2021 March - RA in Bleeding risk, ICS, Liver Failure

Question 1

Conclusion

Answer 1

Vertebral canal haematoma is a rare but potentially catastrophic complication of CNB. Both the AoA and the more recent ASRA guidelines provide excellent advice on safe intervals for the performance of CNB. Differences in some time intervals between these guidelines are relatively minor. There are a number of groups of patients in whom extra care is warranted. There remains no definitive guidance on safe intervals for the performance of PNBs, although the existing guidelines set out a number of useful principles to help direct practice.

Question 2

Key pts

Answer 2

Vertebral canal haematoma is a rare, potentially devastating complication of neuraxial anaesthesia. The risk is higher in patients who are anticoagulated.
*
Major bleeding in peripheral nerve blocks can also have serious sequelae.
*
Guidelines set out recommended time intervals between stopping anticoagulants and performing neuraxial anaesthesia.
*
These guidelines and a recent expert consensus opinion describe the principles underlying risk/benefit decisions in peripheral nerve blocks in anticoagulated patients.
*
Separate guidance exists for patients with acute hip fractures, patients who are pregnant, and patients with chronic pain.

Question 3

Drug gudiance antiplts
ASRA / AOA

Time to be held
Time for next dose

Answer 3

Clopidogrel 5–7 days
Immediately (loading dose: 6 h)

Ticagrelor 5–7 day
Immediately (loading dose: 6 h)

Prasugrel 7–10 days
Immediately (loading dose: 6 h)

Abciximab 24–48 h
No specific guidance

Question 4

Time intervals before and after neuraxial blocks for anticoagulant agents

UFH s.c.

________________

LMWH

Answer 4

UFH i.v.
if >4 days UFH: perform platelet count in addition to the following guidance before CNB:

4–6 h and normal coagulation status

1h
__________________________

If >4 days LMWH: perform platelet count in addition to the following guidance before CNB:

Prophylactic dose: 12 h
resume 4h

Treatment dose: 24 h and consider anti-factor Xa level
24h
48–72 h after high-bleeding-risk surgery; catheters should be removed at least 24 h after needle/catheter

Question 5

Fondaparinux

Answer 5

Only where: single-needle pass, atraumatic needle placement, avoidance of indwelling neuraxial catheters

Prophylactic dose: 36–42 h (consider anti-Xa levels)

6 h

Question 6

Rivaroxaban

Answer 6

72 h; if earlier, consider rivaroxaban or anti-factor Xa level (safe residual level for CNB is unknown)
6 h

Question 7

Apixaban

Answer 7

72 h; if earlier, consider apixaban or anti-factor Xa level (safe residual level for CNB is unknown)
6 h

Question 8

Dabigatran

Answer 8

120 h; if no additional risk factors for bleeding (e.g. age >65 yrs, hypertension and concomitant antiplatelet medications):
6 h

Question 9

Warfarin

Answer 9

Ideally stop INR 5 days before and INR ‘normalise

After catheter removal, suggest continuing neurological observations for 24 h

Question 10

Thrombolytic drugs

Answer 10

(e.g. alteplase and streptokinase) 48 h and documented normal clotting (including fibrinogen)

No recommendation, but note that original contraindications to these drugs state should not be given for 10 days after puncture of non-compressible vessels

Question 11

Thrombolytic drugs

Answer 11

(e.g. alteplase and streptokinase) 48 h and documented normal clotting (including fibrinogen)

No recommendation, but note that original contraindications to these drugs state should not be given for 10 days after puncture of non-compressible vessels

Question 12

PNB techniques

Answer 12

Overall, practitioners considering PNB techniques in patients who are anticoagulated will need to consider the likelihood and consequences of haemorrhagic complications and the compressibility of the site. These risks will also need to be weighed against the risks of stopping the patient’s anticoagulation medication in elective cases and the risks of GA in the particular patient in both elective and emergency cases.

