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Approach to increased intracranial pressure


Post of MSc. Dr. Phan Van Phong - Emergency Doctor - Emergency Resuscitation Department - Vinmec Central Park International General Hospital

Increased intracranial pressure (ICP) can cause cerebral edema, cerebral ischemia, or cerebral collapse very quickly causing death or irreversible damage, so it needs to be diagnosed early and managed aggressively.
In adults, the skull volume is about 1500 ml including (brain organization 80%, blood 10%, cerebrospinal fluid 10%. Normal ICP is 10 mmHg, ICP increases when pressure inside the skull increases. above 15 mmHg Cerebral perfusion pressure (CBP) greater than 60 mmHg: according to the formula ICP = SBP – ICP (SBP: mean blood pressure)

1. Causes of endoscopic hypertension Traumatic brain injury. Cerebral hemorrhage: in the brain parenchyma, ventricles, subarachnoid hemorrhage. Large branch occlusion of cerebral artery: occlusion of internal carotid artery, middle cerebral artery... Brain tumor. Nerve infections: encephalitis, meningitis, brain abscess. Hydrocephalus . Other possible causes of increased intracranial pressure: + Hypercapnia; decreased blood oxygen. + Mechanical ventilation using high PEEP (positive end-expiratory pressure). + Increased body temperature. Hyponatremia. + Convulsions.

2. Symptoms of endoscopic hypertension 2.1. Clinical manifestations Depending on whether the patient is awake or unconscious, there are different disease progressions. Patient awake:
Headache often increases gradually, pain may be diffuse or localized. Vomiting: common in posterior fossa causes. Visual disturbances: double vision, blurred vision, decreased visual acuity, ophthalmoscopy with papilledema. Nervous disorders: somnolence, lethargy. The patient is in a coma:
Being awake suddenly in a coma, or in a deeper coma. There is an increase in muscle tone. Autonomic disturbances (which are serious signs): + Fast or slow heart rate, increased blood pressure or decreased blood pressure. + Respiratory disorders: rapid, deep breathing or Cheyne-Stockes. + Disorders of body temperature regulation: high fever. Signs of brain damage due to brain drop: + Temporomandibular lobe: III cord paralysis, dilated pupils. + Cerebellar amygdala: rapid breathing or stop breathing. + Central cerebral insufficiency: showing damage from top to bottom. 2.2. Laboratory tests Blood tests: can determine the cause of hyponatremia. Computed tomography (CT-scan) of the brain: can see + Cerebral edema, brain structure is pushed, midline structure is changed. + Dilated ventricles: due to obstruction of the circulation of cerebrospinal fluid. + Can see: brain bleeding, cerebral ischemia, brain tumor, brain abscess... Magnetic resonance (MRI) of the brain: gives more information about brain damage. Cerebral angiography: identify cerebral vascular malformations. Lumbar puncture: when meningitis is suspected (pay attention to slowly draining cerebrospinal fluid).
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3. Diagnosis of endoscopic hypertension 3.1. Confirmed Diagnosis Headache is increasing. Nausea or vomiting. There may be accompanying disturbances of consciousness. Ophthalmoscopy: there is optic papilledema. CT scan of the brain or magnetic resonance imaging of the brain: can determine the cause of ITS. 3.2. Differential diagnosis Coma: hyperosmotic coma, ketoacidosis, hypoglycemia, hepatic coma... Blurred vision: physical diseases of the eye. Headache: peripheral nerve causes, vasomotor disorders. 3.3. Diagnosis of the cause of traumatic brain injury: CT scan can show images of brain bleeding, brain damage due to concussion, skull fracture. Brain bleeding: CT scan of the brain shows bleeding in the brain parenchyma, ventricles, subarachnoid hemorrhage. Brain tumor: CT scan or MRI of the brain shows the location, size, and number of tumors. Hydrocephalus: CT scan and MRI have images of dilated ventricles, making the corrugated brain grooves lose wrinkles. Nervous infections : Cerebrospinal fluid test: increased protein accompanied by increased white blood cell count (purulent meningitis). meningitis, brain abscess. Cerebrospinal fluid is normal in encephalitis....MRI can show encephalitis, brain abscess. Other possible causes of increased intracranial pressure: + Increased CO2 in the blood; hypoxemia: blood gas test. + Mechanical ventilation using PEEP (positive end-expiratory pressure). + Hyperthermia: temperature > 40oC, continuous. + Hyponatremia: Electrolyte test showed [Na+] blood < 130 mmol/l. + Convulsions: blood biochemical tests have elevated blood CK.

