Page 1174 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 86: Intracranial Pressure: Monitoring and Management 813

TABLE 86-15 Common Side Effects of Commonly Used Treatment Modalities
Intervention Side Effects
Intracranial pressure Intracranial hemorrhage; infection; pain at insertion site
monitoring
Hyperventilation Autoregulatory dysfunction; cerebral ischemia (regional or global)
Anticonvulsant
Phenobarbital Agitation, confusion, hyperkinesia, ataxia, CNS depression, hallucinations, anxiety, dizziness, headache; hypoventilation, apnea; bradycardia, hypotension,
syncope; nausea, vomiting, constipation; hypersensitivity reactions
Phenytoin Hematologic complications (eg, thrombocytopenia); encephalopathy; sedation; hypotension, cardiac arrhythmia
Valproic acid Headache, somnolence, dizziness, insomnia, nervousness, pain, alopecia, nausea, vomiting, diarrhea, abdominal pain, dyspepsia, anorexia, thrombocytopenia,
tremor, weakness, diplopia, amblyopia
Levetiracetam Behavioral symptoms (confusion, agitation, aggression, anger, anxiety, apathy, depersonalization, depression, emotional lability, hostility, hyperkinesias, irritability,
n ervousness, neurosis, and personality disorder); vomiting; anorexia; weakness; pharyngitis
Lacosamide Dizziness, headache, ataxia, somnolence, tremor, nystagmus, balance disorder, vertigo, diplopia, blurred vision; nausea, vomiting, diarrhea; fatigue, gait
disturbance, asthenia
Hyperosmolar therapy
Mannitol Congestive heart failure; circulatory overload; hypo- or hypertension; chills, convulsions, dizziness, headache; volume depletion; pulmonary and peripheral edema;
electrolyte abnormalities (pseudohyponatremia); osmotic nephropathy (especially when volume depleted); metabolic acidosis, water intoxication; acute tubular
necrosis (>200 g/day; serum osmolality >320 mOsm/L); subdural hematomas that result from shearing of bridging veins due to hyperosmolar contracture of brain
Hypertonic saline CNS changes (encephalopathy, lethargy, seizures, coma); central pontine myelinolysis (often seen in alcoholic and malnutrition patients); congestive heart failure;
transient hypotension (during bolus); electrolyte derangements; cardiac arrhythmias; pulmonary and peripheral edema; hyperchloremic metabolic acidosis;
subdural hematomas that result from shearing of bridging veins due to hyperosmolar brain shrinkage; hemolysis with rapid infusions, resulting in sudden
osmotic gradients in serum; phlebitis with infusion via peripheral route; coagulopathy; rebound hyponatremia leading to cerebral edema with rapid withdrawal
Barbiturates (thiopental/ Respiratory depression and hypercarbia; nausea; vomiting; hypotension and cardiac suppression; infection; confusion, paradoxical reactions, constipation,
pentobarbital) diarrhea, phlebitis
Propofol Hypotension; hypopnea; arrhythmia; decreased cardiac output
Propofol infusion syndrome (PRIS) (acute refractory bradycardia leading to asystole, with one or more of the following: metabolic acidosis, rhabdomyolysis,
hyperlipidemia, enlarged or fatty liver)
Paralytics Clinical examination diminished; myopathy; prolonged paralysis following discontinuation; raised intracranial pressure
Therapeutic hypothermia Electrolyte abnormalities (hypokalemia, hypocalcemia); cardiac suppression, arrhythmias (including asymptomatic electrocardiographic changes); infection
due to immune suppression; reduced creatinine clearance (during the active phase of hypothermia); pancreatitis
CNS, central nervous system.
Some commonly used increased ICP treatment modalities and anticonvulsant medications and their adverse profiles.
that future development of AQP4 modulators may reduce CNS edema in procedures, if used appropriately and timed correctly, are an important
many disease states. Steroids in TBI and stroke patients failed to show part of the management of patients with intracranial hypertension.
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any clinical benefit in outcome and were associated with significant Most of the evidence supporting surgical decompression to lower ICP
morbidity. 152,156 The class I study by Roberts et al studied 10,008 patients is derived from the management of patients with traumatic brain injury
with clinically significant head injury and was terminated by the data from which general guidelines can be extrapolated. Usually, patients
safety monitoring committee due to adverse events and lack of benefit. with extraparenchymal mass lesions that cause significant brain com-
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Furthermore, steroids are of no benefit in patients with intracerebral pression or midline shift should undergo early surgical evacuation and
hemorrhage. 157-159 Steroids benefit patients with brain abscess and bac- decompression as these lesions will contribute to ongoing brain injury
terial or tuberculous meningitis as reduction of acute inflammatory due to persistent, elevated ICP. There is still some disagreement regard-
processes can support ICP-lowering strategies. We also have seen benefit ing the surgical evacuation of intraparenchymal hematomas in TBI
in patients with global brain swelling and acute herniation syndromes patients. Retrospective, single-center studies suggest improved out-
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from fulminant, inflammatory syndromes such as acute disseminated come with evacuation, although results are significantly associated with
encephalomyelitis (ADEM), in which immediate high-dose steroids size and anatomical location of the bleed. Once hematoma evacuation is
serve as an adjunct to ICP management. Dexamethasone is preferred accomplished, an indwelling ICP monitoring device, if not already pres-
due to its low mineralocorticoid activity. It can be administered either ent, should be placed intraoperatively, and ICP should be continuously
parenterally or enterally at a dose of 16 to 24 mg/day in two to four monitored postoperatively.
divided doses. Higher doses can be used safely for brief periods of time Generally, two types of procedures can be employed either in com-
with less clear benefit over more conventional dosing. Possible adverse bination or individually to surgically address intracranial hypertension.
reactions from steroids include hyperglycemia, peptic ulcers, immuno- First, removal of the primary ICP-elevating problem should occur, if
suppression, wound breakdown and poor healing, sleep disturbances, possible (eg, hematoma evacuation, neoplasm excision, etc). In the set-
and psychosis. ting of severe brain injury and global edema with elevated ICP, remov-
ing the skull bone (decompressive hemicraniectomy) with splitting of
■ SURGICAL MANAGEMENT OF INCREASED ICP the dura (durotomy) ipsilateral to the mass or the side with the greatest
swelling in the absence of a focal lesion is beneficial. Factors to be con-
Most centers use surgical interventions (other than EVD placement) sidered in the surgical technique of decompressive craniectomy include
when increased ICP is refractory to neuromedical treatment. Surgical location (ie, frontal, temporal, parietal), size of the decompression,

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