Question 13

Intraop Cell Salvage ICS

Key pts

Answer 13

• Intraoperative cell salvage may be preferable to donor transfusion in the operative setting.

*Consider ICS in cases where estimated blood loss may exceed 500 ml.

• ICS delivers a product containing red cells suspended in saline. Platelets and coagulation factors are removed.
• Neither sepsis nor malignancy are absolute contraindications to ICS.
• Controversies exist regarding the use of ICS in obstetrics and for patients with haemoglobinopathies.

Question 14

Indications

Answer 14

Anticipated blood loss of >500 ml or >10% of estimated blood volume

Patients with low haemoglobin or increased risk factors for bleeding

Patients with multiple antibodies or rare blood groups

Those patients who refuse donor blood products for ethical or religious viewsa or through choice should be considered for ICS when undergoing surgery where blood loss is anticipated.

ICS should be standard equipment for patients experiencing operative massive haemorrhage

Question 15

Contraindications – absolute
ICS

Answer 15

Lack of trained staff to collect or process the aspiratePatient refusal

Question 16

Benefits ICS

Answer 16

1 Avoiding or minimizing allogeneic transfusion

a costs and

b risks
(eg, transfusion reactions, transfusion-transmitted infections

2 Patients who will not accept allogeneic blood –

(i) some Jehovah’s Witnesses
Continuously connected to the patient via intravenous tubing.

ii rare blood type or multiple RBC alloantibodies when crossmatch-compatible blood cannot readily be obtained

3 Increasing number of available units compared with other autologous blood conservation techniques
larger amounts of blood than intraoperative hemodilution, which generally only provides 1 to 3 units of autologous blood

4 Time saving

5 no restrictive transfusion triggers associated with blood management principles,

6 the superior oxygen delivery compared with donor blood

7 ICS offers many financial and healthcare resource benefits, particularly when used with other aspects of PBM.

8 morbidity resulting from reduced oxygen delivery and TRIM-related infection

Question 17

collection, processing, and reinfusion

Answer 17

collection, processing, and reinfusion

Collection
Collection is performed by the surgical team, with the aim of reclaiming the optimal amount of viable red cells and avoiding collection of contaminants or cellular material

wab washings can be used when swabs are expected to collect a significant amount of blood.
normal saline combined with unfractionated heparin

Processing
Processing involves separating the cells through the centrifugation process and then washing them ready for reinfusion.
Separation
There are three systems in existence for the separation process.

Fixed bowl system
Variable volume disk system

Washing
The washing process occurs after separation and the removal of a high proportion of contaminants and other particulate material. The red cell concentrate is washed in normal saline

Reinfusion
Reinfusion should take place within 6 hours of the first collection, in order to protect red cell function and optimise the circulating volume

Monitoring should be similar to that of the intraoperative environment and the attending staff able to detect and treat complications such as reinfusion hypotension

ot be given under pressure as it risks air embolism and bag rupture.

Leucocyte depletion filters (LDFs) are used commonly in cancer surgery and cases where there is concern over heavy bacterial contamination.
Reinfusion hypotension is a well-recognised complication which may be profound when LDFs are used.

Question 18

Disadvantages

Answer 18

Coagulation defects

Transfusion-associated circulatory/volume overload

Infection

Air embolism

Embolism of microaggregates or fat

Training and staff

reinfusion hypotension
?? bradykinin release and acute hypocalcaemia

Major haemorrhage - time

Question 19

Special circumstance

Cancer

Sepsis

Haemoglobinopathies

Answer 19

f the salvaged blood is not required for cardiovascular stability or would not leave the patient requiring a donor transfusion, it may be prudent not to reinfuse.

Sepsis
may be possible that prophylactic broad-spectrum antibiotics contribute to limiting perioperative sepsis when ICS is used, as significant concentrations of bacteria have been isolated from ICS products, but do not appear to result in bacteraemic complications

Hb pathy
This is because of red cell fragility, and the potential for haemolysis or haemoglobin precipitation;
Exchange transfusion before surgery can reduce the percentage of sickle cells and thus reduce the incidence of perioperative sickle crisis. If a patient has undergone exchange transfusion, then there may be benefit in considering ICS during surgery. Such complex decisions should be made on an individual patient basis, after discussion with the regional sickle cell haematology service.

