
Q

What is the coagulation phase?

A

When damage to a blood vessel is so extensive that the platelet plug fails to stop bleeding the blood clotting mechanism commences

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4
Q

What is the Extrinsic Pathway?

A

Chemicals released by damaged cells

outside circulation –FAST response

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5
Q

What is the intrinsic Pathway?

A

inner vessels damaged within the circulation- SLOWER response

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6
Q

What is the common Pathway?

A

Prothrombinase

Prothrombin

Thrombin

Fibrinogen

Fibrin clot

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7
Q

Name the changes in the haemostatic system during pregnancy

A

Cardiac output increased by approx 40%

Blood plasma increased by 50%

Rise in RBC in last two trimesters

Normal pregnancy a state of hypercoagulability - protective mechanism against blood loss at delivery

(Hypercoagulability is increased in the early puerperium and then slowly returns to pre-pregnant state over a few weeks)

Increase in fibrinogen, prothrombin and factors V11, V111, 1X and X

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8
Q

What is Fibrinonlysis?

A

Process which destroys the clot

Factors in the blood activate plasminogen which activates plasmin which digests fibrin threads…fragments then removed by phagocytosis and macrophage

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9
Q

What is Disseminated Intravascular Coagulation?

A

Disseminated Intravascular Coagulation (DIC) also known as consumptive coagulopathy, is an acquired disorder of haemostasis, which often heralds the onset of multi-organ failure

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10
Q

What is the incidence for Disseminated Intravascular Coagulation?

with reference

A

Rare less than 1:1000 pregnancies

Robson & Waugh (2013 p 262)

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11
Q

What is the 10 steps of pathophysiology- coagulation failure in pregnancy

A
  1. Endothelial damage > Release of thromboplastins from damaged cells into maternal circulation (intrinsic pathway)
  2. Extrinsic pathway triggered by activating a coagulation cascade. E.g. Bleeding from placental site or perineal wound.
  3. If tissue damage so severe then clotting occurs at the site of the epithelial damage and throughout the vascular system (micro thrombi)
  4. This process uses large quantities of clotting factors (V and VIII), platelets and fibrinogen
  5. Some small blood vessels can be occluded by micro thrombi which can lead to organ failure
  6. The damaged tissue within the organs also initiates more clotting which makes the situation worse
  7. Eventually all the clotting factors are used up and bleeding occurs
  8. Ironic situation that bleeding cannot be stopped as there is a clotting deficiency despite widespread clotting
  9. Petechiae develop, bleeding from GI tract, nose, GU tract can be observed
  10. If untreated death from haemorrhage
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12
Q

What is petechiae?

A

point flat round red spots under the skin surface caused by intradermal haemorrhage (bleeding into the skin)

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13
Q

list the causes in obstetrics of DIC

A

Major placenta abruption

Major haemorrhage

Pre-eclampsia / eclampsia

Intra-uterine death, missed abortion or trophoblastic disease

Amniotic fluid embolism

Ruptured uterus

Sepsis

HELLP syndrome

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14
Q

list other triggers that can cause DIC, with referance

A

Hydatidiform mole

Acute Fatty Liver of pregnancy

Breast, uterine, ovarian cancer / and metastases

Other infections - viral haemolytic B Strep, E Coli

Mismatched blood transfusion

Other haemoglobinopathies

Immune disorders – snake bite

Burns

Robson & Waugh (2013, p262)

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15
Q

list the complications of DIC

A

Renal failure and anuria

Liver failure and jaundice

Dyspnoea and cyanosis

Convulsions /coma /brain damage

Retinal damage – reduced sight /blindness

Pituitary – Sheehans Syndrome (necrosis of pituitary gland)

Death due to hypovolaemia

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16
Q

provide a list of pre-conception issues and care when a woman has DIC

A

Pre-conception issues and care

History of DIC in previous pregnancy – recurrence risk dependent on cause

F/U and debriefing

Medical conditions such as Von Willebrand’s disease or Thrombocytopenia/Thrombophillia

Women with chronic DIC may be at high risk of pregnancy complications

Needs discussion

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17
Q

What is considered as Major and Severe PPH?

A

Major PPH is more than 1000ml blood loss and severe PPH is blood loss greater than 2000mls

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18
Q

How can you manage a severe haemorrhage?

A

Major PPH is more than 1000ml blood loss and severe PPH is blood loss greater than 2000mls

Anticipate – risk factors – preventative measures – remove causes

Active management of primary PPH

A 14 gauge grey venflon should already be sited in addition to IVI access

Take blood for FBC group, clotting and G & S

If HB less than 9g/dl inform duty registrar and cross match 2 units blood

Active management of the third stage of labour using an oxytocic drug and CCT (reduces PPH risk, NICE 2017)

CALL for MEDICAL HELP – 2222Inform consultant obstetrician & anaesthetist

Inform haematology consultant

Appoint a scribe to record even

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19
Q

What should be done during resuscitation for DIC?