4. Handling 4.1. Principles of management Continuous intracranial pressure monitoring is required to maintain adequate cerebral perfusion pressure. Apply measures to reduce intracranial pressure. Maintain the patient's blood pressure above normal or baseline blood pressure to ensure cerebral perfusion pressure (CPP) between 65-75 mmHg. Maintain blood osmolality 295 to 305 mOsm/L. Minimize complications caused by increased intracranial pressure. Eliminate the cause of increased cranial pressure. 4.2. Initial management and emergency transport Have the patient lie still if the patient is awake. Head elevation 30o - 45o if no hypotension. Provide enough oxygen to the patient: breathe oxygen through glasses. Maintain blood pressure above baseline. + Lower blood pressure: 0.9 % NaCl infusion. + High blood pressure: use antihypertensive drugs (calcium channel blockers, ACE inhibitors). Anti-cerebral edema: glucocorticoids in the presence of brain tumors. + Methylprednisolone: ​​40 - 120 mg intravenously, maintenance 40mg/6 hours. + Dexamethasone: 8 mg intramuscularly or intravenously, maintenance 4mg/6 hours. Treatment of hyperthermia: paracetamol 0.5 grams by inhalation or 1 gram intravenously. Transport when blood pressure and respiration are warranted.
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4.3. Treatment at the Hospital of Internal Medicine: + Let the patient lie down quietly if awake. + Head height 30o - 45o. Correction of electrolyte disturbances. + Treatment of hyperthermia: paracetamol 0.5 grams by nasogastric tube or 1 gram intravenously. + Antibiotics: when there are signs of nerve infection, it is necessary to use antibiotics as soon as possible, choose antibiotics that are permeable to meninges, must be in sufficient dosage, bacteria are still sensitive to that antibiotic, usually 2 combination antibiotics, intravenous drugs, dose adjustment according to glomerular filtration rate. + 3rd generation cephalosporins: ceftazidime 2g/ 8 hours, cefotaxime 2g/ 4-6 hours, ceftriaxone 2g/ 12 hours... + 4th generation cephalosporins: cefepime 2g/8 hours. + Carbapenem group: meropenem 2g / 8 hours. + Chloramphenicol: 4g / 6 hours. + Vancomycin 30-60 mg/kg/day divided into 2-3 times. Often combined with one of the above antibiotics (when no antibiotic chart is available). + Patients with immunodeficiency or over 50 years old: cephalosporin + vancomycin + Ampicillin 2g/4 hours. + Anti-convulsants: (see article on status epilepticus) + Anti-constipation: laxatives such as sorbitol, duphalac... + Urinary retention: catheterization.
Respiratory resuscitation: provide enough oxygen for the patient + The patient is awake: breathe oxygen through glasses. + Patients who are comatose, have respiratory disorders requiring intubation and mechanical ventilation (avoid using PEEP or use low PEEP 5 cm H2O), maintain PaCO2 from 35-45 mmHg. Cardiovascular resuscitation * Attention: maintain blood pressure higher than normal or baseline blood pressure (SBP 140-180 mmHg, DBP <120 mmHg) to ensure cerebral perfusion pressure (CPP: 65-75 mmHg). + If the patient has hypotension: need to insert a 3-lumen central venous catheter. + Adequate fluid infusion: based on ALT, do not give 5% glucose and 0.45% NaCl because of increased intracranial pressure due to increased cerebral edema. + BP still does not meet the requirements: use intravenous dopamine. + Treatment of hypertension when: SBP > 180 mmHg and/or DBP > 120 mmHg with renal failure. + If SBP > 230 mmHg and/or DBP > 140 mmHg: nitroprusside IV: 0.1 - 0.5 g/kg/min, maximum 10 μg/kg/min. Or nicardipine IV: 5 - 15mg/hour. + If SBP 180 - 230 mmHg and/or DBP 105 - 140 mmHg: take a β-blocker (labetalol) if the heart rate is not bradycardia < 60 beats/min. + If SBP < 180 mmHg and/or SBP < 105 mmHg: take a β-blocker (if the heart rate is not bradycardia < 60 beats/min. Or an ACE inhibitor: enalaprin 10 mg/tablet; peridopril 5 mg/tablet). Intravenous furosemide diuretic. If antihypertensive drugs are not effective Anti-cerebral edema: keep blood osmolality 295 - 305 mOsm/L + Mannitol is used only when there is cerebral edema: 0.5 - 1g/kg/6 hours IV infusion over 30 minutes ; Do not use for more than 3 days + Hypertonic saline solution 7.5 - 10% 100 ml/time has the effect of rapidly reducing intracranial pressure, the time of recurrence of increased intracranial pressure is later than that of mannitol 20%. give good results in patients with traumatic brain injury.Do not exceed 3 days. + Intravenous sedation Drugs: phenobacbital or thiopental (100mg/hour), propofol (5-80 μg/kg/min) Effects on anesthetic dose: reduce cerebral edema, reduce brain oxygen demand, anticonvulsant Side effects: deeper coma, lower blood pressure Need to closely monitor consciousness and blood pressure + Glucocorticoid. : indicated in brain tumor, brain abscess.Do not use when there is high blood pressure.Drug c: Synacthen 1mg IM/day (good effect in brain tumor). Methylprednisolone: ​​40 - 120 mg IV, maintenance 40mg/6 hours. Dexamethasone: 8 mg IM or IV, maintenance 4mg/6 hours. Surgery:
When the cause is known, medical treatment does not work.
Hydrocephalus: ventricular drainage surgery. Large hematoma: remove hematoma, resolve bleeding due to malformation. Brain tumor: + Large tumor: surgery to remove the tumor (often difficult). + Small tumor ≤ 2cm: radiotherapy with gamma rays Brain abscess: after stable medical treatment, the abscess is localized. Traumatic brain injury with multiple brain contusions: surgically remove part of the skull from the concussion area to reduce intracranial pressure. Monitoring intracranial pressure:
Through the ventricles: through the ventricular drainage system. In the brain parenchyma: the pressure sensor is placed into the brain parenchyma through a small hole in the skull and connected to a continuous monitor. Subarachnoid: The pressure sensor is placed into the subarachnoid space through a small bore in the skull and connected to a continuous monitor. Epidural: The pressure sensor is placed into the epidural space through a small bore in the skull and connected to a continuous monitor.

