Lernkarten

Christian Brunner
Karten 38 Karten
Lernende 2 Lernende
Sprache Deutsch
Stufe Universität
Erstellt / Aktualisiert 05.09.2014 / 31.03.2016
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0 Exakte Antworten 38 Text Antworten 0 Multiple Choice Antworten

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Zeichen der arteriosclerotic leukencephalopathy?

hypodensity of the white matter with emphasis on periventricular regions

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Welche Formen der häorrhagischen Transformation nach Stroke?

2

Hämorrhagischer Infarkt: petechial or confluent petechial haemorrhage within the infarcted region and normally has few clinical consequences

Parenchymales Hämatom: the region is filled with a mass of blood which may encroach on surrounding structures, resulting in midline shift and clinical deterioration

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Nebenwirkungen der Osmotherapie zur Hirndrucksenkung?

6

  • Aggravation of cerebral oedema related to migration through a permeable blood-brain barrier, reversing the osmotic gradient and exacerbating swelling
  • Dehydration and shrinkage of normal brain tissue, facilitating displacement of brain tissue thereby increasing the risk of herniation
  • Electrolyte imbalances
  • Raised serum osmolarity
  • Hypervolaemia with cardiac failure
  • Renal dysfunction.
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Nachteile der Ventrikeldrainage?

Adäquate Masnahme?

1.Massnahme ist Dekompression durch NCH

2. Drainage:

  • The management of these drainage devices needs special expertise, because it may lead to further brain shifts. 
  • relatively high infection rate of 2-10%, which increases when drainage is maintained beyond ten days.
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Einschlusskriterien i.v.-Thrombolyse?

  • Ischaemic infarct with relevant neurologic deficit (2< NIHSS <25)
  • Symptoms not regressing spontaneously
  • Symptoms not minimal (however no NIHSS limit)
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Ausschlusskritierien i.v.-Thrombolyse?

23!

  • *Time window >3h
  • *Age >80 years
  • *Very severe neurological deficit (i.e. hemiplegia, gaze deviation, coma)
  • Suspicion of subarachnoid haemorrhage**
  • Traumatic head and brain injury within last 3 months
  • Myocardial infarct within last 3 months
  • Gastrointestinal or urogenital bleeding within last 3 weeks
  • Arterial puncture at an incompressible site within last week
  • *Operation within last 2 weeks (NOTE: contact respective surgeons re risk of bleeding)
  • *Seizures at symptom onset
  • *History of intracerebral haemorrhage
  • *Ischaemic stroke within last 3 months
  • Blood pressure >185/100 mmHg despite antihypertensive therapy (In the US, a diastolic BP of >110 is used)
  • Signs of acute bleeding or acute trauma
  • Oral anticoagulant medication and INR >1.5 (in the US: INR=1.7)
  • Heparin for last 48h with aPTT within normal range
  • Platelets <100 000/µl
  • *Diabetics with history of stroke
  • *Large infarct in CT (early signs >1/3 of hemisphere)
  • *Serum glucose <50 mg/dl (2.7 mmol/l) or >400 mg/dl (22.2 mmol/l)
  • Tumour with increased bleeding risk
  • Acute pancreatitis
  • Endocarditis
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Infusionsschema rt-PA?

  • Calculate the total dose of rtPA: 0.9 mg/kg; maximum of 90 mg
  • Administer 10% of the total dose given as a bolus
  • Give the remaining 90% over 60 minutes via an infusion pump
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Zeitfenster für  Lyse?

Was gilt allgemein?

3h (-4.5h, noch nicht freigegeben)

Je früher um so besser

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Welche Massnahmen bei Basilaris-Verschluss?

Zeitfenster?

In the case of basilar artery occlusion:

in specialised centres, intra-arterial therapy using urokinase up to 1.5 million IU or rtPA up to 50 mg may be the treatment of choice.

If cranial CT does not show any demarcated infarction, the time window for thrombolysis may be extended up to 12h

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Was wenn Symptombeginn unklar ist(z.B. beim Aufwachen)?

Individuelle Enscheidung:

demarkiertes Areal im CT?

Abschätzen des Ischämiealters mittels MRI?

Jounger Patient?

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Sekundärprophylaxe nach Stroke?

1. ASS 150-300mg/d

2. Emboliequelle suchen

3. Behandlung der vaskulären Risikofaktoren

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Therapeutisch Heparin nach Stroke?

bisher kein Benefit.

Evtl. erwägen nach thrombembolischen Ereignissen bei Carotisdissektion, VHFli, Sinusvenenthrombose...

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Wann defintiv keine therapeutische Antikoagulation?

  • large infarcts (e.g. more than 50% of middle cerebral artery territory)
  • uncontrollable arterial hypertension
  • advanced microvascular changes in the brain.
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Warum darf man bei septischen Embolien keine ther. Antikoagulation beginnen?

Neigen zu zerebralen Hämorrhagien!

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Welche Emboliequellen brauchen therapeutische Antikoagulation und wann beginnt man?