Question 20

Practice

Answer 20

Obs

The current recommendation from the AoA is that ICS should be used in the ‘collect only’ mode for patients who are identified as having anaemia before surgery. In women who have declined donor blood transfusion or in whom significant blood loss is likely to occur, the risks and benefits of ICS should be weighed and discussed and decisions made on a case-by-case basis.

However, the SALVO trial did not find any statistically significant reduction in the number of donor blood transfusions when ICS was used.

this conclusion by not recommending its routine use in elective or emergency section

Question 21

Trauma

Answer 21

In major trauma centres ICS should be available out-of-hours in the emergency operating theatre, with the greatest benefit being in thoracic, abdominal, and pelvic penetrating trauma.

S has shown significant reduction in the need for donor blood transfusion in orthopaedic surgery, particularly for major pelvic and spinal procedures, major trauma, and major joint revision

Paused during bone cement

Question 22

Cardiac

ICS

Answer 22

Cardiothoracic and vascular surgery
Major blood loss during cardiac surgery is relatively common and the risk is increased because of the coagulopathy and platelet dysfunction that results from cardiac bypass.

However, the routine use of ICS in cardiac surgery has demonstrated a decrease in allogeneic blood transfusion by up to 40% and its use is recommended for all cardiac surgery

restricted to blood loss before and after bypass, as there is evidence that using ICS during bypass instead of direct suction into the cardiotomy reservoir results in a depletion of clotting factors and platelets leading to increased coagulopathy

Question 23

ICS

Safety

Answer 23

Tranexamic acid
Tranexamic acid appears to be useful in reducing operative blood loss as a result of hyperfibrinolysis. NICE advocates the use of tranexamic acid in all cases where ICS is to be used and should be used, unless specific contraindications are identified.

Viral transmission
The need for universal precautions against blood-borne virus transmission should be self-evident and appropriate personal protective equipment should be used in all cases.
.

Reinfusion hypotension
Reinfusion hypotension can result in a rapid and significant decrease in BP. If reinfusion hypotension occurs:
(i)
temporarily stop the reinfusion
(ii)
exclude other causes of hypotension (for example hypovolaemia, drug reactions, embolic events)
(iii)
use standard supportive measures to rectify hypotension (increasing preload, using vasoactive drugs)
(iv)
consider restarting reinfusion at a slower rate.

Question 24

ALF Key points

Answer 24

1 Acute liver failure (ALF) is a rare but severe life-threatening emergency that warrants a multidisciplinary approach and early referral to a liver transplantation centre.
*

2 Liver transplantation has significantly improved outcomes from ALF.
*
3 Transplant-free survival, particularly for ALF caused by paracetamol overdose, has also improved as a result of better organ system support measures.
*
4 The leading causes of ALF globally are hepatitis B and E, whereas in the UK paracetamol-induced liver injury is the predominant aetiology.
*
5 The incidence of intracranial hypertension (ICH) has been continuously decreasing over the years and it is no longer the leading cause of mortality in patients with ALF.

Question 25

Aetiology ALF

Answer 25

1. Viral
   dev world
   Hep B E
2. DILI
   Developed
   -Paracetamol - 70%
   restriction 43% reduction

Subclassified Onset jaundice
development of Hepatic encephalopathy - HE

Hyperacute
Acute
Subacute

Question 26

Hyperacute

Answer 26

<7d
Drug / Toxin
Viral
Preg related
Vascular
Other

Question 27

Acute

Answer 27

8-28d
Drug / Toxin
Viral
Preg related
Vascular
Other

Question 28

Subacute

Answer 28

28-12 weeks
Drug / Toxin
Seroneg hepatitis
Vascular
Other

Question 29

Drugs

Answer 29

1. paracetamol
2. ctx
3. statin
4. Carbamazepine
5. Fluclox
6. TB drugs
7. Ectasy

