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
PESI
Pulmonary embolism severity index (I-V)
26
Treatment of PE
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
27
Classification PE
- High mortality risk PE (high + intermediate-high) | - Non-high mortality risk PE (intermediate-low + low)
28
Systemic thrombolysis agents
- Streptokinase (250 000 IU iv) - Urokinase (4400 IU/kg/10 min) - rt-PA (100 mg/2h)
29
Absolute CI of thrombolytic therapy
- 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
30
Anticoagulation in acute phase
- UFH | - LMWH
31
Anticoagulation subacute/chronic phase
- VKA - LMWH, fondaparinux - NOAC (DTI, DXI)
32
Surgical embolectomy
- If (sub) massive embolus, located centrally - Thrombolysis is CI or ineffective - Within 1 week - Do a median sternotomy - ECMO?
33
What is DIC?
- 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
34
Underlying primary diseases of DIC
- Sepsis - Polytrauma - Malignancy - Obstetric issues - Vascular events - Severe hepatic failure - Severe allergy/intoxication - Severe immunologic reaction
35
4 events required for laboratory diagnosis
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
Organs commonly found to have microthrombi in patients with DIC (9)
Highest percentage to lowest: Kidney, lung, brain, heart, liver, spleen, adrenals, pancreas, gut
37
Phases of acute/subacute DIC
1) Activation phase 2) Early consumption phase 3) Late consumption phase - All three might lead to recovery - 2+3 can lead to death
38
Activation phase of DIC
- No DIC symptoms | - Short aPTT and PT, high fibrinolytic activity
39
Early consumption phase of DIC
- (micro)thrombosis | - Thrombocytopenia, high D-dimer and sol. fibrin
40
Late consumption phase of DIC
- (micro)thrombosis and bleeding | - Severe thrombocytopenia, prolonged aPTT and PT
41
Diagnosis of DIC
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
4 types of DIC
1) Bleeding type - fibrinolysis 2) Asymptomatic type - consumption 3) Massive bleeding type - consumption 4) Organ failure type - coagulation
43
Treatment principles of DIC
1) ABCDE (fluid, hemodynamics, oxygenation, transfusion) 2) Underlying disease 3) Supportive, symptomatic Tx (inc bleeding tendency and augmented coagulation)
44
Tx asymptomatic type of DIC
- Treat underlying condition | - Heparin
45
Tx organ failure type of DIC
- Treat underlying condition | - Natural protease inhibitor
46
Tx bleeding type of DIC
- Treat underlying condition - Blood transfusion - Synthetic protease inhibitor - Antifibrinolytic treatment
47
Tx massive bleeding type of DIC
- Blood transfusion - Synthetic protease inhibitor - Antifibrinolytic treatment
48
Difference in duration: TIA and stroke
- TIA <24h | - Stroke >24h
49
Percentage of the 2 common forms of stroke
- Ischemic 80% | - Hemorrhagic 20%
50
Normal cerebral blood flow
50ml/100g brain tissue/min
51
Cerebral blood flow causing irreversible damage
<10ml/100g brain tissue/min
52
Stroke - chain of survival
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
Signs of occluded ant. cerebral a.
- Contralat leg>arm weakness/numbness | - Dyspraxia
54
Signs of occluded middle cerebral a.
- Contralat face+leg>arm weakness/numbness - Dusarthria - Aphasia in dominant hemisphere - Neglect in non-dominant hemisphere
55
Signs of occluded post cerebral a.
- Contralat visual field loss
56
Signs of occluded basilar a.
- Quadriplegia | - Locked-in syndrome
57
Signs of occlusion: vertebrobasilar syndrome
- Dizziness - Vertigo - Diplopia ataxia
58
Signs of occluded penetrating aa.
- "Lacunar infarcts" | - Pure motor or sensory deficits
59
Cincinatti Prehospital Stroke Scale (CPSS)
Facial asymmetry, arm weakness, disturbed speech
60
Los Angeles Prehospital Stroke Screen (LAPSS)
like CPSS + rule out other cause of decreased level of consciousness
61
DD of stroke
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
Principles of Tx in stroke
1) Initial stabilization/sesuscitation - ABCDE 2) Recanalization of occluded vessel, cerebroprotection 3) Prevention and Tx of comp.
63
Drugs used in stroke Tx
1) IV rtPA 2) Intraarterial lysis (acute MCA/basilar a. occlusion) 3) Aspirin within 24-48h
64
Complications of stroke
1) Cerebral edema, inc ICP 2) Aspiration pneumonia 3) DVT/PE 4) Convulsions 5) Swallowing problems 6) Incontinency
65
Intracerebral hemorrhage: Frontal lobe
1) Frontal headache 2) Contralat arm>leg weakness 3) Behavioral disinhibition
66
Intracerebral hemorrhage: Parietal lobe
1) Parietal headache 2) Contralateral sensory deficits 3) Neglect in nondom. hemisphere 4) Visual field deficits
67
Intracerebral hemorrhage: Temporal lobe
1) Temporal headache 2) Aphasia in dom hemisphere 3) Visual field deficits
68
Intracerebral hemorrhage: Occipital lobe
1) Ipsilateral periorbital headache | 2) Visual field loss
69
Intracerebral hemorrhage: Putamen
1) Contralateral weakness/sensory deficit 2) Aphasia in dominant hemisphere 3) Neglect in nondominant hemisphere
70
Intracerebral hemorrhage: Thalamus
1) Contralateral sensory deficit>weakness | 2) Gaze deviation
71
Intracerebral hemorrhage: Cerebellum
1) Vomiting 2) Ataxia 3) Decreased level of consciousness
72
Intracerebral hemorrhage: Pontine
1) Coma 2) Quadriplegia 3) Posturing 4) Pinpoint pupils
73
Intracerebral hemorrhage Tx
1) ABCDE 2) BP control 3) Coagulation control
74
Complications of intracerebral hemorrhage
1) Herniation 2) Hydrocephalus 3) Dec. level of consciousness
75
Two types of subarachnoid hemorrhage (SAH)
Traumatic and non-traumatic
76
Risk factors of SAH
1) Female 2) HTN 3) Alcohol 4) IV drug abuse 5) Smoking 6) Family history
77
Classic symptoms
- "Worst headache of my life" - Nausea, photophobia, meningeal signs, autonomic instability - Convulsion, diplopia, dec level of consciousness
78
Diagnosing SAH
Imaging (CT, MRA), lumbar puncture?
79
Hunt&Hess classification of SAH
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
Treatment SAH
- BP control (<160/110) - 3H therapy - HTN, hypovolemia, hemodilution - Neurological intervention: open surgery (clipping), endovascular (coiling)
81
Sinus thrombosis
Intracranial form vascular disease on the venous side
82
Risk factors for sinus thrombosis
- Thrombophilia - Pregnancy - Oral contraceptives - Anabolic steroids - Malignancy - Local inflammation
83
Diahnosis of sinus thrombosis
MRI
84
2 sinuses most commonly involved in sinus thrombosis
- Superior sagital sinus | - Transverese (lateral) sinus