Intensive Care After Neurosurgery -

Intensive Care After Neurosurgery -

INTENSIVE CARE AFTER NEUROSURGERY JEAN-LOUIS VINCENT(41) MILLER(94) 1 Saeed Abbasi, MD, FCCM INTENSIVE CARE AFTER NEUROSURGERY Overview Prevention and Management of Systemic Complications After Neurosurgery Prevention and Management of Neurosurgical Postoperative Complications Admission Examination and Monitoring in the

Intensive Care Unit Systemic Monitoring: Cardiopulmonary, Respiratory Status, and Temperature Brain Monitoring and Specific Therapeutic Approaches Neuroprotection 2 Overview Collaboration between various specialists:

neurosurgeons, intensivists, and neuroradiologists Admission policy 3 Priorities and Goals of Postoperative Neurosurgical Care Early detection and treatment of postsurgical

complications Preventing second insults 4 POSTOPERATIVE COMPLICATIONS MAY BE SYSTEMIC OR NEUROSURGICAL 5 Prevention and Management of Systemic Complications After Neurosurgery 6

GENERAL PRINCIPLES AND SECOND INSULTS Follows general principles of intensive care medicine Systemic complications and second insults may initiate or aggravate cerebral damage Conversely, CNS events may induce systemic derangement : response to raised intracranial pressure (ICP)

7 GENERAL PRINCIPLES AND SECOND INSULTS Many drugs routinely used in neurosurgical patients may cause complications or side effects steroids antiepileptic agents Spinal cord injury : loss of autonomic

sympathetic function 8 9 CARDIAC DYSFUNCTION Electrocardiographic (ECG) abnormalities : diffuse ST-segment changes mimicking cardiac ischemia and cardiac arrhythmias, may be caused by SAH, TBI, or raised ICP Takotsubo syndrome : The left ventricle suffers a typical bulging (indicating ischemic

changes and functional impairment) 10 NEUROGENIC PULMONARY EDEMA After a variety of neurosurgical procedures : brain tumors (particularly those resected in the posterior fossa), cysts, hydrocephalus, intracranial hemorrhages, and brainstem lesions 9% mortality rate

Initial 4 hours after the neurologic event More common in women than in men 11 NEUROGENIC PULMONARY EDEMA Mechanisms unclear Sudden central sympathetic discharge may

trigger pulmonary venoconstriction, systemic arterial hypertension, increased left ventricle afterload, increased capillary permeability in the pulmonary vascular bed, and simultaneously cause cardiac ischemia and ventricular failure 12 NEUROGENIC PULMONARY EDEMA Therapeutic measures : Supportive Opioids and sedatives

Supplemental Tracheal oxygen intubation with mechanical ventilation and application of PEEP in 75% of patients Diuretics Vasoactive drugs 13 HYPERCOAGULOPATHY AND THROMBOSIS PROPHYLAXIS

DVT : 18% to 50% PE in 0% to 25% Mechanical therapies carry less associated risk, but pharmacologic approaches are more effective 14 HYPERCOAGULOPATHY AND THROMBOSIS

PROPHYLAXIS Overall, existing evidence, however, shows that the beneficial effects in reducing DVT and in particular PE outweigh a slightly increased risk of clinically significant hemorrhagic complications with anticoagulant prophylaxis 15 16 Prevention and Management of Neurosurgical Postoperative Complications

17 SUPRATENTORIAL PROCEDURES Postoperative Subgaleal Hematoma In up to 11% Can be minimized by routine use of postoperative wound drainage for 24 hours Reoperation

is seldom necessary 18 SUPRATENTORIAL PROCEDURES Intracranial Hemorrhage 1% of procedures Intraparenchymal hematomas (43%-60%), epidural hematomas (28%-33%) and subdural hematomas (5%-7%)

Parenchymal hemorrhages Most frequent Generally occur at the site of operation In rare cases, distant from site of operation Should

be considered in all patients who are not fully alert post anesthesia, as well as in those who exhibit secondary deterioration 19 SUPRATENTORIAL PROCEDURES Postoperative Brain Swelling Predisposing factors

Hypercapnia Arterial hypertension Hyponatremia Obstruction of venous drainage Silent or overt seizures during surgery or in the immediate

postoperative phase Brain swelling due to vasodilation : hyperventilation and barbiturate administration Brain swelling due to cerebral edema : mild hyperventilation and osmotic agents 20 SUPRATENTORIAL PROCEDURES

Tension Pneumocephalus Rewarming of air in the intracranial compartment postoperatively or continuous air leakage due to a cerebrospinal fluid (CSF) fistula of the skull base Clinical symptomatology : decreasing level of consciousness, signs of raised ICP, and occasionally seizures Generally self-limiting and do not require specific

treatment. 21 SUPRATENTORIAL PROCEDURES Seizures Occult seizure activity can occur in 15% to 18% of patients with moderate and severe TBI Prophylactic antiseizure indications are restricted to patients with a higher risk: Cerebrovascular surgery (arteriovenous malformation, aneurysm) Cerebral abscess and subdural empyema Convexity and parafalcial meningiomas