5. Prognosis and complications 5.1. Prognosis Prolonged increase in intracranial pressure will cause irreversible brain damage and poor prognosis. In comatose patients due to traumatic brain injury, a longer duration of elevated intracranial pressure is associated with a worse prognosis. 5.2. Complications Increased intracranial pressure, if not treated promptly, will create a pathological spiral that causes increased intracranial pressure, which can lead to seizures, stroke...irreversible brain damage.. Cerebral palsy is a serious complication that can quickly lead to death. 5.3 Prevention When there are signs of headache, unexplained blurred vision, it is necessary to take a cranial CT scan to rule out the cause of increased intracranial pressure. When there is increased intracranial pressure, the patient should be closely monitored and the cause of the increased intracranial pressure should be treated.

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References: 1. Nguyen Quoc Anh, Ngo Quy Chau and CS. (2011), “Intracranial hypertension”, Guidelines for the diagnosis and treatment of medical diseases, Medical Publishing House, pp. 127-9. 2. Vu Van Dinh (2003), “Diagnosis and management of raised intracranial pressure”, Complete Emergency Resuscitation, Medical Publishing House, pp. 316-27. 3. Frank J.I., Rosengart A.J. (2005), “Intracranial pressure: monitoring and management”, Principles of Critical Care 3rd edition, Pp. 1007-23. 4. Mauritz W., Steltzer H., Bauer P., Aghamanoukjan L.D., Metnitz P. (2008), “Monitoring of intracranial pressure in patients with severe traumatic brain injury: an Austrian prospective multicenter study” Intensive Care Med. Jul, 34(7), Pp. 1208-15. 5. Michael D.B. (2003), “Intracranial Hypertension”, Saunders Manual of Critical care, SaunderSaunders, Pp. 293-297. 6. Kamel H., Navi B.B., Nakagawa .K. et al, (2011) “Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials”, Crit Care Med. 39, Pp. 554-9.

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