RCSI CNS CPC Raised Intracranial Pressure 2024 PDF
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2024
RCSI
Paul Murray
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Summary
This document is an RCSI CNS CPC past paper from November 2024, covering the topic of raised intracranial pressure, including case studies, questions on cerebral oedema, and secondary brain tumors. The document details various clinical presentations and management strategies.
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RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn CPC CNS CPC Raised Intracranial Pressure Class Year 2 Course CNS CPC Lecturer Paul Murray Date November 2024 Case history A 74-year-old man presents to the Emergency Departm...
RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn CPC CNS CPC Raised Intracranial Pressure Class Year 2 Course CNS CPC Lecturer Paul Murray Date November 2024 Case history A 74-year-old man presents to the Emergency Department with new onset seizure Past history lung adenocarcinoma 10 years previously, treated with neoadjuvant chemotherapy and resection Examination Drowsy with rhythmic jerking of the right arm. Four presenting features of brain tumour Seizure Symptoms /signs of raised intracranial pressure (headache especially early morning, vomiting, coma, papilloedema) +/- symptoms/signs of hydrocephalus Focal neurologic deficit Behavioural alteration Brain Imaging – CT brain followed by MRI brain with contrast Ring-enhancing space occupying lesion with oedema The term "ring-enhancing" refers to a specific pattern observed in the imaging of the lesion. It indicates that there is a distinct outer ring or border of enhanced brightness or contrast surrounding a central darker area. This enhancement typically occurs when a contrast agent is used during the imaging procedure. The contrast agent highlights the blood vessels and the outer border of the lesion, creating a "ring" effect. Questions How would you categorise the cerebral oedema in this case? – Localised (rather than generalised) cerebral oedema. Name one cause of generalised cerebral oedema – Hypoxia-ischaemia Presentation of secondary tumour in brain Multiple brain lesions (50% will be solitary) History of systemic malignancy Mass lesion e.g. in the lung – check CXR Questions What is happening at a cellular level in cerebral oedema? 1. Vasogenic oedema = normal blood brain barrier disrupted → increased vascular permeability → fluid escapes from intravascular to intercellular compartments e.g. trauma [Tight Junction Failure] 2. Cytotoxic oedema = increase in intracellular fluid secondary to cellular (neuronal / glial/ endothelial) injury e.g. hypoxia/ischaemia [Pump Failure – which pump?]. Under normal conditions, the Na+/K+ ATPase pump helps maintain the ionic gradient across the cell membrane by pumping sodium ions out of and potassium ions into the neuron. In conditions of hypoxia or ischaemia, the pump cannot function properly because of insufficient ATP supply. As a result, sodium ions accumulate within the cell, leading to an osmotic imbalance that causes water to enter the cell to balance the ion concentration. This water influx increases intracellular volume, causing swelling. Consequences of cerebral oedema Raised Intracranial Pressure Herniation Complications of brain herniation Vascular stretching and compression- as a result of movement of the brain within the skull… Anterior cerebral artery at falx. ACA supplies blood to the frontal lobes. The falx cerebri is a fold of dura mater that descends vertically between the two cerebral hemispheres. The ACA is vulnerable to injury where it comes near the falx Posterior cerebral artery at tentorium. PCA supplies the occipital lobe and the bottom surface of the temporal lobe. The tentorium cerebelli separates the cerebellum from the inferior portion of the occipital lobes. The PCA can be injured, especially where it runs near the tentorium. Perforating vessels in brainstem- small, deep penetrating arteries supply blood to the brainstem. Damage can lead to small but devastating areas of bleeding within the brainstem- Duret haemorrhage: a type of hemorrhage that occurs in the brainstem, typically resulting from its downward displacement. What clinical sign[s] suggest transtentorial uncal herniation? Transtentorial uncal herniation: The uncus, which is part of the medial