Raised Intracranial Pressure

RAISED INTRACRANIAL PRESSURE Causes A.Trauma 1) Haematoma-epidural,subdural,intraventricular, subarachnoid hemorrhage 2) Cerebral edema 3) Depressed skull fractures B. Infections 1) Bacterial-Staphylococcus, streptococcus, Haemophilus, tuberculous meningitis. 2) Parasitic-Cysticercosis, Toxoplasmosis, Echinococcus 3) Fungal-Cryptococcus, histoplasmosis Aspergilosis 4) Intracranial Abscesses C. Neoplastic causes 1. Neuroepithelial tumors; glioma.  Astrocytoma.  Astroblastoma.



Choroid glioma.  Ependymoma  Oligodendroglioma. 2. Pineal region tumors; pineoblastoma. 3. Neuronal and mixed glial tumors 4. Embryonal tumors; medulloblastoma. 5. Meningeal tumors; meningioma. 6. Peripheral neuroblastic tumors; neuroblastoma. 7. Lymphoma and hemopoietic tumors; microglioma. 8. Germ cell tumors; germinoma. 9. Tumors of cranial and spinal nerves; neurofibroma. 10. Metasases; lung, breast, thyroid, renal etc. D.Metabolic 1. Electrolyte imbalances-hyponatriemia 2. Hypoventilation-hypercapnia. E.Others 1) Hypertension 2) Hydrocephalus 3) Dural sinus thrombosis 4) ARDS 5) Seizures and convulsions

Phenytoin is used to prevent or control seizure activity that increases cerebral blood flow and subsequently intracranial pressure. Anticonvulsant medications should be used for 1 week following injury and then discontinued if seizures are not recurrent. 5. Nimodipine The calcium channel blocker reduces death and severe disability when instituted acutely in patients with head injuries 6. Sedatives High dose diazepam may be considered for hemodynamically stable, salvageable, severe head injury patients with intracranial hypertension refractory to maximal medical and surgical therapy. Other narcotics may depress respiration. 7. Relieve and prevent pyrexia This increases intracranial pressure. E.g. NSAIDS Provision of .analgesia has similar effects 8. Steroids Dexamethasone use is controversial in head injury 9. Hyperventilation To blow out the co2 and reduce hypercapnia and keep the partial pressure of co2 between 30-40 mmHg. The use of prophylactic hyperventilation (PaCO2 < 35 mm Hg) therapy during the first 24 hours after severe TBI should be avoided because it can compromise cerebral perfusion during a time when cerebral blood flow (CBF) is reduced. Hyperventilation therapy may be necessary for brief periods when there is acute neurologic deterioration, or for longer periods if there is intracranial hypertension refractory to sedation, paralysis, cerebrospinal fluid (CSF) drainage, and osmotic diuretics.

MANAGEMENT Symptoms 1) -Severe bursting headache 2) -Projectile vomiting 3) -Blurring of vision 4) -Convulsions/seizures 5) -Drowsiness Signs 1) -Vital signs-increased BP and decreased pulse rate (cushings reflex) 2) -Anisocoria-unequal pupils 3) -Papilloedema on fundoscopy

4) 5) 6)

-Nerve palsy e g 3rd and 6th cranial nerves -Tense fontanels. -Irregular breathing/slowed fats

Parameters: Normal ICP = 0-10 mmHg. Treatment threshold > 20-25 mmHg. Goal CPP = 60-70 mmHg. 1. Elevation of head To promote venous drainage from the head. 2.Ventilation o2 by mask Prevention of hypoxia and hypercapnia which increase ICP 3. Mannitol. i. Effective doses range from 0.25-1 gram/kg, given by intermittent bolus infusion every 4-6 hrs. ii. Euvolemia must be maintained. iii. Monitor osmolality. Do not exceed 320mOsm/kg 4. Anticonvulsant therapy JUDY WAWIRA GICHOYA yr 2007

1