Question 30

Preg

Vascular

Other

Answer 30

PET HELLP Fatty liver preg

Hypoxic hpeatitis
Budd chiari

Wilsons
Malgi
AI
HLH
Heat stroke

Question 31

Pathophys

Answer 31

direct hepatocyte damage, necrotic or apoptotic cell damage, and the development of an immune response that is mediated through activated monocytes, macrophages, dendritic, cells and natural killer T cells.

This results in a strong inflammatory response, both locally within the liver and systemically.

Systemic inflammation contributes to the development of extrahepatic manifestations and multiple organ dysfunction syndrome (MODS)..

Hepatic encephalopathy, a hallmark feature of ALF, is characterised by altered cerebral blood flow and dysregulated cerebral autoregulation
progression to cerebral oedema and ICH is not completely understood and is likely to involve a complex interplay between systemic inflammation, circulating neurotoxins (ammonia in particular), and osmolar derangements

Question 32

Hepatic Encephalopathy grade

Answer 32

HE is graded and should be clearly documented for all patients:
*
Grade I: mild confusion, decreased attention, irritability
*
Grade II: disorientation, drowsiness, inappropriate behaviour
*
Grade III: somnolent but rousable, incoherent
*
Grade IV: coma

Question 33

Dx

Answer 33

Diagnosis

Patients present with a range of symptoms including non-specific features of nausea,
vomiting,
lethargy,
abdominal pain,
and feeling generally unwell

Question 34

Ix

Answer 34

Intrahepatic
Aspartate aminotransferase
Alanine transaminase
Alkaline phosphatase

Liver function test
Gamma glutamyl transferase
Bilirubin
Albumin

Severity and presence of hepatocellular and cholestatic injury

Coagulation
INR/prothrombin time
Synthetic marker of liver function

Arterial blood gas
Lactate
Lactate chiefly metabolised by liver and concentrations are increased in liver damage

Biochemistry
Electrolytes; sodium, potassium, chloride, bicarbonate, calcium, magnesium, phosphate
Glucose
Urea/creatinine
Lactate dehydrogenase

Assessment of AKI and another organ dysfunction. General metabolic derangements common in ALF

Haematology
Full blood count
Anaemia, thrombocytopenia, bleeding, concurrent infection

Question 34

Ix

Answer 34

Intrahepatic
Aspartate aminotransferase
Alanine transaminase
Alkaline phosphatase

Liver function test
Gamma glutamyl transferase
Bilirubin
Albumin

Severity and presence of hepatocellular and cholestatic injury

Coagulation
INR/prothrombin time
Synthetic marker of liver function

Arterial blood gas
Lactate
Lactate chiefly metabolised by liver and concentrations are increased in liver damage

Biochemistry
Electrolytes; sodium, potassium, chloride, bicarbonate, calcium, magnesium, phosphate
Glucose
Urea/creatinine
Lactate dehydrogenase

Assessment of AKI and another organ dysfunction. General metabolic derangements common in ALF

Haematology
Full blood count
Anaemia, thrombocytopenia, bleeding, concurrent infection

Question 35

Causative agent

Answer 35

Serological

Hepatitis A, B, C, and E, Epstein–Barr virus, herpes simplex virus, varicella zoster virus and HIV 1 and 2 Viral causes

Antinuclear antibodies
Autoimmune hepatitis

Anti-smooth muscle antibodies
Autoimmune hepatitis

Question 36

Referall to specialist

Answer 36

Thresholds for referral vary but generally include an

INR >3.0, or prothrombin time (PT) >50 s or increasing;

HE;

hyperlactataemia or hypotension despite resuscitation;

pH <7.35;

acute kidney injury (AKI);

bilirubin >300 μmol L−1;

and shrinking liver volume on imaging.