A

IV access 2 x 16 gauge cannulae

Oxygen 10-15 L by mask with reservoir

Elevate legs

Take blood for:FBC, cross match, clotting screen (fibrinogen, APPT) U & Es AND monitoring

Insert indwelling catheter with measuring chamber (30-60 mls per hr)

Monitor fluid intake and output

Monitor pulse, BP, Resps, Temp and Oxygen saturation

Consider CV

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20
Q

List the different types of fluid replacements

A

Crystalloid : e.g. Hartmann’s

Colloid: e.g. Gelofusin until blood available

Blood

Fresh frozen plasma

Cryoprecipitate

Platelet concentrate

Packed cell

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21
Q

Name the steps used to identify and treat the cause of DIC

A

Remove the trigger

Empty the uterus, bimanual compression of the uterus

Repair any tears/episiotomy

Improve uterine tone

Administer uterotonic medication:Oxytocic e.g. syntometrine/ergometrine

Syntocinon 40 IU in 500 mls N/S 125 mls/h

Carboprost (Haemabate) 250 mcg IM

Misoprostol 800 mcg PR

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22
Q

What can be done medically and surgically to treat DIC?

A

Examination under anaesthetic if stable.

Improve tone as mentioned

Uterine compression with B-Lynch suture

Arterial ligation

Hysterectomy – rare if women has severe DIC and already collapsed and compromised

Radial arterial embolisation to control bleeding

Management in HDU

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23
Q

Are there anymore ways of managing DIC?

A

Repeat and check coagulation screen

Evacuation of uterus if RPC

Close liaison with haematologist and blood bank

All blood loss measured and clearly documented

Postnatal observations – HDU 1-1 care

Attention/observations of all wound and cannulation sites for signs of bleeding

Assist mother when well to NNU/SCBU

Obstetric postnatal review – debrief – counselling for future pregnancies – risk factors

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24
Q

Name three inherited haematological diseases

A
  • Von Willebrands Disease (coagulation factor disorder)
  • Factor V leiden disease (thrombophilia)
  • Haemophilia (disease of males but pregnant women may be a carrier)
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25
Q

What is Von Willibrand’s disease?

A

a familial inherited haematological bleeding disorder in pregnancy which is characterised by either a defect or deficiency of the clotting factor V111.

Usually identified in young adults – menorrhagia, bleeding after dental extraction, bruising, nose bleed

26
Q

There are 5 types of Von Willibrand’s disease

True of false?

A

False

there are only three

  1. 75% women quantitative deficiency of VWF (least severe)
  2. 20% women qualitative deficiency
  3. 5% women –severe almost complete deficiency of VWF
27
Q

What type of screening tests could u do for the Von Willibrand disease?

A

FBC

Serum ferritin (iron levels)

Clotting screen PT (normal) activated partial thromboplastin time prolonged

Bleeding time – usually prolonged, normal in mild cases

Platelet aggregation test – measures platelet efficiency

Von Willebrand factor antigen and factor V11

28
Q

How can VWF be managed?

A

Early identification and screening

Observe levels of VWF and factor V111 in mild cases normalise in third trimester

First trimester risk of bleeding – consider risk factors – APH

Regular monitoring of platelet count and bleeding time

Blood taken for group and save x match 2 units

Alert for APH and PPH in labour

Epidural contraindicated in type 3

Prompt removal of cannula following delivery to reduce risk of bleeding

Active management of third stage and complete place

29
Q

How would you manage VWF?

A

Postpartum - fall in VWF and V111 in first 24 hrs – 22% risk of primary PPH

25% risk of secondary risk of PPH > 5 weeks postpartum

Vigilant postnatal observations (MEOWS)

Daily check of neonate for bleeding – cord stump

Avoid neonatal circumcision – check with haematologist

Care with heel prick for Guthrie test – local pressure for 5 mins.

Check for bruising / intracranial bleeding/cephalhaematoa

Neonatal blood screening

30
Q

What is Hemophilia?

A

Hemophillia, also known as factor V111 is a genetic disorder, caused by missing or defective V111 which is a clottting protein.

31
Q

What is Thrombophilia?

A

A disorder of the haemostatic system which results in an increased risk of thrombosis (increased blood clotting)

32
Q

Factor V Leiden (FVL), Inherited or Acquired?

A

Inherited

33
Q

Prothrombin 20210, Inhertited or Acquired?

A

Inherited

34
Q

Antiphospholipid syndrome is inherited, true or false?

A

False it is Acquired

35
Q

Protein C deficiency, Inherited or Acquired?

A

Inherited

36
Q

Protein S deficiency, Inherited or Acquired?

A

Inherited

37
Q

Antithrombin deficiency, Inherited or Acquired?

A

Inherited

38
Q

Sophie suffers from antiphospholipid syndrome, which is a type of thrombopilia, what are considered as complications that Sophie may experience?

A

Venous Thromoembolism
Placental Abruption
Pre-eclampsia
Poor fetal growth

39
Q

Sophie suffers from antiphospholipid syndrome, which is a type of thrombopilia, what methods of management to help Sophie

A

Assessment of risk (VTE score)

Consultant led care - Management with multi-disciplinary team including haematologist

Known condition – anticoagulation Warfarin , non-pregnant, LMWH in pregnancy.