Penetrating brain injury Compound depressed skull fracture some centers recommending a treatment duration of 2 weeks and others continuing for at least 3 months In any case of unexplained neurologic deterioration or delayed awakening from anesthesia, the possibility of 22 seizures should be considered INFRATENTORIAL PROCEDURES

Rapid deterioration because of the relatively small infratentorial volume reserve and the immediate compression of the brainstem Irritation of the brainstem : large swings in arterial BP Lesions of the lower cranial nerves : diminished gag reflex, with increased risk of aspiration and pneumonia 23

INFRATENTORIAL PROCEDURES After any infratentorial procedure, the risk of acute hydrocephalus due to obstruction at the level of the fourth ventricle is present Routine admission of all patients who have undergone posterior fossa surgery to the ICU Particular attention should be paid to the presence of the gag reflex before extubation

and in the early stages after extubation 24 INFRATENTORIAL PROCEDURES Aseptic meningitis Meningeal symptoms, headaches, and an inflammatory response of the CSF in the absence of evidence for infection The origin of this syndrome has not been fully

clarified 25 CEREBROVASCULAR PROCEDURES The main cerebral complications are: 1. Rebleeding 2. Delayed cerebral ischemia 3. Hydrocephalus 26 CEREBROVASCULAR PROCEDURES

Rebleeding first weeks after the aneurysmal rupture Delayed cerebral ischemia (DCI) Angiographic vasospasm : 67% of untreated patients The time of maximum spasm around the end of the first week

DCI cannot always be attributed to vasospasm but more to the occurrence of microthrombosis Oral calcium antagonists in preventing delayed ischemic deficits Triple-H therapy (hypervolemia, hypertension, and hemodilution) 27

CEREBROVASCULAR PROCEDURES Hydrocephalus Not uncommon Spontaneous improvement of hydrocephalus has been reported in approximately half of patients 28 29

Admission Examination and Monitoring in the Intensive Care Unit 30 EARLY EVALUATION Glasgow Coma Scale Pressure on the nail bed and supraorbital pressure 31

EARLY EVALUATION The development of pupillary abnormalities is a sensitive indicator for pressure on the midbrain (tentorial herniation) 32 FURTHER EVALUATION Evaluation is important, since cranial nerve deficits can require immediate treatment Protection

of the ocular bulb to prevent keratitis Avoidance of oral feeding if swallowing is impaired 33 SYSTEMIC MONITORING: CARDIOPULMONARY, RESPIRATORY STATUS, AND TEMPERATURE Invasive arterial BP monitoring is recommended

Hypovolemic shock Skin pallor and poor capillary refill may precede a drop in BP Hematocrit of approximately 30% to 33% as optimal in the acute postoperative period in patients in the neurosurgical ICU After

intracranial or spinal cord procedures aiming at a hemoglobin of at least 9-10 mg/dL 34 SYSTEMIC MONITORING: CARDIOPULMONARY, RESPIRATORY STATUS, AND TEMPERATURE Cardiogenic shock: Elderly patient

Takotsubo Require syndrome sequential echocardiographic follow-up Large pulmonary emboli, sepsis, or spinal paraplegia should also be considered in patients with systemic hypotension 35 SYSTEMIC MONITORING: CARDIOPULMONARY, RESPIRATORY STATUS, AND TEMPERATURE

Spinal distributive shock : Hypotension is associated with bradycardia, with a pulse in the range of 35 to 50 Should not be managed with excessive volume resuscitation but rather with vasopressors to restore -adrenergic peripheral vasomotor tone 36

SYSTEMIC MONITORING: CARDIOPULMONARY, RESPIRATORY STATUS, AND TEMPERATURE The combination of hypertension and bradycardia (Cushing response) Potential of an expanding intracranial lesion and risk of brainstem herniation Antihypertensive agents is contraindicated, and

therapy should be aimed at the raised ICP 37 SYSTEMIC MONITORING: CARDIOPULMONARY, RESPIRATORY STATUS, AND TEMPERATURE Core temperature should be kept lower than 38.0C, using medications (e.g., acetaminophen, paracetamol, diclofenac) and surface or intravascular cooling

Hypothermia may be due to adrenal or pituitary insufficiency, hypothalamic disorders, hypoglycemia, or intraoperative exposure 38 SYSTEMIC MONITORING: CARDIOPULMONARY, RESPIRATORY STATUS, AND TEMPERATURE Hypothermia complications : Cardiovascular instability (mainly arrhythmias)