Question 37

Management

Answer 37

A/B

Early elective tracheal intubation of patients with higher grades of HE (III/IV) is recommended for airway protection especially if being transferred.

Standard airway strategies to minimise increases in ICP should be used during the intubation process

tandard bundles to avoid ventilator associated pneumonia should be strictly adhered to as these patients are at a greater risk of developing infections

Circulation

ALF have profoundly reduced systemic vascular resistance presenting with vasodilatory shock, high cardiac output state, and a clinical picture similar to that seen in SIRS or sepsis.
restore circulating volume and enhance oxygen delivery to tissue by targeting a MAP >65 mmHg

MAP of 80 mmHg should be targeted if there are signs of raised ICP and for patients with uncontrolled chronic hypertension.

Fluid management should be directed by cardiac output monitoring

Noradrenaline (norepinephrine) is recommended as first-line agent for vasopressor support.1 Terlipressin, a commonly used splanchnic vasoconstrictor in patients with cirrhosis, has been implicated in potentially worsening ICP and is not widely used in ALF

Cortisol deficiency is common in ALF and the degree of deficiency correlates with disease severity.

Question 38

Management

Answer 38

A/B

Early elective tracheal intubation of patients with higher grades of HE (III/IV) is recommended for airway protection especially if being transferred.

Standard airway strategies to minimise increases in ICP should be used during the intubation process

tandard bundles to avoid ventilator associated pneumonia should be strictly adhered to as these patients are at a greater risk of developing infections

Circulation

ALF have profoundly reduced systemic vascular resistance presenting with vasodilatory shock, high cardiac output state, and a clinical picture similar to that seen in SIRS or sepsis.
restore circulating volume and enhance oxygen delivery to tissue by targeting a MAP >65 mmHg

MAP of 80 mmHg should be targeted if there are signs of raised ICP and for patients with uncontrolled chronic hypertension.

Fluid management should be directed by cardiac output monitoring

Noradrenaline (norepinephrine) is recommended as first-line agent for vasopressor support.1 Terlipressin, a commonly used splanchnic vasoconstrictor in patients with cirrhosis, has been implicated in potentially worsening ICP and is not widely used in ALF

Cortisol deficiency is common in ALF and the degree of deficiency correlates with disease severity.

Question 39

Renal

Answer 39

Renal
Acute kidney injury occurs in 40–85% of patients with ALF. The incidence is higher in ALF secondary to paracetamol poisoning because of direct paracetamol-mediated tubular toxicity.
]
Rf factors for developing AKI include older age, paracetamol-induced ALF, hypotension, SIRS, and infections.

arly initiation of renal replacement therapy (RRT) is advised for renal support but also for non-renal indications including hyperammonaemia (ammonia concentrations >150 μmol L−1), sodium imbalances, temperature, and metabolic control

RT is preferred to prevent cerebral complications related to fluid shifts. Refractory hyperammonaemia has been shown to respond to higher intensity ultrafiltration

frequent clotting of circuits, and therefore despite coagulopathy most patients will require anticoagulation. Unfractionated heparin, prostacyclin, or both are the most common options.

Regional citrate anticoagulation is generally avoided because of the diminished ability of the liver to metabolise the citrate load

Question 40

CNS

Answer 40

Central nervous system

Intracranial hypertension as a result of cerebral oedema is a major concern in patients with ALF, with a mortality of 55%.

However, the incidence of ICH in the UK has

pathophysiology, pre-emptive institution of targeted cerebral care, and improved organ supportdecreased
from 76% in the 1980s to 19.8

lead to astrocyte swelling, mitochondrial dysfunction, and cerebral oedema, and correlate with the development of raised ICP and HE

Abnormal pupillary responses, spasticity, extensor posturing, and Cushing’s reflex are all late signs of raised ICP.

