Conclusion: The total mannitol dosage required for individual patients with ICH and elevated ICP can be calculated by considering the location of the haemorrhage, the volume of the haematoma and the pretreated ICP reading. Use of this formula in the clinical setting should help reduce the possibility of adverse effects resulting from administration of excessive dosages of mannitol.
Abstract Background and objective: Although mannitol has been widely used in hospitals to treat patients with high intracranial pressure ICP secondary to intracerebral haemorrhage ICH , no universal agreement has been reached regarding the optimal dosage of this agent for achieving appropriate intracranial decompression. Substances Mannitol. It acts by drawing fluid out of tissue into the vascular compartment.
It also reduces blood viscosity and hence increases cerebral blood flow, which results in an autoregulatory vasoconstriction that may reduce ICP. Hyperventilation is one known method of rapidly lowering ICP. Cerebral blood flow is largely dependent on PaCO2. Urine volume can be maintained even when the glomerular filtration GFR rate is low.
Osmotic diuretics are used to lower intracranial pressure and for short-term reduction of intraocular pressure. How does mannitol decrease ICP?
Category: medical health heart and cardiovascular diseases. Mannitol also reduces ICP by reducing cerebral parenchymal cell water, total effect takes min. Sedation decreases anxiety, fear, and response to pain, all of which increase ICP.
How long can you live with cerebral edema? This type of brain swelling occurs alongside acute mountain sickness AMS , ataxia loss of control of body movements , fatigue, and altered mental state. It can progress to a coma or death within 24 hours if not treated. What happens after mannitol administration? Adverse reactions more commonly reported during or after the infusion of mannitol mannitol mannitol injection injection include: Pulmonary congestion, fluid and electrolyte imbalance, acidosis, electrolyte loss, dryness of mouth, thirst, marked diuresis, urinary retention, edema, headache, blurred vision,.
What does mannitol do to sodium? It works as osmotic diuretic and is often used to reduce intracranial pressure and treat oliguric renal failure. At large doses mannitol increases excretion of sodium and potassium. Initially, mannitol acutely raises plasma and extracellular osmolality, which leads to an increase in circulating blood volume.
Why is mannitol given for ICP? What is the action of mannitol? PEEP, which may be needed to improve oxygenation, can increase ICP by impeding venous return and increasing cerebral venous pressure and ICP, and by decreasing blood pressure leading to a reflex increase of cerebral blood volume. The consequences of PEEP on ICP also depend on lung compliance, and minimal consequences for ICP usually are observed when lung compliance is low as in patients with acute lung injury [ 34 ].
Agitation and pain may significantly increase blood pressure and ICP. Adequate sedation and analgesia is an important adjunct treatment. No sedative regimen has clear advantages in this patient population. One consideration in the choice of sedative should be to minimize effects on blood pressure because most available agents can decrease blood pressure. Hypovolemia predisposes to hypotensive side effects and should be treated before administering sedative agents.
Selection of shorter acting agents may have the advantage of allowing brief interruption of sedation to evaluate neurologic status.
Fever during the postinjury period worsens neurologic injury in experimental models of TBI [ 36 ]. In an observational study in patients with TBI, Jones and colleagues [ 37 ] found a significant relationship between fever and a poor neurologic outcome. While a patient is at risk for intracranial hypertension, fever should be controlled with antipyretics and cooling blankets. Infectious causes must be sought and treated with appropriate antibiotics when present.
Elevated blood pressure is seen commonly in patients with intracranial hypertension, especially secondary to head injury, and is characterized by a systolic blood pressure increase greater than diastolic increase.
It is associated with sympathetic hyperactivity [ 38 ]. It is unwise to reduce systemic blood pressure in patients with hypertension associated with untreated intracranial mass lesions because cerebral perfusion is being maintained by the higher blood pressure.
In the absence of an intracranial mass lesion, the decision to treat systemic hypertension is more controversial and may need to be individualized for each patient. In addition, elevated blood pressure may exacerbate cerebral edema and increase the risk of postoperative intracranial hemorrhage.
