4. PE, DIC, stroke Flashcards
3 elements of hemostasis (Virchow)
- Endothelium
- Platelets
- Plasma
3 processes of hemostasis
- Primary: thrombocyte aggregation
- Secondary: coagulation, plasmatic cascade
- Tertiary: fibrinolysis
2 directions of hemostais
Pro/anti or clotting/bleeding
Fibrinogen concentration and substitution
2-4 g/L (no storage)
- Critical if less than 2 g/L
- Diluted by fluid resuscitation
- Substitution: fibrinogen conc. vs FFP
If hemostatic cascades are activated in the dynamic plasma:
DIC
Coaculation 3 (4) steps
- Initiation
- Amplification
- Propagation
- (Stabilisation)
Traditional basic/static lab tests in hemostasis
- PT/aPTT until 5 % throbin formation!
- Platelet, fibrinogen, antithrombin, d-dimer, aFXa
PT/INR vs aPTT
- PT: extrinsic coagulation
- aPTT: intrinsic coagulation
POC examples
- ROTEM/TEG
- Multiplate
Predisposing factors for DVT
- Patient-related (constitutional) or setting-related (transient)
- Provoked if occur within 6 weeks - 3 months
- Can be divided into strong, moderate or weak
Examples of strong predisposing factors for DVT
- Big trauma/surgery, knee/hip prosthesis
- Hospitalized within 3 months due to AMI, CHF, A-fib or A-flu
Examples of moderate predisposing factors for DVT
- Arthroscopic knee surgery, superficial venous thrombosis
- Transfusion, central venous line, chemotherapy!
- IBD, malignancy, infection, HF, oral contraceptives
Examples of weak predisposing factors for DVT
- Bed rest, immobility, varicosity
- Obesity, DM pregnancy etc
Definition and types of shock
Supply doesn´t meet demand (hypoperfusion)
1) Hypovolemic
2) Cardiogenic
3) Distributive
4) Obstructive
Initial risk stratification of PE
Shock or hypotension?
- Yes = high risk
- No = low risk
Clinical presentation PE
- Signs+symptoms, ECG, CXR, ABG
- Clinical probability scores (Geneva, Wells)
- Assess clinical probability (suspected/not suspected?)
Tests PE
- Lab (d-dimer)
- Imaging (CT, scint (V/Q), angio, MRA, echo, doppler)
Clinical probability scores PE
Geneva, Wells
ABG PE
- Typical: type I respiratory failure (hypoxemia+hypocapnia)
- But anything is possible
PE ECG syndrome
McGill-White syndrome: S1Q3T3
Signs of PE on CXR
- Westermark sign
- Hamptons hump (shows pulmonary infarction)
PE labs/biomarkers
- D-dimer
- BNP / NT-proBNP
- Troponin T/I, H-FABP
- (LDH) - outdated
CT triple rule out
AMI, aortic aneurysm, PE
Echo sign specific of PE
McConnell sign: free wall hypokinesis sparing the apex
PESI
Pulmonary embolism severity index (I-V)
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
Classification PE
- High mortality risk PE (high + intermediate-high)
- Non-high mortality risk PE (intermediate-low + low)
Systemic thrombolysis agents
- Streptokinase (250 000 IU iv)
- Urokinase (4400 IU/kg/10 min)
- rt-PA (100 mg/2h)
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
Anticoagulation in acute phase
- UFH
- LMWH
Anticoagulation subacute/chronic phase
- VKA
- LMWH, fondaparinux
- NOAC (DTI, DXI)
Surgical embolectomy
- If (sub) massive embolus, located centrally
- Thrombolysis is CI or ineffective
- Within 1 week
- Do a median sternotomy
- ECMO?
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
Underlying primary diseases of DIC
- Sepsis
- Polytrauma
- Malignancy
- Obstetric issues
- Vascular events
- Severe hepatic failure
- Severe allergy/intoxication
- Severe immunologic reaction
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)
Organs commonly found to have microthrombi in patients with DIC (9)
Highest percentage to lowest: Kidney, lung, brain, heart, liver, spleen, adrenals, pancreas, gut
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
Activation phase of DIC
- No DIC symptoms
- Short aPTT and PT, high fibrinolytic activity
Early consumption phase of DIC
- (micro)thrombosis
- Thrombocytopenia, high D-dimer and sol. fibrin
Late consumption phase of DIC
- (micro)thrombosis and bleeding
- Severe thrombocytopenia, prolonged aPTT and PT
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)
4 types of DIC
1) Bleeding type - fibrinolysis
2) Asymptomatic type - consumption
3) Massive bleeding type - consumption
4) Organ failure type - coagulation
Treatment principles of DIC
1) ABCDE (fluid, hemodynamics, oxygenation, transfusion)
2) Underlying disease
3) Supportive, symptomatic Tx (inc bleeding tendency and augmented coagulation)
Tx asymptomatic type of DIC
- Treat underlying condition
- Heparin
Tx organ failure type of DIC
- Treat underlying condition
- Natural protease inhibitor
Tx bleeding type of DIC
- Treat underlying condition
- Blood transfusion
- Synthetic protease inhibitor
- Antifibrinolytic treatment
Tx massive bleeding type of DIC
- Blood transfusion
- Synthetic protease inhibitor
- Antifibrinolytic treatment
Difference in duration: TIA and stroke
- TIA <24h
- Stroke >24h
Percentage of the 2 common forms of stroke
- Ischemic 80%
- Hemorrhagic 20%
Normal cerebral blood flow
50ml/100g brain tissue/min
Cerebral blood flow causing irreversible damage
<10ml/100g brain tissue/min
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
Signs of occluded ant. cerebral a.
