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Managing Increased Intracranial Pressure. Introduction The cranium is a rigid compartment. Contains the brain, vessels and cerebrospinal fluid. Can not.

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Presentation on theme: "Managing Increased Intracranial Pressure. Introduction The cranium is a rigid compartment. Contains the brain, vessels and cerebrospinal fluid. Can not."— Presentation transcript:

1 Managing Increased Intracranial Pressure

2 Introduction The cranium is a rigid compartment. Contains the brain, vessels and cerebrospinal fluid. Can not expand after closure of the skull sutures. It’s ability to accommodate volume changes is limited.

3 Cranial Contents

4 Monroe-Kellie Doctrine

5

6 Presentation Headache. Visual Symptoms. Vomiting. Altered level of consciousness. Papilledema.

7 Etiology Space occupying lesions. Trauma. Hydrocephalus. Meningitis. Bleeding. Idiopathic intracranial hypertension.

8 Effect on Cerebral Perfusion Normal blood flow to the grey matter is 75 ml/100 gm/min, and 45 ml/100 gm/min. Ischemia ensues at 20 ml/100 gm/min. Irreversible damage at 10 ml/100gm/min. Cerebral Perfusion Pressure is the most significant measure of blood flow.

9 Effect on Cerebral Perfusion CPP: the effective blood pressure gradient across the brain. Calculated as: CPP= MAP-ICP. * CPP: cerebral perfusion pressure, MAP: mean arterial pressure, ICP: intracranial pressure. Increased ICP decreases CPP, leading to ischemia.

10 Cerebral Autoregulation The ability of the brain to maintain blood flow across a wide range of CPPs. Increases in CPP cause vasoconstriction and vice versa. CO 2 tension controls autoregulation. Hyperventilation leads to decreased CO 2 tension leading to vasoconstriction.

11 Cerebral Auto regulation

12 Failure of Autoregulation Autoregulation is limited to CPPs ranging from 50-150 mmHg. Failure of autoregulation occurs when CPP exceeds 150 mmHg. Blood flow increases and leads to vasogenic edema. Hypotension may contribute to worsening of the process. (CPP=MAP- ICP).

13 Monitoring ICP ICP is the most important indicator of morbidity and mortality. Indicated in patients presenting with head trauma and spontaneous subarachnoid hemorrhage, as well as a GCS score between 3-8 and abnormal CT scans. Two main techniques of monitoring: intraventricular and intraparenchymal.

14 Monitoring ICP

15 ICP waveforms

16 ICP Waveforms

17 Treatment Aims at decreasing ICP and optimizing perfusion to brain tissue. Utilizes auto regulatory mechanisms to achieve the required balance. Several targets of therapy lead to synergistic effect on ICP.

18 Non-pharmacological

19 Head Elevation Rapid, easy and effective. Keeping the head elevated at 30-45 o. Uses the force of gravity to promote venous drainage. Head must be forward facing. Contraindicated in hypovolemic patients.

20 Head Elevation

21 Hyperventilation Leads to decreased blood flow to the brain by vasoconstriction. Rapidly decreases ICP. Target Pco 2 : 30-35 mmHg. Sustained hyperventilation may lead to ischemia. Target: Cerebral blood volume.

22 Hyperventilation

23 Hypothermia Core temperature target of 32-35 o for a few days. Controversial, but more centers are starting to embrace it. High incidence of manageable complications. Efficacious. Eurotherm3235 trial currently underway.

24 Hypothermia

25 Hyperbaric Oxygen Class I evidence suggests decreased mortality. Class IV evidence suggest acute decrease in ICP. Functional outcome controversial.

26 Hyperbaric Oxygen

27 Summary of Non- Pharmacologic Management

28 Pharmacologic Management

29 Sedation Intubation indicated when the patient is unable to protect airway or breath spontaneously. Propofol is the agent of choice due to short action and effect on brain metabolism. Target: decreasing cerebral metabolism.

30 Sedation

31 Mannitol Osmotic agent most commonly used in high ICP. Effect is two-fold: 1- Creation of osmotic gradient which increases intravascular volume, leading to vasoconstriction. 2- Cumulative osmotic gradient causes interstitial fluid to enter vasculature leading to decreased edema.

32 Mannitol Given in boluses of 0.25 g to 1 g/kg at 4 to 6-hour intervals. Most useful in the initial 48 to 72 hours. Monitoring of kidney functions, urine osmolality and electrolytes needed.

33 Mannitol

34 Hypertonic Saline Therapy Emerging as an effective alternative to mannitol. Similar efficacy and mechanism of action. May be used beyond 72 hours. Superior to mannitol in hypovolemia and hypotension.

35 Hypertonic Saline Therapy Boluses of 30 ml of 23.4% hypertonic saline Infused over 15 minutes through a central line. Sustained use may lead to electrolyte imbalances.

36 Hypertonic Saline Therapy

37 Barbiturate Coma Controversial. Drug of choice is Thiopental. Requires intensive monitoring of vitals signs. May lead to hypotension.

38 Barbiturate Coma

39 Opioids Conflicting evidence, mostly due to use along with other ICP lowering agents. Used alone, they are thought to increase ICP and CBF. Fentanyl most commonly used, with remifentanyl emerging as a substitute.

40 Opioids

41 Corticosteroids Evidence against use. May increase mortality. Some agents have shown promising results.

42 Corticosteroids

43 Progesterone Therapy Potentially neuroprotective, with very weak evidence on outcome. No effect on ICP, possible better functional outcome.

44 Progesterone Therapy

45 Summary of Pharmacological Therapy

46

47 Surgical Management

48 CSF Drainage Decreases CSF volume. Allows for ICP monitoring.

49 CSF Drainage

50 Decompressive Craniectomy Bifrontal craniectomy or hemicraniectomy including the frontal temporal and parietal bones. Cancels the Monroe-Kellie Doctrine and allows the brain to expand. Evacuation of an underlying hematoma if present. Remains controversial due to lack of class I evidence.

51 Decompressive Craniotomy

52 References 1- Sekhar L, Abdulrauf S, Ellenbogen R. Principles of Neurological Surgery [monograph on the Internet]. Philadelphia, PA: Saunders; 2012. [cited December 30, 2014]. Available from: Discovery eBooks. 2- Qureshi A, Wilson D, Traystman R. Treatment of elevated intracranial pressure in experimental intracerebral hemorrhage: comparison between mannitol and hypertonic saline. Neurosurgery [serial on the Internet]. (1999, May), [cited December 30, 2014]; 44(5): 1055-1063. Available from: MEDLINE Complete. 3-Meyer M, Megyesi J, Teasell R, et al. Acute management of acquired brain injury part I: An evidence-based review of non-pharmacological interventions. Brain Injury [serial online]. May 2010;24(5):694-705. Available from: Academic Search Complete, Ipswich, MA. Accessed December 30, 2014. 4-Meyer M, Megyesi J, Teasell R, et al. Acute management of acquired brain injury part II: An evidence-based review of pharmacological interventions. Brain Injury [serial online]. May 2010;24(5):706-721. Available from: Academic Search Complete, Ipswich, MA. Accessed December 30, 2014. 5- Thomé C. Intracranial pressure and hypothermia. Critical Care 2012;16(Suppl 2):A23. doi:10.1186/cc11281.


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