Coagulopathy Electrolyte Fluid shifts overload Increased risk of infection Shivering 39 BIOCHEMICAL PARAMETERS: ELECTROLYTES,

OSMOLARITY, AND BLOOD GLUCOSE Keeping biochemical parameters within physiologic ranges is obviously desirable, but this apparently simple goal may require a lot of work 40 ELECTROLYTES AND OSMOLARITY General recommendation is that serum osmolarity should be kept below 320 mOsm

Sudden episodes of diabetes insipidus are likely Cerebral salt waisting Fluid restriction for correction should generally be avoided; it is often better to administer hypertonic saline 41 GLUCOSE

In our opinion, the currently available evidence would not support the use of tight glucose control in neurointensive care 42 BRAIN MONITORING AND SPECIFIC THERAPEUTIC APPROACHES ICP and CPP monitoring Cerebral oxygenation

Continuous EEG Magnetic resonance spectroscopy 43 INTRACRANIAL PRESSURE AND CEREBRAL PERFUSION PRESSURE ICP monitoring severe

brain injury (GCS < 8) Abnormalities Normal on the initial CT scan admission CT scan if two or more of the following features are present: Age older than 40 years

Unilateral or bilateral motor posturing Systolic BP less than 90 mm Hg Routine ICP monitoring is not generally indicated in patients with mild or moderate TBI 44 INTRACRANIAL PRESSURE AND CEREBRAL PERFUSION PRESSURE

ICP monitoring is further indicated in poorgrade patients with aneurysmal SAH It may be considered in patients with other intracranial disorders who are sedated and ventilated and in whom the risk of raised ICP is considered present (postoperative swelling, stroke, Reye syndrome) 45 INTRACRANIAL PRESSURE AND CEREBRAL PERFUSION PRESSURE ICP monitoring carries a 0.5% risk of hemorrhage

and a 2% risk of infection Intraventricular catheters are preferable because they are accurate, can be recalibrated, and allow drainage of CSF Intraparenchymal probes are user friendly and accurate Less accurate data are provided by subdural catheters, and epidural probes are unreliable

46 INTRACRANIAL PRESSURE AND CEREBRAL PERFUSION PRESSURE Normal values for ICP are up to 15 mm Hg in adults, and consensus supports maintaining ICP below 20 mm Hg More important is the trend over time and the relation to the arterial BP

MABP ICP = CPP 47 TREATMENT OF CEREBRAL HERNIATION AND ELEVATED ICP The emergency measures to be taken include : Ventricular Bolus CSF drainage (if access available) administration of high-dos hyperosmolar

agents: mannitol: 1 to 1.5 g/kg bodyweight; hypertonic saline (HTS) 1 to 2 mL/ kg body weight 7.5% saline infused over 5 minutes Rapid-sequence hyperventilation intubation and moderate 48 TREATMENT OF CEREBRAL HERNIATION AND ELEVATED ICP Conservative therapy of elevated ICP includes: Sedation,

analgesia, and mild to moderate hyperventilation (30-35 mm Hg) Osmotic therapy: preferably mannitol given in bolus infusions (dose: 0.25-0.5 g/kg bodyweight, or as indicated by monitoring). Alternatively, HTS may be considered. Effective doses as bolus infusion range between 1 and 2 mL/kg of 7.5% saline. Effective doses as a continuous infusion of 3% range between 75 and 150 mL/h.

49 TREATMENT OF CEREBRAL HERNIATION AND ELEVATED ICP CSF fluid drainage Volume expansion and inotropes or vasopressors when arterial BP is insufficient to maintain CPP and CBF in a normovolemic patient 50

TREATMENT OF CEREBRAL HERNIATION AND ELEVATED ICP If these methods fail, second-tier therapies for raised ICP include: Mild or moderate hypothermia Decompressive Administration More surgery of barbiturates

intensive hyperventilation (which should be used with monitoring of cerebral oxygenation to detect cerebral ischemia) 51 TREATMENT OF CEREBRAL HERNIATION AND ELEVATED ICP 52 CEREBRAL BLOOD FLOW Transcranial Doppler (TCD) : Detection

and tracking of cerebral vasospasm, but various studies have shown a disappointing correlation when measured flow velocities are compared with direct measurements of CBF 53 CEREBRAL BLOOD FLOW Vasopressor therapy : Note: The use of dopamine, a precursor of

norepinephrine, has mainly been abandoned because of its interference with hormone secretion 54 CEREBRAL OXYGENATION AND METABOLISM Three approaches Jugular bulb oximetry (Sjvo2) Noninvasive Cerebral

cerebral oximetry parenchymal oximetry monitors 55 CEREBRAL OXYGENATION AND METABOLISM Jugular oximetry Global A cerebral oxygenation decrease in Sjvo2 : brain is extracting more

oxygen : oxygen supply is inadequate for metabolic demands Values below 55% :suggest the presence of ischemia 56 JUGULAR OXIMETRY Interpretation of results of jugular oximetry Requires that both systemic information (e.g., Hb and