- Contralat leg>arm weakness/numbness
- Dyspraxia
Signs of occluded middle cerebral a.
- Contralat face+leg>arm weakness/numbness
- Dusarthria
- Aphasia in dominant hemisphere
- Neglect in non-dominant hemisphere
Signs of occluded post cerebral a.
- Contralat visual field loss
Signs of occluded basilar a.
- Quadriplegia
- Locked-in syndrome
Signs of occlusion: vertebrobasilar syndrome
- Dizziness
- Vertigo
- Diplopia ataxia
Signs of occluded penetrating aa.
- “Lacunar infarcts”
- Pure motor or sensory deficits
Cincinatti Prehospital Stroke Scale (CPSS)
Facial asymmetry, arm weakness, disturbed speech
Los Angeles Prehospital Stroke Screen (LAPSS)
like CPSS + rule out other cause of decreased level of consciousness
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
Principles of Tx in stroke
1) Initial stabilization/sesuscitation - ABCDE
2) Recanalization of occluded vessel, cerebroprotection
3) Prevention and Tx of comp.
Drugs used in stroke Tx
1) IV rtPA
2) Intraarterial lysis (acute MCA/basilar a. occlusion)
3) Aspirin within 24-48h
Complications of stroke
1) Cerebral edema, inc ICP
2) Aspiration pneumonia
3) DVT/PE
4) Convulsions
5) Swallowing problems
6) Incontinency
Intracerebral hemorrhage: Frontal lobe
1) Frontal headache
2) Contralat arm>leg weakness
3) Behavioral disinhibition
Intracerebral hemorrhage: Parietal lobe
1) Parietal headache
2) Contralateral sensory deficits
3) Neglect in nondom. hemisphere
4) Visual field deficits
Intracerebral hemorrhage: Temporal lobe
1) Temporal headache
2) Aphasia in dom hemisphere
3) Visual field deficits
Intracerebral hemorrhage: Occipital lobe
1) Ipsilateral periorbital headache
2) Visual field loss
Intracerebral hemorrhage: Putamen
1) Contralateral weakness/sensory deficit
2) Aphasia in dominant hemisphere
3) Neglect in nondominant hemisphere
Intracerebral hemorrhage: Thalamus
1) Contralateral sensory deficit>weakness
2) Gaze deviation
Intracerebral hemorrhage: Cerebellum
1) Vomiting
2) Ataxia
3) Decreased level of consciousness
Intracerebral hemorrhage: Pontine
1) Coma
2) Quadriplegia
3) Posturing
4) Pinpoint pupils
Intracerebral hemorrhage Tx
1) ABCDE
2) BP control
3) Coagulation control
Complications of intracerebral hemorrhage
1) Herniation
2) Hydrocephalus
3) Dec. level of consciousness
Two types of subarachnoid hemorrhage (SAH)
Traumatic and non-traumatic
Risk factors of SAH
1) Female
2) HTN
3) Alcohol
4) IV drug abuse
5) Smoking
6) Family history
Classic symptoms
- “Worst headache of my life”
- Nausea, photophobia, meningeal signs, autonomic instability
- Convulsion, diplopia, dec level of consciousness
Diagnosing SAH
Imaging (CT, MRA), lumbar puncture?
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
Treatment SAH
- BP control (<160/110)
- 3H therapy - HTN, hypovolemia, hemodilution
- Neurological intervention: open surgery (clipping), endovascular (coiling)
Sinus thrombosis
Intracranial form vascular disease on the venous side
Risk factors for sinus thrombosis
- Thrombophilia
- Pregnancy
- Oral contraceptives
- Anabolic steroids
- Malignancy
- Local inflammation
Diahnosis of sinus thrombosis
MRI
2 sinuses most commonly involved in sinus thrombosis
- Superior sagital sinus
- Transverese (lateral) sinus