temporal lobe, herniates over the tentorium cerebelli. It is serious and potentially life- threatening Pupillary changes: Classic sign is an ipsilateral dilated pupil that does not constrict in response to light due to compression of the third cranial nerve (oculomotor nerve). Altered level of consciousness: ranging from drowsiness to stupor and eventually coma, as a result of brainstem compression. Cushing's triad: This is a late sign of increased intracranial pressure and consists of hypertension, bradycardia, and irregular respirations. Note: Since the tentorial notch is a rigid and narrow structure, any swelling or mass effect in the area of the uncus can lead to these signs and symptoms quickly, and it is considered a neurosurgical emergency. Prompt recognition and treatment are crucial to prevent further neurological deterioration and to save the patient's life. Biopsy of the ring enhancing lesion in the motor cortex carried out Four main diagnostic possibilities: – Metastatic carcinoma – Primary brain tumour – Infection – Negative biopsy– non- diagnostic Presentation of secondary tumour in brain Multiple brain lesions (50% will be solitary) History of systemic malignancy Mass lesion e.g. in the lung – check CXR Biopsy appearance VP N GFAP The tumour demonstrates a densely cellular glioma with mitoses, vascular proliferation [VP] & necrosis [N] and GFAP positivity. There is no gland formation. Diagnosis is GLIOBLASTOMA MULTIFORME What other techniques might be used to examine this tumour for more accurate diagnosis & prognosis? Molecular information impacts on diagnosis and prognosis Molecular analysis Impact BRAF gene fusion 90% posterior fossa pilocytic astrocytoma BRAF gene mutation V600 BRAF inhibitor therapy (clinical trials) IDH1/2 mutation Confers better prognosis in glioma (II-IV) 1p19q co-deletion Defines oligodendroglioma MGMT methylation Predicts responsiveness to temozolamide in glioblastoma/ high grade glioms Histone (H3) mutation Automatically WHO grade IV (paediatrics); dismal prognosis Why might a grade I tumour cause death? Location – Location – Location !!!! Access - Difficult Surgery associated with high morbidity - Brainstem or deep within brain How are patients with brain tumours managed? Gross total resection Radiotherapy Chemotherapy Combinations of 1, 2 and 3 Palliation Seizure control Fill in the blanks! A glioma is a primary brain tumour arising from glial (astrocytes, oligodendrocytes, ependyma) cells. Glioblastoma is the most common malignant glioma in adults. The most common benign primary brain tumour is meningioma, a tumour arising from meningothelial cells in the meninges (covering the brain) Prognosis in meningioma is good. The tumour most likely to metastasize to the brain is melanoma. Metastases from lung and breast primaries are the most common metastatic disease. Contrast agents allows the outer "ring" of a lesion to become more visible because the contrast accumulates in areas where the blood-brain barrier is disrupted (as seen in infections, tumours, or inflammation). This results in a bright ring that outlines the lesion on the scan. The inner, darker area, is usually poorly vascularised and is often necrotic in high grade tumours Transtentorial uncal herniation occurs when the innermost part of the temporal lobe, known as the uncus, is displaced downward through the tentorial notch. This displacement compresses critical structures, notably the brainstem and the third cranial nerve (oculomotor nerve), leading to clinical manifestations; Ipsilateral pupil dilation: Due to compression of the oculomotor nerve, resulting in a fixed and dilated pupil on the same side as the herniation. Contralateral hemiparesis: Weakness on the side opposite to the herniation, stemming from pressure on the cerebral peduncle. Altered consciousness: As the reticular activating system in the brainstem is affected, leading to decreased alertness or coma. Cushing's Triad is a clinical syndrome indicative of increased intracranial pressure and impending brain herniation. It comprises: Hypertension: Elevated blood pressure as a compensatory mechanism to maintain cerebral perfusion. Bradycardia: A slowed heart rate resulting from baroreceptor reflexes responding to increased blood pressure. Irregular respiration: Abnormal breathing patterns due to brainstem compression affecting respiratory centres.