  • VhFi, rheumatische Endokarditis, mechanische Klappen, ventrikelaneurysma
  • PFO

bei TIA/minor Stroke sofort, bei grösseren Infarkten nach 4 Wochen(meistens)

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Welche Massnahmen verbessern das outcome von CVI-Patienten massgeblich?

4

  • Stroke care in specialised units (Stroke units)
  • Platelet inhibitors such as acetylsalicylic acid within 72 hours
  • Intravenous thrombolysis within 4.5 hours
  • Hemicraniectomy within 48 hours (see reference below)
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Welche Patienten sind IPS-pflichtig?

6

  • Large, space-occupying hemispheric infarct
  • Space-occupying cerebellar infarct
  • Basilar artery thrombosis
  • Septic embolic infarction secondary to bacterial endocarditis
  • Stroke associated with cardiothoracic surgery
  • Pre- and post-intervention care of stroke-related angiography.
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Akutes Management von CVI-Patienten?

4

  • Resuscitate, look for  circulation, oxygenation, body temperature and blood glucose.
  • Immediately assess the indication for acute revascularisation.
  • Determine the possible cause of the stroke. This will facilitate institution of optimal secondary prophylaxis, with the aim of preventing early recurrences.
  • Assess the optimal management location – emergency department (ED), stroke unit (SU) or ICU
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Warum akutes Strokemanagement wenn doch Hirnareale längst abgestorben sind? (Ischämiezeit von 3min reichen!)

Sekundäre Prävention:

  1. Erhalten der Penumbra
  2. Vermeiden von Komplikationen, speziell bei TIA
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Welche Patienten machen  respiratorische Probleme in der Akutversorgung?

3

Patienten mit

  1. brainstem infarction
  2. large hemispheric infarctions
  3. space occupying lesions
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Was passiert wenn Blutdruck nach Ischämie zu niederig ist?

Zu hoch?

Zielblutdruck VOR Lyse?

 If the pressure is too high this may exacerbate reperfusion injury to the penumbra and lead to increased oedema, cellular hypoxia or haemorrhagic transformation.

If the pressure is too low, CBF in the penumbra can decrease to a level causing irreversible neuronal damage; additionally, this can cause vessels in intact brain regions to dilate, which can then lead to a potential âsteal-effectâ, further promoting ischaemia in the penumbra.

≤185 mmHg and diastolic blood pressure is ≤110 mmHg

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Blutdruckziele bei intrakranieller Hämorrhagie?

mit vorbekannter /nicht vorbekannter Hypertonie?

-upper recommended limit of 160/95 mmHg in patients without known hypertension. If treatment is necessary, target blood pressure 150/90 mmHg


-upper limit of systolic blood pressure of 180 mmHg if known hypertension and, if treatment is necessary, target blood pressure is 160/100 mmHg.

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Wann müssen Blutdruckvorgaben angepasst werden?

suspected aortic dissection, hypertensive encephalopathy, subarachnoid or intracerebral bleeding, severe heart failure, acute myocardial infarction or unstable angina.

In these situations, a compromise has to be achieved.

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Welche Symptome sprechen FüR intrakranielle Blutung?

4

  • Onset during a hypertensive crisis
  • Progression of symptoms within minutes
  • Early, excessive vomiting
  • Early/immediate loss of consciousness
  • Acute onset of headache
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Führende Symptome bei subarachnoidaler Blutung? 2

occipitaler Kopfschmerz

Meningismus

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Symptome Sinus venosus-Thrombose? 2

Krampfanfälle

Kopfschmerzen

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Lacunäre Infarkte: Pathophysiologie und Verlauf?

Lacuna: Lücke

Penetrating artery occlusions -> develop over a short period of time, typically minutes to hours.

stuttering course may ensue,

symptoms sometimes evolve over several days

lacunar infarction is the main ischemic stroke subtype associated with worsening motor deficits after hospital admission

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Symptome lakunäre Infarkte? 5

Welche nicht?

Keine "kortikalen" Symptome: aphasia, agnosia, neglect, apraxia, or hemianopsia (so-called "cortical" signs). Monoplegia, stupor, coma, loss of consciousness, and seizures also are typically absent

 

Symptome mit hohem prädiktivem Wert für lakunären Infarkt:

  • Pure motor hemiparesis

●Pure sensory stroke

●Ataxic hemiparesis

●Sensorimotor stroke

●Dysarthria-clumsy hand syndrome

Preceding TIAs and nonsudden onset may increase the positive predictive value

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Pathomechanismus systemischer Embolien?

Vorausbestehende kardiale Erkrankung:

mechanical or cardiac valve dysfunction, atrial fibrillation, left atrial and/or ventricular thrombus, dilated cardiomyopathy, recent myocardial infarction (<4 weeks), left ventricular aneurysm, sick sinus syndrome, infective myocarditis, or atrial myxoma

Verschliesst unterschiedliche Gefässregionen

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Typischer Verlauf der Krankengeschichte? 3

  • Sudden onset, with maximal severity at onset
  • Onset usually during activity, in awake state; presentation on awakening is unusual
  • Recurrent TIAs in different anatomical areas