4. PE, DIC, stroke Flashcards

1
Q

3 elements of hemostasis (Virchow)

A
  • Endothelium
  • Platelets
  • Plasma
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2
Q

3 processes of hemostasis

A
  • Primary: thrombocyte aggregation
  • Secondary: coagulation, plasmatic cascade
  • Tertiary: fibrinolysis
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3
Q

2 directions of hemostais

A

Pro/anti or clotting/bleeding

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4
Q

Fibrinogen concentration and substitution

A

2-4 g/L (no storage)

  • Critical if less than 2 g/L
  • Diluted by fluid resuscitation
  • Substitution: fibrinogen conc. vs FFP
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5
Q

If hemostatic cascades are activated in the dynamic plasma:

A

DIC

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6
Q

Coaculation 3 (4) steps

A
  • Initiation
  • Amplification
  • Propagation
  • (Stabilisation)
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7
Q

Traditional basic/static lab tests in hemostasis

A
  • PT/aPTT until 5 % throbin formation!

- Platelet, fibrinogen, antithrombin, d-dimer, aFXa

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8
Q

PT/INR vs aPTT

A
  • PT: extrinsic coagulation

- aPTT: intrinsic coagulation

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9
Q

POC examples

A
  • ROTEM/TEG

- Multiplate

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10
Q

Predisposing factors for DVT

A
  • Patient-related (constitutional) or setting-related (transient)
  • Provoked if occur within 6 weeks - 3 months
  • Can be divided into strong, moderate or weak
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11
Q

Examples of strong predisposing factors for DVT

A
  • Big trauma/surgery, knee/hip prosthesis

- Hospitalized within 3 months due to AMI, CHF, A-fib or A-flu

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12
Q

Examples of moderate predisposing factors for DVT

A
  • Arthroscopic knee surgery, superficial venous thrombosis
  • Transfusion, central venous line, chemotherapy!
  • IBD, malignancy, infection, HF, oral contraceptives
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13
Q

Examples of weak predisposing factors for DVT

A
  • Bed rest, immobility, varicosity

- Obesity, DM pregnancy etc

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14
Q

Definition and types of shock

A

Supply doesn´t meet demand (hypoperfusion)

1) Hypovolemic
2) Cardiogenic
3) Distributive
4) Obstructive

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15
Q

Initial risk stratification of PE

A

Shock or hypotension?

  • Yes = high risk
  • No = low risk
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16
Q

Clinical presentation PE

A
  • Signs+symptoms, ECG, CXR, ABG
  • Clinical probability scores (Geneva, Wells)
  • Assess clinical probability (suspected/not suspected?)
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17
Q

Tests PE

A
  • Lab (d-dimer)

- Imaging (CT, scint (V/Q), angio, MRA, echo, doppler)

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18
Q

Clinical probability scores PE

A

Geneva, Wells

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19
Q

ABG PE

A
  • Typical: type I respiratory failure (hypoxemia+hypocapnia)

- But anything is possible

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20
Q

PE ECG syndrome

A

McGill-White syndrome: S1Q3T3

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21
Q

Signs of PE on CXR

A
  • Westermark sign

- Hamptons hump (shows pulmonary infarction)

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22
Q

PE labs/biomarkers

A
  • D-dimer
  • BNP / NT-proBNP
  • Troponin T/I, H-FABP
  • (LDH) - outdated
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23
Q

CT triple rule out

A

AMI, aortic aneurysm, PE

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24
Q

Echo sign specific of PE

A

McConnell sign: free wall hypokinesis sparing the apex

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25
Q

PESI

A

Pulmonary embolism severity index (I-V)

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26
Q

Treatment of PE

A

High-risk: Primary reperfusion
Intermediate-risk
- Int-high: Anticoag, monitor, rescue reperfusion
- Int-low: Anticoag, hospitalization
Low-risk: Early discharge and home treatment if possible

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27
Q

Classification PE

A
  • High mortality risk PE (high + intermediate-high)

- Non-high mortality risk PE (intermediate-low + low)

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28
Q

Systemic thrombolysis agents

A
  • Streptokinase (250 000 IU iv)
  • Urokinase (4400 IU/kg/10 min)
  • rt-PA (100 mg/2h)
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29
Q

Absolute CI of thrombolytic therapy

A
  • Hemorrhagic stroke or stroke of unknown origin (any time)
  • Ischemic stroke (within 6 months)
  • CNS damage or neoplasms
  • Recent major trauma / surgery / head injury (within 3 weeks)
  • GI bleeding (within 1 month)
  • Known increased risk of bleeding
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30
Q

Anticoagulation in acute phase

A
  • UFH

- LMWH

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31
Q

Anticoagulation subacute/chronic phase

A
  • VKA
  • LMWH, fondaparinux
  • NOAC (DTI, DXI)
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32
Q

Surgical embolectomy

A
  • If (sub) massive embolus, located centrally
  • Thrombolysis is CI or ineffective
  • Within 1 week
  • Do a median sternotomy
  • ECMO?
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33
Q

What is DIC?