SaO2) and intracranial data (e.g., CPP) Continuous monitoring of Sjvo2 with fiberoptic devices is prone to artifact Under conditions of anemia or arteriovenous shunting, hypoxia may be present at the tissue level despite normal values of jugular saturation Sjvo2 is a measure of global cerebral oxygenation and

does not reflect disturbances due to focal lesions 57 58 CEREBRAL OXYGENATION AND METABOLISM near-infrared spectroscopy [NIRS] The main clinical applications are in neonatology and in coronary or carotid artery surgery

59 60 ELECTRICAL MONITORING Continuous EEG (cEEG) monitoring has the potential for detecting nonconvulsive status epilepticus The sensitivity for detecting ischemia and hypoxia is high, but the specificity is low owing to effects of sedative medicationspticus in ICU patients

(BIS) may be useful in assessing the level of sedation in neurocritical care patients 61 NEUROPROTECTION 62 STRATEGIES AIMED AT IMPROVING METABOLISM AND MICROENVIRONMENT

Hypothermia Decreases cerebral blood flow by approximately 5.2% pe degree Stabilization Reduction of the cell membrane of neurotransmitter turnover 63 STRATEGIES AIMED AT IMPROVING METABOLISM

AND MICROENVIRONMENT Hyperosmolar therapy An immediate plasma-expanding effect : reducing hematocrit and blood viscosity : consequently increasing CBF and cerebral oxygen delivery An osmotic effect : delayed for 15 to 30 minutes 64

PLURIPOTENT AGENTS AND COMBINATIONAL THERAPIES various pathophysiologic mechanisms : agents with multiple mechanisms : dirty drugs Corticosteroids Not efficacious in improving cytotoxic edema, a seen after TBI or SAH Barbiturates Magnesium SAH

In TBI, greater mortality and poorer outcome was found in a randomized clinical trial 65 PLURIPOTENT AGENTS AND COMBINATIONAL THERAPIES further clinical evaluation : Erythropoietin (EPO)

Cyclosporine Progesterone 66 STRATEGIES PROMOTING CELL SURVIVAL AND REGENERATION Cellular replacement Gene therapy

Administration of trophic factors 67 68 MILLER-94 The decreased pulmonary compliance necessitating the PEEP will also limit intrathoracic pressure transmission to the cerebral circulation. The net benefit of improved ventilatory efficacy from PEEP outweighs any mild disadvantages from its use.

However, it should be remembered that injudicious PEEP in circumstances of hypovolemia may reduce functional venous return and hence reduce cardiac output with consequent effects on cerebral perfusion. 69 MILLER-94 Hypoxemia below 60 mm Hg is a significant contributor to secondary insult from secondary ICP effects. 70 MILLER-94

The majority of neurosurgical centers insert such devices routinely in the management of traumatic brain injury and SAH, using defined thresholds (e.g., ICP > 25) to trigger treatment interventions, including osmotic agents (e.g., mannitol, or hyper-tonic saline) or operative treatments (e.g., decompressive craniotomy or CSF drainage). 71 MILLER-94 Jugular Bulb Oximetry : Both desaturation (<50%suggesting inadequate

delivery/excess consumption) and abnormally high saturation (>75% suggesting hyperemia or stroke) have been associated with poor outcome. 72 MILLER-94 While bolus usage of hypertonic saline has been shown to be useful, it remains to be seen whether sustained infusions or the practice of persistent-induced hypernatremia offer any improvement in outcome. 73

MILLER-94 The Brain Trauma Foundation for Head Injury: A target Pco2 of between 30 and 35 mm Hg with a CPP of more than 60 mm Hg. It may be prudent to keep glucose below140 mg/ dL. Moderate

hypothermia to33 to 34C generally facilitates control of ICP. 74 MILLER-94 Subarachnoid Hemorrhage Rebleeding peak within the first 24 hours after the initial hemorrhage. Vasospasm tends to develop by the third day,

peak between 5 and 7 days, and generally wanes by 14 days. 75 MILLER-94 Triple H : Induced hypertension (up to and sometimes beyond 180 mm Hg systolic) Aggressive

fluid infusion (4-5 L/day) (hypervolemia) Hematocrit of 30is largely a passive result of hypervolemia andis thought to be less important, and possibly even harmful. 76 MILLER-94 SAH : The

only level 1 evidence from randomized control trial in SAH is regarding the use of nimodipine. For 21 days 77 78 79 MILLER-94

Aneursymal clipping : Maintain the systolic blood pressure in a narrow range between 100 and 120 mm Hg. 80 81

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