The Pathophysiology And Management Of Hemorrhagic Stroke

The Pathophysiology And Management Of Hemorrhagic Stroke

Carotid endarterectomy

Right MCA territory Infarction with mass effect

Case: Refered from tanjung karang on 18/6/2009. 39 years old Indian gentleman, with no known medical illness developed sudden onset of left sided body wekness. He also had vomited few times whereby the vomitus was coffee ground.

Not on any medication. Been unwell since yesterday. Having nausea and persistent vomiting since yesterday. He was unable to tolerate much orally. Today had persistent vomiting too. At about 9 pm, had developed sudden onset of left UL and LL weakness associated with inability to speak. Denies having any headache, No giddiness, No fever, No preceding chest pain or palpitations. Married, Non smoker, occasional alcohol consumption

Examination:

Alert, Obeying commands. Expressive dysphasia. Gag reflex absent. Right UL and LL: dense hemiplegia with hyperreflexia.

Plantar upgoing right side

CVS s1s2 DRNM

lungs clear

PA-soft, non tender

Pupils - equal 3 mms, reactive.

Pulse 92 /min

Respiration 17 /min

Systolic Blood Pressure 117 mmHg Diastolic Blood Pressure 88 mmHg

SPO2 99 %
Analysis / Assessment
:
ECG - sinus rythm, LVH by voltage criteria

CT scan on 18/6/2009

Findings: Large ill defined wedge shaped hypodensity noted in the right fronto-parietal region with effacement of adjacent sulci. No midline shift. Ventricles and CSF-spaces are normal. Visualised paranasal sinuses are clear.

Impression: Right MCA territory recent infarct.

He underwent OGDS on 18/6/2009.

Findings:

Esophagitis LA grade B with gastric metaplasiaChronic atrophic gastritis with antral erosionsDuodenum normal

On the next day noted pupils were unequal. Patient opens eyes, obeys commands, localizing to pain but not verbalizing

Examination:
pupils unequal RT 4mm lt 2mm

BP 150/78

PR 74

Repeat Ct scan on 20/6/2009

Plain CT-brain on 20/6/09. Comparison with CT-scan on 18/6/09. Findings: The previously seen right MCA territory infarct become more well defined with increasing oedema. Associated mass effect to right lateral ventricle with midline shift 13 mm to left side. Hypodensity of midbrain, most likely represent ischaemia. Hyperintensity in basal cisterns and Sylvian fissures, suggestive of subarachnoid haemorrhage which was not seen before. Basal cisterns and sulci are effaced. Left basal ganglia recent infarct as seen before and not increasing in size. Left lateral ventricle is dilated.

He underwent right FTP decompressive cranictomy and left frontal EVD for ICP monitoring

Post-op he underwent cerebral resuscitation. Pupils 3s /2+. ICP maintanied below 20mmHg.

Post-op CT on 21/6/2009

PLAIN CT BRAIN: 21.6.2009 Finding: *** comparison with CT brain dated 20.6.2009. The left lateral ventricle is less dilated with EVD in situ. Lesser degree of midline shift to the leftc with shift of 4mm. Rest of the findings remains similar.

Left cerebellar infarct with hemorrhagic transformation

Case: Referred from KKB. 57 years old malay male with underlying hypertension went to KKB with full GCS, complained of headache, nausea, vomiting, for 2 days with generalised body weakness. no fever. He was started on iv GTN due to uncontraoled hypertension. At 6pm he was confused, having slurred speech with gsc of E4V2M5. He was then referred to HSB for CT brain

PHYSICAL EXAMINATION General : gsc E4V2M6 pupils 3/3

Head and Neck : NAD

CVS : DRNM

Respiratory : Clear Abdomen : soft, nontender, bowel sound heard

Musculoskeletal System : moving all 4 limbs

CT scan on 16/6/2009

Finding: Ill defined hypodense area seen in the left cerebellar hemisphere with perilesional oedema. The cerebellar fovea are effaced with effacement of the 4th ventricle with resultant dilatation of both lateral ventricle * 3rd ventricle. Area of hyperdensity within suggesting intraparenchymal bleed. No midline shift. Quadrigeminal cisterns are narrowed. Visualized sinuses and mastoid air cells are clear.

IMP: With the given presentation, the findings are suggestive of cerebellar infarct with haemorrhagic transformation. Associated with dilatation of lateral ventricles and 3rd ventricle due to mass effect of the 4th ventricle.

He underwent right frontal EVD placement. Right frontal EVD inserted (17/6/09)

Post-op patient alert
E4V3M6
Pupils 3/3 reactive

The next day, Informed by staff nurse that pt was not opening eyes to call / not obeying commands + stridorGCS dropped from 13/15 to 7/15 ( E1V1M5 )Pupil : 3/3 ( reactive )B/P : 240/125PR : 111spo2 : 94 %

He was immediately intubated stat using ETT size 7.5 and started on IV midamorphine infusion 5ml/HLatest B/P : 192/113PR : 98Spo2 : 100%

Repeat Ct scan on 18/6/2009

Finding: ***comparison with CT Brain dated 17/6/09. Evidence of right parietal craniotomy with EVD traversing the right parietal lobe with tip at adjacent to the wall of right lateral ventricle. The previously noted hypodense area seen in the left cerebellar hemisphere with perilesional oedema is now more well defined. The intraparenchymal bleed in the left cerebellum remains similar in appearance.No new bleed. The cerebellar fovea are still effaced with effacement of the 4th ventricle. There is increasing dilatation of both lateral ventricle and 3rd ventricle. No midline shift. Quadrigeminal cistern is more narrowed.

Imp: Increasing hydrocephalus with narrower quadrigeminal cistern. No new bleed/ expansion of bleed.

He was brought to OT for posterior fossa decompression.

Post-op he was on cerebral protection with ICP maintained below 20mmHg.

Post-op CT scan on 19/6/2009

Finding: ***comparison with CT Brain dated 18/6/09. Evidence of right parietal craniotomy with occipital craniectomy . The intraparenchymal bleed in the left cerebellum remains similar in appearance.No new/expansion of bleed. 4th ventricle is no longer effaced. There is minimal reduction in the degree of dilatation of both lateral ventricle and 3rd ventricle. No midline shift. Quadrigeminal cistern is still narrowed.

Imp: Decreasing hydrocephalus. No new bleed/ expansion of bleed.