A
  • always a secondary disease
  • an aquired syndrome
  • intravascular activation of coagulation
  • arising from different causes
  • Can arise from and damage microvasculature
  • Can produce organ dysfunction
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34
Q

Underlying primary diseases of DIC

A
  • Sepsis
  • Polytrauma
  • Malignancy
  • Obstetric issues
  • Vascular events
  • Severe hepatic failure
  • Severe allergy/intoxication
  • Severe immunologic reaction
35
Q

4 events required for laboratory diagnosis

A

1) Procoagulant activation (fibrinopeptide A, B up, plt down)
2) Fibrinolytic activation (d-dimer up, FDP up)
3) Inhibitor consumption (AT-III down)
4) Organ damage (LDH, creat up, pH, pO2 down)

36
Q

Organs commonly found to have microthrombi in patients with DIC (9)

A

Highest percentage to lowest: Kidney, lung, brain, heart, liver, spleen, adrenals, pancreas, gut

37
Q

Phases of acute/subacute DIC

A

1) Activation phase
2) Early consumption phase
3) Late consumption phase
- All three might lead to recovery
- 2+3 can lead to death

38
Q

Activation phase of DIC

A
  • No DIC symptoms

- Short aPTT and PT, high fibrinolytic activity

39
Q

Early consumption phase of DIC

A
  • (micro)thrombosis

- Thrombocytopenia, high D-dimer and sol. fibrin

40
Q

Late consumption phase of DIC

A
  • (micro)thrombosis and bleeding

- Severe thrombocytopenia, prolonged aPTT and PT

41
Q

Diagnosis of DIC

A

1) Proper underlying disease
2) Low (<100 000/uL) or rapidly dec plt count
3) Prolonged coag tests (INR, aPTT)
4) Appearance of fibrin deg products (D-dimer)
5) Low conc of coagulation inhibitors (eg AT-III)

42
Q

4 types of DIC

A

1) Bleeding type - fibrinolysis
2) Asymptomatic type - consumption
3) Massive bleeding type - consumption
4) Organ failure type - coagulation

43
Q

Treatment principles of DIC

A

1) ABCDE (fluid, hemodynamics, oxygenation, transfusion)
2) Underlying disease
3) Supportive, symptomatic Tx (inc bleeding tendency and augmented coagulation)

44
Q

Tx asymptomatic type of DIC

A
  • Treat underlying condition

- Heparin

45
Q

Tx organ failure type of DIC

A
  • Treat underlying condition

- Natural protease inhibitor

46
Q

Tx bleeding type of DIC

A
  • Treat underlying condition
  • Blood transfusion
  • Synthetic protease inhibitor
  • Antifibrinolytic treatment
47
Q

Tx massive bleeding type of DIC

A
  • Blood transfusion
  • Synthetic protease inhibitor
  • Antifibrinolytic treatment
48
Q

Difference in duration: TIA and stroke

A
  • TIA <24h

- Stroke >24h

49
Q

Percentage of the 2 common forms of stroke

A
  • Ischemic 80%

- Hemorrhagic 20%

50
Q

Normal cerebral blood flow

A

50ml/100g brain tissue/min

51
Q

Cerebral blood flow causing irreversible damage

A

<10ml/100g brain tissue/min

52
Q

Stroke - chain of survival

A

1) Detection - symptoms
2) Dispatch - 911
3) Delivery - transported to hospital
4) Door - immediate triage
5) Data - prompt evaluation (lab, imaging)
6) Decision - diagnosis
7) Drug
8) Disposition - timely admission to stroke unit, ICU

53
Q

Signs of occluded ant. cerebral a.

A
  • Contralat leg>arm weakness/numbness

- Dyspraxia

54
Q

Signs of occluded middle cerebral a.

A
  • Contralat face+leg>arm weakness/numbness
  • Dusarthria
  • Aphasia in dominant hemisphere
  • Neglect in non-dominant hemisphere
55
Q

Signs of occluded post cerebral a.

A
  • Contralat visual field loss
56
Q

Signs of occluded basilar a.

