37. HIIT Flashcards
You are asked to see a 60-year-old woman on the High Dependency Unit
who is 6 days post-open abdominal aortic aneurysm repair. She is
acutely short of breath and complaining of pain on inspiration. How
would you approach this situation?
ABC approach adding supplemental oxygen to achieve adequate oxygen
saturation.
In the absence of immediate life-threatening conditions, ascertain the
history and examine the patient.
Review the notes and order appropriate investigations such as an arterial
blood gas, FBC, chest X-ray and an ECG.
What is your differential diagnosis?
Pleuritic pain may indicate a
pulmonary embolism,
infarct, infection or effusion.
DVT should be looked for, although it is common to have a PE
without clinical evidence of a DVT.
Cardiac causes would include an
acute coronary syndrome or pulmonary
oedema from ventricular failure.
There may be abdominal pathology such as
viscus perforation or ischaemia
causing acidosis and peritonitis.
ARDS is a possibility.
Pneumothorax
The drug chart shows that the patient has been on LMW heparin
post-operatively as prophylaxis against thromboembolism. The full blood
count is given to you.
Yes. There is thrombocytopaenia and mild anaemia. This patient has been
exposed to, and treated with, heparin, which in combination with a possible PE would make me suspect a diagnosis of heparin-induced thrombocytopaenia syndrome or HIT.
What do you mean by thrombocytopaenia?
Platelet count below the reference range.
It can broadly be defined as an abnormal fall in platelet count as this can be more relevant.
A decline in platelet count of >50% occurring between 4–14 days after
heparin therapy is suspicious of HIT irrespective of the actual value.
What can you tell me about heparin-induced thrombocytopaenia?
HIT is an acquired disorder of hypercoagulability caused by administration
of heparin.
Types 1 + 2
HIT Type I
Clinically less significant.
It is non-immune-mediated platelet aggregation
and occurs in about 10% of patients on heparin.
The platelet count usually stays above 100 and recovers spontaneously
HIT Type II
Underlying process is antibody-mediated platelet activation
resulting in thrombocytopaenia.
There is an associated increase in thrombin generation,
which overall leads to a high-risk of arterial and venous thrombosis
Heparin-induced thrombocytopaenia – thrombotic (HITT) or Type II
Type II – Autoimmune disorder. After heparin administration, an
immune complex can form between heparin and platelet factor 4
(PF4) that is released by platelets. This heparin–PF4 complex is seen as
‘foreign’ and IgG antibodies are formed against the complex. The
heparin/PF4/IgG complexes cross-link and activate platelets.
More PF4 is released (creating a vicious circle of more complexes) and thrombin generation occurs via the clotting cascade.
Paradoxical high risk of thrombosis (with a low platelet count)
‘White clots’ form as they are platelet rich.
50% of patients develop heparin-dependent antibodies
post-cardiopulmonary by-pass (within 5–10 days).
Only a proportion will get platelet activation.
Antibodies seem to be transient and last 40–100 days. Re-exposure to
heparin before that time can cause rapid onset of HIT.
RF For HIT
Likelihood of developing HIT according to heparin type:
bovine lung UFH > porcine intestinal mucosal
UFH > LMWH.
Patient type:
post-surgical > medical > obstetric patient.
Female > male
How does HIT present?
When
The fall in platelet count typically begins 5–10 days after starting a heparin
course, but in about one-third of patients an abrupt fall in platelets occurs
on giving heparin. This group has usually received heparin within the past
100 days and these patients already have clinically significant levels of HIT
antibodies.
Venous thrombosis such as DVT and PE are more common than arterial
thrombosis, although lower limb arterial thromboses are often seen if
looked for
Sx
Skin lesions at heparin injection sites can occur and range from
erythematous plaques to skin necrosis.
A quarter of patients who receive an intravenous heparin bolus in the
presence of circulating HIT antibodies will have an acute systemic reaction, often with fever, chills, respiratory distress and hypertension.
Circulatory collapse and cardio-respiratory arrest have been reported. The
reaction occurs 5–30 minutes following the bolus injection and is
accompanied by a fall in platelets.
Decompensated DIC can occur, but only in about 10% of cases.
NB: Other causes of thrombocytopaenia are common on intensive care –
especially after cardiac surgery, e.g. intra-aortic balloon pumps, sepsis and
haemofiltration.
How is it diagnosed?
HIT is a clinical syndrome. The diagnosis is based on one or more of the
classical clinical features such as:
Thrombosis
Thrombocytopaenia
The systemic reaction
DIC
The ‘4Ts’ scoring system is frequently used to gauge the clinical likelihood of HIT.
Laboratory diagnosis with enzyme-linked immunosorbent assays that look
at platelet activation are sensitive but not specific. Their negative predictive value is high but their positive predictive value is not so good.
For this reason, testing in the absence of a high clinical suspicion (or worse – screening) is not helpful.
4T score
- Thrombocytopaenia
2 - >50% fall / nadir 20-100 - Timing of platelet count fall or other sequelae
2 - 5-10d / <1d if 100d exposure - Thrombosis or other sequelae (e.g. skin lesions
New thrombosis; skin necrosis;
post heparin bolus acute systemic reaction - Other causes for thrombocytopaenia are not evident
No other cause for platelet count fall is evident
Probability of HIT
6–8 = High
4–5 = Intermediate
0–3 = Low
Does it matter which type of heparin you use?
Type II HIT occurs more frequently with unfractionated heparin,
in approximately 1% of all patients treated. .
Approximately 0.1% of patients treated with low-molecular weight heparin will develop HIT.
How would you manage this lady on the HDU if she were diagnosed
with HIT? Do you need to continue her tinzaparin?
- All heparin should be stopped immediately
when the diagnosis of HIT is suspected or confirmed,
including the heparin in pressure-monitoring lines
and intravenous flushes.
The patient was probably on LMWH as prophylaxis against
DVT in the post-operative period and the risk of this occurring
increases once the heparin is stopped.
- There is also a high risk of thrombosis with established HIT
(50% over 30 days if not anticoagulated by other means)
and so immediate substitution with an alternative non-heparin anticoagulant is required. - Platelet transfusions should be avoided – this may ‘fuel the fire’.