The management and prevention of raised ICP includes reducing cerebral oxygen consumption through adequate sedation, maintaining normocapnia and normoglycaemia, minimising venous congestion through 30° head elevation and loosening endotracheal ties, and avoiding hyperthermia. Serum sodium should be maintained between 145 and 150 mmol L−

1 using boluses or a continuous infusion of sodium chloride 30% if needed.1,9 RRT should be initiated early with the aim of keeping the serum ammonia <100 μmol

with a bolus of hypertonic saline (200 ml 3% or 20 ml of 30%) or rarely mannitol

Question 41

Coagulation ALF

Answer 41

Coagulation
Acute liver failure often presents with deranged INR/PT, thrombocytopenia, and reduced circulating pro- and anticoagulant proteins and fibrinogen concentrations

Reduced synthesis of procoagulant clotting factors by the diseased liver is compensated by a simultaneous reduction of natural anticoagulants

This collectively leads to a state of rebalanced haemostasis.

OC testing is therefore recommended, as standard laboratory measurements of coagulation such as INR measurements may fail to reveal the true haemostatic state

Routine correction of INR/PT should be avoided as these are important markers of synthetic liver function. Platelets and fibrinogen are more sensitive indicators of bleeding risk and should be corrected as required

For insertion of intravascular catheters, a platelet count of >30×109 L−1 and a fibrinogen concentration of >1–1.5 g L−1 are generally adequate

Question 42

Sepsis

Answer 42

Acute liver failure is associated with an immune dysfunction leading to altered macrophage and neutrophil function, reduction in complement and impaired phagocytosis, and opsonisation.

Prophylactic use of antibiotics and antifungals does not have an impact on survival outcome but does reduce the incidence of sepsis and HE, and is therefore recommended.1,9 This is particularly important for those listed for super urgent liver transplants as development of infections may lead to delisting.1

Question 43

Metabolic and nutrition ALF

Answer 43

Metabolic and nutrition
Hypoglycaemia is frequently present in patients with ALF and is associated with increased mortality. The clinical presentation is often similar to that of HE, and therefore blood glucose should be monitored regularly. Prompt treatment should be provided in the form of i.v. low volume, high concentration glucose solutions, avoiding infusion of large volume of hypotonic solutions, which could worsen cerebral oedema and hyponatraemia

Acute liver failure leads to increased energy expenditure and protein catabolism; early initiation of nutritional support is necessary. Enteral feeding is often the preferred route with a daily calorie target of 25–30 kcal kg−1 day

Question 44

Spec Tx

Answer 44

N-acetyl cysteine

There is strong evidence for the early use of N-acetyl cysteine (NAC) in patients with established paracetamol overdose.1 It provides cysteine, which is a glutathione precursor. This neutralises N-acetyl-p-benzoquinone imine (NAPQI), which is responsible for hepatocyte toxicity. In 2012 the UK’s Commission on Human Medicine (CHM) offered simpler guidelines with a single nomogram treatment line (patient risk stratification no longer required) resulting in greater treatment consistency among different centres.

AIH and steroids
Autoimmune hepatitis is a hepatic necrotic-inflammatory condition that often presents chronically, but approximately 20% of cases present as ALF with extensive necrosis.24 The diagnosis is often challenging, and a significant proportion of patients will require a LT. If diagnosis is suspected, early referral to a specialist centre is crucial for a diagnostic biopsy and potential steroid therapy.

Question 45

ALF and Liver tplx

Answer 45

Liver transplantation
Liver transplantation has been a significant leap in the management of ALF with dramatic effects on survival outcomes. Ten percent of all liver transplants are performed for ALF, and the 5 yr survival of these patients in the UK is 82%

ALF caused by paracetamol toxicity
pH <7.25 (after 24 h of fluid resuscitation)Lactate >3.0 mmol L−1 (after 24 h of fluid resuscitation)

All of the following:
*
Prothrombin time >100 s (INR >6.5)
*
Creatinine >300 μmol L−1
*
Grade III or IV HE

_____________________________

ALF not caused by paracetamol toxicity

Prothrombin time >100 s (INR > 6.5)