Systemic hypertension may resolve with sedation. If the decision is made to treat systemic hypertension, the choice of antihypertensive agent is important. Vasodilating drugs, such as nitroprusside, nitroglycerin, and nifedipine, can be expected to increase ICP and may reflexively increase plasma catecholamines, which may be deleterious to the marginally perfused injured brain.
Agents with a short half-life have an advantage when the blood pressure is labile. Anecdotal cases have been reported of patients with severe anemia presenting with symptoms of increased ICP and signs of papilledema, which resolve with treatment of the anemia [ 39 ]. The mechanism is thought to be related to the marked increase in CBF that is required to maintain cerebral oxygen delivery when anemia is severe.
Seizures can increase cerebral metabolic rate and ICP, but there is no clear relationship between the occurrence of early seizures and a worse neurologic outcome [ 41 ]. Significant risk factors for later seizures are brain contusions, subdural hematoma, depressed skull fracture, penetrating head wound, loss of consciousness or amnesia for more than 1 day, and age 65 years or older. In a randomized clinical trial, phenytoin reduced the incidence of seizures during the first week after trauma, but not thereafter [ 43 ].
Based on this study, seizure prophylaxis for patients with severe brain injury is recommended for the first 7 days after injury. Treatment with anticonvulsants beyond 7 days should be reserved for patients who develop late seizures [ 44 ].
Emergent surgical management should be considered whenever intracranial hypertension occurs suddenly or is refractory to medical management. Routine paralysis of patients with neurosurgical disorders is not indicated; however, intracranial hypertension caused by agitation, posturing, or coughing can be prevented by sedation and nondepolarizing muscle relaxants that do not alter cerebrovascular resistance [ 45 ].
Although a disadvantage of this therapy is that the neurologic examination cannot be monitored closely, the sedatives and muscle relaxants can be interrupted once a day, usually before morning rounds, to allow neurologic assessments.
Major complications of neuromuscular blockade are myopathy, polyneuropathy, and prolonged neuromuscular blockade. Myopathy is associated with the use of neuromuscular blocking agents, particularly in combination with corticosteroids [ 46 ]. Polyneuropathy has been observed in patients with sepsis and multiple organ failure. Prolonged neuromuscular blockade is seen in patients with multiple organ failure especially with kidney and liver dysfunction.
Recommendations to minimize these complications are limiting the use and dose of neuromuscular blocking agents, train-of-four monitoring, measuring creatine phosphokinase daily, and stopping the drug daily to evaluate motor response [ 47 ]. Mannitol is the most commonly used hyperosmolar agent for the treatment of intracranial hypertension. More recently, hypertonic saline also has been used in this circumstance. A few studies have compared the relative effectiveness of these two hyperosmotic agents, but more work is needed.
Intravenous bolus administration of mannitol lowers the ICP in 1 to 5 minutes with a peak effect at 20 to 60 minutes. The effect of mannitol on ICP lasts 1. Mannitol usually is given as a bolus of 0. Two prospective clinical trials, one in patients with subdural hematoma and the other in patients who have herniated from diffuse brain swelling, have suggested that a higher dose of mannitol 1.
When long-term reduction of ICP is needed, 0. Mannitol has rheologic and osmotic effects. Immediately after infusion of mannitol, there is an expansion of plasma volume and a reduction in hematocrit and in blood viscosity, which may increase CBF and on balance increase oxygen delivery to the brain.
These rheologic effects of mannitol depend on the status of pressure autoregulation [ 51 ]. In patients with intact pressure autoregulation, infusion of mannitol induces cerebral vasoconstriction, which maintains CBF constant, and the decrease in ICP is large.
In patients with absent pressure autoregulation, infusion of mannitol increases CBF, and the decrease in ICP is less pronounced. Mannitol also may improve microcirculatory rheology [ 50 ] and has free radical scavenging effects. The osmotic effect of mannitol increases serum tonicity, which draws edema fluid from cerebral parenchyma. This process takes 15 to 30 minutes until gradients are established.
