Lernkarten

Christian Brunner
Karten 38 Karten
Lernende 2 Lernende
Sprache Deutsch
Stufe Universität
Erstellt / Aktualisiert 05.09.2014 / 31.03.2016
Lizenzierung Keine Angabe
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0 Exakte Antworten 38 Text Antworten 0 Multiple Choice Antworten
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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
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Symptome bei Verschluss der cerebri media?

  • Contralateral motor and/or sensory deficit of face and arm more than leg
  • Higher cerebral dysfunction (aphasia, apraxia)
  • Conjugated ipsilateral eye deviation in large infarcts
  • Homonymous visual field defects, alone or in combination with above
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Symptome bei Verschluss der cerebri anterior?

  • Contralateral hemiparesis with emphasis on the lower limb
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Symptome bei Verschluss der cerebri posterior?

  • Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit
  • Bilateral motor and/or sensory deficit
  • Disorder or conjugate eye movement (vertical=midbrain, horizontal=pons)
  • Cerebellar dysfunction without ipsilateral long-tract deficit
  • Altered consciousness
  • Dysarthrophonia, dysphagia
  • Horner syndrome (also in carotid artery dissection)
  • Isolated homonymous visual field defect
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Verlauf von grossen thrombarteriellen Verschlüssen? 3

ähnlich wie bei thrombembolischen Ereignissen bis auf:

  • Typical atherogenic risk factors
  • Frequent TIAs, e.g. amaurosis fugax (internal carotid artery stenosis), in the same arterial territory
  • Onset often during sleep or atherothrombotic stroke during activity, a gradual progression or stepwise course over minutes to hours is characteristic (attributable to gradual accumulation of thrombus or to lowering of blood pressure, e.g. following antihypertensive therapy).
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Risikofaktor für Dissektionen?

3

  • Recent trauma
  • Previous infection
  • Signs of connective tissue abnormalities (hyperextensible joints, Marfan syndrome, known mitral valve prolapse)
  • Younger Patients!
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Klinscher Verlauf der Dissektionen? 4

is a focal neurological syndrome

  • + unilateral headache or neck pain
  • + pulsatile tinnitus
  • 1 ipsilateral Horner syndrome in the case of internal carotid artery dissection
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Early signs of ischaemia?

Aussagekraft?

Hypoattenuation involving one-third or more of the middle cerebral artery (MCA) territory

●Obscuration of the lentiform nucleus

●Cortical sulcal effacement

●Focal parenchymal hypoattenuation

●Loss of the insular ribbon or obscuration of the Sylvian fissure

●Hyperattenuation of large vessel (eg, "hyperdense MCA sign")

●Loss of gray-white matter differentiation in the basal ganglia

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Ab welchem Befund eher keine Lyse mehr?

Early signs of ischaemia + Ischaemieareal >1/3 des cerebri media -Territoriums

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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