Any three of the following:
*
Age <10 or >40 yr
*
Seronegative or drug-induced ALF
*
Jaundice to encephalopathy >7 days
*
Prothrombin time >50 s (INR >3.5)
*
Bilirubin >300 μmol L

Question 46

VTE in pregnancy

Answer 46

Venous thromboembolism is the leading cause of direct maternal death in the UK.
*

Pregnancy itself is an independent risk factor for venous thromboembolism and can increase the risk by four to five times.
*

Signs and symptoms may be non-specific and often mimic normal symptoms of pregnancy.
*

Risk assessment tools are useful in the prevention of venous thromboembolism, and risk must be reassessed at each admission.
*

Anticoagulation with low molecular weight heparin is the treatment of choice, although caution must be exercised around its timing and delivery.

Question 47

Obs risk accesment

High

Inter

Low

Answer 47

High ——————> requires antenatal prophylaxis - r/f
Previous VTE
(except related to surgery)

Inter

1 Hospital admission

2 Single previous VTE - Maj surgery

3 Med comorbs
Ca
Hfail
SLE iBd

4. OHSS

5.

Question 48

Obs risk accesment

High

Inter

Low

Answer 48

High ——————> requires antenatal prophylaxis - r/f
Previous VTE
(except related to surgery)

Inter —————-> Consider prophylaxis w/ LMWH

1 Hospital admission

2 Single previous VTE - Maj surgery

3 Med comorbs
Ca
Hfail
SLE iBd

4. OHSS
5. Surgical procedure

4=> RF: —-> First trimester
3 - prophylaxis 28/40

Obestiy >30

Age>35

Parity 3+

Smoker

VV

PET

Imoobbility

fh unprovoked dvt - 1st degree relative

Low risj thrmbophilia

Multiple preg

IVF

<3 - mobilise and avoid dehydration

Question 49

Postnatal assessment

Answer 49

High risk————-> Min 6/52 prophylaxis:

Any previous VTE

Anyone require antenatal

High risk thrombophilia

Low risk thrombophilia + Fhx

Inter risk ———–> Min 10/7 prophylaxis

Csection in labour

bmi >30

Readmission or prolonged admission

any surgical procedure

Medical comorbs

Other rf

Question 50

Inx VTE preg

Answer 50

VTE is suspected clinically and delivery is not imminent, then treatment with low molecular weight heparin (LMWH) should be commenced immediately, before investigations are carried out to confirm or exclude the diagnosis.

basic investigations including an ECG and a chest X-ray.6 Routine measurement of D-dimer not recommended

A compression duplex ultrasound scan should be performed if a woman presents with a suspected PE and also has signs and symptoms of DVT. If a DVT is confirmed, treatment for DVT should continue and further investigation is unnecessary.

Local guidelines, radiology availability, and clinician or patient preferences will dictate whether a V˙/Q˙ scan or a CTPA are performed

clinical suspicion of PE, CTPA should be performed in preference to a V˙/Q˙ sca

Question 51

Rx

Answer 51

Signs or symptoms suggestive of VTE should be discussed with a senior clinician and commenced on anticoagulation until a diagnosis of VTE is excluded

LMWH is the treatment of choice in acute VTE unless there is a clinical suspicion that labour or delivery may occur within the next 24 h or if the patient is acutely ill

unfractionated heparin (UFH) may be more appropriate, as its effect can be reversed more easily using protamine

LMWH, the booking weight of the patient is used.

Question 52

Dosing

Answer 52

Enoxaparin

<50
20 mg once daily

50-90
40 mg once daily

90-130
60 mg once dailya

130-170
80 mg once dailya

> 170
0.6 mg kg−1 once dailya

Question 53

Tinzaparin

Answer 53

175 units kg−1 once dail

Question 54

Monitoring and maintenance of treatment

Answer 54

Therapeutic s.c. LMWH should continue for the rest of the pregnancy and usually no additional blood test monitoring is required. However, patients at the extremes of weight or those with recurrent VTE, antithrombin deficiency, or renal disease may require dosage adjustment and monitoring of anti-Xa concentrations.