Serum osmolarity seems to be optimal when increased to to mOsm and should be kept at less than mOsm to avoid side effects of therapy, such as hypovolemia, hyperosmolarity, and renal failure. Mannitol opens the blood-brain barrier, and mannitol that has crossed the blood-brain barrier may draw fluid into the central nervous system, which can aggravate vasogenic edema.
For this reason, when it is time to stop mannitol, it should be tapered to prevent a rebound in cerebral edema and ICP. The adverse effects of mannitol are most likely when mannitol is present in the circulation for extended periods, such as in slow or continuous infusions or with repeated administration of higher than necessary doses. In some studies, hypertonic saline has been more effective at reducing ICP than mannitol [ 52 , 53 ]. Hypertonic saline has a clear advantage over mannitol in hypovolemic and hypotensive patients.
Mannitol is relatively contraindicated in hypovolemic patients because of the diuretic effects, whereas hypertonic saline augments intravascular volume and may increase blood pressure in addition to decreasing ICP. Hypertonic saline was not associated with improved neurologic outcomes, however, when given as a prehospital bolus to hypotensive patients with severe TBI [ 54 ].
Adverse effects of hypertonic saline administration include hematologic and electrolyte abnormalities, such as bleeding secondary to decreased platelet aggregation and prolonged coagulation times, hypokalemia, and hyperchloremic acidosis [ 55 ]. Hyponatremia should be excluded before administering hypertonic saline to reduce the risk of central pontine myelinolysis. The resulting reduction in cerebral blood volume decreases ICP. Hyperventilation has limited use in the management of intracranial hypertension, however, because this effect on ICP is time limited, and because hyperventilation may produce a sufficient decrease in CBF to induce ischemia.
The vasoconstrictive effect on cerebral arterioles lasts only 11 to 20 hours because the pH of the CSF rapidly equilibrates to the new PaCO 2 level. As the CSF pH equilibrates, the cerebral arterioles redilate, possibly to a larger caliber than at baseline, and the initial reduction in cerebral blood volume comes at the cost of a possible rebound phase of increased ICP [ 57 , 58 ]. For this reason, the most effective use of hyperventilation is acutely to allow time for other, more definitive treatments to be put into action.
When hypocarbia is induced and maintained for several hours, it should be reversed slowly, over several days, to minimize this rebound hyperemia [ 59 ]. Hyperventilation decreases CBF, but whether this reduction in flow is sufficient to induce ischemia in injured brain is controversial.
Although hyperventilation-induced ischemia has not been clearly shown, routine chronic hyperventilation to PaCO 2 of 20—25 mm Hg had a detrimental effect on outcome in one randomized clinical trial [ 59 ]. The authors of this study recommended using hyperventilation only in patients with intracranial hypertension, rather than as a routine in all head-injured patients.
This view is reinforced in TBI guidelines. Barbiturate coma should only be considered for patients with refractory intracranial hypertension because of the serious complications associated with high-dose barbiturates, and because the neurologic examination becomes unavailable for several days [ 62 ]. Although routine use of barbiturates in unselected patients has not been consistently effective in reducing morbidity or mortality after severe head injury [ 63 , 64 ], a randomized multicenter trial showed that instituting barbiturate coma in patients with refractory intracranial hypertension resulted in a twofold greater chance of controlling the ICP [ 65 ].
Studies by Messeter and colleagues [ 66 , 67 ] have suggested that the reduction in ICP with barbiturates is closely tied to the retention of carbon dioxide reactivity by the brain. Hypotension caused by pentobarbital should be treated first with volume replacement and then with vasopressors if necessary.
Experimental studies suggest that for the treatment of hypotension associated with barbiturate coma, volume resuscitation may be better than dopamine [ 69 ] because dopamine infusion increased cerebral metabolic requirements and partially offset the beneficial effects of barbiturates on CMRO 2.