Women taught self-injection technique

TED stockings

Management and care as for PE and DVT

40
Q

What is VTE?

A

VTE is Venous Thromboebolism, this is a condition that includeds DVT or PE and it invloves blood clotting, in particular areas of the body.

41
Q

How many maternal deaths during 2013-2015 were caused by VTE with ref?

A

26 Maternal Deaths

MBRRACE,2017

42
Q

In maternity PE, is a type of exercise True or false?

A

False Its pulmonary Embolism YOU CHICKEN

43
Q

Within the MMBRACE how many maternal deaths occured during 2009-2013 from VTE?

A

64 Maternal deaths

44
Q

Within the MMBRACE how many maternal deaths occured during pregnancy from VTE?

A

48 deaths

45
Q

Within the MMBRACE how many maternal deaths occured antenatally from VTE?

A

50% of deaths

46
Q

Within the MMBRACE how many maternal deaths occured postnatal from VTE?

A

50% postnatal deaths delivered by CS section

47
Q

Within the MMBRACE how many maternal deaths occured with no risk factors from VTE?

A

17% deaths

48
Q

Within the MMBRACE how many maternal deaths occured from VTE? Where the women were obese?

A

53% were obese

49
Q

List the 9 types of people, that are at higher risk of VTE?

A
  • Thrombophilia
  • Previous VTE
  • Obesity
  • Smoking
  • Surgery
  • Immobility
  • Dehydration
  • (pregnancy increases risk of a VTE 10 fold and up to 25 fold in the puerperium (Robson & Waugh, 2013)
50
Q

What is DVT?

A

DVT, Deep Vein Thrombosis

DVT is a blood clot in one of the deep veins in the leg (usually in the left leg in pregnant women)

51
Q

Why are pregnant women more susceptible to developing DVT?

A
  1. Reduction of blood flow
  2. Hypercoagulability
  3. Abnormalities/damage to the vessel
52
Q

what do the RCOG Green-top Guidelines 37a (2015) suggests in regards to the assessment of VTE?

A

•All women should have Risk assessment for venous thrombosis (VTE) undertaken at booking and repeated at any hospital admission, intrapartum or immediately postpartum and before discharge from hospital

53
Q

What should be given to women who have an increased risk of VTE?

A

May require prophylactic LMWH (e.g. fragmin, clexane), TED stockings in AN period, and/or PN period

54
Q

Name the symptoms of DVT?

A

PAIN

Unilateral swelling (occasionally bilateral)

Redness or discolouration

Difficulty weight bearing on the affected leg

Low grade pyrexia

Occasionally lower abdo pain

55
Q

How would you diagnose DVT?

A
  • If a DVT is suspected through observation then urgent referral needed
  • Doppler ultrasound recommended
  • D-dimer testing not recommended by RCOG ( D-dimers are breakdown products of fibrin found in the blood)
56
Q

How can DVT be treated?

A
  • IV heparin regime should be commenced as soon as possible
  • Pain relief
  • MEOWS
  • Compression (TED) stockings
  • Avoid dehydration
  • LMWH regime (warfarin is not recommended in pregnancy)- dosage dependent on weight
  • Avoid air travel
57
Q

What is PE?

A

Pulmonary Embolism .A PE is a clot that has formed in the pulmonary circulation, usually from a clot that was a DVT and has travelled through the circulatory system

58
Q

What is the symptoms of PE?

A

Chest Pain

Shortness of breath

Cough with blood

59
Q

How is PE diagnosed and treated?

A
  • If DVT already diagnosed then presumptive diagnosis can be made with symptoms
  • If not diagnosis by CXR or VQ scan

Treatment:-

  • Urgent referral
  • IV heparin
  • Then LMWH thromboprophylaxis
  • See local Trust policy
60
Q

What intrapartum care would u give to an VTE?

A
  • If an A/N VTE then women will be taught to self inject LMWH as outpatient once stabilised
  • Before labour starts LMWH must be stopped
  • If spontaneous labour women should stop administration as soon as possible
  • If elective IOL, LMWH should be stopped 24 hours before
  • Epidural/spinal anaesthetic to be discussed with senior anaesthetist and Should not be administered within 24 hours of last dose of LMWH
  • MEOWS and close monitoring
  • After delivery recommence LMWH (BD)
61
Q

What puerperium care would u give to an VTE?

A
  • Thromboprophylaxis should continue for at least 6 weeks postnatal until at least 3 months of anticoagulant therapy has been given
  • Can be offered LMWH or warfarin(If commence warfarin will need INR tests)
  • TEDs should continue to be worn on the affected leg for up to 2 years after the event
  • Prescriptions for the entire postnatal course of LMWH should be issued in secondary care.
  • This will help ensure that women receive the full course without the need to visit their GP to obtain another prescription.
  • This also provides a double safety net since the prescription will be checked by a hospital pharmacist, who ensures the correct weight-appropriate dose is dispensed

Midwifery emergencies (8 decks)

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