Question 55

Prevention

Answer 55

n general, all women should be encouraged to mobilise and avoid dehydration throughout pregnancy and the puerperium. For those in whom antenatal thromboprophylaxis is indicated, it should begin as early as practical. Thromboprophylaxis can be mechanical or pharmacological. Mechanical thromboprophylaxis in the form of graduated compression stockings should be used for all hospitalised pregnant women with contraindications to LMWH, and for some high-risk inpatients in conjunction with LMWH.

Question 56

Anticoagulation and implications for neuraxial block

Answer 56

The most feared complication when performing neuraxial anaesthesia in the setting of anticoagulation is the complication of vertebral canal haematoma.

his can result in paralysis if not diagnosed and treated within 12 h. The third National Audit Project reported the incidence of vertebral canal haematoma causing permanent harm to be very rare at one in 140,
000

Most women should be advised to discontinue their LMWH as soon as labour commences and further dosing should be prescribed by medical staff after assessment

n the outpatient setting they suggest switching from LMWH to low-dose UFH 5,000 units s.c. twice daily, at 36 weeks of gestation or earlie

Question 56

Anticoagulation and implications for neuraxial block

Answer 56

The most feared complication when performing neuraxial anaesthesia in the setting of anticoagulation is the complication of vertebral canal haematoma.

his can result in paralysis if not diagnosed and treated within 12 h. The third National Audit Project reported the incidence of vertebral canal haematoma causing permanent harm to be very rare at one in 140,
000

Most women should be advised to discontinue their LMWH as soon as labour commences and further dosing should be prescribed by medical staff after assessment

n the outpatient setting they suggest switching from LMWH to low-dose UFH 5,000 units s.c. twice daily, at 36 weeks of gestation or earlier

Ongoing monitoring of neurological function, especially in the context of recent anticoagulation, is also very important as early detection is crucial to avoid permanent damage.

Question 57

LMWH—prophylactic dose

Answer 57

LMWH—prophylactic dose
>12 h
6–12 h
<6 h <6 h

Question 58

LMWH—therapeutic dose

Answer 58

> 24 h 12–24 h 6–12 h

Question 59

UFH—

Answer 59

UFH—infusion Stopped >4 h and APTTR≤ 1.4

Answer 60

i) during labour, the anaesthetist should be alerted if a woman is unable to straight-leg raise;

(ii) during the recovery phase after a spinal anaesthetic or epidural top-up for a procedure, straight-leg raising should be used as a screening method to assess motor block. If the woman is unable to straight-leg raise at 4 h from the last dose of epidural/spinal local anaesthetic, the anaesthetist should be called;

(iii) women should be informed of the likely timescale for resolution of their neuraxial block and encouraged to alert staff should this be delayed; and

(iv) each maternity unit should have a guideline or policy in place to guide the escalation of care, depending on local resources and referral pathways’.1

Question 61

Management of massive life-threatening thrombosis in pregnancy

Answer 61

A woman with an acute massive PE in pregnancy or the perinatal period may present in a collapsed or shocked state or in cardiac arrest and will require immediate and urgent care and investigations. A multidisciplinary team comprised of experienced clinicians including consultant obstetrician, consultant anaesthetist, and consultant haematologist should decide on a patient-specific basis whether i.v. UFH or thrombolysis is required. I.V. UFH is the optimal treatment in massive PE with haemodynamic instability because of its speed of onset of action. If thrombolysis is given, there is also the option for dose adjusting UFH therapy. Thrombolysis should be considered in women with life-threatening PE and haemodynamic compromise. I.V. UFH should be commenced promptly after thrombolysis. Once stability is established, UFH can be converted to LMWH. The risk of maternal and fetal bleeding complications is approximately 2–3%, similar to in non-pregnant patients.