Although a multicenter randomized clinical trial of moderate hypothermia in severe TBI did not show a beneficial effect on neurologic outcome, it was noted that fewer patients randomized to moderate hypothermia had intracranial hypertension [ 70 ]. A pilot randomized clinical trial of hypothermia in children with TBI produced similar findings—no improvement in neurologic outcome, but a reduction in ICP during the hypothermia treatment [ 71 ].
Although routine induction of hypothermia is not indicated at present, hypothermia may be an effective adjunctive treatment for increased ICP refractory to other medical management. Steroids commonly are used for primary and metastastic brain tumors, to decrease vasogenic cerebral edema.
Focal neurologic signs and decreased mental status owing to surrounding edema typically begin to improve within hours [ 72 ]. Increased ICP, when present, decreases over the following 2 to 5 days, in some cases to normal. The most commonly used regimen is intravenous dexamethasone, 4 mg every 6 hours. For other neurosurgical disorders, such as TBI or spontaneous intracerebral hemorrhage, steroids have not been shown to have a benefit [ 73 , 74 ] and in some studies have had a detrimental effect [ 75 , 76 ].
Administration of methylprednisolone resulted in a significant increase in the risk of death from This trial confirmed previous studies and guidelines that routine administration of steroids is not indicated for patients with TBI. Intracranial masses producing elevated ICP should be removed when possible.
Acute epidural and subdural hematomas are a hyperacute surgical emergency, especially epidural hematoma because the bleeding is under arterial pressure. Brain abscess must be drained, and pneumocephalus must be evacuated if it is under sufficient tension to increase ICP.
Surgical management of spontaneous intracerebral bleeding is controversial [ 77 ]. CSF drainage lowers ICP immediately by reducing intracranial volume and more long-term by allowing edema fluid to drain into the ventricular system. Drainage of even a small volume of CSF can lower ICP significantly, especially when intracranial compliance is reduced by injury.
This modality can be an important adjunct therapy for lowering ICP. If the brain is diffusely swollen, the ventricles may collapse, and this modality then has limited utility. The surgical removal of part of the calvaria to create a window in the cranial vault is the most radical intervention for intracranial hypertension, negating the Monro-Kellie doctrine of fixed intracranial volume and allowing for herniation of swollen brain through the bone window to relieve pressure.
Decompressive craniectomy has been used to treat uncontrolled intracranial hypertension of various origins, including cerebral infarction [ 78 ], trauma, subarachnoid hemorrhage, and spontaneous hemorrhage. Patient selection, timing of operation, type of surgery, and severity of clinical and radiologic brain injury all are factors that determine the outcome of this procedure. Sahuquillo and Arikan [ 79 ] reviewed the evidence in the literature for studies evaluating the effectiveness of decompressive craniectomy after TBI.
They found only one small randomized clinical trial in 27 children with TBI [ 80 ]. This trial found a reduced risk ratio for death of 0. All of the available studies in adults are either case series or cohorts with historical controls.
Brain oxygenation measured by tissue PO 2 and blood flow estimated by middle cerebral artery flow velocity also are usually improved after decompressive craniectomy [ 83 , 84 ]. Reported complications include hydrocephalus, hemorrhagic swelling ipsilateral to the craniectomy site, and subdural hygroma [ 81 ]. A case report of paradoxical herniation also has been reported after a lumbar puncture in a patient with a decompressive craniectomy [ 85 ].
There are limited results from randomized trials to confirm or refute the effectiveness of decompressive craniectomy in adults. Reports suggest, however, that decompressive craniectomy may be a useful option when maximal medical treatment has failed to control ICP. In a pooled analysis of randomized trials in patients with malignant MCA infarction, decompressive surgery undertaken within 48 h of stroke was associated with reduced mortality and an increased proportion of patients with a favourable functional outcome [ 87 ].
Effective treatment of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased ICP. When ICP becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. Medical management of increased ICP should include sedation, drainage of CSF, and osmotherapy with either mannitol or hypertonic saline.
Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from TBI. PMC documents will be made available for review after conversion approx. Any corrections that need to be made will be done at that time.
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