A
  • Quadriplegia

- Locked-in syndrome

57
Q

Signs of occlusion: vertebrobasilar syndrome

A
  • Dizziness
  • Vertigo
  • Diplopia ataxia
58
Q

Signs of occluded penetrating aa.

A
  • “Lacunar infarcts”

- Pure motor or sensory deficits

59
Q

Cincinatti Prehospital Stroke Scale (CPSS)

A

Facial asymmetry, arm weakness, disturbed speech

60
Q

Los Angeles Prehospital Stroke Screen (LAPSS)

A

like CPSS + rule out other cause of decreased level of consciousness

61
Q

DD of stroke

A

1) Psychogenic
2) Seizures
3) Hypoglycemia
4) Migraine with aura
5) Hypertensive encephalopathy
6) Wernickes encephalopathy
7) CNS abscess
8) CNS tmor
9) Drug toxicity

62
Q

Principles of Tx in stroke

A

1) Initial stabilization/sesuscitation - ABCDE
2) Recanalization of occluded vessel, cerebroprotection
3) Prevention and Tx of comp.

63
Q

Drugs used in stroke Tx

A

1) IV rtPA
2) Intraarterial lysis (acute MCA/basilar a. occlusion)
3) Aspirin within 24-48h

64
Q

Complications of stroke

A

1) Cerebral edema, inc ICP
2) Aspiration pneumonia
3) DVT/PE
4) Convulsions
5) Swallowing problems
6) Incontinency

65
Q

Intracerebral hemorrhage: Frontal lobe

A

1) Frontal headache
2) Contralat arm>leg weakness
3) Behavioral disinhibition

66
Q

Intracerebral hemorrhage: Parietal lobe

A

1) Parietal headache
2) Contralateral sensory deficits
3) Neglect in nondom. hemisphere
4) Visual field deficits

67
Q

Intracerebral hemorrhage: Temporal lobe

A

1) Temporal headache
2) Aphasia in dom hemisphere
3) Visual field deficits

68
Q

Intracerebral hemorrhage: Occipital lobe

A

1) Ipsilateral periorbital headache

2) Visual field loss

69
Q

Intracerebral hemorrhage: Putamen

A

1) Contralateral weakness/sensory deficit
2) Aphasia in dominant hemisphere
3) Neglect in nondominant hemisphere

70
Q

Intracerebral hemorrhage: Thalamus

A

1) Contralateral sensory deficit>weakness

2) Gaze deviation

71
Q

Intracerebral hemorrhage: Cerebellum

A

1) Vomiting
2) Ataxia
3) Decreased level of consciousness

72
Q

Intracerebral hemorrhage: Pontine

A

1) Coma
2) Quadriplegia
3) Posturing
4) Pinpoint pupils

73
Q

Intracerebral hemorrhage Tx

A

1) ABCDE
2) BP control
3) Coagulation control

74
Q

Complications of intracerebral hemorrhage

A

1) Herniation
2) Hydrocephalus
3) Dec. level of consciousness

75
Q

Two types of subarachnoid hemorrhage (SAH)

A

Traumatic and non-traumatic

76
Q

Risk factors of SAH

A

1) Female
2) HTN
3) Alcohol
4) IV drug abuse
5) Smoking
6) Family history

77
Q

Classic symptoms

A
  • “Worst headache of my life”
  • Nausea, photophobia, meningeal signs, autonomic instability
  • Convulsion, diplopia, dec level of consciousness
78
Q

Diagnosing SAH

A

Imaging (CT, MRA), lumbar puncture?

79
Q

Hunt&Hess classification of SAH

A

I. Symptomatic or mild headache and slight nuchal rigidity
II. Mod.-severe headache, stiff neck, no neurologic deficit except CN palsy
III. Drowsy or confused, mild neurologic deficit
IV. Stupor, moderate to severe hemiparesis
V. Deep coma, decerebrate posturing

80
Q

Treatment SAH

A
  • BP control (<160/110)
  • 3H therapy - HTN, hypovolemia, hemodilution
  • Neurological intervention: open surgery (clipping), endovascular (coiling)
81
Q

Sinus thrombosis

A

Intracranial form vascular disease on the venous side

82
Q

Risk factors for sinus thrombosis

A
  • Thrombophilia
  • Pregnancy
  • Oral contraceptives
  • Anabolic steroids
  • Malignancy
  • Local inflammation
83
Q

Diahnosis of sinus thrombosis

A

MRI

84
Q

2 sinuses most commonly involved in sinus thrombosis

A
  • Superior sagital sinus

- Transverese (lateral) sinus